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First treat-to-target gout trial supports allopurinol dose escalation
Gradual dose escalation of allopurinol achieved target serum urate levels without causing excess adverse effects in patients with gout who tolerated but responded inadequately to creatinine clearance–based dosing, including in patients with chronic kidney disease, investigators reported in Annals of the Rheumatic Diseases.
The study is the first randomized, controlled trial to examine treat-to-target allopurinol dose escalation in gout. “We believe this approach can be undertaken in all patients who tolerate allopurinol,” lead investigator Lisa Stamp, MD, said in an interview. However, it is important to monitor kidney and liver function.”
To help settle these debates, Dr. Stamp and her associates recruited 183 patients with gout whose serum urate levels averaged 7.15 mg/dL (standard deviation, 1.6 mg/dL) despite at least 1 month of at least a creatinine clearance–based allopurinol dose (average, 269 mg/day). For the next 12 months, patients either continued this dose or increased it monthly until serum urate fell below 6 mg/dL (Ann Rheum Dis. 2017 March 17. doi: 10.1136/annrheumdis-2016-210872).
At month 12, 69% of dose-escalation patients and 32% of controls reached this target (P less than .001; odds ratio, 4.3; 95% confidence interval, 2.4-7.9). Serum urate levels dropped by a mean of 1.5 mg/dL with dose escalation and by 0.34 mg/dL in controls (P less than .001). Thus, dose escalation cut serum urate levels by an additional 1.2 mg/dL (95% CI, 0.67-1.5 mg/dL; P less than .001). The average final daily allopurinol dose was 413 mg (range, 0-900 mg) with dose escalation and 288 mg (0-600 mg) for controls.
Notably, renal function measures did not differ between arms. “There has been long-standing concern about whether it is safe to escalate allopurinol doses in persons with chronic kidney disease,” said Kenneth Saag, MD, of the University of Alabama at Birmingham, who was not involved in the trial. “This study contributes to the limited literature supporting the practice of treating to serum urate targets, even in patients with underlying kidney disease.”
Fully 52% of trial participants had chronic kidney disease, and 44% had tophi. “Thus, our population is representative of people with gout, represents real-life clinical practice, and the results are generalizable to other gout populations,” the investigators wrote.
The findings support the ACR recommendation to gradually titrate urate-lowering therapy while performing close laboratory monitoring, said Tuhina Neogi, MD, of Boston University, who was not involved in the study. This approach is “efficacious and relatively safe for patients who have already tolerated lower doses of allopurinol, but have not yet achieved their serum urate target,” she said. “This is akin to finding the right regimen and titrating doses of medications for patients with diabetes or hypertension in a patient-centered manner.”
Patients in both groups developed mild increases in liver function tests, and a few in the dose escalation group developed more pronounced rises in gamma glutamyl transferase (GGT), as previously reported in the LASSO trial (Semin Arthritis Rheum. 2015 Oct;45[2]:174-83). Allopurinol has been linked to liver enzyme abnormalities, and the GGT finding is of unclear significance, but laboratory monitoring is important, Dr. Neogi said. If primary care providers who treat gout cannot routinely measure serum urate and other relevant laboratory measures, they should consider referring patients to a rheumatologist, she added.
Gradual dose escalation meant that patients did not reach the serum urate target until month 7, Dr. Neogi added. “Since the trial was 12 months long, the time over which serum urate was less than 6 mg/dL was not long enough to demonstrate the benefits on flares and tophi,” she said. The open-label extension phase of the trial should shed more insight on these important questions, she added.
For now, providers should know that “patients with gout are not well served if their serum urate levels remain elevated, as that means they are at ongoing risk for flares and tophi,” Dr. Neogi said. “This trial provides evidence and further support for the feasibility, efficacy, and relative safety of escalating allopurinol beyond creatinine-clearance dosing to achieve this important and critical goal for gout management.”
The Health Research Council of New Zealand funded the study. Dr. Stamp and two coinvestigators disclosed grant support from the Health Research Council of New Zealand. Dr. Stamp also disclosed grants from Ardea Biosciences and the Health Research Council of New Zealand outside the submitted work, and her coinvestigators disclosed grants and personal fees from AstraZeneca, Ardea Biosciences, Takeda, and several other pharmaceutical companies. Dr. Neogi had no disclosures. Dr. Saag has received meal compensation from Eli Lilly.
Gradual dose escalation of allopurinol achieved target serum urate levels without causing excess adverse effects in patients with gout who tolerated but responded inadequately to creatinine clearance–based dosing, including in patients with chronic kidney disease, investigators reported in Annals of the Rheumatic Diseases.
The study is the first randomized, controlled trial to examine treat-to-target allopurinol dose escalation in gout. “We believe this approach can be undertaken in all patients who tolerate allopurinol,” lead investigator Lisa Stamp, MD, said in an interview. However, it is important to monitor kidney and liver function.”
To help settle these debates, Dr. Stamp and her associates recruited 183 patients with gout whose serum urate levels averaged 7.15 mg/dL (standard deviation, 1.6 mg/dL) despite at least 1 month of at least a creatinine clearance–based allopurinol dose (average, 269 mg/day). For the next 12 months, patients either continued this dose or increased it monthly until serum urate fell below 6 mg/dL (Ann Rheum Dis. 2017 March 17. doi: 10.1136/annrheumdis-2016-210872).
At month 12, 69% of dose-escalation patients and 32% of controls reached this target (P less than .001; odds ratio, 4.3; 95% confidence interval, 2.4-7.9). Serum urate levels dropped by a mean of 1.5 mg/dL with dose escalation and by 0.34 mg/dL in controls (P less than .001). Thus, dose escalation cut serum urate levels by an additional 1.2 mg/dL (95% CI, 0.67-1.5 mg/dL; P less than .001). The average final daily allopurinol dose was 413 mg (range, 0-900 mg) with dose escalation and 288 mg (0-600 mg) for controls.
Notably, renal function measures did not differ between arms. “There has been long-standing concern about whether it is safe to escalate allopurinol doses in persons with chronic kidney disease,” said Kenneth Saag, MD, of the University of Alabama at Birmingham, who was not involved in the trial. “This study contributes to the limited literature supporting the practice of treating to serum urate targets, even in patients with underlying kidney disease.”
Fully 52% of trial participants had chronic kidney disease, and 44% had tophi. “Thus, our population is representative of people with gout, represents real-life clinical practice, and the results are generalizable to other gout populations,” the investigators wrote.
The findings support the ACR recommendation to gradually titrate urate-lowering therapy while performing close laboratory monitoring, said Tuhina Neogi, MD, of Boston University, who was not involved in the study. This approach is “efficacious and relatively safe for patients who have already tolerated lower doses of allopurinol, but have not yet achieved their serum urate target,” she said. “This is akin to finding the right regimen and titrating doses of medications for patients with diabetes or hypertension in a patient-centered manner.”
Patients in both groups developed mild increases in liver function tests, and a few in the dose escalation group developed more pronounced rises in gamma glutamyl transferase (GGT), as previously reported in the LASSO trial (Semin Arthritis Rheum. 2015 Oct;45[2]:174-83). Allopurinol has been linked to liver enzyme abnormalities, and the GGT finding is of unclear significance, but laboratory monitoring is important, Dr. Neogi said. If primary care providers who treat gout cannot routinely measure serum urate and other relevant laboratory measures, they should consider referring patients to a rheumatologist, she added.
Gradual dose escalation meant that patients did not reach the serum urate target until month 7, Dr. Neogi added. “Since the trial was 12 months long, the time over which serum urate was less than 6 mg/dL was not long enough to demonstrate the benefits on flares and tophi,” she said. The open-label extension phase of the trial should shed more insight on these important questions, she added.
For now, providers should know that “patients with gout are not well served if their serum urate levels remain elevated, as that means they are at ongoing risk for flares and tophi,” Dr. Neogi said. “This trial provides evidence and further support for the feasibility, efficacy, and relative safety of escalating allopurinol beyond creatinine-clearance dosing to achieve this important and critical goal for gout management.”
The Health Research Council of New Zealand funded the study. Dr. Stamp and two coinvestigators disclosed grant support from the Health Research Council of New Zealand. Dr. Stamp also disclosed grants from Ardea Biosciences and the Health Research Council of New Zealand outside the submitted work, and her coinvestigators disclosed grants and personal fees from AstraZeneca, Ardea Biosciences, Takeda, and several other pharmaceutical companies. Dr. Neogi had no disclosures. Dr. Saag has received meal compensation from Eli Lilly.
Gradual dose escalation of allopurinol achieved target serum urate levels without causing excess adverse effects in patients with gout who tolerated but responded inadequately to creatinine clearance–based dosing, including in patients with chronic kidney disease, investigators reported in Annals of the Rheumatic Diseases.
The study is the first randomized, controlled trial to examine treat-to-target allopurinol dose escalation in gout. “We believe this approach can be undertaken in all patients who tolerate allopurinol,” lead investigator Lisa Stamp, MD, said in an interview. However, it is important to monitor kidney and liver function.”
To help settle these debates, Dr. Stamp and her associates recruited 183 patients with gout whose serum urate levels averaged 7.15 mg/dL (standard deviation, 1.6 mg/dL) despite at least 1 month of at least a creatinine clearance–based allopurinol dose (average, 269 mg/day). For the next 12 months, patients either continued this dose or increased it monthly until serum urate fell below 6 mg/dL (Ann Rheum Dis. 2017 March 17. doi: 10.1136/annrheumdis-2016-210872).
At month 12, 69% of dose-escalation patients and 32% of controls reached this target (P less than .001; odds ratio, 4.3; 95% confidence interval, 2.4-7.9). Serum urate levels dropped by a mean of 1.5 mg/dL with dose escalation and by 0.34 mg/dL in controls (P less than .001). Thus, dose escalation cut serum urate levels by an additional 1.2 mg/dL (95% CI, 0.67-1.5 mg/dL; P less than .001). The average final daily allopurinol dose was 413 mg (range, 0-900 mg) with dose escalation and 288 mg (0-600 mg) for controls.
Notably, renal function measures did not differ between arms. “There has been long-standing concern about whether it is safe to escalate allopurinol doses in persons with chronic kidney disease,” said Kenneth Saag, MD, of the University of Alabama at Birmingham, who was not involved in the trial. “This study contributes to the limited literature supporting the practice of treating to serum urate targets, even in patients with underlying kidney disease.”
Fully 52% of trial participants had chronic kidney disease, and 44% had tophi. “Thus, our population is representative of people with gout, represents real-life clinical practice, and the results are generalizable to other gout populations,” the investigators wrote.
The findings support the ACR recommendation to gradually titrate urate-lowering therapy while performing close laboratory monitoring, said Tuhina Neogi, MD, of Boston University, who was not involved in the study. This approach is “efficacious and relatively safe for patients who have already tolerated lower doses of allopurinol, but have not yet achieved their serum urate target,” she said. “This is akin to finding the right regimen and titrating doses of medications for patients with diabetes or hypertension in a patient-centered manner.”
Patients in both groups developed mild increases in liver function tests, and a few in the dose escalation group developed more pronounced rises in gamma glutamyl transferase (GGT), as previously reported in the LASSO trial (Semin Arthritis Rheum. 2015 Oct;45[2]:174-83). Allopurinol has been linked to liver enzyme abnormalities, and the GGT finding is of unclear significance, but laboratory monitoring is important, Dr. Neogi said. If primary care providers who treat gout cannot routinely measure serum urate and other relevant laboratory measures, they should consider referring patients to a rheumatologist, she added.
Gradual dose escalation meant that patients did not reach the serum urate target until month 7, Dr. Neogi added. “Since the trial was 12 months long, the time over which serum urate was less than 6 mg/dL was not long enough to demonstrate the benefits on flares and tophi,” she said. The open-label extension phase of the trial should shed more insight on these important questions, she added.
For now, providers should know that “patients with gout are not well served if their serum urate levels remain elevated, as that means they are at ongoing risk for flares and tophi,” Dr. Neogi said. “This trial provides evidence and further support for the feasibility, efficacy, and relative safety of escalating allopurinol beyond creatinine-clearance dosing to achieve this important and critical goal for gout management.”
The Health Research Council of New Zealand funded the study. Dr. Stamp and two coinvestigators disclosed grant support from the Health Research Council of New Zealand. Dr. Stamp also disclosed grants from Ardea Biosciences and the Health Research Council of New Zealand outside the submitted work, and her coinvestigators disclosed grants and personal fees from AstraZeneca, Ardea Biosciences, Takeda, and several other pharmaceutical companies. Dr. Neogi had no disclosures. Dr. Saag has received meal compensation from Eli Lilly.
FROM ANNALS OF THE RHEUMATIC DISEASES
Key clinical point:
Major finding: At month 12, 69% of dose escalation patients and 32% of controls had serum urate levels below 6 mg/dL (P less than .001). Dose escalation did not increase the risk of serious adverse effects.
Data source: A 12-month, open-label, randomized, controlled, parallel-group, comparative trial of 186 patients with gout.
Disclosures: The Health Research Council of New Zealand funded the study. Dr. Stamp and two coinvestigators disclosed grant support from Health Research Council of New Zealand. Dr. Stamp also disclosed grants from Ardea Biosciences and Health Research Council of New Zealand outside the submitted work, and her coinvestigators disclosed grants and personal fees from AstraZeneca, Ardea Biosciences, Takeda, and several other pharmaceutical companies. Dr. Neogi had no disclosures. Dr. Saag has received meal compensation from Eli Lilly.
Omalizumab effects rapid, often complete, clearance of refractory bullous pemphigoid
ORLANDO – Omalizumab, a monoclonal anti-IgE antibody, may be a good option for patients with treatment-refractory bullous pemphigoid.
Patients who received omalizumab (Xolair) experienced rapid improvements, with 30%-50% lesion clearance within a week and complete clearance by 3 weeks, Kenneth Yu, MD, said at the annual meeting of the American Academy of Dermatology. With regular injections, they were kept symptom free for months. Some patients did flare, but were then easily controlled on standard treatment. Omalizumab, approved by the Food and Drug Administration in 2003, is indicated for moderate to severe persistent asthma and chronic idiopathic urticaria.
“We have now treated six patients with omalizumab with very good results with five of them. These are not your garden-variety BP patients, but people with very treatment-resistant disease who have failed treatment with corticosteroids alone, and in combination with other immunosuppressants.”
The rapid clinical improvements, along with observations that eosinophilia decreased with treatment, “strengthen the evidence that BP is an IgE-mediated, organ-specific autoimmune disease,” said Dr. Yu, senior resident in dermatology at the University of Michigan, Ann Arbor.
“Would I use this as a first-line treatment for BP? Probably not. But if you are seeing someone who’s nonresponsive to therapy, you might want to check IgE and eosinophil levels and if those are elevated, you might consider omalizumab as an adjunct treatment – and you might observe a fairly dramatic response.”
Three of Dr. Yu’s patients received omalizumab as monotherapy, and three received it in conjunction with other immunosuppressants. He described their disease presentation, treatment, and progression.
In general, Dr. Yu reserves omalizumab for patients with refractory disease and two particular clinical characteristics: high eosinophil count and elevated serum IgE. The initial dosing is based on the asthma treatment nomogram for the drug; he titrates it according to clinical response. “We don’t alter the total dose given, but we do adjust the frequency with which we give it.”
His first patient was a 70-year-old woman with a 1-year history of poorly controlled BP; she had failed prednisone, azathioprine, and minocycline. She also had a history of steroid-related vertebral compression fractures. She presented with an eosinophil count of over 400 cells/microL.
“We treated her with subcutaneous injections of 300 mg every 2 weeks for 16 weeks,” Dr. Yu said. Within 1 week, she had a 44% reduction in blisters; within 4 weeks, she had gone from 50% body surface area involvement to 5%.
After eight injections, the patient was disease free and Dr. Yu discontinued treatment. She remained clear until week 32 after treatment initiation; she had a flare manifested by increased pruritus and recurrence of lesions. Dr. Yu restarted omalizumab and the lesions cleared within 2 weeks. From weeks 35-72, the patient received five more injections and remained disease free.
“After that, she did have another flare, so we used omalizumab again,” but without the same excellent results. “She had an initial decrease in pruritus, and symptom improvement, but her disease subsequently worsened. We restarted her on prednisone and azathioprine and she has done well.”
Dr. Yu said he made “a couple of interesting observations on this case.”
“We saw no real correlation between disease activity score, and the levels of serum IgG antibodies. But we did notice a parallel correlation with the level of eosinophil and disease severity and also treatment response,” he said. “It was quite clear that immediately after injection, she had a dramatic drop in eosinophils” from 1,600 to 60 cells/microL within 24 hours.
His next case was a 72-year-old woman with a history of somewhat controlled essential tremor, and 6 months of highly pruritic BP blistering. She had been treated with 60 mg/day prednisone, but didn’t tolerate it well, developing steroid-induced psychosis with agitation and violence, and a worsening of her tremor. The steroid was tapered to 40 mg/day and azathioprine was added, but she was did not respond to this change and continued to develop new blisters each day. She was admitted to the hospital for plasmapheresis, which was not helpful. Nor did she respond to six cycles of cyclophosphamide.
At that point, Dr. Yu drew IgE and eosinophil levels: Her absolute eosinophil count was 1,600 cells/microL and IgE was 287 units/mL. He then gave the patient 300 mg omalizumab subcutaneously.
“Ten days after a single injection, her blisters had almost completely resolved,” he said. “To briefly describe her disease course, the blisters went away, and she had resolution of her pruritus. She was discharged with 1 month of prednisone, but we tapered that and have been able to maintain her on omalizumab alone. She had one mild flare, which was readily controlled with prednisone. The last time we saw her, she was disease free.”
He also described four other steroid-refractory BP patients treated with omalizumab.“Their commonalities were that they all had steroid-refractory disease that was resistant to immunosuppressants, had a high level of IgE, and most of them also had eosinophilia.”
Dr. Yu’s descriptions:
• A 78-year-old woman with refractory BP of 1.5 years responded well to three initial injections spaced 6 and 4 weeks apart, and has been well maintained for 20 months with 300-mL injections administered once a month. One relapse was easily controlled.
• A 72-year-old woman with 3.5 years of refractory BP responded well to 375 mg injections every 4 weeks and has been symptom free for a year on that maintenance dose.
• A 55-year-old woman with a 7-month history of refractory BP experienced a 30% reduction in body surface area blistering within 1 week of her first 375-mg injection. By 3 weeks, she was clear. She had three injections, 2 weeks apart, and was disease free for 3 months.
• An 86-year-old woman with longstanding refractory BP experienced a 22% reduction in blister count within a week of her first 375-mL injection. After a series of injections every 2 weeks, however, she developed an exacerbation of her preexisting chronic obstructive pulmonary disease, which was due primarily to tapering her prednisone. However, she no longer uses omalizumab.
“It is difficult to make recommendations because of the limitations of our data,” Dr. Yu said. “But based on the small number of patients we have treated, I would consider using omalizumab in patients with resistant disease who have an elevated IgE and eosinophil count. The optimal dosing regimen is not yet determined. Our approach is to start out with the asthma dosing and titrate until we see improvement. We use the highest dose indicated for the patient’s weight and IgE levels, typically 300-375 mg subcutaneously every 2-8 weeks, and start tapering when the patient gets control.”
He had no financial disclosures.
[email protected]
On Twitter @Alz_Gal
ORLANDO – Omalizumab, a monoclonal anti-IgE antibody, may be a good option for patients with treatment-refractory bullous pemphigoid.
Patients who received omalizumab (Xolair) experienced rapid improvements, with 30%-50% lesion clearance within a week and complete clearance by 3 weeks, Kenneth Yu, MD, said at the annual meeting of the American Academy of Dermatology. With regular injections, they were kept symptom free for months. Some patients did flare, but were then easily controlled on standard treatment. Omalizumab, approved by the Food and Drug Administration in 2003, is indicated for moderate to severe persistent asthma and chronic idiopathic urticaria.
“We have now treated six patients with omalizumab with very good results with five of them. These are not your garden-variety BP patients, but people with very treatment-resistant disease who have failed treatment with corticosteroids alone, and in combination with other immunosuppressants.”
The rapid clinical improvements, along with observations that eosinophilia decreased with treatment, “strengthen the evidence that BP is an IgE-mediated, organ-specific autoimmune disease,” said Dr. Yu, senior resident in dermatology at the University of Michigan, Ann Arbor.
“Would I use this as a first-line treatment for BP? Probably not. But if you are seeing someone who’s nonresponsive to therapy, you might want to check IgE and eosinophil levels and if those are elevated, you might consider omalizumab as an adjunct treatment – and you might observe a fairly dramatic response.”
Three of Dr. Yu’s patients received omalizumab as monotherapy, and three received it in conjunction with other immunosuppressants. He described their disease presentation, treatment, and progression.
In general, Dr. Yu reserves omalizumab for patients with refractory disease and two particular clinical characteristics: high eosinophil count and elevated serum IgE. The initial dosing is based on the asthma treatment nomogram for the drug; he titrates it according to clinical response. “We don’t alter the total dose given, but we do adjust the frequency with which we give it.”
His first patient was a 70-year-old woman with a 1-year history of poorly controlled BP; she had failed prednisone, azathioprine, and minocycline. She also had a history of steroid-related vertebral compression fractures. She presented with an eosinophil count of over 400 cells/microL.
“We treated her with subcutaneous injections of 300 mg every 2 weeks for 16 weeks,” Dr. Yu said. Within 1 week, she had a 44% reduction in blisters; within 4 weeks, she had gone from 50% body surface area involvement to 5%.
After eight injections, the patient was disease free and Dr. Yu discontinued treatment. She remained clear until week 32 after treatment initiation; she had a flare manifested by increased pruritus and recurrence of lesions. Dr. Yu restarted omalizumab and the lesions cleared within 2 weeks. From weeks 35-72, the patient received five more injections and remained disease free.
“After that, she did have another flare, so we used omalizumab again,” but without the same excellent results. “She had an initial decrease in pruritus, and symptom improvement, but her disease subsequently worsened. We restarted her on prednisone and azathioprine and she has done well.”
Dr. Yu said he made “a couple of interesting observations on this case.”
“We saw no real correlation between disease activity score, and the levels of serum IgG antibodies. But we did notice a parallel correlation with the level of eosinophil and disease severity and also treatment response,” he said. “It was quite clear that immediately after injection, she had a dramatic drop in eosinophils” from 1,600 to 60 cells/microL within 24 hours.
His next case was a 72-year-old woman with a history of somewhat controlled essential tremor, and 6 months of highly pruritic BP blistering. She had been treated with 60 mg/day prednisone, but didn’t tolerate it well, developing steroid-induced psychosis with agitation and violence, and a worsening of her tremor. The steroid was tapered to 40 mg/day and azathioprine was added, but she was did not respond to this change and continued to develop new blisters each day. She was admitted to the hospital for plasmapheresis, which was not helpful. Nor did she respond to six cycles of cyclophosphamide.
At that point, Dr. Yu drew IgE and eosinophil levels: Her absolute eosinophil count was 1,600 cells/microL and IgE was 287 units/mL. He then gave the patient 300 mg omalizumab subcutaneously.
“Ten days after a single injection, her blisters had almost completely resolved,” he said. “To briefly describe her disease course, the blisters went away, and she had resolution of her pruritus. She was discharged with 1 month of prednisone, but we tapered that and have been able to maintain her on omalizumab alone. She had one mild flare, which was readily controlled with prednisone. The last time we saw her, she was disease free.”
He also described four other steroid-refractory BP patients treated with omalizumab.“Their commonalities were that they all had steroid-refractory disease that was resistant to immunosuppressants, had a high level of IgE, and most of them also had eosinophilia.”
Dr. Yu’s descriptions:
• A 78-year-old woman with refractory BP of 1.5 years responded well to three initial injections spaced 6 and 4 weeks apart, and has been well maintained for 20 months with 300-mL injections administered once a month. One relapse was easily controlled.
• A 72-year-old woman with 3.5 years of refractory BP responded well to 375 mg injections every 4 weeks and has been symptom free for a year on that maintenance dose.
• A 55-year-old woman with a 7-month history of refractory BP experienced a 30% reduction in body surface area blistering within 1 week of her first 375-mg injection. By 3 weeks, she was clear. She had three injections, 2 weeks apart, and was disease free for 3 months.
• An 86-year-old woman with longstanding refractory BP experienced a 22% reduction in blister count within a week of her first 375-mL injection. After a series of injections every 2 weeks, however, she developed an exacerbation of her preexisting chronic obstructive pulmonary disease, which was due primarily to tapering her prednisone. However, she no longer uses omalizumab.
“It is difficult to make recommendations because of the limitations of our data,” Dr. Yu said. “But based on the small number of patients we have treated, I would consider using omalizumab in patients with resistant disease who have an elevated IgE and eosinophil count. The optimal dosing regimen is not yet determined. Our approach is to start out with the asthma dosing and titrate until we see improvement. We use the highest dose indicated for the patient’s weight and IgE levels, typically 300-375 mg subcutaneously every 2-8 weeks, and start tapering when the patient gets control.”
He had no financial disclosures.
[email protected]
On Twitter @Alz_Gal
ORLANDO – Omalizumab, a monoclonal anti-IgE antibody, may be a good option for patients with treatment-refractory bullous pemphigoid.
Patients who received omalizumab (Xolair) experienced rapid improvements, with 30%-50% lesion clearance within a week and complete clearance by 3 weeks, Kenneth Yu, MD, said at the annual meeting of the American Academy of Dermatology. With regular injections, they were kept symptom free for months. Some patients did flare, but were then easily controlled on standard treatment. Omalizumab, approved by the Food and Drug Administration in 2003, is indicated for moderate to severe persistent asthma and chronic idiopathic urticaria.
“We have now treated six patients with omalizumab with very good results with five of them. These are not your garden-variety BP patients, but people with very treatment-resistant disease who have failed treatment with corticosteroids alone, and in combination with other immunosuppressants.”
The rapid clinical improvements, along with observations that eosinophilia decreased with treatment, “strengthen the evidence that BP is an IgE-mediated, organ-specific autoimmune disease,” said Dr. Yu, senior resident in dermatology at the University of Michigan, Ann Arbor.
“Would I use this as a first-line treatment for BP? Probably not. But if you are seeing someone who’s nonresponsive to therapy, you might want to check IgE and eosinophil levels and if those are elevated, you might consider omalizumab as an adjunct treatment – and you might observe a fairly dramatic response.”
Three of Dr. Yu’s patients received omalizumab as monotherapy, and three received it in conjunction with other immunosuppressants. He described their disease presentation, treatment, and progression.
In general, Dr. Yu reserves omalizumab for patients with refractory disease and two particular clinical characteristics: high eosinophil count and elevated serum IgE. The initial dosing is based on the asthma treatment nomogram for the drug; he titrates it according to clinical response. “We don’t alter the total dose given, but we do adjust the frequency with which we give it.”
His first patient was a 70-year-old woman with a 1-year history of poorly controlled BP; she had failed prednisone, azathioprine, and minocycline. She also had a history of steroid-related vertebral compression fractures. She presented with an eosinophil count of over 400 cells/microL.
“We treated her with subcutaneous injections of 300 mg every 2 weeks for 16 weeks,” Dr. Yu said. Within 1 week, she had a 44% reduction in blisters; within 4 weeks, she had gone from 50% body surface area involvement to 5%.
After eight injections, the patient was disease free and Dr. Yu discontinued treatment. She remained clear until week 32 after treatment initiation; she had a flare manifested by increased pruritus and recurrence of lesions. Dr. Yu restarted omalizumab and the lesions cleared within 2 weeks. From weeks 35-72, the patient received five more injections and remained disease free.
“After that, she did have another flare, so we used omalizumab again,” but without the same excellent results. “She had an initial decrease in pruritus, and symptom improvement, but her disease subsequently worsened. We restarted her on prednisone and azathioprine and she has done well.”
Dr. Yu said he made “a couple of interesting observations on this case.”
“We saw no real correlation between disease activity score, and the levels of serum IgG antibodies. But we did notice a parallel correlation with the level of eosinophil and disease severity and also treatment response,” he said. “It was quite clear that immediately after injection, she had a dramatic drop in eosinophils” from 1,600 to 60 cells/microL within 24 hours.
His next case was a 72-year-old woman with a history of somewhat controlled essential tremor, and 6 months of highly pruritic BP blistering. She had been treated with 60 mg/day prednisone, but didn’t tolerate it well, developing steroid-induced psychosis with agitation and violence, and a worsening of her tremor. The steroid was tapered to 40 mg/day and azathioprine was added, but she was did not respond to this change and continued to develop new blisters each day. She was admitted to the hospital for plasmapheresis, which was not helpful. Nor did she respond to six cycles of cyclophosphamide.
At that point, Dr. Yu drew IgE and eosinophil levels: Her absolute eosinophil count was 1,600 cells/microL and IgE was 287 units/mL. He then gave the patient 300 mg omalizumab subcutaneously.
“Ten days after a single injection, her blisters had almost completely resolved,” he said. “To briefly describe her disease course, the blisters went away, and she had resolution of her pruritus. She was discharged with 1 month of prednisone, but we tapered that and have been able to maintain her on omalizumab alone. She had one mild flare, which was readily controlled with prednisone. The last time we saw her, she was disease free.”
He also described four other steroid-refractory BP patients treated with omalizumab.“Their commonalities were that they all had steroid-refractory disease that was resistant to immunosuppressants, had a high level of IgE, and most of them also had eosinophilia.”
Dr. Yu’s descriptions:
• A 78-year-old woman with refractory BP of 1.5 years responded well to three initial injections spaced 6 and 4 weeks apart, and has been well maintained for 20 months with 300-mL injections administered once a month. One relapse was easily controlled.
• A 72-year-old woman with 3.5 years of refractory BP responded well to 375 mg injections every 4 weeks and has been symptom free for a year on that maintenance dose.
• A 55-year-old woman with a 7-month history of refractory BP experienced a 30% reduction in body surface area blistering within 1 week of her first 375-mg injection. By 3 weeks, she was clear. She had three injections, 2 weeks apart, and was disease free for 3 months.
• An 86-year-old woman with longstanding refractory BP experienced a 22% reduction in blister count within a week of her first 375-mL injection. After a series of injections every 2 weeks, however, she developed an exacerbation of her preexisting chronic obstructive pulmonary disease, which was due primarily to tapering her prednisone. However, she no longer uses omalizumab.
“It is difficult to make recommendations because of the limitations of our data,” Dr. Yu said. “But based on the small number of patients we have treated, I would consider using omalizumab in patients with resistant disease who have an elevated IgE and eosinophil count. The optimal dosing regimen is not yet determined. Our approach is to start out with the asthma dosing and titrate until we see improvement. We use the highest dose indicated for the patient’s weight and IgE levels, typically 300-375 mg subcutaneously every 2-8 weeks, and start tapering when the patient gets control.”
He had no financial disclosures.
[email protected]
On Twitter @Alz_Gal
AT AAD 17
Psoriasis Symptoms With the Greatest Impact on Patients
Flaking/scaling and itching, followed by dry cracked skin that may bleed, pain or soreness, and burning/stinging were noted by psoriasis patients as the symptoms with the most significant impact on daily life in a public meeting hosted by the US Food and Drug Administration (FDA) to hear patient perspectives on psoriasis. Approximately 70 psoriasis patients or patient representatives attended the meeting in person and others attended through a live webcast.
More than two-thirds of respondents identified flaking/scaling as one of their most significant symptoms of psoriasis, either localized to psoriasis-prone areas such as the elbows and knees or more widespread. Patients reported that this symptom is constant, leaving them to absentmindedly rub certain areas of the skin.
A similar number of respondents indicated that itching was their most significant symptom. One patient called it “an intense subcutaneous itch… deep down in the skin,” a description that resonated with other patients in the room.
Nearly 40% identified dry cracked skin that may bleed as a significant symptom, noting that areas where skin is thinner are affected more, such as the folds of the body. Patients described this symptom as interrelated with other symptoms such as itching. “The thicker the scales get on my skin, the more they itch, and the more they itch, the more I am likely to scratch them, and the more I scratch them, the more they start to crack, and then more come back and it keeps going and going,” one patient said.
More than one-quarter of respondents indicated that pain, soreness, or burning/stinging were the most significant symptoms. Patients indicated that the stinging/burning was more episodic, while the pain was more constant, with the pain being under the skin.
Triggers of these symptoms included stress (primary trigger), changes in weather, hormonal changes, diet, lotions, prolonged exposure to sunlight, sweat, aging, and other medical conditions.
Dermatologists may use these patient insights to prescribe therapies that target these symptoms.
The psoriasis public meeting in March 2016 was the FDA’s 18th patient-focused drug development meeting. The FDA sought this information to have a greater understanding of the burden of psoriasis on patients and the treatments currently used to treat psoriasis and its symptoms. This information will help guide the FDA as they consider future drug approvals.
Flaking/scaling and itching, followed by dry cracked skin that may bleed, pain or soreness, and burning/stinging were noted by psoriasis patients as the symptoms with the most significant impact on daily life in a public meeting hosted by the US Food and Drug Administration (FDA) to hear patient perspectives on psoriasis. Approximately 70 psoriasis patients or patient representatives attended the meeting in person and others attended through a live webcast.
More than two-thirds of respondents identified flaking/scaling as one of their most significant symptoms of psoriasis, either localized to psoriasis-prone areas such as the elbows and knees or more widespread. Patients reported that this symptom is constant, leaving them to absentmindedly rub certain areas of the skin.
A similar number of respondents indicated that itching was their most significant symptom. One patient called it “an intense subcutaneous itch… deep down in the skin,” a description that resonated with other patients in the room.
Nearly 40% identified dry cracked skin that may bleed as a significant symptom, noting that areas where skin is thinner are affected more, such as the folds of the body. Patients described this symptom as interrelated with other symptoms such as itching. “The thicker the scales get on my skin, the more they itch, and the more they itch, the more I am likely to scratch them, and the more I scratch them, the more they start to crack, and then more come back and it keeps going and going,” one patient said.
More than one-quarter of respondents indicated that pain, soreness, or burning/stinging were the most significant symptoms. Patients indicated that the stinging/burning was more episodic, while the pain was more constant, with the pain being under the skin.
Triggers of these symptoms included stress (primary trigger), changes in weather, hormonal changes, diet, lotions, prolonged exposure to sunlight, sweat, aging, and other medical conditions.
Dermatologists may use these patient insights to prescribe therapies that target these symptoms.
The psoriasis public meeting in March 2016 was the FDA’s 18th patient-focused drug development meeting. The FDA sought this information to have a greater understanding of the burden of psoriasis on patients and the treatments currently used to treat psoriasis and its symptoms. This information will help guide the FDA as they consider future drug approvals.
Flaking/scaling and itching, followed by dry cracked skin that may bleed, pain or soreness, and burning/stinging were noted by psoriasis patients as the symptoms with the most significant impact on daily life in a public meeting hosted by the US Food and Drug Administration (FDA) to hear patient perspectives on psoriasis. Approximately 70 psoriasis patients or patient representatives attended the meeting in person and others attended through a live webcast.
More than two-thirds of respondents identified flaking/scaling as one of their most significant symptoms of psoriasis, either localized to psoriasis-prone areas such as the elbows and knees or more widespread. Patients reported that this symptom is constant, leaving them to absentmindedly rub certain areas of the skin.
A similar number of respondents indicated that itching was their most significant symptom. One patient called it “an intense subcutaneous itch… deep down in the skin,” a description that resonated with other patients in the room.
Nearly 40% identified dry cracked skin that may bleed as a significant symptom, noting that areas where skin is thinner are affected more, such as the folds of the body. Patients described this symptom as interrelated with other symptoms such as itching. “The thicker the scales get on my skin, the more they itch, and the more they itch, the more I am likely to scratch them, and the more I scratch them, the more they start to crack, and then more come back and it keeps going and going,” one patient said.
More than one-quarter of respondents indicated that pain, soreness, or burning/stinging were the most significant symptoms. Patients indicated that the stinging/burning was more episodic, while the pain was more constant, with the pain being under the skin.
Triggers of these symptoms included stress (primary trigger), changes in weather, hormonal changes, diet, lotions, prolonged exposure to sunlight, sweat, aging, and other medical conditions.
Dermatologists may use these patient insights to prescribe therapies that target these symptoms.
The psoriasis public meeting in March 2016 was the FDA’s 18th patient-focused drug development meeting. The FDA sought this information to have a greater understanding of the burden of psoriasis on patients and the treatments currently used to treat psoriasis and its symptoms. This information will help guide the FDA as they consider future drug approvals.
Tocilizumab shows promise for GVHD prevention
ORLANDO – Tocilizumab plus standard immune suppression appears to drive down the risk for graft-versus-host disease (GVHD), according to results from a phase II study of 35 adults undergoing allogeneic stem cell transplants.
The effect was particularly pronounced for prevention of GVHD in the colon, William Drobyski, MD, reported at the combined annual meetings of the Center for International Blood & Marrow Transplant Research and the American Society for Blood and Marrow Transplantation.
The incidence rate of grades II-IV and III-IV acute GVHD was 12% at day 100 in patients given standard prophylaxis of tacrolimus/methotrexate (Tac/MTX) and 3% in patients given Tac/MTX plus 8 mg/kg of tocilizumab (Toc, capped at 800 mg), said Dr. Drobyski of the Medical College of Wisconsin, Milwaukee.
To provide further context to the results, Dr. Drobyski and his colleagues performed a matched case-control analysis using contemporary controls in the Center for International Blood & Marrow Transplant Research from 2000 to 2014. The same eligibility criteria used for the trial were applied to the matched controls except for the use of Tac/MTX as GVHD prophylaxis. Patients were otherwise matched based on age, performance score, disease, and donor type.
The incidence of grades II-IV acute GVHD at day 100 was significantly lower in the Toc/Tac/MTX group than in the Tac/MTX control population (12% vs. 41%). The incidence of grades III-IV acute GVHD was slightly lower with tocilizumab, but the difference between the groups was not statistically significant, Dr. Drobyski said.
The probability of grade II-IV acute GVHD–free survival, which was the primary endpoint of the study, was significantly higher in the Toc/Tac/MTX group (79% vs 52%), he said.
Five patients developed grade 2 acute GVHD of the skin or upper GI tract, and one patient died of grade 4 acute GVHD of the skin in the first 100 days. Notably, there were no cases of acute GVHD of the lower GI tract during that time, although two cases did occur between days 130 and 180, he said.
“There was no difference in transplant-related mortality, relapse, disease-free survival, or overall survival,” he said, adding that preliminary data suggest there were no differences in chronic GVHD between the groups.
Causes of death also were similar between the two cohorts with respect to disease- and transplant-related complications.
Patients in the tocilizumab study were enrolled between January 2015 and June 2016; the median age was 66 years. Diseases represented in the cohort included de novo acute myeloid leukemia (13 patients), AML (6 patients), chronic myelomonocytic leukemia (6 patients), acute lymphoblastic leukemia (4 patients), myelodysplastic syndrome (3 patients), and T-cell lymphoma, chronic myeloid leukemia, and NK/T cell lymphoma (in 1 patient each). Most patients were classified as high risk (9 patients) or intermediate risk (22 patients) by the disease risk index.
Conditioning was entirely busulfan based. Myeloablative conditioning was with busulfan and cyclophosphamide (Cytoxan) in 5 patients, or fludarabine and 4 days of busulfan in 10 patients, and reduced-intensity conditioning was with fludarabine and 2 days of busulfan in 18 patients. Transplants were with either HLA-matched related or unrelated donor grafts. Most patients (29 of 35) received peripheral stem cell grafts.
Tocilizumab, an interleuken-6 receptor blocker that is approved for treatment of rheumatoid arthritis, was administered after completion of conditioning and on the day prior to stem cell infusion.
In a pilot clinical trial of tocilizumab for the treatment of steroid-resistant acute GVHD in patients who had primarily had lower GI tract disease, “we were able to demonstrate responses in a majority of these patients,” Dr. Drobyski said, noting that a recent study presented at the 2016 annual meeting of the American Society of Hematology also showed efficacy in the treatment of lower tract GI GVHD, “providing evidence that tocilizumab had activity in acute GVHD, and perhaps in the treatment of steroid-refractory lower GI GVHD.”
Elevated IL-6 levels in the peripheral blood are correlated with an increased incidence and severity of GVHD; administration of an anti-IL-6 receptor antibody has been shown in preclinical studies to protect mice from lethal GVHD. The current open-label study was performed to “try to advance this concept” by assessing whether inhibition of IL-6 signaling could also prevent acute GVHD.
The findings confirm those of a 2014 study by Kennedy et al. in Lancet Oncology (2014;15:1451-9), and imply that tocilizumab warrants a randomized trial as prophylaxis for acute GVHD, he concluded.
Dr. Drobyski reported having no disclosures.
ORLANDO – Tocilizumab plus standard immune suppression appears to drive down the risk for graft-versus-host disease (GVHD), according to results from a phase II study of 35 adults undergoing allogeneic stem cell transplants.
The effect was particularly pronounced for prevention of GVHD in the colon, William Drobyski, MD, reported at the combined annual meetings of the Center for International Blood & Marrow Transplant Research and the American Society for Blood and Marrow Transplantation.
The incidence rate of grades II-IV and III-IV acute GVHD was 12% at day 100 in patients given standard prophylaxis of tacrolimus/methotrexate (Tac/MTX) and 3% in patients given Tac/MTX plus 8 mg/kg of tocilizumab (Toc, capped at 800 mg), said Dr. Drobyski of the Medical College of Wisconsin, Milwaukee.
To provide further context to the results, Dr. Drobyski and his colleagues performed a matched case-control analysis using contemporary controls in the Center for International Blood & Marrow Transplant Research from 2000 to 2014. The same eligibility criteria used for the trial were applied to the matched controls except for the use of Tac/MTX as GVHD prophylaxis. Patients were otherwise matched based on age, performance score, disease, and donor type.
The incidence of grades II-IV acute GVHD at day 100 was significantly lower in the Toc/Tac/MTX group than in the Tac/MTX control population (12% vs. 41%). The incidence of grades III-IV acute GVHD was slightly lower with tocilizumab, but the difference between the groups was not statistically significant, Dr. Drobyski said.
The probability of grade II-IV acute GVHD–free survival, which was the primary endpoint of the study, was significantly higher in the Toc/Tac/MTX group (79% vs 52%), he said.
Five patients developed grade 2 acute GVHD of the skin or upper GI tract, and one patient died of grade 4 acute GVHD of the skin in the first 100 days. Notably, there were no cases of acute GVHD of the lower GI tract during that time, although two cases did occur between days 130 and 180, he said.
“There was no difference in transplant-related mortality, relapse, disease-free survival, or overall survival,” he said, adding that preliminary data suggest there were no differences in chronic GVHD between the groups.
Causes of death also were similar between the two cohorts with respect to disease- and transplant-related complications.
Patients in the tocilizumab study were enrolled between January 2015 and June 2016; the median age was 66 years. Diseases represented in the cohort included de novo acute myeloid leukemia (13 patients), AML (6 patients), chronic myelomonocytic leukemia (6 patients), acute lymphoblastic leukemia (4 patients), myelodysplastic syndrome (3 patients), and T-cell lymphoma, chronic myeloid leukemia, and NK/T cell lymphoma (in 1 patient each). Most patients were classified as high risk (9 patients) or intermediate risk (22 patients) by the disease risk index.
Conditioning was entirely busulfan based. Myeloablative conditioning was with busulfan and cyclophosphamide (Cytoxan) in 5 patients, or fludarabine and 4 days of busulfan in 10 patients, and reduced-intensity conditioning was with fludarabine and 2 days of busulfan in 18 patients. Transplants were with either HLA-matched related or unrelated donor grafts. Most patients (29 of 35) received peripheral stem cell grafts.
Tocilizumab, an interleuken-6 receptor blocker that is approved for treatment of rheumatoid arthritis, was administered after completion of conditioning and on the day prior to stem cell infusion.
In a pilot clinical trial of tocilizumab for the treatment of steroid-resistant acute GVHD in patients who had primarily had lower GI tract disease, “we were able to demonstrate responses in a majority of these patients,” Dr. Drobyski said, noting that a recent study presented at the 2016 annual meeting of the American Society of Hematology also showed efficacy in the treatment of lower tract GI GVHD, “providing evidence that tocilizumab had activity in acute GVHD, and perhaps in the treatment of steroid-refractory lower GI GVHD.”
Elevated IL-6 levels in the peripheral blood are correlated with an increased incidence and severity of GVHD; administration of an anti-IL-6 receptor antibody has been shown in preclinical studies to protect mice from lethal GVHD. The current open-label study was performed to “try to advance this concept” by assessing whether inhibition of IL-6 signaling could also prevent acute GVHD.
The findings confirm those of a 2014 study by Kennedy et al. in Lancet Oncology (2014;15:1451-9), and imply that tocilizumab warrants a randomized trial as prophylaxis for acute GVHD, he concluded.
Dr. Drobyski reported having no disclosures.
ORLANDO – Tocilizumab plus standard immune suppression appears to drive down the risk for graft-versus-host disease (GVHD), according to results from a phase II study of 35 adults undergoing allogeneic stem cell transplants.
The effect was particularly pronounced for prevention of GVHD in the colon, William Drobyski, MD, reported at the combined annual meetings of the Center for International Blood & Marrow Transplant Research and the American Society for Blood and Marrow Transplantation.
The incidence rate of grades II-IV and III-IV acute GVHD was 12% at day 100 in patients given standard prophylaxis of tacrolimus/methotrexate (Tac/MTX) and 3% in patients given Tac/MTX plus 8 mg/kg of tocilizumab (Toc, capped at 800 mg), said Dr. Drobyski of the Medical College of Wisconsin, Milwaukee.
To provide further context to the results, Dr. Drobyski and his colleagues performed a matched case-control analysis using contemporary controls in the Center for International Blood & Marrow Transplant Research from 2000 to 2014. The same eligibility criteria used for the trial were applied to the matched controls except for the use of Tac/MTX as GVHD prophylaxis. Patients were otherwise matched based on age, performance score, disease, and donor type.
The incidence of grades II-IV acute GVHD at day 100 was significantly lower in the Toc/Tac/MTX group than in the Tac/MTX control population (12% vs. 41%). The incidence of grades III-IV acute GVHD was slightly lower with tocilizumab, but the difference between the groups was not statistically significant, Dr. Drobyski said.
The probability of grade II-IV acute GVHD–free survival, which was the primary endpoint of the study, was significantly higher in the Toc/Tac/MTX group (79% vs 52%), he said.
Five patients developed grade 2 acute GVHD of the skin or upper GI tract, and one patient died of grade 4 acute GVHD of the skin in the first 100 days. Notably, there were no cases of acute GVHD of the lower GI tract during that time, although two cases did occur between days 130 and 180, he said.
“There was no difference in transplant-related mortality, relapse, disease-free survival, or overall survival,” he said, adding that preliminary data suggest there were no differences in chronic GVHD between the groups.
Causes of death also were similar between the two cohorts with respect to disease- and transplant-related complications.
Patients in the tocilizumab study were enrolled between January 2015 and June 2016; the median age was 66 years. Diseases represented in the cohort included de novo acute myeloid leukemia (13 patients), AML (6 patients), chronic myelomonocytic leukemia (6 patients), acute lymphoblastic leukemia (4 patients), myelodysplastic syndrome (3 patients), and T-cell lymphoma, chronic myeloid leukemia, and NK/T cell lymphoma (in 1 patient each). Most patients were classified as high risk (9 patients) or intermediate risk (22 patients) by the disease risk index.
Conditioning was entirely busulfan based. Myeloablative conditioning was with busulfan and cyclophosphamide (Cytoxan) in 5 patients, or fludarabine and 4 days of busulfan in 10 patients, and reduced-intensity conditioning was with fludarabine and 2 days of busulfan in 18 patients. Transplants were with either HLA-matched related or unrelated donor grafts. Most patients (29 of 35) received peripheral stem cell grafts.
Tocilizumab, an interleuken-6 receptor blocker that is approved for treatment of rheumatoid arthritis, was administered after completion of conditioning and on the day prior to stem cell infusion.
In a pilot clinical trial of tocilizumab for the treatment of steroid-resistant acute GVHD in patients who had primarily had lower GI tract disease, “we were able to demonstrate responses in a majority of these patients,” Dr. Drobyski said, noting that a recent study presented at the 2016 annual meeting of the American Society of Hematology also showed efficacy in the treatment of lower tract GI GVHD, “providing evidence that tocilizumab had activity in acute GVHD, and perhaps in the treatment of steroid-refractory lower GI GVHD.”
Elevated IL-6 levels in the peripheral blood are correlated with an increased incidence and severity of GVHD; administration of an anti-IL-6 receptor antibody has been shown in preclinical studies to protect mice from lethal GVHD. The current open-label study was performed to “try to advance this concept” by assessing whether inhibition of IL-6 signaling could also prevent acute GVHD.
The findings confirm those of a 2014 study by Kennedy et al. in Lancet Oncology (2014;15:1451-9), and imply that tocilizumab warrants a randomized trial as prophylaxis for acute GVHD, he concluded.
Dr. Drobyski reported having no disclosures.
Key clinical point:
Major finding: The probability of grade II-IV acute GVHD-free survival was 79% vs. 52% in the tocilizumab group vs. age-matched controls.
Data source: An open-label phase II study of 35 patients.
Disclosures: Dr. Drobyski reported having no disclosures.
Hepatitis B, C appear to raise Parkinson’s risk
Hepatitis B and C appear to raise the risk of later Parkinson’s disease (PD), according to a report published in Neurology.
The etiology of Parkinson’s disease is complex, and several factors, including environmental toxins and head trauma, have been proposed that may increase risk for the disorder. Two recent epidemiologic studies in Taiwan found an association between hepatitis C and Parkinson’s risk, said Julia Pakpoor, BM BCh, of the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford (England), and her associates.
To further explore that association, the investigators performed a retrospective cohort study using data from National Health Service hospitals across England for 1999-2011. They assessed the risk for developing PD among 21,633 people with hepatitis B, 48,428 with hepatitis C, 6,225 with autoimmune hepatitis, 4,234 with chronic active hepatitis, 19,870 with HIV, and 6,132,124 control subjects with other disorders.
The risk of developing PD was elevated for only 1 or more years following hospitalization for hepatitis B (relative risk, 1.76) or hepatitis C (RR, 1.51). “These findings may be explained by a specific aspect of viral hepatitis (rather than a general hepatic inflammatory process or general use of antivirals), but whether this reflects shared disease mechanisms, shared genetic or environmental susceptibility, sequelae of viral hepatitis per se, or a consequence of treatment remains to be determined,” Dr. Pakpoor and her associates said (Neurology. 2017;88:1-4).
The reason for this association is not yet known. “Neurotropic features of hepatitis C have been described previously and include the potential for cognitive impairment, independent of hepatic encephalopathy. Further, all essential hepatitis C virus receptors have been shown to be expressed on the brain microvascular endothelium. … suggesting one mechanism by which the virus may affect the CNS,” they noted.
In addition, parkinsonism has been described as an adverse effect of treatment with interferon and ribavirin, which are commonly used in hepatitis C infection. Parkinsonism also is known to develop in association with liver cirrhosis, and cirrhosis status was not available for the members of this study cohort.
More studies are needed to confirm this association and verify that it is causal. Such research will also provide insight into pathophysiologic pathways of PD, “which may be important to understanding the development of PD more broadly,” Dr. Pakpoor and her associates said.
The English National Institute for Health Research supported the study. Dr. Pakpoor and her associates reported having no relevant financial disclosures.
The findings presented by Dr. Pakpoor and her associates justify performing deep-sequencing studies in brain tissue samples at autopsy or in cerebrospinal fluid samples from patients with PD, to detect possible links with infectious agents such as viral hepatitis.
However, for any such link to be considered conclusive, future research also must show that direct-acting antiviral therapies for chronic HCV improve PD symptoms, or epidemiology studies must demonstrate a strong association with specific hepatitis virus.
Julian Benito-Leon, MD, PhD, is in the department of neurology at Complutense University Hospital, Madrid. He reported having no relevant financial disclosures. Dr. Benito-Leon made these remarks in an editorial accompanying Dr. Pakpoor’s report (Neurology. 2017;88:1-2).
The findings presented by Dr. Pakpoor and her associates justify performing deep-sequencing studies in brain tissue samples at autopsy or in cerebrospinal fluid samples from patients with PD, to detect possible links with infectious agents such as viral hepatitis.
However, for any such link to be considered conclusive, future research also must show that direct-acting antiviral therapies for chronic HCV improve PD symptoms, or epidemiology studies must demonstrate a strong association with specific hepatitis virus.
Julian Benito-Leon, MD, PhD, is in the department of neurology at Complutense University Hospital, Madrid. He reported having no relevant financial disclosures. Dr. Benito-Leon made these remarks in an editorial accompanying Dr. Pakpoor’s report (Neurology. 2017;88:1-2).
The findings presented by Dr. Pakpoor and her associates justify performing deep-sequencing studies in brain tissue samples at autopsy or in cerebrospinal fluid samples from patients with PD, to detect possible links with infectious agents such as viral hepatitis.
However, for any such link to be considered conclusive, future research also must show that direct-acting antiviral therapies for chronic HCV improve PD symptoms, or epidemiology studies must demonstrate a strong association with specific hepatitis virus.
Julian Benito-Leon, MD, PhD, is in the department of neurology at Complutense University Hospital, Madrid. He reported having no relevant financial disclosures. Dr. Benito-Leon made these remarks in an editorial accompanying Dr. Pakpoor’s report (Neurology. 2017;88:1-2).
Hepatitis B and C appear to raise the risk of later Parkinson’s disease (PD), according to a report published in Neurology.
The etiology of Parkinson’s disease is complex, and several factors, including environmental toxins and head trauma, have been proposed that may increase risk for the disorder. Two recent epidemiologic studies in Taiwan found an association between hepatitis C and Parkinson’s risk, said Julia Pakpoor, BM BCh, of the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford (England), and her associates.
To further explore that association, the investigators performed a retrospective cohort study using data from National Health Service hospitals across England for 1999-2011. They assessed the risk for developing PD among 21,633 people with hepatitis B, 48,428 with hepatitis C, 6,225 with autoimmune hepatitis, 4,234 with chronic active hepatitis, 19,870 with HIV, and 6,132,124 control subjects with other disorders.
The risk of developing PD was elevated for only 1 or more years following hospitalization for hepatitis B (relative risk, 1.76) or hepatitis C (RR, 1.51). “These findings may be explained by a specific aspect of viral hepatitis (rather than a general hepatic inflammatory process or general use of antivirals), but whether this reflects shared disease mechanisms, shared genetic or environmental susceptibility, sequelae of viral hepatitis per se, or a consequence of treatment remains to be determined,” Dr. Pakpoor and her associates said (Neurology. 2017;88:1-4).
The reason for this association is not yet known. “Neurotropic features of hepatitis C have been described previously and include the potential for cognitive impairment, independent of hepatic encephalopathy. Further, all essential hepatitis C virus receptors have been shown to be expressed on the brain microvascular endothelium. … suggesting one mechanism by which the virus may affect the CNS,” they noted.
In addition, parkinsonism has been described as an adverse effect of treatment with interferon and ribavirin, which are commonly used in hepatitis C infection. Parkinsonism also is known to develop in association with liver cirrhosis, and cirrhosis status was not available for the members of this study cohort.
More studies are needed to confirm this association and verify that it is causal. Such research will also provide insight into pathophysiologic pathways of PD, “which may be important to understanding the development of PD more broadly,” Dr. Pakpoor and her associates said.
The English National Institute for Health Research supported the study. Dr. Pakpoor and her associates reported having no relevant financial disclosures.
Hepatitis B and C appear to raise the risk of later Parkinson’s disease (PD), according to a report published in Neurology.
The etiology of Parkinson’s disease is complex, and several factors, including environmental toxins and head trauma, have been proposed that may increase risk for the disorder. Two recent epidemiologic studies in Taiwan found an association between hepatitis C and Parkinson’s risk, said Julia Pakpoor, BM BCh, of the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford (England), and her associates.
To further explore that association, the investigators performed a retrospective cohort study using data from National Health Service hospitals across England for 1999-2011. They assessed the risk for developing PD among 21,633 people with hepatitis B, 48,428 with hepatitis C, 6,225 with autoimmune hepatitis, 4,234 with chronic active hepatitis, 19,870 with HIV, and 6,132,124 control subjects with other disorders.
The risk of developing PD was elevated for only 1 or more years following hospitalization for hepatitis B (relative risk, 1.76) or hepatitis C (RR, 1.51). “These findings may be explained by a specific aspect of viral hepatitis (rather than a general hepatic inflammatory process or general use of antivirals), but whether this reflects shared disease mechanisms, shared genetic or environmental susceptibility, sequelae of viral hepatitis per se, or a consequence of treatment remains to be determined,” Dr. Pakpoor and her associates said (Neurology. 2017;88:1-4).
The reason for this association is not yet known. “Neurotropic features of hepatitis C have been described previously and include the potential for cognitive impairment, independent of hepatic encephalopathy. Further, all essential hepatitis C virus receptors have been shown to be expressed on the brain microvascular endothelium. … suggesting one mechanism by which the virus may affect the CNS,” they noted.
In addition, parkinsonism has been described as an adverse effect of treatment with interferon and ribavirin, which are commonly used in hepatitis C infection. Parkinsonism also is known to develop in association with liver cirrhosis, and cirrhosis status was not available for the members of this study cohort.
More studies are needed to confirm this association and verify that it is causal. Such research will also provide insight into pathophysiologic pathways of PD, “which may be important to understanding the development of PD more broadly,” Dr. Pakpoor and her associates said.
The English National Institute for Health Research supported the study. Dr. Pakpoor and her associates reported having no relevant financial disclosures.
FROM NEUROLOGY
Key clinical point:
Major finding: The risk of developing PD was significantly elevated for only 1 or more years following hospitalization for hepatitis B (RR, 1.76) or hepatitis C (RR, 1.51).
Data source: A retrospective cohort study involving 70,061 people in the general U.K. population with hepatitis B or C, 6,225 with autoimmune hepatitis, 4,234 with chronic active hepatitis, 19,870 with HIV, and 6,132,124 control subjects hospitalized during 1999-2011.
Disclosures: The English National Institute for Health Research supported the study. Dr. Pakpoor and her associates reported having no relevant financial disclosures.
Evolution of a movement
One of the most enduring lessons I have learned during my time in hospital medicine is that hospitalists are always evolving, much like the specialty and healthcare system of which they are a part. And during my time as president of the Society of Hospital Medicine (SHM), I have come to realize how SHM provides its members with the resources to help us continue that evolution through our career journeys as a part of the hospital medicine movement.
Over a year ago, I ascended to president of SHM’s board of directors at HM16, the annual meeting in San Diego. Now, I am eagerly looking forward to HM17 next month, in Las Vegas, which we expect to be, yet again, the biggest, best, most innovative and most energetic gathering of hospitalists. As that meeting will mark the end of my tenure as president of the board, I’m also inclined to look back and survey what has happened over the last year, both personally and professionally.
The personal perspective is easy. I have a different position within my organization: president of Cleveland Clinic Akron General and the Southern Region, one which I would and could never have anticipated a year ago. It challenges, exhausts, exhilarates, and teaches me every day. I am also celebrating my 15th wedding anniversary and have three amazing children who seem to evolve in front of my eyes every day.
And, professionally, at HM16 (and on these pages a year ago), I framed what I felt were four critical directions for SHM and have a few thoughts on the work we have done over the last year.
1. Expand and engage SHM’s membership. SHM continues to be the envy of professional organizations, growing each year. More important than sole growth is our pursuit of connecting hospitalists to SHM’s resources and to each other; we have been incredibly active this past year. For instance, SHM is embarking on an engagement survey of HM groups, and is investing in new technologies to support membership. We are now a CME-accrediting organization and are moving the SHM Learning Portal to a new, enhanced platform. We launched a long-term communications strategy that is tied to engagement and a more nimble and mobile experience for our members. The SHM Leadership Academy sold out. HM17 is poised to be another success. And finally, we are increasingly appreciating that a strong SHM must have a vibrant chapter structure to ensure connections between our membership, staff, and board.
2. Focus on patient- and family-centered care. A look at the HM17 curriculum reinforces SHM’s awareness that patients and hospitalists must be more assertive in developing skills in communication and empathy. By doing so, they support a culture and environment wherein patients are active participants their care. Members of our Patient Experience Committee are presenting courses and workshops in Las Vegas, and last year’s annual meeting featured an entire pre-course on communication skills. Hospitalists play a signature role in the Cleveland Clinic’s national conference on improving the patient experience, and the committee has an advisory council of patients and advocates to guide their work.
3. Move assertively to define our role in an era of risk and reform. Last year’s national election will probably create policy upheavals that are difficult to either anticipate or plan for. However, the evolution of Medicare, Medicaid, and commercial payers toward passing risk (and reward) onto physicians, hospitals, and systems, likely is unstoppable. SHM held a board retreat with key hospital leaders (including Patrick Conway, MD, MSc, MHM, deputy administrator for Innovation and Quality at CMS and director of the Center for Medicare and Medicaid Innovation, and a keynote speaker at HM17) to outline a framework to engage and educate our membership by leveraging the work of our Public Policy, Education, and Practice Management committees.
4. Define our stance regarding specialty recognition: The complexities of this issue are political as well as logistical. SHM has continued to build out the infrastructure for Recognition of Focused Practice with the launch of SPARK ONE (our Focused Practice in Hospital Medicine exam preparation product), but the gaps between the curricula of internal medicine and family medicine residencies, and our daily clinical realities, will continue to exist for the foreseeable future. Pediatrics has established a board requirement for pediatric hospital medicine, but it is still unclear if this is the future of adult hospital medicine.
In sum
As I prepare to the pass to baton to Dr. Ron Greeno for 2017-18, I am reminded of one of the pearls of a former boss and mentor of mine who preached that career satisfaction comes from finding opportunities to achieve three goals: addressing meaningful challenges, working with compelling individuals, and learning something new every day. I would like to thank the board, SHM CEO Larry Wellikson, MD, MHM, and the society staff and volunteers, and, most of all, the many SHM members with whom I have met and spoken over the last year for providing me with exactly that opportunity.
I look forward to continuing to serve an active role in SHM, an organization that can provide you with those same opportunities and resources to help you grow, evolve and be an active participant in the hospital medicine movement.
One of the most enduring lessons I have learned during my time in hospital medicine is that hospitalists are always evolving, much like the specialty and healthcare system of which they are a part. And during my time as president of the Society of Hospital Medicine (SHM), I have come to realize how SHM provides its members with the resources to help us continue that evolution through our career journeys as a part of the hospital medicine movement.
Over a year ago, I ascended to president of SHM’s board of directors at HM16, the annual meeting in San Diego. Now, I am eagerly looking forward to HM17 next month, in Las Vegas, which we expect to be, yet again, the biggest, best, most innovative and most energetic gathering of hospitalists. As that meeting will mark the end of my tenure as president of the board, I’m also inclined to look back and survey what has happened over the last year, both personally and professionally.
The personal perspective is easy. I have a different position within my organization: president of Cleveland Clinic Akron General and the Southern Region, one which I would and could never have anticipated a year ago. It challenges, exhausts, exhilarates, and teaches me every day. I am also celebrating my 15th wedding anniversary and have three amazing children who seem to evolve in front of my eyes every day.
And, professionally, at HM16 (and on these pages a year ago), I framed what I felt were four critical directions for SHM and have a few thoughts on the work we have done over the last year.
1. Expand and engage SHM’s membership. SHM continues to be the envy of professional organizations, growing each year. More important than sole growth is our pursuit of connecting hospitalists to SHM’s resources and to each other; we have been incredibly active this past year. For instance, SHM is embarking on an engagement survey of HM groups, and is investing in new technologies to support membership. We are now a CME-accrediting organization and are moving the SHM Learning Portal to a new, enhanced platform. We launched a long-term communications strategy that is tied to engagement and a more nimble and mobile experience for our members. The SHM Leadership Academy sold out. HM17 is poised to be another success. And finally, we are increasingly appreciating that a strong SHM must have a vibrant chapter structure to ensure connections between our membership, staff, and board.
2. Focus on patient- and family-centered care. A look at the HM17 curriculum reinforces SHM’s awareness that patients and hospitalists must be more assertive in developing skills in communication and empathy. By doing so, they support a culture and environment wherein patients are active participants their care. Members of our Patient Experience Committee are presenting courses and workshops in Las Vegas, and last year’s annual meeting featured an entire pre-course on communication skills. Hospitalists play a signature role in the Cleveland Clinic’s national conference on improving the patient experience, and the committee has an advisory council of patients and advocates to guide their work.
3. Move assertively to define our role in an era of risk and reform. Last year’s national election will probably create policy upheavals that are difficult to either anticipate or plan for. However, the evolution of Medicare, Medicaid, and commercial payers toward passing risk (and reward) onto physicians, hospitals, and systems, likely is unstoppable. SHM held a board retreat with key hospital leaders (including Patrick Conway, MD, MSc, MHM, deputy administrator for Innovation and Quality at CMS and director of the Center for Medicare and Medicaid Innovation, and a keynote speaker at HM17) to outline a framework to engage and educate our membership by leveraging the work of our Public Policy, Education, and Practice Management committees.
4. Define our stance regarding specialty recognition: The complexities of this issue are political as well as logistical. SHM has continued to build out the infrastructure for Recognition of Focused Practice with the launch of SPARK ONE (our Focused Practice in Hospital Medicine exam preparation product), but the gaps between the curricula of internal medicine and family medicine residencies, and our daily clinical realities, will continue to exist for the foreseeable future. Pediatrics has established a board requirement for pediatric hospital medicine, but it is still unclear if this is the future of adult hospital medicine.
In sum
As I prepare to the pass to baton to Dr. Ron Greeno for 2017-18, I am reminded of one of the pearls of a former boss and mentor of mine who preached that career satisfaction comes from finding opportunities to achieve three goals: addressing meaningful challenges, working with compelling individuals, and learning something new every day. I would like to thank the board, SHM CEO Larry Wellikson, MD, MHM, and the society staff and volunteers, and, most of all, the many SHM members with whom I have met and spoken over the last year for providing me with exactly that opportunity.
I look forward to continuing to serve an active role in SHM, an organization that can provide you with those same opportunities and resources to help you grow, evolve and be an active participant in the hospital medicine movement.
One of the most enduring lessons I have learned during my time in hospital medicine is that hospitalists are always evolving, much like the specialty and healthcare system of which they are a part. And during my time as president of the Society of Hospital Medicine (SHM), I have come to realize how SHM provides its members with the resources to help us continue that evolution through our career journeys as a part of the hospital medicine movement.
Over a year ago, I ascended to president of SHM’s board of directors at HM16, the annual meeting in San Diego. Now, I am eagerly looking forward to HM17 next month, in Las Vegas, which we expect to be, yet again, the biggest, best, most innovative and most energetic gathering of hospitalists. As that meeting will mark the end of my tenure as president of the board, I’m also inclined to look back and survey what has happened over the last year, both personally and professionally.
The personal perspective is easy. I have a different position within my organization: president of Cleveland Clinic Akron General and the Southern Region, one which I would and could never have anticipated a year ago. It challenges, exhausts, exhilarates, and teaches me every day. I am also celebrating my 15th wedding anniversary and have three amazing children who seem to evolve in front of my eyes every day.
And, professionally, at HM16 (and on these pages a year ago), I framed what I felt were four critical directions for SHM and have a few thoughts on the work we have done over the last year.
1. Expand and engage SHM’s membership. SHM continues to be the envy of professional organizations, growing each year. More important than sole growth is our pursuit of connecting hospitalists to SHM’s resources and to each other; we have been incredibly active this past year. For instance, SHM is embarking on an engagement survey of HM groups, and is investing in new technologies to support membership. We are now a CME-accrediting organization and are moving the SHM Learning Portal to a new, enhanced platform. We launched a long-term communications strategy that is tied to engagement and a more nimble and mobile experience for our members. The SHM Leadership Academy sold out. HM17 is poised to be another success. And finally, we are increasingly appreciating that a strong SHM must have a vibrant chapter structure to ensure connections between our membership, staff, and board.
2. Focus on patient- and family-centered care. A look at the HM17 curriculum reinforces SHM’s awareness that patients and hospitalists must be more assertive in developing skills in communication and empathy. By doing so, they support a culture and environment wherein patients are active participants their care. Members of our Patient Experience Committee are presenting courses and workshops in Las Vegas, and last year’s annual meeting featured an entire pre-course on communication skills. Hospitalists play a signature role in the Cleveland Clinic’s national conference on improving the patient experience, and the committee has an advisory council of patients and advocates to guide their work.
3. Move assertively to define our role in an era of risk and reform. Last year’s national election will probably create policy upheavals that are difficult to either anticipate or plan for. However, the evolution of Medicare, Medicaid, and commercial payers toward passing risk (and reward) onto physicians, hospitals, and systems, likely is unstoppable. SHM held a board retreat with key hospital leaders (including Patrick Conway, MD, MSc, MHM, deputy administrator for Innovation and Quality at CMS and director of the Center for Medicare and Medicaid Innovation, and a keynote speaker at HM17) to outline a framework to engage and educate our membership by leveraging the work of our Public Policy, Education, and Practice Management committees.
4. Define our stance regarding specialty recognition: The complexities of this issue are political as well as logistical. SHM has continued to build out the infrastructure for Recognition of Focused Practice with the launch of SPARK ONE (our Focused Practice in Hospital Medicine exam preparation product), but the gaps between the curricula of internal medicine and family medicine residencies, and our daily clinical realities, will continue to exist for the foreseeable future. Pediatrics has established a board requirement for pediatric hospital medicine, but it is still unclear if this is the future of adult hospital medicine.
In sum
As I prepare to the pass to baton to Dr. Ron Greeno for 2017-18, I am reminded of one of the pearls of a former boss and mentor of mine who preached that career satisfaction comes from finding opportunities to achieve three goals: addressing meaningful challenges, working with compelling individuals, and learning something new every day. I would like to thank the board, SHM CEO Larry Wellikson, MD, MHM, and the society staff and volunteers, and, most of all, the many SHM members with whom I have met and spoken over the last year for providing me with exactly that opportunity.
I look forward to continuing to serve an active role in SHM, an organization that can provide you with those same opportunities and resources to help you grow, evolve and be an active participant in the hospital medicine movement.
In an uncertain health care climate, will you advocate for women's health outside your office?
In her February 2017 article, Lucia DiVenere interviewed the current and incoming ACOG Presidents, Drs. Thomas Gellhaus and Haywood Brown. The Presidents called for advocacy on behalf of the “melting pot” of women’s health specialists and subspecialists. “We cannot sit on the sidelines and expect others to speak for us,” said Dr. Gellhaus. “If we are not part of the solution, then we need to cede our future to others and have no right to complain about the result. Our members need to commit to advocating outside their exam rooms.”
Answer the poll below:
[polldaddy:9703185]
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
In her February 2017 article, Lucia DiVenere interviewed the current and incoming ACOG Presidents, Drs. Thomas Gellhaus and Haywood Brown. The Presidents called for advocacy on behalf of the “melting pot” of women’s health specialists and subspecialists. “We cannot sit on the sidelines and expect others to speak for us,” said Dr. Gellhaus. “If we are not part of the solution, then we need to cede our future to others and have no right to complain about the result. Our members need to commit to advocating outside their exam rooms.”
Answer the poll below:
[polldaddy:9703185]
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
In her February 2017 article, Lucia DiVenere interviewed the current and incoming ACOG Presidents, Drs. Thomas Gellhaus and Haywood Brown. The Presidents called for advocacy on behalf of the “melting pot” of women’s health specialists and subspecialists. “We cannot sit on the sidelines and expect others to speak for us,” said Dr. Gellhaus. “If we are not part of the solution, then we need to cede our future to others and have no right to complain about the result. Our members need to commit to advocating outside their exam rooms.”
Answer the poll below:
[polldaddy:9703185]
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Diagnosing Gastric Plasmacytoma
Extramedullary plasmacytomas are rare ( > 5% of all plasma cell neoplasms), and the gastric version is even more rare. That rarity combined with unspecific symptoms that mimic other tumors “can mislead the clinician into a diagnosis of a more aggressive tumor,” say clinicians from University Hospital Center of Coimbra in Portugal. They reported on a patient who presented that diagnostic puzzle.
The patient arrived in the emergency department with symptoms of upper gastrointestinal bleeding. He had a history of tongue carcinoma, cirrhosis, diabetes mellitus, chronic gastritis, and obesity, among other health conditions, and was taking a panoply of medications. The patient’s family history included a grandmother with breast cancer and an aunt with head and neck cancer.
Related: Treatment and Management of Multiple Myeloma
The clinicians embarked on an extensive diagnostic process of elimination. Endoscopy, immunohistochemistry, and other tests helped rule out Helicobacter pylori infection, lymphoma, carcinoma, melanoma, and neuroendocrine carcinoma. “Rethinking our possibilities,” the clinicians say, and taking into account the presence of mature and immature plasmocytes in the periphery, they next considered plasmacytoma/multiple myeloma (MM). On the third immunohistochemical panel, they got the evidence they needed for the diagnosis: gastric plasmacytoma (GP)/ involvement by MM.
Gastric plasmacytomas have a good prognosis. Surgical excision normally is the treatment of choice with good results, the clinicians say. After endoscopic polypectomy without radiation, the patient was discharged with no further therapy. Although diagnosed with prostate cancer in the 6 years following, the patient has had no signs of plasmacytic relapse.
Related: Rare Cancer Gets Timely Right Treatment
Due to their cellular similarity, GP needs to be differentiated from MM. But GP may be the initial manifestation of a MM, the clinicians note. Therefore, the patient must undergo systemic evaluation to exclude bone marrow involvement and to make sure there is no clinical or laboratory evidence of myeloma.
Sources:
1. Oliveira RC, Amaro P, Julião MJ, Cipriano MA. BMJ Case Rep. 2017. pii: bcr2016218967.
doi: 10.1136/bcr-2016-218967.
2. International Myeloma Working Group. Br J Haematol. 2003;12(5):749-57.
doi: 10.1046/j.1365-2141.2003.04355.x
3. Kilciksiz S, Karakoyun-Celik O, Agaoglu FY, Haydaroglu A. A review for solitary
plasmacytoma of bone and extramedullary plasmacytoma. Sci World J. 2012;2012:895765.
doi: 10.1100/2012/895765.
Extramedullary plasmacytomas are rare ( > 5% of all plasma cell neoplasms), and the gastric version is even more rare. That rarity combined with unspecific symptoms that mimic other tumors “can mislead the clinician into a diagnosis of a more aggressive tumor,” say clinicians from University Hospital Center of Coimbra in Portugal. They reported on a patient who presented that diagnostic puzzle.
The patient arrived in the emergency department with symptoms of upper gastrointestinal bleeding. He had a history of tongue carcinoma, cirrhosis, diabetes mellitus, chronic gastritis, and obesity, among other health conditions, and was taking a panoply of medications. The patient’s family history included a grandmother with breast cancer and an aunt with head and neck cancer.
Related: Treatment and Management of Multiple Myeloma
The clinicians embarked on an extensive diagnostic process of elimination. Endoscopy, immunohistochemistry, and other tests helped rule out Helicobacter pylori infection, lymphoma, carcinoma, melanoma, and neuroendocrine carcinoma. “Rethinking our possibilities,” the clinicians say, and taking into account the presence of mature and immature plasmocytes in the periphery, they next considered plasmacytoma/multiple myeloma (MM). On the third immunohistochemical panel, they got the evidence they needed for the diagnosis: gastric plasmacytoma (GP)/ involvement by MM.
Gastric plasmacytomas have a good prognosis. Surgical excision normally is the treatment of choice with good results, the clinicians say. After endoscopic polypectomy without radiation, the patient was discharged with no further therapy. Although diagnosed with prostate cancer in the 6 years following, the patient has had no signs of plasmacytic relapse.
Related: Rare Cancer Gets Timely Right Treatment
Due to their cellular similarity, GP needs to be differentiated from MM. But GP may be the initial manifestation of a MM, the clinicians note. Therefore, the patient must undergo systemic evaluation to exclude bone marrow involvement and to make sure there is no clinical or laboratory evidence of myeloma.
Sources:
1. Oliveira RC, Amaro P, Julião MJ, Cipriano MA. BMJ Case Rep. 2017. pii: bcr2016218967.
doi: 10.1136/bcr-2016-218967.
2. International Myeloma Working Group. Br J Haematol. 2003;12(5):749-57.
doi: 10.1046/j.1365-2141.2003.04355.x
3. Kilciksiz S, Karakoyun-Celik O, Agaoglu FY, Haydaroglu A. A review for solitary
plasmacytoma of bone and extramedullary plasmacytoma. Sci World J. 2012;2012:895765.
doi: 10.1100/2012/895765.
Extramedullary plasmacytomas are rare ( > 5% of all plasma cell neoplasms), and the gastric version is even more rare. That rarity combined with unspecific symptoms that mimic other tumors “can mislead the clinician into a diagnosis of a more aggressive tumor,” say clinicians from University Hospital Center of Coimbra in Portugal. They reported on a patient who presented that diagnostic puzzle.
The patient arrived in the emergency department with symptoms of upper gastrointestinal bleeding. He had a history of tongue carcinoma, cirrhosis, diabetes mellitus, chronic gastritis, and obesity, among other health conditions, and was taking a panoply of medications. The patient’s family history included a grandmother with breast cancer and an aunt with head and neck cancer.
Related: Treatment and Management of Multiple Myeloma
The clinicians embarked on an extensive diagnostic process of elimination. Endoscopy, immunohistochemistry, and other tests helped rule out Helicobacter pylori infection, lymphoma, carcinoma, melanoma, and neuroendocrine carcinoma. “Rethinking our possibilities,” the clinicians say, and taking into account the presence of mature and immature plasmocytes in the periphery, they next considered plasmacytoma/multiple myeloma (MM). On the third immunohistochemical panel, they got the evidence they needed for the diagnosis: gastric plasmacytoma (GP)/ involvement by MM.
Gastric plasmacytomas have a good prognosis. Surgical excision normally is the treatment of choice with good results, the clinicians say. After endoscopic polypectomy without radiation, the patient was discharged with no further therapy. Although diagnosed with prostate cancer in the 6 years following, the patient has had no signs of plasmacytic relapse.
Related: Rare Cancer Gets Timely Right Treatment
Due to their cellular similarity, GP needs to be differentiated from MM. But GP may be the initial manifestation of a MM, the clinicians note. Therefore, the patient must undergo systemic evaluation to exclude bone marrow involvement and to make sure there is no clinical or laboratory evidence of myeloma.
Sources:
1. Oliveira RC, Amaro P, Julião MJ, Cipriano MA. BMJ Case Rep. 2017. pii: bcr2016218967.
doi: 10.1136/bcr-2016-218967.
2. International Myeloma Working Group. Br J Haematol. 2003;12(5):749-57.
doi: 10.1046/j.1365-2141.2003.04355.x
3. Kilciksiz S, Karakoyun-Celik O, Agaoglu FY, Haydaroglu A. A review for solitary
plasmacytoma of bone and extramedullary plasmacytoma. Sci World J. 2012;2012:895765.
doi: 10.1100/2012/895765.
Reusing Syringes: Not Safe, Not Cost-Effective
In 2015, the Texas Department of State Health Services was notified that a hospital telemetry unit nurse had been reusing saline flush prefilled syringes in patients’ IV lines. Mistakenly believing that it was safe and that she was saving the hospital money, she had been reusing syringes for 6 months. This was not the hospital’s practice.
Because she had been putting patients at risk for bloodborne pathogens, the state, regional, and local health departments with consultation from the CDC worked with the hospital to investigate. The hospital notified 392 patients, advising them of potential exposure and offering them free testing for hepatitis B (HBV), hepatitis C (HCV), and HIV. A year after the exposure, 262 had completed initial screening and 182 had completed all recommended testing.
Two patients had newly diagnosed HBV and 2 had HCV. A patient with known preexisting chronic HCV infection had been hospitalized on the telemetry unit on the same day as one of the patients with newly diagnosed HCV. That second patient did not share overlapping days with any patient with known HCV infection, nor did the 2 with newly diagnosed HBV infection share with each other or any other patient with a known HBV infection. No epidemiologic evidence linked the patients with newly diagnosed infections to a potential source patient. But when specimens were tested, the results indicated transmission linkage between the patient with chronic HCV infection and one of the patients with newly diagnosed HCV infection.
Taken together, the CDC concluded, the findings indicated that at least 1 HCV infection was “likely transmitted” in the telemetry unit as a result of the inappropriate reuse and sharing of syringes. The investigation, the CDC adds, illustrates a need for ongoing education and oversight of health care providers regarding safe injection practices.
In 2015, the Texas Department of State Health Services was notified that a hospital telemetry unit nurse had been reusing saline flush prefilled syringes in patients’ IV lines. Mistakenly believing that it was safe and that she was saving the hospital money, she had been reusing syringes for 6 months. This was not the hospital’s practice.
Because she had been putting patients at risk for bloodborne pathogens, the state, regional, and local health departments with consultation from the CDC worked with the hospital to investigate. The hospital notified 392 patients, advising them of potential exposure and offering them free testing for hepatitis B (HBV), hepatitis C (HCV), and HIV. A year after the exposure, 262 had completed initial screening and 182 had completed all recommended testing.
Two patients had newly diagnosed HBV and 2 had HCV. A patient with known preexisting chronic HCV infection had been hospitalized on the telemetry unit on the same day as one of the patients with newly diagnosed HCV. That second patient did not share overlapping days with any patient with known HCV infection, nor did the 2 with newly diagnosed HBV infection share with each other or any other patient with a known HBV infection. No epidemiologic evidence linked the patients with newly diagnosed infections to a potential source patient. But when specimens were tested, the results indicated transmission linkage between the patient with chronic HCV infection and one of the patients with newly diagnosed HCV infection.
Taken together, the CDC concluded, the findings indicated that at least 1 HCV infection was “likely transmitted” in the telemetry unit as a result of the inappropriate reuse and sharing of syringes. The investigation, the CDC adds, illustrates a need for ongoing education and oversight of health care providers regarding safe injection practices.
In 2015, the Texas Department of State Health Services was notified that a hospital telemetry unit nurse had been reusing saline flush prefilled syringes in patients’ IV lines. Mistakenly believing that it was safe and that she was saving the hospital money, she had been reusing syringes for 6 months. This was not the hospital’s practice.
Because she had been putting patients at risk for bloodborne pathogens, the state, regional, and local health departments with consultation from the CDC worked with the hospital to investigate. The hospital notified 392 patients, advising them of potential exposure and offering them free testing for hepatitis B (HBV), hepatitis C (HCV), and HIV. A year after the exposure, 262 had completed initial screening and 182 had completed all recommended testing.
Two patients had newly diagnosed HBV and 2 had HCV. A patient with known preexisting chronic HCV infection had been hospitalized on the telemetry unit on the same day as one of the patients with newly diagnosed HCV. That second patient did not share overlapping days with any patient with known HCV infection, nor did the 2 with newly diagnosed HBV infection share with each other or any other patient with a known HBV infection. No epidemiologic evidence linked the patients with newly diagnosed infections to a potential source patient. But when specimens were tested, the results indicated transmission linkage between the patient with chronic HCV infection and one of the patients with newly diagnosed HCV infection.
Taken together, the CDC concluded, the findings indicated that at least 1 HCV infection was “likely transmitted” in the telemetry unit as a result of the inappropriate reuse and sharing of syringes. The investigation, the CDC adds, illustrates a need for ongoing education and oversight of health care providers regarding safe injection practices.