Key clinical point: Temporarily discontinuing endocrine therapy (ET) to attempt pregnancy did not increase the recurrence risk for breast cancer (BC) in young women with early hormone receptor-positive (HR+) BC.

Major finding: After a median follow-up of 41 months, 44 patients had BC and the incidence of BC events was not higher among patients who interrupted ET vs control individuals with BC from an external cohort who received treatment with different adjuvant endocrine strategies (hazard ratio 0.81; 95% CI 0.57-1.15). Pregnancy was reported by 368 patients and 317 patients had ≥1 live birth.

Study details: Findings are from a single-group trial including 516 premenopausal women aged ≤42 years with stage I, II, or III HR+ BC treated with ET for 18-30 months who discontinued ET to attempt pregnancy.

Disclosures: This study was supported by the ETOP IBCSG Partners Foundation and other sources. Some authors declared serving as consultants; receiving grants, contracts, or travel support; or having other ties with several sources.

Source: Partridge AH et al for the International Breast Cancer Study Group, and the POSITIVE Trial Collaborators. Interrupting endocrine therapy to attempt pregnancy after breast cancer. N Engl J Med. 2023;388(18):1645-1656 (May 4). Doi: 10.1056/NEJMoa2212856

Key clinical point: Temporarily discontinuing endocrine therapy (ET) to attempt pregnancy did not increase the recurrence risk for breast cancer (BC) in young women with early hormone receptor-positive (HR+) BC.

Major finding: After a median follow-up of 41 months, 44 patients had BC and the incidence of BC events was not higher among patients who interrupted ET vs control individuals with BC from an external cohort who received treatment with different adjuvant endocrine strategies (hazard ratio 0.81; 95% CI 0.57-1.15). Pregnancy was reported by 368 patients and 317 patients had ≥1 live birth.

Study details: Findings are from a single-group trial including 516 premenopausal women aged ≤42 years with stage I, II, or III HR+ BC treated with ET for 18-30 months who discontinued ET to attempt pregnancy.

Disclosures: This study was supported by the ETOP IBCSG Partners Foundation and other sources. Some authors declared serving as consultants; receiving grants, contracts, or travel support; or having other ties with several sources.

Source: Partridge AH et al for the International Breast Cancer Study Group, and the POSITIVE Trial Collaborators. Interrupting endocrine therapy to attempt pregnancy after breast cancer. N Engl J Med. 2023;388(18):1645-1656 (May 4). Doi: 10.1056/NEJMoa2212856

Key clinical point: Temporarily discontinuing endocrine therapy (ET) to attempt pregnancy did not increase the recurrence risk for breast cancer (BC) in young women with early hormone receptor-positive (HR+) BC.

Major finding: After a median follow-up of 41 months, 44 patients had BC and the incidence of BC events was not higher among patients who interrupted ET vs control individuals with BC from an external cohort who received treatment with different adjuvant endocrine strategies (hazard ratio 0.81; 95% CI 0.57-1.15). Pregnancy was reported by 368 patients and 317 patients had ≥1 live birth.

Study details: Findings are from a single-group trial including 516 premenopausal women aged ≤42 years with stage I, II, or III HR+ BC treated with ET for 18-30 months who discontinued ET to attempt pregnancy.

Disclosures: This study was supported by the ETOP IBCSG Partners Foundation and other sources. Some authors declared serving as consultants; receiving grants, contracts, or travel support; or having other ties with several sources.

Source: Partridge AH et al for the International Breast Cancer Study Group, and the POSITIVE Trial Collaborators. Interrupting endocrine therapy to attempt pregnancy after breast cancer. N Engl J Med. 2023;388(18):1645-1656 (May 4). Doi: 10.1056/NEJMoa2212856

To the Editor:

A 67-year-old woman presented to the hospital with painful hands and feet. Two weeks prior, the patient experienced a few days of intermittent purple discoloration of the fingers, followed by black discoloration of the fingers, toes, and nose with notable pain. She reported no illness preceding the presenting symptoms, and there was no progression of symptoms in the days preceding presentation.

The patient had a history of smoking. She had a medical history of chronic obstructive pulmonary disease as well as recurrent non–small cell lung cancer that was treated most recently with a 1-year course of the programmed death-ligand 1 (PD-L1) immune checkpoint inhibitor durvalumab (last treatment was 4 months prior to the current presentation).

Physical examination revealed necrosis of the tips of the second, third, and fourth fingers of the left hand, as well as the tips of the third and fourth fingers of the right hand, progressing to purpura proximally on all involved fingers (Figure, A); scattered purpura and necrotic papules on the toe pads (Figure, B); and a 2- to 3-cm black plaque on the nasal tip. The patient was afebrile.

An embolic and vascular workup was performed. Transthoracic echocardiography was negative for thrombi, ankle brachial indices were within reference range, and computed tomography angiography revealed a few nonocclusive coronary plaques. Conventional angiography was not performed.

Laboratory testing revealed a mildly elevated level of cryofibrinogens (cryocrit, 2.5%); cold agglutinins (1:32); mild monoclonal κ IgG gammopathy (0.1 g/dL); and elevated inflammatory markers (C-reactive protein, 76 mg/L [reference range, 0–10 mg/L]; erythrocyte sedimentation rate, 38 mm/h [reference range, 0–20 mm/h]; fibrinogen, 571 mg/dL [reference range, 150–450 mg/dL]; and ferritin, 394 ng/mL [reference range, 10–180 ng/mL]). Additional laboratory studies were negative or within reference range, including tests of anti-RNA polymerase antibody, rheumatoid factor, antinuclear antibody, anticardiolipin antibody, anti-β₂ glycoprotein antibody, antineutrophil cytoplasmic antibodies (myeloperoxidase and proteinase-3), cryoglobulins, and complement; human immunodeficiency virus and hepatitis B and C virus serologic studies; prothrombin time, partial thromboplastin time, and lupus anticoagulant; and a heparin-induced thrombocytopenia panel.

A skin biopsy adjacent to an area of necrosis on the finger showed thickened walls of dermal vessels, sparse leukocytoclastic debris, and evidence of recanalizing medium-sized vessels. Direct immunofluorescence studies were negative.

Based on the clinical history and histologic findings showing an absence of vasculitis, a diagnosis of acral necrosis associated with the PD-L1 immune checkpoint inhibitor durvalumab—a delayed immune-related event (DIRE)—was favored. The calcium channel blocker amlodipine was started at a dosage of 2.5 mg/d orally. Necrosis of the toes resolved over the course of 1 week; however, necrosis of the fingers remained unchanged. After 1 week of hospitalization, the patient was discharged at her request.

Acral necrosis following immune checkpoint inhibitor therapy has been reported as a rare and recalcitrant immune-related adverse event (AE).^1-4 However, our patient’s symptoms occurred months after treatment was discontinued, which is consistent with a DIRE.⁵ The course of acral necrosis begins with acrocyanosis (a Raynaud disease–like phenomenon) of the fingers that progresses to necrosis. A history of Raynaud disease or other autoimmune disorder generally is absent.¹ Our patient’s history indicated actively smoking at the time of presentation, similar to a case described by Khaddour et al.¹ Similarly, in a case presented by Comont et al,³ the patient also had a history of smoking. In a recent study of acute vascular events associated with immune checkpoint inhibitors, 16 of 31 patients had a history of smoking.⁶

No definitive diagnostic laboratory or pathologic findings are associated with acral necrosis following immune checkpoint inhibitor therapy. Histopathologic analysis does not demonstrate vasculitis or other overt vascular pathology.^2,3

The optimal treatment of immune checkpoint inhibitor–associated digital necrosis is unclear. Corticosteroids and discontinuation of the immune checkpoint inhibitor generally are employed,^1-4 though treatment response has been variable. Other therapies such as calcium channel blockers (as in our case), sympathectomy,¹ epoprostenol, botulinum injection, rituximab,² and alprostadil⁴ have been attempted without clear effect.

We considered a diagnosis of paraneoplastic acral vascular syndrome in our patient, which was ruled out because the syndrome typically occurs in the setting of a worsening underlying malignancy⁷; our patient’s cancer was stable to improved. Thromboangiitis obliterans was ruled out by the absence of a characteristic thrombus on biopsy, the patient’s older age, and involvement of the nose.

We report an unusual case of acral necrosis occurring as a DIRE in response to administration of an immune checkpoint inhibitor. Further description is needed to clarify the diagnostic criteria for and treatment of this rare autoimmune phenomenon.

To the Editor:

A 67-year-old woman presented to the hospital with painful hands and feet. Two weeks prior, the patient experienced a few days of intermittent purple discoloration of the fingers, followed by black discoloration of the fingers, toes, and nose with notable pain. She reported no illness preceding the presenting symptoms, and there was no progression of symptoms in the days preceding presentation.

The patient had a history of smoking. She had a medical history of chronic obstructive pulmonary disease as well as recurrent non–small cell lung cancer that was treated most recently with a 1-year course of the programmed death-ligand 1 (PD-L1) immune checkpoint inhibitor durvalumab (last treatment was 4 months prior to the current presentation).

Physical examination revealed necrosis of the tips of the second, third, and fourth fingers of the left hand, as well as the tips of the third and fourth fingers of the right hand, progressing to purpura proximally on all involved fingers (Figure, A); scattered purpura and necrotic papules on the toe pads (Figure, B); and a 2- to 3-cm black plaque on the nasal tip. The patient was afebrile.

An embolic and vascular workup was performed. Transthoracic echocardiography was negative for thrombi, ankle brachial indices were within reference range, and computed tomography angiography revealed a few nonocclusive coronary plaques. Conventional angiography was not performed.

Laboratory testing revealed a mildly elevated level of cryofibrinogens (cryocrit, 2.5%); cold agglutinins (1:32); mild monoclonal κ IgG gammopathy (0.1 g/dL); and elevated inflammatory markers (C-reactive protein, 76 mg/L [reference range, 0–10 mg/L]; erythrocyte sedimentation rate, 38 mm/h [reference range, 0–20 mm/h]; fibrinogen, 571 mg/dL [reference range, 150–450 mg/dL]; and ferritin, 394 ng/mL [reference range, 10–180 ng/mL]). Additional laboratory studies were negative or within reference range, including tests of anti-RNA polymerase antibody, rheumatoid factor, antinuclear antibody, anticardiolipin antibody, anti-β₂ glycoprotein antibody, antineutrophil cytoplasmic antibodies (myeloperoxidase and proteinase-3), cryoglobulins, and complement; human immunodeficiency virus and hepatitis B and C virus serologic studies; prothrombin time, partial thromboplastin time, and lupus anticoagulant; and a heparin-induced thrombocytopenia panel.

A skin biopsy adjacent to an area of necrosis on the finger showed thickened walls of dermal vessels, sparse leukocytoclastic debris, and evidence of recanalizing medium-sized vessels. Direct immunofluorescence studies were negative.

Based on the clinical history and histologic findings showing an absence of vasculitis, a diagnosis of acral necrosis associated with the PD-L1 immune checkpoint inhibitor durvalumab—a delayed immune-related event (DIRE)—was favored. The calcium channel blocker amlodipine was started at a dosage of 2.5 mg/d orally. Necrosis of the toes resolved over the course of 1 week; however, necrosis of the fingers remained unchanged. After 1 week of hospitalization, the patient was discharged at her request.

Acral necrosis following immune checkpoint inhibitor therapy has been reported as a rare and recalcitrant immune-related adverse event (AE).^1-4 However, our patient’s symptoms occurred months after treatment was discontinued, which is consistent with a DIRE.⁵ The course of acral necrosis begins with acrocyanosis (a Raynaud disease–like phenomenon) of the fingers that progresses to necrosis. A history of Raynaud disease or other autoimmune disorder generally is absent.¹ Our patient’s history indicated actively smoking at the time of presentation, similar to a case described by Khaddour et al.¹ Similarly, in a case presented by Comont et al,³ the patient also had a history of smoking. In a recent study of acute vascular events associated with immune checkpoint inhibitors, 16 of 31 patients had a history of smoking.⁶

No definitive diagnostic laboratory or pathologic findings are associated with acral necrosis following immune checkpoint inhibitor therapy. Histopathologic analysis does not demonstrate vasculitis or other overt vascular pathology.^2,3

The optimal treatment of immune checkpoint inhibitor–associated digital necrosis is unclear. Corticosteroids and discontinuation of the immune checkpoint inhibitor generally are employed,^1-4 though treatment response has been variable. Other therapies such as calcium channel blockers (as in our case), sympathectomy,¹ epoprostenol, botulinum injection, rituximab,² and alprostadil⁴ have been attempted without clear effect.

We considered a diagnosis of paraneoplastic acral vascular syndrome in our patient, which was ruled out because the syndrome typically occurs in the setting of a worsening underlying malignancy⁷; our patient’s cancer was stable to improved. Thromboangiitis obliterans was ruled out by the absence of a characteristic thrombus on biopsy, the patient’s older age, and involvement of the nose.

We report an unusual case of acral necrosis occurring as a DIRE in response to administration of an immune checkpoint inhibitor. Further description is needed to clarify the diagnostic criteria for and treatment of this rare autoimmune phenomenon.

To the Editor:

A 67-year-old woman presented to the hospital with painful hands and feet. Two weeks prior, the patient experienced a few days of intermittent purple discoloration of the fingers, followed by black discoloration of the fingers, toes, and nose with notable pain. She reported no illness preceding the presenting symptoms, and there was no progression of symptoms in the days preceding presentation.

The patient had a history of smoking. She had a medical history of chronic obstructive pulmonary disease as well as recurrent non–small cell lung cancer that was treated most recently with a 1-year course of the programmed death-ligand 1 (PD-L1) immune checkpoint inhibitor durvalumab (last treatment was 4 months prior to the current presentation).

Physical examination revealed necrosis of the tips of the second, third, and fourth fingers of the left hand, as well as the tips of the third and fourth fingers of the right hand, progressing to purpura proximally on all involved fingers (Figure, A); scattered purpura and necrotic papules on the toe pads (Figure, B); and a 2- to 3-cm black plaque on the nasal tip. The patient was afebrile.

An embolic and vascular workup was performed. Transthoracic echocardiography was negative for thrombi, ankle brachial indices were within reference range, and computed tomography angiography revealed a few nonocclusive coronary plaques. Conventional angiography was not performed.

Laboratory testing revealed a mildly elevated level of cryofibrinogens (cryocrit, 2.5%); cold agglutinins (1:32); mild monoclonal κ IgG gammopathy (0.1 g/dL); and elevated inflammatory markers (C-reactive protein, 76 mg/L [reference range, 0–10 mg/L]; erythrocyte sedimentation rate, 38 mm/h [reference range, 0–20 mm/h]; fibrinogen, 571 mg/dL [reference range, 150–450 mg/dL]; and ferritin, 394 ng/mL [reference range, 10–180 ng/mL]). Additional laboratory studies were negative or within reference range, including tests of anti-RNA polymerase antibody, rheumatoid factor, antinuclear antibody, anticardiolipin antibody, anti-β₂ glycoprotein antibody, antineutrophil cytoplasmic antibodies (myeloperoxidase and proteinase-3), cryoglobulins, and complement; human immunodeficiency virus and hepatitis B and C virus serologic studies; prothrombin time, partial thromboplastin time, and lupus anticoagulant; and a heparin-induced thrombocytopenia panel.

A skin biopsy adjacent to an area of necrosis on the finger showed thickened walls of dermal vessels, sparse leukocytoclastic debris, and evidence of recanalizing medium-sized vessels. Direct immunofluorescence studies were negative.

Based on the clinical history and histologic findings showing an absence of vasculitis, a diagnosis of acral necrosis associated with the PD-L1 immune checkpoint inhibitor durvalumab—a delayed immune-related event (DIRE)—was favored. The calcium channel blocker amlodipine was started at a dosage of 2.5 mg/d orally. Necrosis of the toes resolved over the course of 1 week; however, necrosis of the fingers remained unchanged. After 1 week of hospitalization, the patient was discharged at her request.

Acral necrosis following immune checkpoint inhibitor therapy has been reported as a rare and recalcitrant immune-related adverse event (AE).^1-4 However, our patient’s symptoms occurred months after treatment was discontinued, which is consistent with a DIRE.⁵ The course of acral necrosis begins with acrocyanosis (a Raynaud disease–like phenomenon) of the fingers that progresses to necrosis. A history of Raynaud disease or other autoimmune disorder generally is absent.¹ Our patient’s history indicated actively smoking at the time of presentation, similar to a case described by Khaddour et al.¹ Similarly, in a case presented by Comont et al,³ the patient also had a history of smoking. In a recent study of acute vascular events associated with immune checkpoint inhibitors, 16 of 31 patients had a history of smoking.⁶

No definitive diagnostic laboratory or pathologic findings are associated with acral necrosis following immune checkpoint inhibitor therapy. Histopathologic analysis does not demonstrate vasculitis or other overt vascular pathology.^2,3

The optimal treatment of immune checkpoint inhibitor–associated digital necrosis is unclear. Corticosteroids and discontinuation of the immune checkpoint inhibitor generally are employed,^1-4 though treatment response has been variable. Other therapies such as calcium channel blockers (as in our case), sympathectomy,¹ epoprostenol, botulinum injection, rituximab,² and alprostadil⁴ have been attempted without clear effect.

We considered a diagnosis of paraneoplastic acral vascular syndrome in our patient, which was ruled out because the syndrome typically occurs in the setting of a worsening underlying malignancy⁷; our patient’s cancer was stable to improved. Thromboangiitis obliterans was ruled out by the absence of a characteristic thrombus on biopsy, the patient’s older age, and involvement of the nose.

We report an unusual case of acral necrosis occurring as a DIRE in response to administration of an immune checkpoint inhibitor. Further description is needed to clarify the diagnostic criteria for and treatment of this rare autoimmune phenomenon.

To the Editor:

Programmed cell death protein 1 (PD-1) inhibitors have been widely used in the treatment of various cancers. Programmed cell death-ligand 1 (PD-L1) and programmed cell death-ligand 2 located on cancer cells will bind to PD-1 receptors on T cells and suppress them, which will prevent cancer cell destruction. Programmed cell death protein 1 inhibitors block the binding of PD-L1 to cancer cells, which then prevents T-cell immunosuppression.¹ However, cutaneous adverse effects have been associated with PD-1 inhibitors. Dermatitis associated with PD-1 inhibitor therapy occurs more frequently in patients with cutaneous tumors such as melanoma compared to those with head and neck cancers.² Curry et al¹ reported that treatment with an immune checkpoint blockade can lead to immune-related adverse effects, most commonly affecting the gastrointestinal tract, liver, and skin. The same report cited dermatologic toxicity as an adverse effect in approximately 39% of patients treated with anti–PD-1 and approximately 17% of anti–PD-L1.¹ The 4 main categories of dermatologic toxicities to immunotherapies in general include inflammatory disorders, immunobullous disorders, alterations of keratinocytes, and alteration of melanocytes. The most common adverse effects from the use of the PD-1 inhibitor nivolumab were skin rashes, not otherwise specified (14%–20%), pruritus (13%–18%), and vitiligo (~8%).¹ Of the cutaneous dermatitic reactions to PD-1 and PD-L1 inhibitors that were biopsied, the 2 most common were lichenoid dermatitis and spongiotic dermatitis.² Seldomly, there have been reports of keratoacanthomas (KAs) in association with anti–PD-1 therapy.³

A KA is a common skin tumor that appears most frequently as a solitary lesion and is thought to arise from the hair follicle.⁴ It resembles squamous cell carcinoma and commonly regresses within months without intervention. Exposure to UV light is a known risk factor for the development of KAs.

Eruptive KAs have been found in association with 10 cases of various cancers treated with the PD-1 inhibitors pembrolizumab and nivolumab.³ Multiple lesions on photodistributed areas of the body were reported in all 10 cases. Various treatments were used in these 10 cases—doxycycline and niacinamide, electrodesiccation and curettage, clobetasol ointment and/or intralesional triamcinolone, cryotherapy, imiquimod, or no treatment—as well as the cessation of PD-1 inhibitor therapy, with 4 cases continuing therapy and 6 cases discontinuing therapy. Nine cases regressed by 6 months; electrodesiccation and curettage of the lesions was used in the tenth case.³ We report a case of eruptive KA after 1 cycle of nivolumab therapy for metastatic melanoma.

A 79-year-old woman with stage III melanoma presented to her dermatologist after developing generalized pruritic lichenoid eruptions involving the torso, arms, and legs, as well as erosions on the lips, buccal mucosa, and palate 1 month after starting nivolumab therapy. The patient initially presented to dermatology with an irregularly shaped lesion on the left upper back 3 months prior. Biopsy results at that time revealed a diagnosis of malignant melanoma, lentigo maligna type. The lesion was 1.5-mm thick and classified as Clark level IV with a mitotic count of 6 per mm². Molecular genetic studies showed expression of PD-L1 and no expression of c-KIT. The patient underwent wide local excision, and a sentinel lymph node biopsy was positive. Positron emission tomography did not show any hypermetabolic lesions, and magnetic resonance imaging did not indicate brain metastasis. The patient underwent an axillary dissection, which did not show any residual melanoma. She was started on adjuvant immunotherapy with intravenous nivolumab 480 mg monthly and developed pruritic crusted lesions on the arms, legs, and torso 1 month later, which prompted follow-up to dermatology.

At the current presentation 4 months after the onset of lesions, physical examination revealed lichenoid patches with serous crusting that were concentrated on the torso but also affected the arms and legs. She developed erosions on the upper and lower lips, buccal mucosa, and hard and soft palates, as well as painful, erythematous, dome-shaped papules and nodules on the legs (Figure 1). Her oncologist previously had initiated treatment at the onset of the lesions with clobetasol cream and valacyclovir for the lesions, but the patient showed no improvement.

Four months after the onset of the lesions, the patient was re-referred to her dermatologist, and a biopsy was performed on the left lower leg that showed squamous cell carcinoma, KA type. Additionally, flat erythematous patches were seen on the legs that were consistent with a lichenoid drug eruption. Two weeks later, she was started on halobetasol propionate ointment 0.05% for treatment of the KAs. At 2-week follow-up, 5 months after the onset of the lesions, the patient showed no signs of improvement. An oral prednisone taper of 60 mg for 3 days, 40 mg for 3 days, and then 20 mg daily for a total of 4 weeks was started to treat the lichenoid dermatitis and eruptive KAs. At the next follow-up 6.5 months following the first eruptive KAs, she was no longer using topical or oral steroids, she did not have any new eruptive KAs, and old lesions showed regression (Figure 2). The patient still experienced postinflammatory erythema and hyperpigmentation at the location of the KAs but showed improvement of the lichenoid drug eruption.

We describe a case of eruptive KAs after use of a PD-1 inhibitor for treatment of melanoma. Our patient developed eruptive KAs after only 1 nivolumab treatment. Another report described onset of eruptive KAs after 1 month of nivolumab infusions.³ The KAs experienced by our patient took 6.5 months to regress, which is unusual compared to other case reports in which the KAs self-resolved within a few months, though one other case described lesions that persisted for 6 months.³

Our patient was treated with topical steroids and an oral steroid taper for the concomitant lichenoid drug eruption. It is unknown if the steroids affected the course of the KAs or if they spontaneously regressed on their own. Freites-Martinez et al⁵ described that regression of KAs may be related to an immune response, but corticosteroids are inherently immunosuppressive. They hypothesized that corticosteroids help to temper the heightened immune response of eruptive KAs.⁵

Our patient had oral ulcers, which may have been indicative of an oral lichenoid drug eruption, as well as skin lesions representative of a cutaneous lichenoid drug eruption. This is a favorable reaction, as lichenoid dermatitis is thought to represent successful PD-1 inhibition and therefore a better response to oncologic therapies.² Comorbid lichenoid drug eruption lesions and eruptive KAs may be suggestive of increased T-cell activity,^2,6,7 though some prior case studies have reported eruptive KAs in isolation.³

Discontinuation of immunotherapy due to development of eruptive KAs presents a challenge in the treatment of underlying malignancies such as melanoma. Immunotherapy was discontinued in 7 of 11 cases due to these cutaneous reactions.³ Similarly, our patient underwent only 1 cycle of immunotherapy before developing eruptive KAs and discontinuing PD-1 inhibitor therapy. If we are better able to treat eruptive KAs, then patients can remain on immunotherapy to treat underlying malignancies. Crow et al⁸ showed improvement in lesions when 3 patients with eruptive KAs were treated with hydroxychloroquine; the Goeckerman regimen consisting of steroids, UVB phototherapy, and crude coal tar; and Unna boots with zinc oxide and compression stockings. The above may be added to a list of possible treatments to consider for hastening the regression of eruptive KAs.

Our patient’s clinical course was similar to reports on the regressive nature of eruptive KAs within 6 months after initial eruption. Although it is likely that KAs will regress on their own, treatment modalities that speed up recovery are a future source for research.

To the Editor:

Programmed cell death protein 1 (PD-1) inhibitors have been widely used in the treatment of various cancers. Programmed cell death-ligand 1 (PD-L1) and programmed cell death-ligand 2 located on cancer cells will bind to PD-1 receptors on T cells and suppress them, which will prevent cancer cell destruction. Programmed cell death protein 1 inhibitors block the binding of PD-L1 to cancer cells, which then prevents T-cell immunosuppression.¹ However, cutaneous adverse effects have been associated with PD-1 inhibitors. Dermatitis associated with PD-1 inhibitor therapy occurs more frequently in patients with cutaneous tumors such as melanoma compared to those with head and neck cancers.² Curry et al¹ reported that treatment with an immune checkpoint blockade can lead to immune-related adverse effects, most commonly affecting the gastrointestinal tract, liver, and skin. The same report cited dermatologic toxicity as an adverse effect in approximately 39% of patients treated with anti–PD-1 and approximately 17% of anti–PD-L1.¹ The 4 main categories of dermatologic toxicities to immunotherapies in general include inflammatory disorders, immunobullous disorders, alterations of keratinocytes, and alteration of melanocytes. The most common adverse effects from the use of the PD-1 inhibitor nivolumab were skin rashes, not otherwise specified (14%–20%), pruritus (13%–18%), and vitiligo (~8%).¹ Of the cutaneous dermatitic reactions to PD-1 and PD-L1 inhibitors that were biopsied, the 2 most common were lichenoid dermatitis and spongiotic dermatitis.² Seldomly, there have been reports of keratoacanthomas (KAs) in association with anti–PD-1 therapy.³

A KA is a common skin tumor that appears most frequently as a solitary lesion and is thought to arise from the hair follicle.⁴ It resembles squamous cell carcinoma and commonly regresses within months without intervention. Exposure to UV light is a known risk factor for the development of KAs.

Eruptive KAs have been found in association with 10 cases of various cancers treated with the PD-1 inhibitors pembrolizumab and nivolumab.³ Multiple lesions on photodistributed areas of the body were reported in all 10 cases. Various treatments were used in these 10 cases—doxycycline and niacinamide, electrodesiccation and curettage, clobetasol ointment and/or intralesional triamcinolone, cryotherapy, imiquimod, or no treatment—as well as the cessation of PD-1 inhibitor therapy, with 4 cases continuing therapy and 6 cases discontinuing therapy. Nine cases regressed by 6 months; electrodesiccation and curettage of the lesions was used in the tenth case.³ We report a case of eruptive KA after 1 cycle of nivolumab therapy for metastatic melanoma.

A 79-year-old woman with stage III melanoma presented to her dermatologist after developing generalized pruritic lichenoid eruptions involving the torso, arms, and legs, as well as erosions on the lips, buccal mucosa, and palate 1 month after starting nivolumab therapy. The patient initially presented to dermatology with an irregularly shaped lesion on the left upper back 3 months prior. Biopsy results at that time revealed a diagnosis of malignant melanoma, lentigo maligna type. The lesion was 1.5-mm thick and classified as Clark level IV with a mitotic count of 6 per mm². Molecular genetic studies showed expression of PD-L1 and no expression of c-KIT. The patient underwent wide local excision, and a sentinel lymph node biopsy was positive. Positron emission tomography did not show any hypermetabolic lesions, and magnetic resonance imaging did not indicate brain metastasis. The patient underwent an axillary dissection, which did not show any residual melanoma. She was started on adjuvant immunotherapy with intravenous nivolumab 480 mg monthly and developed pruritic crusted lesions on the arms, legs, and torso 1 month later, which prompted follow-up to dermatology.

At the current presentation 4 months after the onset of lesions, physical examination revealed lichenoid patches with serous crusting that were concentrated on the torso but also affected the arms and legs. She developed erosions on the upper and lower lips, buccal mucosa, and hard and soft palates, as well as painful, erythematous, dome-shaped papules and nodules on the legs (Figure 1). Her oncologist previously had initiated treatment at the onset of the lesions with clobetasol cream and valacyclovir for the lesions, but the patient showed no improvement.

Four months after the onset of the lesions, the patient was re-referred to her dermatologist, and a biopsy was performed on the left lower leg that showed squamous cell carcinoma, KA type. Additionally, flat erythematous patches were seen on the legs that were consistent with a lichenoid drug eruption. Two weeks later, she was started on halobetasol propionate ointment 0.05% for treatment of the KAs. At 2-week follow-up, 5 months after the onset of the lesions, the patient showed no signs of improvement. An oral prednisone taper of 60 mg for 3 days, 40 mg for 3 days, and then 20 mg daily for a total of 4 weeks was started to treat the lichenoid dermatitis and eruptive KAs. At the next follow-up 6.5 months following the first eruptive KAs, she was no longer using topical or oral steroids, she did not have any new eruptive KAs, and old lesions showed regression (Figure 2). The patient still experienced postinflammatory erythema and hyperpigmentation at the location of the KAs but showed improvement of the lichenoid drug eruption.

We describe a case of eruptive KAs after use of a PD-1 inhibitor for treatment of melanoma. Our patient developed eruptive KAs after only 1 nivolumab treatment. Another report described onset of eruptive KAs after 1 month of nivolumab infusions.³ The KAs experienced by our patient took 6.5 months to regress, which is unusual compared to other case reports in which the KAs self-resolved within a few months, though one other case described lesions that persisted for 6 months.³

Our patient was treated with topical steroids and an oral steroid taper for the concomitant lichenoid drug eruption. It is unknown if the steroids affected the course of the KAs or if they spontaneously regressed on their own. Freites-Martinez et al⁵ described that regression of KAs may be related to an immune response, but corticosteroids are inherently immunosuppressive. They hypothesized that corticosteroids help to temper the heightened immune response of eruptive KAs.⁵

Our patient had oral ulcers, which may have been indicative of an oral lichenoid drug eruption, as well as skin lesions representative of a cutaneous lichenoid drug eruption. This is a favorable reaction, as lichenoid dermatitis is thought to represent successful PD-1 inhibition and therefore a better response to oncologic therapies.² Comorbid lichenoid drug eruption lesions and eruptive KAs may be suggestive of increased T-cell activity,^2,6,7 though some prior case studies have reported eruptive KAs in isolation.³

Discontinuation of immunotherapy due to development of eruptive KAs presents a challenge in the treatment of underlying malignancies such as melanoma. Immunotherapy was discontinued in 7 of 11 cases due to these cutaneous reactions.³ Similarly, our patient underwent only 1 cycle of immunotherapy before developing eruptive KAs and discontinuing PD-1 inhibitor therapy. If we are better able to treat eruptive KAs, then patients can remain on immunotherapy to treat underlying malignancies. Crow et al⁸ showed improvement in lesions when 3 patients with eruptive KAs were treated with hydroxychloroquine; the Goeckerman regimen consisting of steroids, UVB phototherapy, and crude coal tar; and Unna boots with zinc oxide and compression stockings. The above may be added to a list of possible treatments to consider for hastening the regression of eruptive KAs.

Our patient’s clinical course was similar to reports on the regressive nature of eruptive KAs within 6 months after initial eruption. Although it is likely that KAs will regress on their own, treatment modalities that speed up recovery are a future source for research.

To the Editor:

Programmed cell death protein 1 (PD-1) inhibitors have been widely used in the treatment of various cancers. Programmed cell death-ligand 1 (PD-L1) and programmed cell death-ligand 2 located on cancer cells will bind to PD-1 receptors on T cells and suppress them, which will prevent cancer cell destruction. Programmed cell death protein 1 inhibitors block the binding of PD-L1 to cancer cells, which then prevents T-cell immunosuppression.¹ However, cutaneous adverse effects have been associated with PD-1 inhibitors. Dermatitis associated with PD-1 inhibitor therapy occurs more frequently in patients with cutaneous tumors such as melanoma compared to those with head and neck cancers.² Curry et al¹ reported that treatment with an immune checkpoint blockade can lead to immune-related adverse effects, most commonly affecting the gastrointestinal tract, liver, and skin. The same report cited dermatologic toxicity as an adverse effect in approximately 39% of patients treated with anti–PD-1 and approximately 17% of anti–PD-L1.¹ The 4 main categories of dermatologic toxicities to immunotherapies in general include inflammatory disorders, immunobullous disorders, alterations of keratinocytes, and alteration of melanocytes. The most common adverse effects from the use of the PD-1 inhibitor nivolumab were skin rashes, not otherwise specified (14%–20%), pruritus (13%–18%), and vitiligo (~8%).¹ Of the cutaneous dermatitic reactions to PD-1 and PD-L1 inhibitors that were biopsied, the 2 most common were lichenoid dermatitis and spongiotic dermatitis.² Seldomly, there have been reports of keratoacanthomas (KAs) in association with anti–PD-1 therapy.³

A KA is a common skin tumor that appears most frequently as a solitary lesion and is thought to arise from the hair follicle.⁴ It resembles squamous cell carcinoma and commonly regresses within months without intervention. Exposure to UV light is a known risk factor for the development of KAs.

Eruptive KAs have been found in association with 10 cases of various cancers treated with the PD-1 inhibitors pembrolizumab and nivolumab.³ Multiple lesions on photodistributed areas of the body were reported in all 10 cases. Various treatments were used in these 10 cases—doxycycline and niacinamide, electrodesiccation and curettage, clobetasol ointment and/or intralesional triamcinolone, cryotherapy, imiquimod, or no treatment—as well as the cessation of PD-1 inhibitor therapy, with 4 cases continuing therapy and 6 cases discontinuing therapy. Nine cases regressed by 6 months; electrodesiccation and curettage of the lesions was used in the tenth case.³ We report a case of eruptive KA after 1 cycle of nivolumab therapy for metastatic melanoma.

A 79-year-old woman with stage III melanoma presented to her dermatologist after developing generalized pruritic lichenoid eruptions involving the torso, arms, and legs, as well as erosions on the lips, buccal mucosa, and palate 1 month after starting nivolumab therapy. The patient initially presented to dermatology with an irregularly shaped lesion on the left upper back 3 months prior. Biopsy results at that time revealed a diagnosis of malignant melanoma, lentigo maligna type. The lesion was 1.5-mm thick and classified as Clark level IV with a mitotic count of 6 per mm². Molecular genetic studies showed expression of PD-L1 and no expression of c-KIT. The patient underwent wide local excision, and a sentinel lymph node biopsy was positive. Positron emission tomography did not show any hypermetabolic lesions, and magnetic resonance imaging did not indicate brain metastasis. The patient underwent an axillary dissection, which did not show any residual melanoma. She was started on adjuvant immunotherapy with intravenous nivolumab 480 mg monthly and developed pruritic crusted lesions on the arms, legs, and torso 1 month later, which prompted follow-up to dermatology.

At the current presentation 4 months after the onset of lesions, physical examination revealed lichenoid patches with serous crusting that were concentrated on the torso but also affected the arms and legs. She developed erosions on the upper and lower lips, buccal mucosa, and hard and soft palates, as well as painful, erythematous, dome-shaped papules and nodules on the legs (Figure 1). Her oncologist previously had initiated treatment at the onset of the lesions with clobetasol cream and valacyclovir for the lesions, but the patient showed no improvement.

Four months after the onset of the lesions, the patient was re-referred to her dermatologist, and a biopsy was performed on the left lower leg that showed squamous cell carcinoma, KA type. Additionally, flat erythematous patches were seen on the legs that were consistent with a lichenoid drug eruption. Two weeks later, she was started on halobetasol propionate ointment 0.05% for treatment of the KAs. At 2-week follow-up, 5 months after the onset of the lesions, the patient showed no signs of improvement. An oral prednisone taper of 60 mg for 3 days, 40 mg for 3 days, and then 20 mg daily for a total of 4 weeks was started to treat the lichenoid dermatitis and eruptive KAs. At the next follow-up 6.5 months following the first eruptive KAs, she was no longer using topical or oral steroids, she did not have any new eruptive KAs, and old lesions showed regression (Figure 2). The patient still experienced postinflammatory erythema and hyperpigmentation at the location of the KAs but showed improvement of the lichenoid drug eruption.

We describe a case of eruptive KAs after use of a PD-1 inhibitor for treatment of melanoma. Our patient developed eruptive KAs after only 1 nivolumab treatment. Another report described onset of eruptive KAs after 1 month of nivolumab infusions.³ The KAs experienced by our patient took 6.5 months to regress, which is unusual compared to other case reports in which the KAs self-resolved within a few months, though one other case described lesions that persisted for 6 months.³

Our patient was treated with topical steroids and an oral steroid taper for the concomitant lichenoid drug eruption. It is unknown if the steroids affected the course of the KAs or if they spontaneously regressed on their own. Freites-Martinez et al⁵ described that regression of KAs may be related to an immune response, but corticosteroids are inherently immunosuppressive. They hypothesized that corticosteroids help to temper the heightened immune response of eruptive KAs.⁵

Our patient had oral ulcers, which may have been indicative of an oral lichenoid drug eruption, as well as skin lesions representative of a cutaneous lichenoid drug eruption. This is a favorable reaction, as lichenoid dermatitis is thought to represent successful PD-1 inhibition and therefore a better response to oncologic therapies.² Comorbid lichenoid drug eruption lesions and eruptive KAs may be suggestive of increased T-cell activity,^2,6,7 though some prior case studies have reported eruptive KAs in isolation.³

Discontinuation of immunotherapy due to development of eruptive KAs presents a challenge in the treatment of underlying malignancies such as melanoma. Immunotherapy was discontinued in 7 of 11 cases due to these cutaneous reactions.³ Similarly, our patient underwent only 1 cycle of immunotherapy before developing eruptive KAs and discontinuing PD-1 inhibitor therapy. If we are better able to treat eruptive KAs, then patients can remain on immunotherapy to treat underlying malignancies. Crow et al⁸ showed improvement in lesions when 3 patients with eruptive KAs were treated with hydroxychloroquine; the Goeckerman regimen consisting of steroids, UVB phototherapy, and crude coal tar; and Unna boots with zinc oxide and compression stockings. The above may be added to a list of possible treatments to consider for hastening the regression of eruptive KAs.

Our patient’s clinical course was similar to reports on the regressive nature of eruptive KAs within 6 months after initial eruption. Although it is likely that KAs will regress on their own, treatment modalities that speed up recovery are a future source for research.

Inpatient dermatology consultation services are becoming increasingly prevalent in hospital institutions.^1-3 Although often underutilized as a consulting service, dermatology-related admissions cost hundreds of millions of dollars for the health care system.^1,2 Misdiagnosis, prolonged hospital stays, and incorrect treatment are common results of lack of involvement by a skin expert.^1-3 The importance of consultative inpatient dermatology cannot be understated. Accreditation Council for Graduate Medical Education requirements for proficiency in dermatology residency include exposure to inpatient dermatology, and it is our duty as residents to aid our colleagues in the management and treatment of cutaneous disease.

Although exposure to inpatient dermatology varies across residency programs, nearly every dermatology resident is bound to perform a consultation and be involved in the care of a hospitalized patient. At our program at the University of Utah (Salt Lake City), we have robust inpatient exposure, and after numerous hours spent on the forefront of inpatient dermatology, I have accrued a list of specific tips and techniques that have aided me as a resident clinician.

Pre-Rounding More Thoroughly

When I started as a postgraduate year 2 (PGY-2) on the inpatient dermatology rotation, I found myself perplexed. I had learned how to round in internal medicine but was unaccustomed to the nuances of specialty rounds. My list included calciphylaxis, small vessel vasculitis, cellulitis, stasis dermatitis, toxic epidermal necrolysis, and atypical mycobacterial infection. The first few days of service were undeniably difficult due to the daily consultations, complexity of admitted patients, and need for efficiency. I sometimes overlooked important laboratory test results, medication changes, and interdisciplinary discussions that prolonged rounding. As dermatologists, we are responsible for the largest organ of the body, and it is important to approach patients in a comprehensive manner. Pre-rounding should include reviewing interdisciplinary notes, laboratory values/results, and medications, and performing a focused skin examination with a review of systems during the encounter. Importantly, most electronic medical record systems offer an automated rounding sheet. In Epic (Epic Systems Corporation), I would use the bone marrow transplant rounding sheet, which includes laboratory test results, vitals, and medications. After printing out the rounding sheet, I would note important updates for each patient. Although pre-rounding and chart review requires time and effort, it aided me in providing elevated patient care and becoming more efficient during rounds. Over time I have come to strongly appreciate the term dermatology hospitalist. Cutaneous manifestations of systemic disease require thoughtful consideration and workup.

New Patient Consultations: Must-Ask Questions

Holding the university inpatient pager can be stressful. At the University of Utah, we often carry 5 to 10 patients on our list and receive 3 to 4 new consultations a day, sometimes right before 5 pm. When receiving new consultations, it is important to obtain the whole story from the requesting provider. Some of the questions may seem obvious, but I am frequently reminded of the inefficiencies I encountered as a first-year dermatology resident. Remember to always be kind to your consulting colleagues. Dermatology is a difficult discipline, and describing rashes is no easy task. Here is my systematic approach to questions that should be asked of the requesting provider during each new patient consultation:

• What is the patient’s name, room number, and medical record number?
• Is this patient getting admitted or admitted currently?
• Is the rash the reason for admission? (This can greatly help with triaging the urgency of evaluation.)
• Is the rash painful?
• Is this patient ill?
• How would you describe the rash?

When evaluating new patients, it is crucial to remember the morphology camps. Formulating a differential diagnosis on a complex patient can be difficult; however, remembering the morphology camps of acneiform, dermal, eczematous, erythematous, subcutaneous, vasculitic, vasculopathic, and vesiculobullous lesions can be extremely helpful. Additionally, it is crucial to perform a thorough and complete skin examination on every patient. When emphasizing the importance of this, I often am reminded of a humbling moment early in my training. Our team was consulted on a patient with cellulitis and stasis dermatitis. It was a busy day, and my examination was quick and focused on the lower and upper extremities, chest, and back. The patient improved from a cutaneous standpoint and was discharged. At follow-up the next week, one of my attending providers biopsied an atypical macule on the retroauricular region, which was found to be consistent with a stage 1A melanoma. Even on the longest and most tiring hospital days, it is important to perform a full-body skin examination on each patient. You may end up saving a life.

An Organized Toolbox: What to Carry

Similar to our ophthalmology colleagues who are seen carrying around a suitcase in the hospital, I highly recommend some form of a toolbox or bag for performing inpatient biopsies (Table). Carrying around an organized bag, albeit bulky and unfashionable, has saved me numerous trips back to clinic for unexpected complications including fixing leaky vessels, closing stubborn ulcers, and coordinating sedated biopsies in the operating room.

Final Thoughts

As I near the completion of my residency journey, I hope these tips will aid budding and current dermatology residents at excelling as dermatology hospitalists during inpatient rotations. Dermatologists can make a profound impact on a variety of patients, especially when treating hospitalized patients on the clinical forefront. Our role extends beyond the skin, as cutaneous manifestations of internal disease are not uncommon.

Inpatient dermatology consultation services are becoming increasingly prevalent in hospital institutions.^1-3 Although often underutilized as a consulting service, dermatology-related admissions cost hundreds of millions of dollars for the health care system.^1,2 Misdiagnosis, prolonged hospital stays, and incorrect treatment are common results of lack of involvement by a skin expert.^1-3 The importance of consultative inpatient dermatology cannot be understated. Accreditation Council for Graduate Medical Education requirements for proficiency in dermatology residency include exposure to inpatient dermatology, and it is our duty as residents to aid our colleagues in the management and treatment of cutaneous disease.

Although exposure to inpatient dermatology varies across residency programs, nearly every dermatology resident is bound to perform a consultation and be involved in the care of a hospitalized patient. At our program at the University of Utah (Salt Lake City), we have robust inpatient exposure, and after numerous hours spent on the forefront of inpatient dermatology, I have accrued a list of specific tips and techniques that have aided me as a resident clinician.

Pre-Rounding More Thoroughly

When I started as a postgraduate year 2 (PGY-2) on the inpatient dermatology rotation, I found myself perplexed. I had learned how to round in internal medicine but was unaccustomed to the nuances of specialty rounds. My list included calciphylaxis, small vessel vasculitis, cellulitis, stasis dermatitis, toxic epidermal necrolysis, and atypical mycobacterial infection. The first few days of service were undeniably difficult due to the daily consultations, complexity of admitted patients, and need for efficiency. I sometimes overlooked important laboratory test results, medication changes, and interdisciplinary discussions that prolonged rounding. As dermatologists, we are responsible for the largest organ of the body, and it is important to approach patients in a comprehensive manner. Pre-rounding should include reviewing interdisciplinary notes, laboratory values/results, and medications, and performing a focused skin examination with a review of systems during the encounter. Importantly, most electronic medical record systems offer an automated rounding sheet. In Epic (Epic Systems Corporation), I would use the bone marrow transplant rounding sheet, which includes laboratory test results, vitals, and medications. After printing out the rounding sheet, I would note important updates for each patient. Although pre-rounding and chart review requires time and effort, it aided me in providing elevated patient care and becoming more efficient during rounds. Over time I have come to strongly appreciate the term dermatology hospitalist. Cutaneous manifestations of systemic disease require thoughtful consideration and workup.

New Patient Consultations: Must-Ask Questions

Holding the university inpatient pager can be stressful. At the University of Utah, we often carry 5 to 10 patients on our list and receive 3 to 4 new consultations a day, sometimes right before 5 pm. When receiving new consultations, it is important to obtain the whole story from the requesting provider. Some of the questions may seem obvious, but I am frequently reminded of the inefficiencies I encountered as a first-year dermatology resident. Remember to always be kind to your consulting colleagues. Dermatology is a difficult discipline, and describing rashes is no easy task. Here is my systematic approach to questions that should be asked of the requesting provider during each new patient consultation:

• What is the patient’s name, room number, and medical record number?
• Is this patient getting admitted or admitted currently?
• Is the rash the reason for admission? (This can greatly help with triaging the urgency of evaluation.)
• Is the rash painful?
• Is this patient ill?
• How would you describe the rash?

When evaluating new patients, it is crucial to remember the morphology camps. Formulating a differential diagnosis on a complex patient can be difficult; however, remembering the morphology camps of acneiform, dermal, eczematous, erythematous, subcutaneous, vasculitic, vasculopathic, and vesiculobullous lesions can be extremely helpful. Additionally, it is crucial to perform a thorough and complete skin examination on every patient. When emphasizing the importance of this, I often am reminded of a humbling moment early in my training. Our team was consulted on a patient with cellulitis and stasis dermatitis. It was a busy day, and my examination was quick and focused on the lower and upper extremities, chest, and back. The patient improved from a cutaneous standpoint and was discharged. At follow-up the next week, one of my attending providers biopsied an atypical macule on the retroauricular region, which was found to be consistent with a stage 1A melanoma. Even on the longest and most tiring hospital days, it is important to perform a full-body skin examination on each patient. You may end up saving a life.

An Organized Toolbox: What to Carry

Similar to our ophthalmology colleagues who are seen carrying around a suitcase in the hospital, I highly recommend some form of a toolbox or bag for performing inpatient biopsies (Table). Carrying around an organized bag, albeit bulky and unfashionable, has saved me numerous trips back to clinic for unexpected complications including fixing leaky vessels, closing stubborn ulcers, and coordinating sedated biopsies in the operating room.

Final Thoughts

As I near the completion of my residency journey, I hope these tips will aid budding and current dermatology residents at excelling as dermatology hospitalists during inpatient rotations. Dermatologists can make a profound impact on a variety of patients, especially when treating hospitalized patients on the clinical forefront. Our role extends beyond the skin, as cutaneous manifestations of internal disease are not uncommon.

Inpatient dermatology consultation services are becoming increasingly prevalent in hospital institutions.^1-3 Although often underutilized as a consulting service, dermatology-related admissions cost hundreds of millions of dollars for the health care system.^1,2 Misdiagnosis, prolonged hospital stays, and incorrect treatment are common results of lack of involvement by a skin expert.^1-3 The importance of consultative inpatient dermatology cannot be understated. Accreditation Council for Graduate Medical Education requirements for proficiency in dermatology residency include exposure to inpatient dermatology, and it is our duty as residents to aid our colleagues in the management and treatment of cutaneous disease.

Although exposure to inpatient dermatology varies across residency programs, nearly every dermatology resident is bound to perform a consultation and be involved in the care of a hospitalized patient. At our program at the University of Utah (Salt Lake City), we have robust inpatient exposure, and after numerous hours spent on the forefront of inpatient dermatology, I have accrued a list of specific tips and techniques that have aided me as a resident clinician.

Pre-Rounding More Thoroughly

When I started as a postgraduate year 2 (PGY-2) on the inpatient dermatology rotation, I found myself perplexed. I had learned how to round in internal medicine but was unaccustomed to the nuances of specialty rounds. My list included calciphylaxis, small vessel vasculitis, cellulitis, stasis dermatitis, toxic epidermal necrolysis, and atypical mycobacterial infection. The first few days of service were undeniably difficult due to the daily consultations, complexity of admitted patients, and need for efficiency. I sometimes overlooked important laboratory test results, medication changes, and interdisciplinary discussions that prolonged rounding. As dermatologists, we are responsible for the largest organ of the body, and it is important to approach patients in a comprehensive manner. Pre-rounding should include reviewing interdisciplinary notes, laboratory values/results, and medications, and performing a focused skin examination with a review of systems during the encounter. Importantly, most electronic medical record systems offer an automated rounding sheet. In Epic (Epic Systems Corporation), I would use the bone marrow transplant rounding sheet, which includes laboratory test results, vitals, and medications. After printing out the rounding sheet, I would note important updates for each patient. Although pre-rounding and chart review requires time and effort, it aided me in providing elevated patient care and becoming more efficient during rounds. Over time I have come to strongly appreciate the term dermatology hospitalist. Cutaneous manifestations of systemic disease require thoughtful consideration and workup.

New Patient Consultations: Must-Ask Questions

Holding the university inpatient pager can be stressful. At the University of Utah, we often carry 5 to 10 patients on our list and receive 3 to 4 new consultations a day, sometimes right before 5 pm. When receiving new consultations, it is important to obtain the whole story from the requesting provider. Some of the questions may seem obvious, but I am frequently reminded of the inefficiencies I encountered as a first-year dermatology resident. Remember to always be kind to your consulting colleagues. Dermatology is a difficult discipline, and describing rashes is no easy task. Here is my systematic approach to questions that should be asked of the requesting provider during each new patient consultation:

• What is the patient’s name, room number, and medical record number?
• Is this patient getting admitted or admitted currently?
• Is the rash the reason for admission? (This can greatly help with triaging the urgency of evaluation.)
• Is the rash painful?
• Is this patient ill?
• How would you describe the rash?

When evaluating new patients, it is crucial to remember the morphology camps. Formulating a differential diagnosis on a complex patient can be difficult; however, remembering the morphology camps of acneiform, dermal, eczematous, erythematous, subcutaneous, vasculitic, vasculopathic, and vesiculobullous lesions can be extremely helpful. Additionally, it is crucial to perform a thorough and complete skin examination on every patient. When emphasizing the importance of this, I often am reminded of a humbling moment early in my training. Our team was consulted on a patient with cellulitis and stasis dermatitis. It was a busy day, and my examination was quick and focused on the lower and upper extremities, chest, and back. The patient improved from a cutaneous standpoint and was discharged. At follow-up the next week, one of my attending providers biopsied an atypical macule on the retroauricular region, which was found to be consistent with a stage 1A melanoma. Even on the longest and most tiring hospital days, it is important to perform a full-body skin examination on each patient. You may end up saving a life.

An Organized Toolbox: What to Carry

Similar to our ophthalmology colleagues who are seen carrying around a suitcase in the hospital, I highly recommend some form of a toolbox or bag for performing inpatient biopsies (Table). Carrying around an organized bag, albeit bulky and unfashionable, has saved me numerous trips back to clinic for unexpected complications including fixing leaky vessels, closing stubborn ulcers, and coordinating sedated biopsies in the operating room.

Final Thoughts

As I near the completion of my residency journey, I hope these tips will aid budding and current dermatology residents at excelling as dermatology hospitalists during inpatient rotations. Dermatologists can make a profound impact on a variety of patients, especially when treating hospitalized patients on the clinical forefront. Our role extends beyond the skin, as cutaneous manifestations of internal disease are not uncommon.

The investigational drug brepocitinib showed superior symptom reduction in adults with moderate to severe active psoriatic arthritis (PsA), compared with placebo, by meeting primary and secondary endpoints of a phase 2b trial at 16 weeks, which persisted out to 1 year, according to data from 218 individuals.

Brepocitinib, a combination tyrosine kinase 2 and Janus kinase 1 inhibitor, is being studied for the treatment of several immunologic diseases including PsA, wrote Philip Mease, MD, of the Swedish Medical Center/Providence St. Joseph Health and the University of Washington, both in Seattle.

Previous studies in patients with PsA support the use of Janus kinase inhibitors and demonstrate the efficacy of tyrosine kinase 2 inhibitors, but more data are needed in patients with active PsA, the researchers noted.

In a study published in Arthritis & Rheumatology, the researchers randomized adults aged 18-75 years with moderate to severe PsA to once-daily oral doses of brepocitinib at 10 mg, 30 mg, or 60 mg, or a placebo for 16 weeks to assess safety, efficacy, and dose response. Placebo-treated patients were advanced to 30 mg or 60 mg of brepocitinib at week 16. Baseline demographics and disease characteristics were similar among the treatment groups. The mean Psoriatic Arthritis Disease Activity Score (PASDAS) and Disease Activity Index for PsA scores were 5.6 and 38.2, respectively, for the overall study population. Approximately two-thirds (64.7%) had a baseline Psoriasis Area and Severity Index (PASI) score greater than 0 and 3% or more of their body surface area affected by psoriasis.

The primary endpoint was the proportion of patients achieving 20% improvement in American College of Rheumatology response criteria (ACR 20) at week 16. Secondary endpoints included rates of patients meeting ACR 50 and ACR 70 response criteria, the proportion of patients achieving 75% and 90% improvement in PASI scores (PASI 70 and 90), as well as the rates of patients meeting Minimal Disease Activity (MDA) criteria at 16 and 52 weeks.

At week 16, ACR 20 response rates were significantly higher in the brepocitinib 30-mg and 60-mg groups, compared with the placebo group (66.7% and 74.6%, respectively, vs. 43.3%), but not for those who received brepocitinib 10 mg (64.5%).

Response rates for ACR 50, ACR 70, PASI 75, PASI 90, and MDA were similarly higher in the 30-mg and 60-mg brepocitinib groups, compared with placebo, and these responses persisted at week 52. Notably, significant differences in PASI 75 and PASI 90 were observed in patients taking 30 mg and 60 mg brepocitinib, compared with placebo, as early as weeks 4 and 8, respectively, the researchers said.

In addition, disease activity based on PASDAS improved significantly more from baseline to week 16 in all brepocitinib groups, compared with placebo.

The overall safety data were consistent with previous brepocitinib studies, and most of the adverse events were mild or moderate, the researchers said. A total of 12 participants (5.5%) experienced a total of 15 serious adverse events, including 6 infections with brepocitinib 30 mg or 60 mg. No major adverse cardiovascular events or deaths occurred during the study period.

The findings were limited by several factors, including the use of clinics in a limited geographic area (11 countries in Europe), small sample size, and mainly White population, the researchers noted. Other limitations included the large placebo effect and relatively short placebo-controlled period.

The study was supported by Pfizer. Dr. Mease disclosed relationships with Pfizer and other companies including AbbVie, Amgen, Bristol-Myers Squibb, Boehringer Ingelheim, Galapagos, Gilead, GlaxoSmithKline, Inmagene, Janssen, Lilly, Novartis, Sun, and UCB. Many coauthors were employees of Pfizer, and others reported financial relationships with Pfizer and other pharmaceutical companies.

The investigational drug brepocitinib showed superior symptom reduction in adults with moderate to severe active psoriatic arthritis (PsA), compared with placebo, by meeting primary and secondary endpoints of a phase 2b trial at 16 weeks, which persisted out to 1 year, according to data from 218 individuals.

Brepocitinib, a combination tyrosine kinase 2 and Janus kinase 1 inhibitor, is being studied for the treatment of several immunologic diseases including PsA, wrote Philip Mease, MD, of the Swedish Medical Center/Providence St. Joseph Health and the University of Washington, both in Seattle.

Previous studies in patients with PsA support the use of Janus kinase inhibitors and demonstrate the efficacy of tyrosine kinase 2 inhibitors, but more data are needed in patients with active PsA, the researchers noted.

In a study published in Arthritis & Rheumatology, the researchers randomized adults aged 18-75 years with moderate to severe PsA to once-daily oral doses of brepocitinib at 10 mg, 30 mg, or 60 mg, or a placebo for 16 weeks to assess safety, efficacy, and dose response. Placebo-treated patients were advanced to 30 mg or 60 mg of brepocitinib at week 16. Baseline demographics and disease characteristics were similar among the treatment groups. The mean Psoriatic Arthritis Disease Activity Score (PASDAS) and Disease Activity Index for PsA scores were 5.6 and 38.2, respectively, for the overall study population. Approximately two-thirds (64.7%) had a baseline Psoriasis Area and Severity Index (PASI) score greater than 0 and 3% or more of their body surface area affected by psoriasis.

The primary endpoint was the proportion of patients achieving 20% improvement in American College of Rheumatology response criteria (ACR 20) at week 16. Secondary endpoints included rates of patients meeting ACR 50 and ACR 70 response criteria, the proportion of patients achieving 75% and 90% improvement in PASI scores (PASI 70 and 90), as well as the rates of patients meeting Minimal Disease Activity (MDA) criteria at 16 and 52 weeks.

At week 16, ACR 20 response rates were significantly higher in the brepocitinib 30-mg and 60-mg groups, compared with the placebo group (66.7% and 74.6%, respectively, vs. 43.3%), but not for those who received brepocitinib 10 mg (64.5%).

Response rates for ACR 50, ACR 70, PASI 75, PASI 90, and MDA were similarly higher in the 30-mg and 60-mg brepocitinib groups, compared with placebo, and these responses persisted at week 52. Notably, significant differences in PASI 75 and PASI 90 were observed in patients taking 30 mg and 60 mg brepocitinib, compared with placebo, as early as weeks 4 and 8, respectively, the researchers said.

In addition, disease activity based on PASDAS improved significantly more from baseline to week 16 in all brepocitinib groups, compared with placebo.

The overall safety data were consistent with previous brepocitinib studies, and most of the adverse events were mild or moderate, the researchers said. A total of 12 participants (5.5%) experienced a total of 15 serious adverse events, including 6 infections with brepocitinib 30 mg or 60 mg. No major adverse cardiovascular events or deaths occurred during the study period.

The findings were limited by several factors, including the use of clinics in a limited geographic area (11 countries in Europe), small sample size, and mainly White population, the researchers noted. Other limitations included the large placebo effect and relatively short placebo-controlled period.

The study was supported by Pfizer. Dr. Mease disclosed relationships with Pfizer and other companies including AbbVie, Amgen, Bristol-Myers Squibb, Boehringer Ingelheim, Galapagos, Gilead, GlaxoSmithKline, Inmagene, Janssen, Lilly, Novartis, Sun, and UCB. Many coauthors were employees of Pfizer, and others reported financial relationships with Pfizer and other pharmaceutical companies.

The investigational drug brepocitinib showed superior symptom reduction in adults with moderate to severe active psoriatic arthritis (PsA), compared with placebo, by meeting primary and secondary endpoints of a phase 2b trial at 16 weeks, which persisted out to 1 year, according to data from 218 individuals.

Brepocitinib, a combination tyrosine kinase 2 and Janus kinase 1 inhibitor, is being studied for the treatment of several immunologic diseases including PsA, wrote Philip Mease, MD, of the Swedish Medical Center/Providence St. Joseph Health and the University of Washington, both in Seattle.

Previous studies in patients with PsA support the use of Janus kinase inhibitors and demonstrate the efficacy of tyrosine kinase 2 inhibitors, but more data are needed in patients with active PsA, the researchers noted.

In a study published in Arthritis & Rheumatology, the researchers randomized adults aged 18-75 years with moderate to severe PsA to once-daily oral doses of brepocitinib at 10 mg, 30 mg, or 60 mg, or a placebo for 16 weeks to assess safety, efficacy, and dose response. Placebo-treated patients were advanced to 30 mg or 60 mg of brepocitinib at week 16. Baseline demographics and disease characteristics were similar among the treatment groups. The mean Psoriatic Arthritis Disease Activity Score (PASDAS) and Disease Activity Index for PsA scores were 5.6 and 38.2, respectively, for the overall study population. Approximately two-thirds (64.7%) had a baseline Psoriasis Area and Severity Index (PASI) score greater than 0 and 3% or more of their body surface area affected by psoriasis.

The primary endpoint was the proportion of patients achieving 20% improvement in American College of Rheumatology response criteria (ACR 20) at week 16. Secondary endpoints included rates of patients meeting ACR 50 and ACR 70 response criteria, the proportion of patients achieving 75% and 90% improvement in PASI scores (PASI 70 and 90), as well as the rates of patients meeting Minimal Disease Activity (MDA) criteria at 16 and 52 weeks.

At week 16, ACR 20 response rates were significantly higher in the brepocitinib 30-mg and 60-mg groups, compared with the placebo group (66.7% and 74.6%, respectively, vs. 43.3%), but not for those who received brepocitinib 10 mg (64.5%).

Response rates for ACR 50, ACR 70, PASI 75, PASI 90, and MDA were similarly higher in the 30-mg and 60-mg brepocitinib groups, compared with placebo, and these responses persisted at week 52. Notably, significant differences in PASI 75 and PASI 90 were observed in patients taking 30 mg and 60 mg brepocitinib, compared with placebo, as early as weeks 4 and 8, respectively, the researchers said.

In addition, disease activity based on PASDAS improved significantly more from baseline to week 16 in all brepocitinib groups, compared with placebo.

The overall safety data were consistent with previous brepocitinib studies, and most of the adverse events were mild or moderate, the researchers said. A total of 12 participants (5.5%) experienced a total of 15 serious adverse events, including 6 infections with brepocitinib 30 mg or 60 mg. No major adverse cardiovascular events or deaths occurred during the study period.

The findings were limited by several factors, including the use of clinics in a limited geographic area (11 countries in Europe), small sample size, and mainly White population, the researchers noted. Other limitations included the large placebo effect and relatively short placebo-controlled period.

The study was supported by Pfizer. Dr. Mease disclosed relationships with Pfizer and other companies including AbbVie, Amgen, Bristol-Myers Squibb, Boehringer Ingelheim, Galapagos, Gilead, GlaxoSmithKline, Inmagene, Janssen, Lilly, Novartis, Sun, and UCB. Many coauthors were employees of Pfizer, and others reported financial relationships with Pfizer and other pharmaceutical companies.

CHICAGO – An analysis of posts on TikTok about cirrhosis finds that approximately 40% of these posts include misinformation, according to a study presented at the annual Digestive Disease Week® (DDW).

TikTok’s short video format is increasingly becoming a major source for news and information, especially for adolescents and young adults. In 2022 the technology news website The Verge reported that about 10% of all U.S. adults regularly get news from TikTok, including an estimated 26% of adults under 30.

“Our study highlights the alarming prevalence of misinformation related to liver disease and cirrhosis on the TikTok platform. This misinformation can potentially lead to harm and poor health outcomes for individuals seeking accurate information about their conditions,” wrote the study authors in their abstract.

The study, which was led by Macklin Loveland, MD, an internal medicine resident at the University of Arizona, Tucson, found that, among 2,223 TikTok posts related to liver disease or cirrhosis as of November 2022, 60.3% were found to have accurate medical information, but the remaining 39.7% contained misinformation.

Some of the misinformation offered highly dubious and potentially dangerous advice, such as “Reishi mushrooms can reverse liver damage,” when in fact there is evidence to suggest that reishi mushrooms, especially in powder form, may be toxic to the liver and may even cause fatal fulminant hepatitis.

In an interview, Dr. Loveland said that much of the good information about liver disease on TikTok seems to come from patients with cirrhosis or other liver diseases who post videos chronicling their experiences, whereas bad information seems to come from people who are trying to pitch a product such as “natural” or “alternative” medicine.

“People who have real-life, firsthand experiences with cirrhosis have a really nice platform to talk about their disease process and share information with other people with similar disease processes, and the majority of them are accurate,” he said. “Where the inaccuracies come in are when people are trying to profit off a product or sell a dietary supplement, and then things go by the wayside.”

It’s important for TikTok users to understand the intentions of other users, he said, and expressed the hope that content mediators within TikTok would help to keep misinformation at bay.

Skyler B. Johnson, MD, assistant professor of radiation oncology at the University of Utah Huntsman Cancer Institute, Salt Lake City, has studied misinformation about cancer on social media, and as he and colleagues reported in the Journal of the National Cancer Institute, of 200 articles on cancer posted on social media sites, 32.5% contained misinformation and 30.5% contained harmful information.

In an interview, Dr. Johnson, who was not involved in the study by Dr. Loveland and colleagues, offered advice for colleagues about countering misinformation.

“What we’re trying to do, as part of our research group, is encourage physicians to take an active role in addressing misinformation with their patients and also in their social networking interactions,” he said. “When I see a new patient with a new diagnosis of cancer, I warn them that they’re going to encounter things online that may or may not be true.”

He noted that, often when physicians instruct patients not to go online to research their disease, the first thing the vast majority of patients do after leaving the office is to jump online.

Instead, Dr. Johnson recommended inoculating patients against misinformation – not to discourage them from going online, but to inform them about the myriad good and bad information sources, and steer them toward trustworthy sites such as government agencies (the National Institutes of Health, Centers for Disease Control and Prevention, etc), academic medical center sites, or select nonprofit organizations, foundations, and medical associations.

“But at the end of the day, even those you have to be somewhat vigilant about, because there are some unscrupulous providers who exploit even those sites,” he added.
 

Study details

Dr. Loveland and colleagues used the TikTok search engine to look for posts containing the terms “cirrhosis” and “liver disease,” and watched all such videos that turned up in the search from beginning to end. They classified each post as either educational in intent or whether it depicted a firsthand experience with liver disease.

They determined whether each post was accurate or erroneous according to guidelines from the American Association for the Study of Liver Disease, American College of Gastroenterology, and American Gastroenterological Association. They also recorded the number of likes, comments, and the number of times that each video was shared.

Accurate posts were viewed and liked significantly more often than inaccurate ones, and accurate posts had significantly more comments that faulty posts.

However, both accurate and inaccurate posts were shared a similar number of times, suggesting that bad-quality information can metastasize just as easily as good information can be disseminated.

Dr. Loveland and colleagues echoed the recommendations of Dr. Johnson, stating that “health care provides should be aware of the potential for misinformation on social media and should strive to provide their patients with accurate and evidence-based information to inform their health care decisions.”

The study was internally funded. Dr. Loveland and Dr. Johnson reported having no conflicts of interest to disclose.

DDW is sponsored by the American Association for the Study of Liver Diseases, the AGA, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

CHICAGO – An analysis of posts on TikTok about cirrhosis finds that approximately 40% of these posts include misinformation, according to a study presented at the annual Digestive Disease Week® (DDW).

TikTok’s short video format is increasingly becoming a major source for news and information, especially for adolescents and young adults. In 2022 the technology news website The Verge reported that about 10% of all U.S. adults regularly get news from TikTok, including an estimated 26% of adults under 30.

“Our study highlights the alarming prevalence of misinformation related to liver disease and cirrhosis on the TikTok platform. This misinformation can potentially lead to harm and poor health outcomes for individuals seeking accurate information about their conditions,” wrote the study authors in their abstract.

The study, which was led by Macklin Loveland, MD, an internal medicine resident at the University of Arizona, Tucson, found that, among 2,223 TikTok posts related to liver disease or cirrhosis as of November 2022, 60.3% were found to have accurate medical information, but the remaining 39.7% contained misinformation.

Some of the misinformation offered highly dubious and potentially dangerous advice, such as “Reishi mushrooms can reverse liver damage,” when in fact there is evidence to suggest that reishi mushrooms, especially in powder form, may be toxic to the liver and may even cause fatal fulminant hepatitis.

In an interview, Dr. Loveland said that much of the good information about liver disease on TikTok seems to come from patients with cirrhosis or other liver diseases who post videos chronicling their experiences, whereas bad information seems to come from people who are trying to pitch a product such as “natural” or “alternative” medicine.

“People who have real-life, firsthand experiences with cirrhosis have a really nice platform to talk about their disease process and share information with other people with similar disease processes, and the majority of them are accurate,” he said. “Where the inaccuracies come in are when people are trying to profit off a product or sell a dietary supplement, and then things go by the wayside.”

It’s important for TikTok users to understand the intentions of other users, he said, and expressed the hope that content mediators within TikTok would help to keep misinformation at bay.

Skyler B. Johnson, MD, assistant professor of radiation oncology at the University of Utah Huntsman Cancer Institute, Salt Lake City, has studied misinformation about cancer on social media, and as he and colleagues reported in the Journal of the National Cancer Institute, of 200 articles on cancer posted on social media sites, 32.5% contained misinformation and 30.5% contained harmful information.

In an interview, Dr. Johnson, who was not involved in the study by Dr. Loveland and colleagues, offered advice for colleagues about countering misinformation.

“What we’re trying to do, as part of our research group, is encourage physicians to take an active role in addressing misinformation with their patients and also in their social networking interactions,” he said. “When I see a new patient with a new diagnosis of cancer, I warn them that they’re going to encounter things online that may or may not be true.”

He noted that, often when physicians instruct patients not to go online to research their disease, the first thing the vast majority of patients do after leaving the office is to jump online.

Instead, Dr. Johnson recommended inoculating patients against misinformation – not to discourage them from going online, but to inform them about the myriad good and bad information sources, and steer them toward trustworthy sites such as government agencies (the National Institutes of Health, Centers for Disease Control and Prevention, etc), academic medical center sites, or select nonprofit organizations, foundations, and medical associations.

“But at the end of the day, even those you have to be somewhat vigilant about, because there are some unscrupulous providers who exploit even those sites,” he added.
 

Study details

Dr. Loveland and colleagues used the TikTok search engine to look for posts containing the terms “cirrhosis” and “liver disease,” and watched all such videos that turned up in the search from beginning to end. They classified each post as either educational in intent or whether it depicted a firsthand experience with liver disease.

They determined whether each post was accurate or erroneous according to guidelines from the American Association for the Study of Liver Disease, American College of Gastroenterology, and American Gastroenterological Association. They also recorded the number of likes, comments, and the number of times that each video was shared.

Accurate posts were viewed and liked significantly more often than inaccurate ones, and accurate posts had significantly more comments that faulty posts.

However, both accurate and inaccurate posts were shared a similar number of times, suggesting that bad-quality information can metastasize just as easily as good information can be disseminated.

Dr. Loveland and colleagues echoed the recommendations of Dr. Johnson, stating that “health care provides should be aware of the potential for misinformation on social media and should strive to provide their patients with accurate and evidence-based information to inform their health care decisions.”

The study was internally funded. Dr. Loveland and Dr. Johnson reported having no conflicts of interest to disclose.

DDW is sponsored by the American Association for the Study of Liver Diseases, the AGA, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

CHICAGO – An analysis of posts on TikTok about cirrhosis finds that approximately 40% of these posts include misinformation, according to a study presented at the annual Digestive Disease Week® (DDW).

TikTok’s short video format is increasingly becoming a major source for news and information, especially for adolescents and young adults. In 2022 the technology news website The Verge reported that about 10% of all U.S. adults regularly get news from TikTok, including an estimated 26% of adults under 30.

“Our study highlights the alarming prevalence of misinformation related to liver disease and cirrhosis on the TikTok platform. This misinformation can potentially lead to harm and poor health outcomes for individuals seeking accurate information about their conditions,” wrote the study authors in their abstract.

The study, which was led by Macklin Loveland, MD, an internal medicine resident at the University of Arizona, Tucson, found that, among 2,223 TikTok posts related to liver disease or cirrhosis as of November 2022, 60.3% were found to have accurate medical information, but the remaining 39.7% contained misinformation.

Some of the misinformation offered highly dubious and potentially dangerous advice, such as “Reishi mushrooms can reverse liver damage,” when in fact there is evidence to suggest that reishi mushrooms, especially in powder form, may be toxic to the liver and may even cause fatal fulminant hepatitis.

In an interview, Dr. Loveland said that much of the good information about liver disease on TikTok seems to come from patients with cirrhosis or other liver diseases who post videos chronicling their experiences, whereas bad information seems to come from people who are trying to pitch a product such as “natural” or “alternative” medicine.

“People who have real-life, firsthand experiences with cirrhosis have a really nice platform to talk about their disease process and share information with other people with similar disease processes, and the majority of them are accurate,” he said. “Where the inaccuracies come in are when people are trying to profit off a product or sell a dietary supplement, and then things go by the wayside.”

It’s important for TikTok users to understand the intentions of other users, he said, and expressed the hope that content mediators within TikTok would help to keep misinformation at bay.

Skyler B. Johnson, MD, assistant professor of radiation oncology at the University of Utah Huntsman Cancer Institute, Salt Lake City, has studied misinformation about cancer on social media, and as he and colleagues reported in the Journal of the National Cancer Institute, of 200 articles on cancer posted on social media sites, 32.5% contained misinformation and 30.5% contained harmful information.

In an interview, Dr. Johnson, who was not involved in the study by Dr. Loveland and colleagues, offered advice for colleagues about countering misinformation.

“What we’re trying to do, as part of our research group, is encourage physicians to take an active role in addressing misinformation with their patients and also in their social networking interactions,” he said. “When I see a new patient with a new diagnosis of cancer, I warn them that they’re going to encounter things online that may or may not be true.”

He noted that, often when physicians instruct patients not to go online to research their disease, the first thing the vast majority of patients do after leaving the office is to jump online.

Instead, Dr. Johnson recommended inoculating patients against misinformation – not to discourage them from going online, but to inform them about the myriad good and bad information sources, and steer them toward trustworthy sites such as government agencies (the National Institutes of Health, Centers for Disease Control and Prevention, etc), academic medical center sites, or select nonprofit organizations, foundations, and medical associations.

“But at the end of the day, even those you have to be somewhat vigilant about, because there are some unscrupulous providers who exploit even those sites,” he added.
 

Study details

Dr. Loveland and colleagues used the TikTok search engine to look for posts containing the terms “cirrhosis” and “liver disease,” and watched all such videos that turned up in the search from beginning to end. They classified each post as either educational in intent or whether it depicted a firsthand experience with liver disease.

They determined whether each post was accurate or erroneous according to guidelines from the American Association for the Study of Liver Disease, American College of Gastroenterology, and American Gastroenterological Association. They also recorded the number of likes, comments, and the number of times that each video was shared.

Accurate posts were viewed and liked significantly more often than inaccurate ones, and accurate posts had significantly more comments that faulty posts.

However, both accurate and inaccurate posts were shared a similar number of times, suggesting that bad-quality information can metastasize just as easily as good information can be disseminated.

Dr. Loveland and colleagues echoed the recommendations of Dr. Johnson, stating that “health care provides should be aware of the potential for misinformation on social media and should strive to provide their patients with accurate and evidence-based information to inform their health care decisions.”

The study was internally funded. Dr. Loveland and Dr. Johnson reported having no conflicts of interest to disclose.

DDW is sponsored by the American Association for the Study of Liver Diseases, the AGA, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

CHICAGO – Preoperative clinical diagnoses of pancreatic cystic neoplasms (PCNs) are frequently found to be in error when patients go to surgery as recommended under international guidelines, data from a retrospective study show.

An analysis of all pancreatic resections performed for presumed PCN at the Verona Pancreas Institute, Italy, from 2011 through 2020 showed a high degree of discrepancy between the preoperative clinical diagnosis and the final postoperative pathology, with some lesions being misdiagnosed in nearly two-thirds of cases, reported Anna Burelli, MD, of the department of general and pancreatic surgery at the University of Verona.

“Diagnostic errors are still common for resected PCNs. Morphological and clinical information alone still poorly frame actual targets for surgery, and hopefully the development of new reliable biomarkers will represent the next evolution in pancreatic cystic neoplasm management,” she said in an oral abstract session at the annual Digestive Disease Week^® (DDW).

Diagnostic errors are significant issues in care of patients with PCN, because clinicians must balance the need for prompt, definitive treatment when necessary with the need for avoiding the significant morbidity of pancreatic resection for patients with lesions that turn out to be nonmalignant.

The investigators define “misdiagnosis” as a discrepancy between the preoperative clinical diagnosis and the postoperative pathology, and “mismatch” as a discrepancy between the preoperative suspicion of malignant or benign disease and the final pathology.
 

Checkered history

In previous cases series from Massachusetts General Hospital in Boston (2010) and the Verona Pancreas Institute (2012) – both experienced, high-volume centers – PCN misdiagnosis rates were 30% and 21%, respectively, and results from the current study show that things haven’t changed much since then, Dr. Burelli said.

PCNs are divided into neoplastic and nonneoplastic categories, with mucin-producing subtypes considered to be precancerous lesions that require accurate diagnosis and close monitoring.

Examples of neoplastic PCNs are intraductal papillary mucinous neoplasms (IPMNs) of the main pancreatic duct or side branch and mucinous cystadenomas. In contrast, serous cystadenomas, considered nonneoplastic, are mostly benign lesions discovered incidentally during abdominal imaging for another indication. It is very difficult, however, to distinguish between the two PCN subtypes clinically.

For example, Dr. Burelli showed images from a patient who received a preoperative diagnosis of mixed IPMN that was in fact found to be chronic pancreatitis on postoperative pathology.

Dr. Burelli noted that AGA and joint European guidelines for management of PCNs have been updated over the past decade, with the latest AGA iteration in 2015.

A 2017 study evaluating the 2015 AGA guidelines for management of asymptomatic PCNs found that following the guidelines in a large multicenter cohort “would have resulted in 60 % fewer patients being referred for surgical resection, and accurately recommended surveillance in 95% of patients with asymptomatic PCNs.”

Misdiagnosis and mismatch common

In the current study, Dr. Burelli and colleagues reviewed all pancreatic resections performed for PCNs at their center from 2011 through 2020.

Of 601 patients included in the retrospective study, 301 underwent endoscopic ultrasound (EUS).

The investigators identified misdiagnosis in 19% of cases and mismatch in 34%, and there was no significant improvement in diagnostic accuracy among the 50% of patients who underwent EUS.

The most frequently misdiagnosed lesions were cystic neuroendocrine tumors, in 61% of cases. The least misdiagnosed lesions were pseudopapillary tumors, in 6% of cases.

Many of the diagnostic errors were clinically important. For example, seven cases presumed to be serous cystic neoplasms (an almost always benign lesion) were found on final pathology to have a different, malignant histology.

Mismatch examples included 50 IPMNs with high-risk stigmata that were presumed to be malignant before surgery but were nonmalignant on final pathology, and 38 IPMNs without high-risk stigmata which were thought on clinical examination to be benign but turned out to be malignant on final pathology.

“Our results are in line with the current literature,” Dr. Burelli said, citing a recent meta-analysis showing that among 3,292 patients who underwent resection for mucinous cystic neoplasms (MCNs), the pooled rate of malignancy was 16.1%, yet the 2012 International Association of Pancreatology guidelines recommend surgery for all fit patients with MCNs, and joint European evidence-based guidelines from 2018 recommend surgery for MCNs 40 mm or larger, those with mural nodules, and for patients who are symptomatic.

The 16.1% pooled malignancy rate suggests “that there is space for surveillance in most cases of MCNs,” she said.

In addition, morphologic and clinical evaluation for IPMN with high-risk stigmata have been shown to have low specificity and low sensitivity, “so should guideline recommendations be revised?” Dr. Burelli said.

She pointed to a recent multi-institutional study in Gastroenterology showing that real-time next-generation sequencing of pancreatic cyst fluid “is sensitive and specific for various pancreatic cyst types and advanced neoplasia arising from mucinous cysts, but also reveals the diversity of genomic alterations seen in pancreatic cysts and their clinical significance.”

“This is not the future; this is the present,” she concluded.

Invited discussant R. Matthew Walsh, MD, a surgeon specializing in pancreatic and cancer surgery at the Cleveland Clinic, complimented the contributions of her group.

“The patient that you showed with chronic pancreatitis could have very well benefited from the operation regardless of the diagnosis if they were symptomatic,” he said, addressing Dr. Burelli. “So what is the group that is the regrettable surgical patients, and where are you aiming your studies? Is it really the 24% with high-risk features in IPMN that have low-grade dysplasia, or is it the 58% who we’re not sure why they were operated on because they didn’t have high-grade features who had low-grade dysplasia?”

She replied that “the goal here is to avoid surgery for benign entities, and we know that the only true benign entities are serous cystic neoplasms, and all the others have a malignant potential, but we think at Verona Pancreas Institute there is no reason to operate on low-grade dysplasia free patients. This is what we really would like to avoid.”

Dr. Walsh also asked, given their finding that EUS did not appear to offer a benefit to patients or change decision making, which patients should still get EUS.

“I think that only patients in which the diagnosis is uncertain or in which there are some worrisome features or high-risk stigmata should undergo EUS before surgery, and also to continue follow-up,” Dr. Burelli said. “I don’t think that the conclusion is that EUS is not useful, but it’s not useful in all.”

For example, large, microcystic lesions can be readily identified radiographically, but other, more complex cases may still require EUS to help nail down or refine a diagnosis, she said.

The study was internally funded. Dr. Burelli and Dr. Walsh reported having no conflicts of interest.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – Preoperative clinical diagnoses of pancreatic cystic neoplasms (PCNs) are frequently found to be in error when patients go to surgery as recommended under international guidelines, data from a retrospective study show.

An analysis of all pancreatic resections performed for presumed PCN at the Verona Pancreas Institute, Italy, from 2011 through 2020 showed a high degree of discrepancy between the preoperative clinical diagnosis and the final postoperative pathology, with some lesions being misdiagnosed in nearly two-thirds of cases, reported Anna Burelli, MD, of the department of general and pancreatic surgery at the University of Verona.

“Diagnostic errors are still common for resected PCNs. Morphological and clinical information alone still poorly frame actual targets for surgery, and hopefully the development of new reliable biomarkers will represent the next evolution in pancreatic cystic neoplasm management,” she said in an oral abstract session at the annual Digestive Disease Week^® (DDW).

Diagnostic errors are significant issues in care of patients with PCN, because clinicians must balance the need for prompt, definitive treatment when necessary with the need for avoiding the significant morbidity of pancreatic resection for patients with lesions that turn out to be nonmalignant.

The investigators define “misdiagnosis” as a discrepancy between the preoperative clinical diagnosis and the postoperative pathology, and “mismatch” as a discrepancy between the preoperative suspicion of malignant or benign disease and the final pathology.
 

Checkered history

In previous cases series from Massachusetts General Hospital in Boston (2010) and the Verona Pancreas Institute (2012) – both experienced, high-volume centers – PCN misdiagnosis rates were 30% and 21%, respectively, and results from the current study show that things haven’t changed much since then, Dr. Burelli said.

PCNs are divided into neoplastic and nonneoplastic categories, with mucin-producing subtypes considered to be precancerous lesions that require accurate diagnosis and close monitoring.

Examples of neoplastic PCNs are intraductal papillary mucinous neoplasms (IPMNs) of the main pancreatic duct or side branch and mucinous cystadenomas. In contrast, serous cystadenomas, considered nonneoplastic, are mostly benign lesions discovered incidentally during abdominal imaging for another indication. It is very difficult, however, to distinguish between the two PCN subtypes clinically.

For example, Dr. Burelli showed images from a patient who received a preoperative diagnosis of mixed IPMN that was in fact found to be chronic pancreatitis on postoperative pathology.

Dr. Burelli noted that AGA and joint European guidelines for management of PCNs have been updated over the past decade, with the latest AGA iteration in 2015.

A 2017 study evaluating the 2015 AGA guidelines for management of asymptomatic PCNs found that following the guidelines in a large multicenter cohort “would have resulted in 60 % fewer patients being referred for surgical resection, and accurately recommended surveillance in 95% of patients with asymptomatic PCNs.”

Misdiagnosis and mismatch common

In the current study, Dr. Burelli and colleagues reviewed all pancreatic resections performed for PCNs at their center from 2011 through 2020.

Of 601 patients included in the retrospective study, 301 underwent endoscopic ultrasound (EUS).

The investigators identified misdiagnosis in 19% of cases and mismatch in 34%, and there was no significant improvement in diagnostic accuracy among the 50% of patients who underwent EUS.

The most frequently misdiagnosed lesions were cystic neuroendocrine tumors, in 61% of cases. The least misdiagnosed lesions were pseudopapillary tumors, in 6% of cases.

Many of the diagnostic errors were clinically important. For example, seven cases presumed to be serous cystic neoplasms (an almost always benign lesion) were found on final pathology to have a different, malignant histology.

Mismatch examples included 50 IPMNs with high-risk stigmata that were presumed to be malignant before surgery but were nonmalignant on final pathology, and 38 IPMNs without high-risk stigmata which were thought on clinical examination to be benign but turned out to be malignant on final pathology.

“Our results are in line with the current literature,” Dr. Burelli said, citing a recent meta-analysis showing that among 3,292 patients who underwent resection for mucinous cystic neoplasms (MCNs), the pooled rate of malignancy was 16.1%, yet the 2012 International Association of Pancreatology guidelines recommend surgery for all fit patients with MCNs, and joint European evidence-based guidelines from 2018 recommend surgery for MCNs 40 mm or larger, those with mural nodules, and for patients who are symptomatic.

The 16.1% pooled malignancy rate suggests “that there is space for surveillance in most cases of MCNs,” she said.

In addition, morphologic and clinical evaluation for IPMN with high-risk stigmata have been shown to have low specificity and low sensitivity, “so should guideline recommendations be revised?” Dr. Burelli said.

She pointed to a recent multi-institutional study in Gastroenterology showing that real-time next-generation sequencing of pancreatic cyst fluid “is sensitive and specific for various pancreatic cyst types and advanced neoplasia arising from mucinous cysts, but also reveals the diversity of genomic alterations seen in pancreatic cysts and their clinical significance.”

“This is not the future; this is the present,” she concluded.

Invited discussant R. Matthew Walsh, MD, a surgeon specializing in pancreatic and cancer surgery at the Cleveland Clinic, complimented the contributions of her group.

“The patient that you showed with chronic pancreatitis could have very well benefited from the operation regardless of the diagnosis if they were symptomatic,” he said, addressing Dr. Burelli. “So what is the group that is the regrettable surgical patients, and where are you aiming your studies? Is it really the 24% with high-risk features in IPMN that have low-grade dysplasia, or is it the 58% who we’re not sure why they were operated on because they didn’t have high-grade features who had low-grade dysplasia?”

She replied that “the goal here is to avoid surgery for benign entities, and we know that the only true benign entities are serous cystic neoplasms, and all the others have a malignant potential, but we think at Verona Pancreas Institute there is no reason to operate on low-grade dysplasia free patients. This is what we really would like to avoid.”

Dr. Walsh also asked, given their finding that EUS did not appear to offer a benefit to patients or change decision making, which patients should still get EUS.

“I think that only patients in which the diagnosis is uncertain or in which there are some worrisome features or high-risk stigmata should undergo EUS before surgery, and also to continue follow-up,” Dr. Burelli said. “I don’t think that the conclusion is that EUS is not useful, but it’s not useful in all.”

For example, large, microcystic lesions can be readily identified radiographically, but other, more complex cases may still require EUS to help nail down or refine a diagnosis, she said.

The study was internally funded. Dr. Burelli and Dr. Walsh reported having no conflicts of interest.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – Preoperative clinical diagnoses of pancreatic cystic neoplasms (PCNs) are frequently found to be in error when patients go to surgery as recommended under international guidelines, data from a retrospective study show.

An analysis of all pancreatic resections performed for presumed PCN at the Verona Pancreas Institute, Italy, from 2011 through 2020 showed a high degree of discrepancy between the preoperative clinical diagnosis and the final postoperative pathology, with some lesions being misdiagnosed in nearly two-thirds of cases, reported Anna Burelli, MD, of the department of general and pancreatic surgery at the University of Verona.

“Diagnostic errors are still common for resected PCNs. Morphological and clinical information alone still poorly frame actual targets for surgery, and hopefully the development of new reliable biomarkers will represent the next evolution in pancreatic cystic neoplasm management,” she said in an oral abstract session at the annual Digestive Disease Week^® (DDW).

Diagnostic errors are significant issues in care of patients with PCN, because clinicians must balance the need for prompt, definitive treatment when necessary with the need for avoiding the significant morbidity of pancreatic resection for patients with lesions that turn out to be nonmalignant.

The investigators define “misdiagnosis” as a discrepancy between the preoperative clinical diagnosis and the postoperative pathology, and “mismatch” as a discrepancy between the preoperative suspicion of malignant or benign disease and the final pathology.
 

Checkered history

In previous cases series from Massachusetts General Hospital in Boston (2010) and the Verona Pancreas Institute (2012) – both experienced, high-volume centers – PCN misdiagnosis rates were 30% and 21%, respectively, and results from the current study show that things haven’t changed much since then, Dr. Burelli said.

PCNs are divided into neoplastic and nonneoplastic categories, with mucin-producing subtypes considered to be precancerous lesions that require accurate diagnosis and close monitoring.

Examples of neoplastic PCNs are intraductal papillary mucinous neoplasms (IPMNs) of the main pancreatic duct or side branch and mucinous cystadenomas. In contrast, serous cystadenomas, considered nonneoplastic, are mostly benign lesions discovered incidentally during abdominal imaging for another indication. It is very difficult, however, to distinguish between the two PCN subtypes clinically.

For example, Dr. Burelli showed images from a patient who received a preoperative diagnosis of mixed IPMN that was in fact found to be chronic pancreatitis on postoperative pathology.

Dr. Burelli noted that AGA and joint European guidelines for management of PCNs have been updated over the past decade, with the latest AGA iteration in 2015.

A 2017 study evaluating the 2015 AGA guidelines for management of asymptomatic PCNs found that following the guidelines in a large multicenter cohort “would have resulted in 60 % fewer patients being referred for surgical resection, and accurately recommended surveillance in 95% of patients with asymptomatic PCNs.”

Misdiagnosis and mismatch common

In the current study, Dr. Burelli and colleagues reviewed all pancreatic resections performed for PCNs at their center from 2011 through 2020.

Of 601 patients included in the retrospective study, 301 underwent endoscopic ultrasound (EUS).

The investigators identified misdiagnosis in 19% of cases and mismatch in 34%, and there was no significant improvement in diagnostic accuracy among the 50% of patients who underwent EUS.

The most frequently misdiagnosed lesions were cystic neuroendocrine tumors, in 61% of cases. The least misdiagnosed lesions were pseudopapillary tumors, in 6% of cases.

Many of the diagnostic errors were clinically important. For example, seven cases presumed to be serous cystic neoplasms (an almost always benign lesion) were found on final pathology to have a different, malignant histology.

Mismatch examples included 50 IPMNs with high-risk stigmata that were presumed to be malignant before surgery but were nonmalignant on final pathology, and 38 IPMNs without high-risk stigmata which were thought on clinical examination to be benign but turned out to be malignant on final pathology.

“Our results are in line with the current literature,” Dr. Burelli said, citing a recent meta-analysis showing that among 3,292 patients who underwent resection for mucinous cystic neoplasms (MCNs), the pooled rate of malignancy was 16.1%, yet the 2012 International Association of Pancreatology guidelines recommend surgery for all fit patients with MCNs, and joint European evidence-based guidelines from 2018 recommend surgery for MCNs 40 mm or larger, those with mural nodules, and for patients who are symptomatic.

The 16.1% pooled malignancy rate suggests “that there is space for surveillance in most cases of MCNs,” she said.

In addition, morphologic and clinical evaluation for IPMN with high-risk stigmata have been shown to have low specificity and low sensitivity, “so should guideline recommendations be revised?” Dr. Burelli said.

She pointed to a recent multi-institutional study in Gastroenterology showing that real-time next-generation sequencing of pancreatic cyst fluid “is sensitive and specific for various pancreatic cyst types and advanced neoplasia arising from mucinous cysts, but also reveals the diversity of genomic alterations seen in pancreatic cysts and their clinical significance.”

“This is not the future; this is the present,” she concluded.

Invited discussant R. Matthew Walsh, MD, a surgeon specializing in pancreatic and cancer surgery at the Cleveland Clinic, complimented the contributions of her group.

“The patient that you showed with chronic pancreatitis could have very well benefited from the operation regardless of the diagnosis if they were symptomatic,” he said, addressing Dr. Burelli. “So what is the group that is the regrettable surgical patients, and where are you aiming your studies? Is it really the 24% with high-risk features in IPMN that have low-grade dysplasia, or is it the 58% who we’re not sure why they were operated on because they didn’t have high-grade features who had low-grade dysplasia?”

She replied that “the goal here is to avoid surgery for benign entities, and we know that the only true benign entities are serous cystic neoplasms, and all the others have a malignant potential, but we think at Verona Pancreas Institute there is no reason to operate on low-grade dysplasia free patients. This is what we really would like to avoid.”

Dr. Walsh also asked, given their finding that EUS did not appear to offer a benefit to patients or change decision making, which patients should still get EUS.

“I think that only patients in which the diagnosis is uncertain or in which there are some worrisome features or high-risk stigmata should undergo EUS before surgery, and also to continue follow-up,” Dr. Burelli said. “I don’t think that the conclusion is that EUS is not useful, but it’s not useful in all.”

For example, large, microcystic lesions can be readily identified radiographically, but other, more complex cases may still require EUS to help nail down or refine a diagnosis, she said.

The study was internally funded. Dr. Burelli and Dr. Walsh reported having no conflicts of interest.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

A version of this article first appeared on Medscape.com.

“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

A version of this article first appeared on Medscape.com.

“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

A version of this article first appeared on Medscape.com.

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

The Food and Drug Administration has expanded the indication for Abbott Laboratories’ spinal cord stimulation (SCS) devices to include treatment of chronic back pain in patients who have not had, or are not eligible for, back surgery, the company has announced.
 

The new indication spans all of Abbott’s SCS devices in the United States, which include the recharge-free Proclaim SCS family and the rechargeable Eterna SCS platform.

The devices feature the company’s proprietary, low-energy BurstDR stimulation waveform, a form of stimulation therapy that uses bursts of mild electrical energy without causing an abnormal tingling sensation to help disrupt pain signals before they can reach the brain, the company explained.

The expanded indication was supported by results from the DISTINCT study, which enrolled 270 adults suffering from severe, disabling chronic back pain for an average of more than 12 years and who were not eligible for surgery.

The study showed that significantly more patients who were treated with SCS achieved significant improvements in back pain, function, quality of life, and psychological status than peers treated with conservative medical management.

“To date, we have struggled with how to treat people who weren’t considered a good surgical candidate because we didn’t have clear, data-driven treatment options for non-surgical back pain,” Timothy Deer, MD, president and CEO of the Spine and Nerve Centers of the Virginias in Charleston, W.Va., said in a news release.

“This new indication for Abbott’s SCS devices, together with BurstDR stimulation, allows physicians the ability to identify and treat a new group of people, providing them with relief from chronic back pain,” Dr. Deer said.

A version of this article first appeared on Medscape.com.

The Food and Drug Administration has expanded the indication for Abbott Laboratories’ spinal cord stimulation (SCS) devices to include treatment of chronic back pain in patients who have not had, or are not eligible for, back surgery, the company has announced.
 

The new indication spans all of Abbott’s SCS devices in the United States, which include the recharge-free Proclaim SCS family and the rechargeable Eterna SCS platform.

The devices feature the company’s proprietary, low-energy BurstDR stimulation waveform, a form of stimulation therapy that uses bursts of mild electrical energy without causing an abnormal tingling sensation to help disrupt pain signals before they can reach the brain, the company explained.

The expanded indication was supported by results from the DISTINCT study, which enrolled 270 adults suffering from severe, disabling chronic back pain for an average of more than 12 years and who were not eligible for surgery.

The study showed that significantly more patients who were treated with SCS achieved significant improvements in back pain, function, quality of life, and psychological status than peers treated with conservative medical management.

“To date, we have struggled with how to treat people who weren’t considered a good surgical candidate because we didn’t have clear, data-driven treatment options for non-surgical back pain,” Timothy Deer, MD, president and CEO of the Spine and Nerve Centers of the Virginias in Charleston, W.Va., said in a news release.

“This new indication for Abbott’s SCS devices, together with BurstDR stimulation, allows physicians the ability to identify and treat a new group of people, providing them with relief from chronic back pain,” Dr. Deer said.

A version of this article first appeared on Medscape.com.

The Food and Drug Administration has expanded the indication for Abbott Laboratories’ spinal cord stimulation (SCS) devices to include treatment of chronic back pain in patients who have not had, or are not eligible for, back surgery, the company has announced.
 

The new indication spans all of Abbott’s SCS devices in the United States, which include the recharge-free Proclaim SCS family and the rechargeable Eterna SCS platform.

The devices feature the company’s proprietary, low-energy BurstDR stimulation waveform, a form of stimulation therapy that uses bursts of mild electrical energy without causing an abnormal tingling sensation to help disrupt pain signals before they can reach the brain, the company explained.

The expanded indication was supported by results from the DISTINCT study, which enrolled 270 adults suffering from severe, disabling chronic back pain for an average of more than 12 years and who were not eligible for surgery.

The study showed that significantly more patients who were treated with SCS achieved significant improvements in back pain, function, quality of life, and psychological status than peers treated with conservative medical management.

“To date, we have struggled with how to treat people who weren’t considered a good surgical candidate because we didn’t have clear, data-driven treatment options for non-surgical back pain,” Timothy Deer, MD, president and CEO of the Spine and Nerve Centers of the Virginias in Charleston, W.Va., said in a news release.

“This new indication for Abbott’s SCS devices, together with BurstDR stimulation, allows physicians the ability to identify and treat a new group of people, providing them with relief from chronic back pain,” Dr. Deer said.

A version of this article first appeared on Medscape.com.