Blood donation

Photo by Marja Helander

Canadian Blood Services has made several changes to its blood donor policies in an attempt to broaden the pool of eligible donors in the country.

The agency has eliminated the upper age limit for donating blood, and donors over the age of 71 no longer need to have their physician fill out an assessment form before donating.

People with a history of most cancers are now eligible to donate blood if they have been cancer-free for 5 years.

However, this change does not apply to those with a history of hematologic malignancies.

People who have recently received most vaccines, such as a flu shot, will no longer need to wait 2 days before donating blood.

People who were born in or lived in some African countries (Central African Republic, Chad, Congo, Equatorial Guinea, Gabon, Niger, and Nigeria) are now eligible to donate blood. According to Canadian Blood Services, HIV testing performed on blood donors can now detect HIV strains found in these countries.

Canadian Blood Services has also revised geographic deferrals affecting Western Europe based on scientific evidence that indicates the risk of variant Creutzfeldt-Jakob disease has decreased since January 2008.

People who spent 5 years or more in Western Europe since 1980 are deferred from donating blood, but Canadian Blood Services is now including an end date of 2007. People who reached the 5-year limit in Western Europe after 2007 are now eligible to donate.

“Canadian Blood Services regularly reviews the criteria used to determine if someone is eligible to donate blood, including geographic and age restrictions, based on new scientific information,” said Mindy Goldman, medical director of donor and clinical services with Canadian Blood Services.

“These restrictions are no longer necessary. We estimate that about 3000 people who try to donate each year but cannot will now be eligible to donate due to these changes.”

The complete policy changes are available at www.blood.ca/en/blood/recent-changes-donation-criteria.

Blood donation

Photo by Marja Helander

Canadian Blood Services has made several changes to its blood donor policies in an attempt to broaden the pool of eligible donors in the country.

The agency has eliminated the upper age limit for donating blood, and donors over the age of 71 no longer need to have their physician fill out an assessment form before donating.

People with a history of most cancers are now eligible to donate blood if they have been cancer-free for 5 years.

However, this change does not apply to those with a history of hematologic malignancies.

People who have recently received most vaccines, such as a flu shot, will no longer need to wait 2 days before donating blood.

People who were born in or lived in some African countries (Central African Republic, Chad, Congo, Equatorial Guinea, Gabon, Niger, and Nigeria) are now eligible to donate blood. According to Canadian Blood Services, HIV testing performed on blood donors can now detect HIV strains found in these countries.

Canadian Blood Services has also revised geographic deferrals affecting Western Europe based on scientific evidence that indicates the risk of variant Creutzfeldt-Jakob disease has decreased since January 2008.

People who spent 5 years or more in Western Europe since 1980 are deferred from donating blood, but Canadian Blood Services is now including an end date of 2007. People who reached the 5-year limit in Western Europe after 2007 are now eligible to donate.

“Canadian Blood Services regularly reviews the criteria used to determine if someone is eligible to donate blood, including geographic and age restrictions, based on new scientific information,” said Mindy Goldman, medical director of donor and clinical services with Canadian Blood Services.

“These restrictions are no longer necessary. We estimate that about 3000 people who try to donate each year but cannot will now be eligible to donate due to these changes.”

The complete policy changes are available at www.blood.ca/en/blood/recent-changes-donation-criteria.

Blood donation

Photo by Marja Helander

Canadian Blood Services has made several changes to its blood donor policies in an attempt to broaden the pool of eligible donors in the country.

The agency has eliminated the upper age limit for donating blood, and donors over the age of 71 no longer need to have their physician fill out an assessment form before donating.

People with a history of most cancers are now eligible to donate blood if they have been cancer-free for 5 years.

However, this change does not apply to those with a history of hematologic malignancies.

People who have recently received most vaccines, such as a flu shot, will no longer need to wait 2 days before donating blood.

People who were born in or lived in some African countries (Central African Republic, Chad, Congo, Equatorial Guinea, Gabon, Niger, and Nigeria) are now eligible to donate blood. According to Canadian Blood Services, HIV testing performed on blood donors can now detect HIV strains found in these countries.

Canadian Blood Services has also revised geographic deferrals affecting Western Europe based on scientific evidence that indicates the risk of variant Creutzfeldt-Jakob disease has decreased since January 2008.

People who spent 5 years or more in Western Europe since 1980 are deferred from donating blood, but Canadian Blood Services is now including an end date of 2007. People who reached the 5-year limit in Western Europe after 2007 are now eligible to donate.

“Canadian Blood Services regularly reviews the criteria used to determine if someone is eligible to donate blood, including geographic and age restrictions, based on new scientific information,” said Mindy Goldman, medical director of donor and clinical services with Canadian Blood Services.

“These restrictions are no longer necessary. We estimate that about 3000 people who try to donate each year but cannot will now be eligible to donate due to these changes.”

The complete policy changes are available at www.blood.ca/en/blood/recent-changes-donation-criteria.

Doctor consults with cancer

patient and her father

Photo by Rhoda Baer

A new study indicates that delirium is relatively frequent and underdiagnosed in patients with advanced cancer visiting the emergency department.

The research showed that delirium was similarly common among older and younger patients.

According to researchers, this suggests that, in the setting of advanced cancer, all patients should be considered at higher risk for delirium.

The researchers reported their findings in Cancer.

For this study, the team assessed a random sample of 243 advanced cancer patients who presented to the emergency department. They were 19 to 89 years old.

All patients were assessed with 2 methods: the Confusion Assessment Method (CAM) to screen for delirium and the Memorial Delirium Assessment Scale (MDAS) to measure delirium severity (mild ≤15, moderate 16-22, and severe ≥23).

In all, 22 patients (9%) had CAM-positive delirium and a median MDAS score of 14. Among CAM-positive patients, delirium was mild in 18 (82%) and moderate in 4 (18%) according to the MDAS.

Of the 99 patients age 65 and older, 10 (10%) had CAM-positive delirium, compared with 12 (8%) of 144 patients younger than 65.

Emergency department physicians failed to detect delirium in 9 (41%) CAM-positive delirious patients.

“We found evidence of delirium in 1 of every 10 patients with advanced cancer who are treated in the emergency department,” said study author Knox Todd, MD, of The University of Texas MD Anderson Cancer Center in Houston.

“Given that we could only study patients who were able to give consent to enter our study, even 10% is likely to be a low estimate. We also identified many psychoactive medications that could have contributed to delirium, and sharing this information with treating oncologists may help them avoid such complications in the next patient they treat.”

Doctor consults with cancer

patient and her father

Photo by Rhoda Baer

A new study indicates that delirium is relatively frequent and underdiagnosed in patients with advanced cancer visiting the emergency department.

The research showed that delirium was similarly common among older and younger patients.

According to researchers, this suggests that, in the setting of advanced cancer, all patients should be considered at higher risk for delirium.

The researchers reported their findings in Cancer.

For this study, the team assessed a random sample of 243 advanced cancer patients who presented to the emergency department. They were 19 to 89 years old.

All patients were assessed with 2 methods: the Confusion Assessment Method (CAM) to screen for delirium and the Memorial Delirium Assessment Scale (MDAS) to measure delirium severity (mild ≤15, moderate 16-22, and severe ≥23).

In all, 22 patients (9%) had CAM-positive delirium and a median MDAS score of 14. Among CAM-positive patients, delirium was mild in 18 (82%) and moderate in 4 (18%) according to the MDAS.

Of the 99 patients age 65 and older, 10 (10%) had CAM-positive delirium, compared with 12 (8%) of 144 patients younger than 65.

Emergency department physicians failed to detect delirium in 9 (41%) CAM-positive delirious patients.

“We found evidence of delirium in 1 of every 10 patients with advanced cancer who are treated in the emergency department,” said study author Knox Todd, MD, of The University of Texas MD Anderson Cancer Center in Houston.

“Given that we could only study patients who were able to give consent to enter our study, even 10% is likely to be a low estimate. We also identified many psychoactive medications that could have contributed to delirium, and sharing this information with treating oncologists may help them avoid such complications in the next patient they treat.”

Doctor consults with cancer

patient and her father

Photo by Rhoda Baer

A new study indicates that delirium is relatively frequent and underdiagnosed in patients with advanced cancer visiting the emergency department.

The research showed that delirium was similarly common among older and younger patients.

According to researchers, this suggests that, in the setting of advanced cancer, all patients should be considered at higher risk for delirium.

The researchers reported their findings in Cancer.

For this study, the team assessed a random sample of 243 advanced cancer patients who presented to the emergency department. They were 19 to 89 years old.

All patients were assessed with 2 methods: the Confusion Assessment Method (CAM) to screen for delirium and the Memorial Delirium Assessment Scale (MDAS) to measure delirium severity (mild ≤15, moderate 16-22, and severe ≥23).

In all, 22 patients (9%) had CAM-positive delirium and a median MDAS score of 14. Among CAM-positive patients, delirium was mild in 18 (82%) and moderate in 4 (18%) according to the MDAS.

Of the 99 patients age 65 and older, 10 (10%) had CAM-positive delirium, compared with 12 (8%) of 144 patients younger than 65.

Emergency department physicians failed to detect delirium in 9 (41%) CAM-positive delirious patients.

“We found evidence of delirium in 1 of every 10 patients with advanced cancer who are treated in the emergency department,” said study author Knox Todd, MD, of The University of Texas MD Anderson Cancer Center in Houston.

“Given that we could only study patients who were able to give consent to enter our study, even 10% is likely to be a low estimate. We also identified many psychoactive medications that could have contributed to delirium, and sharing this information with treating oncologists may help them avoid such complications in the next patient they treat.”

THE CASE

An 85-year-old woman sought care at our outpatient clinic for a 9-month history of severe pruritus and crusted lesions on her face, extremities, and trunk. She had been diagnosed with hepatitis C virus (HCV) infection one year ago and was not taking any medication. The patient, who had been living with her family, had visited various clinics for her complaints and was diagnosed as having contact dermatitis and senile pruritus. She was prescribed topical mometasone furoate and moisturizers.

After 6 months of using this therapy, widespread grey-white plaques and minimal excoriation appeared on her face, scalp, and trunk. This was diagnosed as psoriasis, and the patient was prescribed topical corticosteroids, which she used for 9 months until she came to our clinic. She said the lesions regressed minimally with the topical corticosteroids, but did not fully clear.

Dermatologic examination revealed widespread erythema and grey-white, cohesive, thick, pruritic plaques on her scalp, face, trunk, and bilateral extremities (FIGURE 1). A punch biopsy specimen was taken from the border of a plaque on her trunk.

THE DIAGNOSIS

A complete blood cell count and wide biochemistry panel, including tumor markers and viral serology for human immunodeficiency virus (HIV), were normal. The patient had lymphadenopathy in her posterior cervical, bilateral preauricular, and bilateral inguinal regions.

Histopathologic examination revealed hyperkeratosis, acanthosis, and spongiotic edema in the epidermis, and vesiculation and mites in the stratum corneum. The dermal changes consisted of perivascular and diffuse cell infiltrates that were mainly mononuclear cells and eosinophilic granulocytes.

Based on the dermatologic examination and the histopathologic findings, we diagnosed the patient with crusted (Norwegian) scabies.

DISCUSSION

Crusted (Norwegian) scabies is a rare, highly contagious form of scabies that is characterized by the presence of millions of Sarcoptes scabiei var hominis mites in the epidermis.¹ This variant of scabies can affect individuals of any age, gender, or race.² It was first described by Boeck and Danielssen in 1848 in Norway and was named Norwegian scabies by von Hebra in 1862.³ In 2010, more than 200 cases of crusted scabies were reported in the literature.⁴

Crusted scabies is usually seen in immunocompromised patients, such as the elderly, those who’ve had solid organ transplantation, and those with HIV, malignancy, or malnutrition. Crusted scabies may also occur in patients with decreased sensory function (such as those with leprosy) or decreased ability to scratch, intellectual disabilities, and in those who use biologic agents or systemic/topical corticosteroids.^4-8

Crusted scabies is associated with increased morbidity and mortality, especially in children and the elderly, because of complications such as secondary bacterial infections and sepsis.^1,3 Widespread inflammation may also cause erythroderma, which can lead to metabolic disorders.

Distinguish it from other pruritic papulosquamous diseases

The differential diagnosis for crusted scabies includes psoriasis, eczema, cutaneous lymphoma, Darier disease, and adverse drug reactions.⁹ Crusted scabies can be differentiated from these other diagnoses by its clinical presentation and histopathological examination.

Crusted scabies is characterized by hyperkeratosis and wart-like crusts that are due to extreme proliferation of mites in the stratum corneum of the epidermis.² Lesions are usually localized on acral sites (especially the hands), although the entire body, including the face and the scalp, can be involved.¹ Psoriasiform or bullous pemphigoid-like eruptions have also been reported in the literature.^5,9

Our patient presented with widespread erythema and psoriasiform grey-white crusts on her scalp, face, chest, periareolar region, and extremities. In addition, she did not have an immunosuppressant disease or medication history.

However, the fact that our patient was using topical corticosteroids for so long explained the extent of her condition. Topical corticosteroids have been linked to scabies incognito.¹⁰ Topical or systemic corticosteroid use for long periods of time may alter the skin immune system by suppressing cellular immunity, thereby reducing the inflammatory response. This may lead to progression of the regular variant of scabies to crusted scabies, as our patient had.

Topical treatments, oral ivermectin proven to be effective

Topical keratolytics, permethrin 5%, lindane 1%, crotamiton 10%, sulfur ointment (5%-10%), malathion 0.5%, benzyl benzoate (10%-25%), oral ivermectin (2 doses of 200 mcg/kg/dose), and systemic antihistamines are appropriate therapies.³ While oral ivermectin is effective, it is not available in Turkey.

Because of our patient’s hepatic disorder, we opted for a topical, rather than a systemic, treatment and recommended repeated applications of topical permethrin. Repeated treatment with topical permethrin is often sufficient in patients who are unable to take systemic therapy. In fact, Binic et al⁴ reported a case in which an elderly patient with crusted scabies (who had previously been treated with systemic and topical corticosteroids) responded well to repeated topical treatment with lindane 1%, 25% benzyl benzoate, and 10% precipitated sulfur.

Our patient. We prescribed topical 5% permethrin lotion for our patient to apply to her entire body 4 times a week and advised her to wash her clothing and bed linens at 140° F. She was scheduled for biweekly check-ups. We also advised the patient’s family to use the same topical therapy 2 times per week because crusted scabies is highly contagious. One month later, our patient’s lesions had resolved (FIGURE 2).

THE TAKEAWAY

Early diagnosis and treatment of crusted scabies is important, both for the treatment of the patient and to stop the spread of the disease. Although rare, crusted scabies should be included in the differential diagnosis of long-term pruritic papulosquamous diseases, and the possibility of an atypical presentation in all patients should be considered—whether their immunity is compromised or not. Scabies should also be considered in patients with a positive family history of the disease and in those with chronic pruritus that is unresponsive to topical therapies.

THE CASE

An 85-year-old woman sought care at our outpatient clinic for a 9-month history of severe pruritus and crusted lesions on her face, extremities, and trunk. She had been diagnosed with hepatitis C virus (HCV) infection one year ago and was not taking any medication. The patient, who had been living with her family, had visited various clinics for her complaints and was diagnosed as having contact dermatitis and senile pruritus. She was prescribed topical mometasone furoate and moisturizers.

After 6 months of using this therapy, widespread grey-white plaques and minimal excoriation appeared on her face, scalp, and trunk. This was diagnosed as psoriasis, and the patient was prescribed topical corticosteroids, which she used for 9 months until she came to our clinic. She said the lesions regressed minimally with the topical corticosteroids, but did not fully clear.

Dermatologic examination revealed widespread erythema and grey-white, cohesive, thick, pruritic plaques on her scalp, face, trunk, and bilateral extremities (FIGURE 1). A punch biopsy specimen was taken from the border of a plaque on her trunk.

THE DIAGNOSIS

A complete blood cell count and wide biochemistry panel, including tumor markers and viral serology for human immunodeficiency virus (HIV), were normal. The patient had lymphadenopathy in her posterior cervical, bilateral preauricular, and bilateral inguinal regions.

Histopathologic examination revealed hyperkeratosis, acanthosis, and spongiotic edema in the epidermis, and vesiculation and mites in the stratum corneum. The dermal changes consisted of perivascular and diffuse cell infiltrates that were mainly mononuclear cells and eosinophilic granulocytes.

Based on the dermatologic examination and the histopathologic findings, we diagnosed the patient with crusted (Norwegian) scabies.

DISCUSSION

Crusted (Norwegian) scabies is a rare, highly contagious form of scabies that is characterized by the presence of millions of Sarcoptes scabiei var hominis mites in the epidermis.¹ This variant of scabies can affect individuals of any age, gender, or race.² It was first described by Boeck and Danielssen in 1848 in Norway and was named Norwegian scabies by von Hebra in 1862.³ In 2010, more than 200 cases of crusted scabies were reported in the literature.⁴

Crusted scabies is usually seen in immunocompromised patients, such as the elderly, those who’ve had solid organ transplantation, and those with HIV, malignancy, or malnutrition. Crusted scabies may also occur in patients with decreased sensory function (such as those with leprosy) or decreased ability to scratch, intellectual disabilities, and in those who use biologic agents or systemic/topical corticosteroids.^4-8

Crusted scabies is associated with increased morbidity and mortality, especially in children and the elderly, because of complications such as secondary bacterial infections and sepsis.^1,3 Widespread inflammation may also cause erythroderma, which can lead to metabolic disorders.

Distinguish it from other pruritic papulosquamous diseases

The differential diagnosis for crusted scabies includes psoriasis, eczema, cutaneous lymphoma, Darier disease, and adverse drug reactions.⁹ Crusted scabies can be differentiated from these other diagnoses by its clinical presentation and histopathological examination.

Crusted scabies is characterized by hyperkeratosis and wart-like crusts that are due to extreme proliferation of mites in the stratum corneum of the epidermis.² Lesions are usually localized on acral sites (especially the hands), although the entire body, including the face and the scalp, can be involved.¹ Psoriasiform or bullous pemphigoid-like eruptions have also been reported in the literature.^5,9

Our patient presented with widespread erythema and psoriasiform grey-white crusts on her scalp, face, chest, periareolar region, and extremities. In addition, she did not have an immunosuppressant disease or medication history.

However, the fact that our patient was using topical corticosteroids for so long explained the extent of her condition. Topical corticosteroids have been linked to scabies incognito.¹⁰ Topical or systemic corticosteroid use for long periods of time may alter the skin immune system by suppressing cellular immunity, thereby reducing the inflammatory response. This may lead to progression of the regular variant of scabies to crusted scabies, as our patient had.

Topical treatments, oral ivermectin proven to be effective

Topical keratolytics, permethrin 5%, lindane 1%, crotamiton 10%, sulfur ointment (5%-10%), malathion 0.5%, benzyl benzoate (10%-25%), oral ivermectin (2 doses of 200 mcg/kg/dose), and systemic antihistamines are appropriate therapies.³ While oral ivermectin is effective, it is not available in Turkey.

Because of our patient’s hepatic disorder, we opted for a topical, rather than a systemic, treatment and recommended repeated applications of topical permethrin. Repeated treatment with topical permethrin is often sufficient in patients who are unable to take systemic therapy. In fact, Binic et al⁴ reported a case in which an elderly patient with crusted scabies (who had previously been treated with systemic and topical corticosteroids) responded well to repeated topical treatment with lindane 1%, 25% benzyl benzoate, and 10% precipitated sulfur.

Our patient. We prescribed topical 5% permethrin lotion for our patient to apply to her entire body 4 times a week and advised her to wash her clothing and bed linens at 140° F. She was scheduled for biweekly check-ups. We also advised the patient’s family to use the same topical therapy 2 times per week because crusted scabies is highly contagious. One month later, our patient’s lesions had resolved (FIGURE 2).

THE TAKEAWAY

Early diagnosis and treatment of crusted scabies is important, both for the treatment of the patient and to stop the spread of the disease. Although rare, crusted scabies should be included in the differential diagnosis of long-term pruritic papulosquamous diseases, and the possibility of an atypical presentation in all patients should be considered—whether their immunity is compromised or not. Scabies should also be considered in patients with a positive family history of the disease and in those with chronic pruritus that is unresponsive to topical therapies.

THE CASE

An 85-year-old woman sought care at our outpatient clinic for a 9-month history of severe pruritus and crusted lesions on her face, extremities, and trunk. She had been diagnosed with hepatitis C virus (HCV) infection one year ago and was not taking any medication. The patient, who had been living with her family, had visited various clinics for her complaints and was diagnosed as having contact dermatitis and senile pruritus. She was prescribed topical mometasone furoate and moisturizers.

After 6 months of using this therapy, widespread grey-white plaques and minimal excoriation appeared on her face, scalp, and trunk. This was diagnosed as psoriasis, and the patient was prescribed topical corticosteroids, which she used for 9 months until she came to our clinic. She said the lesions regressed minimally with the topical corticosteroids, but did not fully clear.

Dermatologic examination revealed widespread erythema and grey-white, cohesive, thick, pruritic plaques on her scalp, face, trunk, and bilateral extremities (FIGURE 1). A punch biopsy specimen was taken from the border of a plaque on her trunk.

THE DIAGNOSIS

A complete blood cell count and wide biochemistry panel, including tumor markers and viral serology for human immunodeficiency virus (HIV), were normal. The patient had lymphadenopathy in her posterior cervical, bilateral preauricular, and bilateral inguinal regions.

Histopathologic examination revealed hyperkeratosis, acanthosis, and spongiotic edema in the epidermis, and vesiculation and mites in the stratum corneum. The dermal changes consisted of perivascular and diffuse cell infiltrates that were mainly mononuclear cells and eosinophilic granulocytes.

Based on the dermatologic examination and the histopathologic findings, we diagnosed the patient with crusted (Norwegian) scabies.

DISCUSSION

Crusted (Norwegian) scabies is a rare, highly contagious form of scabies that is characterized by the presence of millions of Sarcoptes scabiei var hominis mites in the epidermis.¹ This variant of scabies can affect individuals of any age, gender, or race.² It was first described by Boeck and Danielssen in 1848 in Norway and was named Norwegian scabies by von Hebra in 1862.³ In 2010, more than 200 cases of crusted scabies were reported in the literature.⁴

Crusted scabies is usually seen in immunocompromised patients, such as the elderly, those who’ve had solid organ transplantation, and those with HIV, malignancy, or malnutrition. Crusted scabies may also occur in patients with decreased sensory function (such as those with leprosy) or decreased ability to scratch, intellectual disabilities, and in those who use biologic agents or systemic/topical corticosteroids.^4-8

Crusted scabies is associated with increased morbidity and mortality, especially in children and the elderly, because of complications such as secondary bacterial infections and sepsis.^1,3 Widespread inflammation may also cause erythroderma, which can lead to metabolic disorders.

Distinguish it from other pruritic papulosquamous diseases

The differential diagnosis for crusted scabies includes psoriasis, eczema, cutaneous lymphoma, Darier disease, and adverse drug reactions.⁹ Crusted scabies can be differentiated from these other diagnoses by its clinical presentation and histopathological examination.

Crusted scabies is characterized by hyperkeratosis and wart-like crusts that are due to extreme proliferation of mites in the stratum corneum of the epidermis.² Lesions are usually localized on acral sites (especially the hands), although the entire body, including the face and the scalp, can be involved.¹ Psoriasiform or bullous pemphigoid-like eruptions have also been reported in the literature.^5,9

Our patient presented with widespread erythema and psoriasiform grey-white crusts on her scalp, face, chest, periareolar region, and extremities. In addition, she did not have an immunosuppressant disease or medication history.

However, the fact that our patient was using topical corticosteroids for so long explained the extent of her condition. Topical corticosteroids have been linked to scabies incognito.¹⁰ Topical or systemic corticosteroid use for long periods of time may alter the skin immune system by suppressing cellular immunity, thereby reducing the inflammatory response. This may lead to progression of the regular variant of scabies to crusted scabies, as our patient had.

Topical treatments, oral ivermectin proven to be effective

Topical keratolytics, permethrin 5%, lindane 1%, crotamiton 10%, sulfur ointment (5%-10%), malathion 0.5%, benzyl benzoate (10%-25%), oral ivermectin (2 doses of 200 mcg/kg/dose), and systemic antihistamines are appropriate therapies.³ While oral ivermectin is effective, it is not available in Turkey.

Because of our patient’s hepatic disorder, we opted for a topical, rather than a systemic, treatment and recommended repeated applications of topical permethrin. Repeated treatment with topical permethrin is often sufficient in patients who are unable to take systemic therapy. In fact, Binic et al⁴ reported a case in which an elderly patient with crusted scabies (who had previously been treated with systemic and topical corticosteroids) responded well to repeated topical treatment with lindane 1%, 25% benzyl benzoate, and 10% precipitated sulfur.

Our patient. We prescribed topical 5% permethrin lotion for our patient to apply to her entire body 4 times a week and advised her to wash her clothing and bed linens at 140° F. She was scheduled for biweekly check-ups. We also advised the patient’s family to use the same topical therapy 2 times per week because crusted scabies is highly contagious. One month later, our patient’s lesions had resolved (FIGURE 2).

THE TAKEAWAY

Early diagnosis and treatment of crusted scabies is important, both for the treatment of the patient and to stop the spread of the disease. Although rare, crusted scabies should be included in the differential diagnosis of long-term pruritic papulosquamous diseases, and the possibility of an atypical presentation in all patients should be considered—whether their immunity is compromised or not. Scabies should also be considered in patients with a positive family history of the disease and in those with chronic pruritus that is unresponsive to topical therapies.

THE CASE

A 63-year-old woman with a history of hyperlipidemia presented to our hospital with a swollen right hand. The patient noted that she had closed her hand in a car door one week earlier, causing minor trauma to the right third metacarpophalangeal joint. Shortly after injuring her hand, she’d sought care at an outpatient facility, where she was given a diagnosis of cellulitis and a prescription for an oral antibiotic. The swelling, however, worsened, prompting her visit to our hospital. She was admitted for further work-up and started on intravenous (IV) antibiotics.

Her family history included a sister with deep vein thrombosis (DVT) and a maternal aunt with breast cancer. The patient denied oral contraceptive use or a personal history of malignancy. On physical examination, her right hand and forearm were swollen, tender, and erythematous.

THE DIAGNOSIS

Laboratory data showed a normal complete blood count and complete metabolic panel. The patient’s sedimentation rate and C-reactive protein level were elevated at 65 mm/hr and 110 mg/L, respectively. The patient was not improving on IV antibiotics, so we performed a right upper extremity venous duplex ultrasound. The ultrasound showed an occlusive thrombus in the right ulnar and radial veins (FIGURES 1 AND 2), and we diagnosed the patient with upper extremity deep vein thrombosis (UEDVT). (The timing of the diagnosis, relative to the injury to the patient’s hand, appeared to have been coincidental.)

Further work-up revealed normal complement C3 and C4 tests, as well as negative antinuclear, anti-double stranded DNA, anti-Smith, and anticardiolipin antibody tests. Similarly, a factor II DNA analysis was negative. However, the patient was positive for the factor V Leiden heterozygous mutation.

DISCUSSION

More than 350,000 people are diagnosed with DVT or pulmonary embolism (PE) in the United States each year.¹ Up to 4% of all DVTs involve the upper extremities.² Secondary UEDVT, which occurs in patients with central venous catheters, malignancies, and thrombophilia, accounts for the majority of UEDVT cases; primary UEDVT is less common.³

Large epidemiologic studies have demonstrated that hypercoagulability is a risk factor for lower extremity DVT, but few data exist on the role of coagulation abnormalities in patients with primary UEDVT. The prevalence of clotting abnormalities in patients with primary UEDVT ranges from 8% to 43%.^4,5 Factor V Leiden is the most common cause of inherited thrombophilia. Patients with heterozygous factor V Leiden mutation have a 7-fold increased risk of venous thrombosis.⁶

Héron and colleagues⁷ reported that 16 of 51 patients with at least one clotting abnormality had primary UEDVT. Factor V Leiden was found in 5 of those patients (20%). Interestingly, 3 of the 5 carriers of the factor V Leiden mutation were older than 45 years. Our patient was 63, which was consistent with these findings.

Malignancy is also an important risk factor for UEDVT.^8,9 In patients with a DVT in an unusual location, age- and sex-appropriate cancer screenings are strongly recommended. (Our patient had undergone a colonoscopy 8 years earlier, which was normal. She’d also had a recent mammogram and Pap smear, which were normal, as well.)

It’s often difficult to distinguish between cellulitis and UEDVT

The differential diagnosis for UEDVT includes effort thrombosis (also known as Paget-Schroetter syndrome) and cellulitis.

Effort thrombosis usually occurs in young, otherwise healthy individuals and almost exclusively in the axillary and subclavian veins. Our patient’s age and a venous duplex ultrasound ruled out any thrombosis in these locations.

Distinguishing cellulitis from UEDVT based on clinical features can be difficult. In both conditions, the limb is swollen and painful and the skin is warm and erythematous. As a result, each condition is often misdiagnosed as the other.

But there are features that distinguish the 2. In patients with UEDVT, you’re likely to see limb pain and a palpable cord (a hard, thickened palpable vein along the line of the deep veins). On the other hand, patients with cellulitis tend to have more systemic symptoms, such as fever, chills, and swollen lymph nodes, as well as skin breakdown, ulcers, and pus.

The American College of Chest Physicians (ACCP) recommends that the initial evaluation for patients with suspected UEDVT be a combined modality ultrasound (compression with either Doppler or color Doppler) rather than D-dimer or venography.¹⁰ Quickly arriving at a proper diagnosis is critical, given that up to one-third of patients with UEDVT will develop a PE.⁷ Other complications include superior vena cava syndrome, septic thrombophlebitis, thoracic duct obstruction, and brachial plexopathy.¹¹

Treat with anticoagulants for no longer than 3 months

The ACCP also recommends that patients who have UEDVT that isn’t associated with a central venous catheter or with cancer be treated with anticoagulation for no longer than 3 months.¹⁰

Our patient was started on enoxaparin and warfarin. After 5 days at our hospital, she was taken off the enoxaparin and discharged home on warfarin 5 mg/d. The swelling completely resolved one week later.

THE TAKEAWAY

Ulnar and radial DVT in a patient with factor V Leiden mutation is a rare condition. UEDVT should be included in the differential diagnosis for cellulitis whenever the diagnosis is uncertain or the patient doesn’t respond to antibiotics. Factor V Leiden mutation appears to be a risk factor in UEDVT and testing for it should be considered.

THE CASE

A 63-year-old woman with a history of hyperlipidemia presented to our hospital with a swollen right hand. The patient noted that she had closed her hand in a car door one week earlier, causing minor trauma to the right third metacarpophalangeal joint. Shortly after injuring her hand, she’d sought care at an outpatient facility, where she was given a diagnosis of cellulitis and a prescription for an oral antibiotic. The swelling, however, worsened, prompting her visit to our hospital. She was admitted for further work-up and started on intravenous (IV) antibiotics.

Her family history included a sister with deep vein thrombosis (DVT) and a maternal aunt with breast cancer. The patient denied oral contraceptive use or a personal history of malignancy. On physical examination, her right hand and forearm were swollen, tender, and erythematous.

THE DIAGNOSIS

Laboratory data showed a normal complete blood count and complete metabolic panel. The patient’s sedimentation rate and C-reactive protein level were elevated at 65 mm/hr and 110 mg/L, respectively. The patient was not improving on IV antibiotics, so we performed a right upper extremity venous duplex ultrasound. The ultrasound showed an occlusive thrombus in the right ulnar and radial veins (FIGURES 1 AND 2), and we diagnosed the patient with upper extremity deep vein thrombosis (UEDVT). (The timing of the diagnosis, relative to the injury to the patient’s hand, appeared to have been coincidental.)

Further work-up revealed normal complement C3 and C4 tests, as well as negative antinuclear, anti-double stranded DNA, anti-Smith, and anticardiolipin antibody tests. Similarly, a factor II DNA analysis was negative. However, the patient was positive for the factor V Leiden heterozygous mutation.

DISCUSSION

More than 350,000 people are diagnosed with DVT or pulmonary embolism (PE) in the United States each year.¹ Up to 4% of all DVTs involve the upper extremities.² Secondary UEDVT, which occurs in patients with central venous catheters, malignancies, and thrombophilia, accounts for the majority of UEDVT cases; primary UEDVT is less common.³

Large epidemiologic studies have demonstrated that hypercoagulability is a risk factor for lower extremity DVT, but few data exist on the role of coagulation abnormalities in patients with primary UEDVT. The prevalence of clotting abnormalities in patients with primary UEDVT ranges from 8% to 43%.^4,5 Factor V Leiden is the most common cause of inherited thrombophilia. Patients with heterozygous factor V Leiden mutation have a 7-fold increased risk of venous thrombosis.⁶

Héron and colleagues⁷ reported that 16 of 51 patients with at least one clotting abnormality had primary UEDVT. Factor V Leiden was found in 5 of those patients (20%). Interestingly, 3 of the 5 carriers of the factor V Leiden mutation were older than 45 years. Our patient was 63, which was consistent with these findings.

Malignancy is also an important risk factor for UEDVT.^8,9 In patients with a DVT in an unusual location, age- and sex-appropriate cancer screenings are strongly recommended. (Our patient had undergone a colonoscopy 8 years earlier, which was normal. She’d also had a recent mammogram and Pap smear, which were normal, as well.)

It’s often difficult to distinguish between cellulitis and UEDVT

The differential diagnosis for UEDVT includes effort thrombosis (also known as Paget-Schroetter syndrome) and cellulitis.

Effort thrombosis usually occurs in young, otherwise healthy individuals and almost exclusively in the axillary and subclavian veins. Our patient’s age and a venous duplex ultrasound ruled out any thrombosis in these locations.

Distinguishing cellulitis from UEDVT based on clinical features can be difficult. In both conditions, the limb is swollen and painful and the skin is warm and erythematous. As a result, each condition is often misdiagnosed as the other.

But there are features that distinguish the 2. In patients with UEDVT, you’re likely to see limb pain and a palpable cord (a hard, thickened palpable vein along the line of the deep veins). On the other hand, patients with cellulitis tend to have more systemic symptoms, such as fever, chills, and swollen lymph nodes, as well as skin breakdown, ulcers, and pus.

The American College of Chest Physicians (ACCP) recommends that the initial evaluation for patients with suspected UEDVT be a combined modality ultrasound (compression with either Doppler or color Doppler) rather than D-dimer or venography.¹⁰ Quickly arriving at a proper diagnosis is critical, given that up to one-third of patients with UEDVT will develop a PE.⁷ Other complications include superior vena cava syndrome, septic thrombophlebitis, thoracic duct obstruction, and brachial plexopathy.¹¹

Treat with anticoagulants for no longer than 3 months

The ACCP also recommends that patients who have UEDVT that isn’t associated with a central venous catheter or with cancer be treated with anticoagulation for no longer than 3 months.¹⁰

Our patient was started on enoxaparin and warfarin. After 5 days at our hospital, she was taken off the enoxaparin and discharged home on warfarin 5 mg/d. The swelling completely resolved one week later.

THE TAKEAWAY

Ulnar and radial DVT in a patient with factor V Leiden mutation is a rare condition. UEDVT should be included in the differential diagnosis for cellulitis whenever the diagnosis is uncertain or the patient doesn’t respond to antibiotics. Factor V Leiden mutation appears to be a risk factor in UEDVT and testing for it should be considered.

THE CASE

A 63-year-old woman with a history of hyperlipidemia presented to our hospital with a swollen right hand. The patient noted that she had closed her hand in a car door one week earlier, causing minor trauma to the right third metacarpophalangeal joint. Shortly after injuring her hand, she’d sought care at an outpatient facility, where she was given a diagnosis of cellulitis and a prescription for an oral antibiotic. The swelling, however, worsened, prompting her visit to our hospital. She was admitted for further work-up and started on intravenous (IV) antibiotics.

Her family history included a sister with deep vein thrombosis (DVT) and a maternal aunt with breast cancer. The patient denied oral contraceptive use or a personal history of malignancy. On physical examination, her right hand and forearm were swollen, tender, and erythematous.

THE DIAGNOSIS

Laboratory data showed a normal complete blood count and complete metabolic panel. The patient’s sedimentation rate and C-reactive protein level were elevated at 65 mm/hr and 110 mg/L, respectively. The patient was not improving on IV antibiotics, so we performed a right upper extremity venous duplex ultrasound. The ultrasound showed an occlusive thrombus in the right ulnar and radial veins (FIGURES 1 AND 2), and we diagnosed the patient with upper extremity deep vein thrombosis (UEDVT). (The timing of the diagnosis, relative to the injury to the patient’s hand, appeared to have been coincidental.)

Further work-up revealed normal complement C3 and C4 tests, as well as negative antinuclear, anti-double stranded DNA, anti-Smith, and anticardiolipin antibody tests. Similarly, a factor II DNA analysis was negative. However, the patient was positive for the factor V Leiden heterozygous mutation.

DISCUSSION

More than 350,000 people are diagnosed with DVT or pulmonary embolism (PE) in the United States each year.¹ Up to 4% of all DVTs involve the upper extremities.² Secondary UEDVT, which occurs in patients with central venous catheters, malignancies, and thrombophilia, accounts for the majority of UEDVT cases; primary UEDVT is less common.³

Large epidemiologic studies have demonstrated that hypercoagulability is a risk factor for lower extremity DVT, but few data exist on the role of coagulation abnormalities in patients with primary UEDVT. The prevalence of clotting abnormalities in patients with primary UEDVT ranges from 8% to 43%.^4,5 Factor V Leiden is the most common cause of inherited thrombophilia. Patients with heterozygous factor V Leiden mutation have a 7-fold increased risk of venous thrombosis.⁶

Héron and colleagues⁷ reported that 16 of 51 patients with at least one clotting abnormality had primary UEDVT. Factor V Leiden was found in 5 of those patients (20%). Interestingly, 3 of the 5 carriers of the factor V Leiden mutation were older than 45 years. Our patient was 63, which was consistent with these findings.

Malignancy is also an important risk factor for UEDVT.^8,9 In patients with a DVT in an unusual location, age- and sex-appropriate cancer screenings are strongly recommended. (Our patient had undergone a colonoscopy 8 years earlier, which was normal. She’d also had a recent mammogram and Pap smear, which were normal, as well.)

It’s often difficult to distinguish between cellulitis and UEDVT

The differential diagnosis for UEDVT includes effort thrombosis (also known as Paget-Schroetter syndrome) and cellulitis.

Effort thrombosis usually occurs in young, otherwise healthy individuals and almost exclusively in the axillary and subclavian veins. Our patient’s age and a venous duplex ultrasound ruled out any thrombosis in these locations.

Distinguishing cellulitis from UEDVT based on clinical features can be difficult. In both conditions, the limb is swollen and painful and the skin is warm and erythematous. As a result, each condition is often misdiagnosed as the other.

But there are features that distinguish the 2. In patients with UEDVT, you’re likely to see limb pain and a palpable cord (a hard, thickened palpable vein along the line of the deep veins). On the other hand, patients with cellulitis tend to have more systemic symptoms, such as fever, chills, and swollen lymph nodes, as well as skin breakdown, ulcers, and pus.

The American College of Chest Physicians (ACCP) recommends that the initial evaluation for patients with suspected UEDVT be a combined modality ultrasound (compression with either Doppler or color Doppler) rather than D-dimer or venography.¹⁰ Quickly arriving at a proper diagnosis is critical, given that up to one-third of patients with UEDVT will develop a PE.⁷ Other complications include superior vena cava syndrome, septic thrombophlebitis, thoracic duct obstruction, and brachial plexopathy.¹¹

Treat with anticoagulants for no longer than 3 months

The ACCP also recommends that patients who have UEDVT that isn’t associated with a central venous catheter or with cancer be treated with anticoagulation for no longer than 3 months.¹⁰

Our patient was started on enoxaparin and warfarin. After 5 days at our hospital, she was taken off the enoxaparin and discharged home on warfarin 5 mg/d. The swelling completely resolved one week later.

THE TAKEAWAY

Ulnar and radial DVT in a patient with factor V Leiden mutation is a rare condition. UEDVT should be included in the differential diagnosis for cellulitis whenever the diagnosis is uncertain or the patient doesn’t respond to antibiotics. Factor V Leiden mutation appears to be a risk factor in UEDVT and testing for it should be considered.

Growing teratoma syndrome (GTS) is a rare condition seen in patients with germ-cell tumors (GCT) who present with enlarging masses during or after appropriate chemotherapy with normalized serum markers.1 Three defining criteria for GTS are: a persistently growing tumor mass or evolving new mass during or after chemotherapy, normalization of tumor markers, and presence of only mature teratoma in the resected specimen on the final histopathological examination.1 Growing teratomas lack the metastatic potential; however, their relentless local growth causes compression and infiltration of adjacent organs, which produces symptoms.

Click on the PDF icon at the top of this introduction to read the full article. 

Growing teratoma syndrome (GTS) is a rare condition seen in patients with germ-cell tumors (GCT) who present with enlarging masses during or after appropriate chemotherapy with normalized serum markers.1 Three defining criteria for GTS are: a persistently growing tumor mass or evolving new mass during or after chemotherapy, normalization of tumor markers, and presence of only mature teratoma in the resected specimen on the final histopathological examination.1 Growing teratomas lack the metastatic potential; however, their relentless local growth causes compression and infiltration of adjacent organs, which produces symptoms.

Click on the PDF icon at the top of this introduction to read the full article. 

Growing teratoma syndrome (GTS) is a rare condition seen in patients with germ-cell tumors (GCT) who present with enlarging masses during or after appropriate chemotherapy with normalized serum markers.1 Three defining criteria for GTS are: a persistently growing tumor mass or evolving new mass during or after chemotherapy, normalization of tumor markers, and presence of only mature teratoma in the resected specimen on the final histopathological examination.1 Growing teratomas lack the metastatic potential; however, their relentless local growth causes compression and infiltration of adjacent organs, which produces symptoms.

Click on the PDF icon at the top of this introduction to read the full article. 

While we can imagine what a high-quality, state-of- the-art cancer care system might deliver in terms of value-based care and how it might yield exceptional patient outcomes and job satisfaction for our staff, most of us are struggling with the processes and tools needed to achieve defined outcomes that can be benchmarked and further refined – all within the limits of our already hectic 12-, 14,- 16+-hour days. As more community practices, academic centers, and hospitals align to share and leverage expertise in their efforts to form more streamlined, patient-centered delivery systems for cancer care, we need to set up, refine, and integrate pathways into pathway programs that will pave the way to the delivery of value-based care.

Click on the PDF icon at the top of this introduction to read the full article.

While we can imagine what a high-quality, state-of- the-art cancer care system might deliver in terms of value-based care and how it might yield exceptional patient outcomes and job satisfaction for our staff, most of us are struggling with the processes and tools needed to achieve defined outcomes that can be benchmarked and further refined – all within the limits of our already hectic 12-, 14,- 16+-hour days. As more community practices, academic centers, and hospitals align to share and leverage expertise in their efforts to form more streamlined, patient-centered delivery systems for cancer care, we need to set up, refine, and integrate pathways into pathway programs that will pave the way to the delivery of value-based care.

Click on the PDF icon at the top of this introduction to read the full article.

While we can imagine what a high-quality, state-of- the-art cancer care system might deliver in terms of value-based care and how it might yield exceptional patient outcomes and job satisfaction for our staff, most of us are struggling with the processes and tools needed to achieve defined outcomes that can be benchmarked and further refined – all within the limits of our already hectic 12-, 14,- 16+-hour days. As more community practices, academic centers, and hospitals align to share and leverage expertise in their efforts to form more streamlined, patient-centered delivery systems for cancer care, we need to set up, refine, and integrate pathways into pathway programs that will pave the way to the delivery of value-based care.

Click on the PDF icon at the top of this introduction to read the full article.

MIAMI – Reaching a consensus on measurement and assessment of flare in psoriatic arthritis remains challenging, especially with no widely accepted definition and differing opinions among patients and physicians. But getting standard evaluation of flare under control is critical for both clinical and research outcomes.

Through a series of patient interviews, physician surveys, and lessons learned in rheumatoid arthritis, the GRAPPA Flare Project is close to a validated flare instrument. A 10-question flare assessment tool is now in the final validation stage, according to a presentation at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

“Flare is a clearly personal experience and varies from patient to patient. It’s clear that physicians and patients have clearly different ideas of what flare is. Bringing those two worlds together was a challenge,” Philip Helliwell, MD, of Leeds (England) University and GRAPPA president, said at the meeting.

James Heilman, MD/Wikimedia Commons/CC BY-SA 3.0

“Some societies – I’m not going to mention any names – have gone down the route of a definition of flare linked to disease activity measures. We have not done this,” Dr. Helliwell said.

Instead, the Flare Project is taking a patient-driven and physician-reviewed approach. Investigators cast a wide net, identifying 79 factors important to patients in six major domains: skin, joint, emotional, participation, fatigue, and unclassified. The results were published in 2015 (Rheumatology [Oxford]. 2015 Aug;54[8]:1448-53). Through a Delphi survey, physicians reviewed these considerations. Then GRAPPA identified items important to both patients and physicians and developed a preliminary flare instrument.

Unlike most assessment tools for psoriatic disease, the new instrument includes patient-reported emotional well-being. Niti Goel, MD, of Duke University, Durham, N.C., said that physicians do not always ask patients about the psychological impact of their disease, so the tool “could provide additional information.”

Another goal of the project is to provide standard answers to some of the common questions related to psoriatic arthritis, including: What exactly is a flare? Does the definition truly capture the worsening of disease? Are there different types of flares? Is flare different if you start from a point of high disease activity? What self-management and other interventions are effective for flare?

GRAPPA adopted a definition of flare developed from rheumatoid arthritis, stating that flare is any worsening of disease activity that would, if persistent, in most cases lead to initiation or change of therapy (J Rheumatol. 2009 Oct;36[10]:2335-41).

“It took [them] some time to get to that definition,” Dr. Helliwell said. “We know from rheumatoid arthritis that there is a lot more to a flare than joint swelling and pain.”

The GRAPPA flare tool is now in the validation stage, Dr. Helliwell said, and will be tested in several studies, including a prospective multicenter study where the 10-item questionnaire will be administered to patients.

A meeting attendee commented that the patient and physician global scales are sufficient and asked: “Is there really a need for a flare instrument?”

“I accept what you are saying, but I would also retort that knowledge is power, and the more information we get, the more we know about what we are doing,” Dr. Helliwell said. “We are going to collect all our information – physician global, patient global, composite disease measures – everything within that study.”

Dr. Helliwell and Dr. Goel reported having no relevant financial disclosures.

MIAMI – Reaching a consensus on measurement and assessment of flare in psoriatic arthritis remains challenging, especially with no widely accepted definition and differing opinions among patients and physicians. But getting standard evaluation of flare under control is critical for both clinical and research outcomes.

Through a series of patient interviews, physician surveys, and lessons learned in rheumatoid arthritis, the GRAPPA Flare Project is close to a validated flare instrument. A 10-question flare assessment tool is now in the final validation stage, according to a presentation at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

“Flare is a clearly personal experience and varies from patient to patient. It’s clear that physicians and patients have clearly different ideas of what flare is. Bringing those two worlds together was a challenge,” Philip Helliwell, MD, of Leeds (England) University and GRAPPA president, said at the meeting.

James Heilman, MD/Wikimedia Commons/CC BY-SA 3.0

“Some societies – I’m not going to mention any names – have gone down the route of a definition of flare linked to disease activity measures. We have not done this,” Dr. Helliwell said.

Instead, the Flare Project is taking a patient-driven and physician-reviewed approach. Investigators cast a wide net, identifying 79 factors important to patients in six major domains: skin, joint, emotional, participation, fatigue, and unclassified. The results were published in 2015 (Rheumatology [Oxford]. 2015 Aug;54[8]:1448-53). Through a Delphi survey, physicians reviewed these considerations. Then GRAPPA identified items important to both patients and physicians and developed a preliminary flare instrument.

Unlike most assessment tools for psoriatic disease, the new instrument includes patient-reported emotional well-being. Niti Goel, MD, of Duke University, Durham, N.C., said that physicians do not always ask patients about the psychological impact of their disease, so the tool “could provide additional information.”

Another goal of the project is to provide standard answers to some of the common questions related to psoriatic arthritis, including: What exactly is a flare? Does the definition truly capture the worsening of disease? Are there different types of flares? Is flare different if you start from a point of high disease activity? What self-management and other interventions are effective for flare?

GRAPPA adopted a definition of flare developed from rheumatoid arthritis, stating that flare is any worsening of disease activity that would, if persistent, in most cases lead to initiation or change of therapy (J Rheumatol. 2009 Oct;36[10]:2335-41).

“It took [them] some time to get to that definition,” Dr. Helliwell said. “We know from rheumatoid arthritis that there is a lot more to a flare than joint swelling and pain.”

The GRAPPA flare tool is now in the validation stage, Dr. Helliwell said, and will be tested in several studies, including a prospective multicenter study where the 10-item questionnaire will be administered to patients.

A meeting attendee commented that the patient and physician global scales are sufficient and asked: “Is there really a need for a flare instrument?”

“I accept what you are saying, but I would also retort that knowledge is power, and the more information we get, the more we know about what we are doing,” Dr. Helliwell said. “We are going to collect all our information – physician global, patient global, composite disease measures – everything within that study.”

Dr. Helliwell and Dr. Goel reported having no relevant financial disclosures.

MIAMI – Reaching a consensus on measurement and assessment of flare in psoriatic arthritis remains challenging, especially with no widely accepted definition and differing opinions among patients and physicians. But getting standard evaluation of flare under control is critical for both clinical and research outcomes.

Through a series of patient interviews, physician surveys, and lessons learned in rheumatoid arthritis, the GRAPPA Flare Project is close to a validated flare instrument. A 10-question flare assessment tool is now in the final validation stage, according to a presentation at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

“Flare is a clearly personal experience and varies from patient to patient. It’s clear that physicians and patients have clearly different ideas of what flare is. Bringing those two worlds together was a challenge,” Philip Helliwell, MD, of Leeds (England) University and GRAPPA president, said at the meeting.

James Heilman, MD/Wikimedia Commons/CC BY-SA 3.0

“Some societies – I’m not going to mention any names – have gone down the route of a definition of flare linked to disease activity measures. We have not done this,” Dr. Helliwell said.

Instead, the Flare Project is taking a patient-driven and physician-reviewed approach. Investigators cast a wide net, identifying 79 factors important to patients in six major domains: skin, joint, emotional, participation, fatigue, and unclassified. The results were published in 2015 (Rheumatology [Oxford]. 2015 Aug;54[8]:1448-53). Through a Delphi survey, physicians reviewed these considerations. Then GRAPPA identified items important to both patients and physicians and developed a preliminary flare instrument.

Unlike most assessment tools for psoriatic disease, the new instrument includes patient-reported emotional well-being. Niti Goel, MD, of Duke University, Durham, N.C., said that physicians do not always ask patients about the psychological impact of their disease, so the tool “could provide additional information.”

Another goal of the project is to provide standard answers to some of the common questions related to psoriatic arthritis, including: What exactly is a flare? Does the definition truly capture the worsening of disease? Are there different types of flares? Is flare different if you start from a point of high disease activity? What self-management and other interventions are effective for flare?

GRAPPA adopted a definition of flare developed from rheumatoid arthritis, stating that flare is any worsening of disease activity that would, if persistent, in most cases lead to initiation or change of therapy (J Rheumatol. 2009 Oct;36[10]:2335-41).

“It took [them] some time to get to that definition,” Dr. Helliwell said. “We know from rheumatoid arthritis that there is a lot more to a flare than joint swelling and pain.”

The GRAPPA flare tool is now in the validation stage, Dr. Helliwell said, and will be tested in several studies, including a prospective multicenter study where the 10-item questionnaire will be administered to patients.

A meeting attendee commented that the patient and physician global scales are sufficient and asked: “Is there really a need for a flare instrument?”

“I accept what you are saying, but I would also retort that knowledge is power, and the more information we get, the more we know about what we are doing,” Dr. Helliwell said. “We are going to collect all our information – physician global, patient global, composite disease measures – everything within that study.”

Dr. Helliwell and Dr. Goel reported having no relevant financial disclosures.

One-third of the individuals who received a multicomponent meningococcal B vaccine during an outbreak did not show a protective response against the outbreak strain, though they also did not contract the disease, a study showed.

“This level of seropositivity was lower than expected, given the antigenic similarity between the outbreak strain and the components of the vaccine and given that the Meningococcal Antigen Typing System predicted that 4CMenB would induce responses against the outbreak strain,” Nicole E. Basta, PhD, of the University of Minnesota, Minneapolis, and her associates wrote in the New England Journal of Medicine (2016;375:220-8. doi:10.1056/NEJMoa1514866).

©Steve Mann/thinkstockphotos.com

“Our results indicate that knowledge of [human complement serum bactericidal antibodies] immunity against the vaccine reference strains is not sufficient to predict individual-level immunity against an outbreak strain, even when the strain expresses one or more antigens that are closely related to the vaccine antigens,” the investigators added.

Amidst an outbreak of meningococcal B at Princeton (N.J.) University in the winter of 2013, the Food and Drug Administration allowed use of the meningococcal serogroup B (4CMenB) vaccine before its licensure, in an attempt to control the outbreak. Two strains of meningitis were used in developing this vaccine: 5/99 strain, which was not at all similar to the outbreak strain, and 44/76-SL, which was 96% genetically similar to the outbreak strain.

Among 535 people who completed the study, 499 individuals received two doses of 4CMenB 10 weeks apart, 17 received one dose of the vaccine, and 19 were unvaccinated. When the fully vaccinated individuals were tested for titers 8 weeks after their second dose, two-thirds (66.1%) had low-level seropositivity for the outbreak strain, with a geometric mean titer (GMT) of 7.6. One in five of the unvaccinated people (21.1%) had low seropositivity for the outbreak strain (GMT, 2.8), and 58.8% of the partly vaccinated individuals had seropositivity with a GMT of 5.4.

The researchers then assessed titers for the two strains used in developing 4CMenB in 61 fully vaccinated individuals, all randomly selected from the one-third of fully vaccinated people who did not have a detectable response to the outbreak strain. Most of them (86.9%) were seropositive for the 44/76-SL strain with a GMT of 17.4, and all of them were seropositive for the 5/99 strain, with a considerably larger GMT of 256.3.

Among those fully vaccinated who responded to the outbreak strain with titers above 8, all had seropositivity for 44/76-SL (GMT, 178.8), and 96.7% had seropositivity for the 5/99 strain (GMT, 214.2). Among the 18 unvaccinated individuals, just 1 had very low seropositivity to the 5/99 strain (GMT, 1.2), and 6 of them (33.3%) responded to the 44/76-SL strain (GMT, 3.2).

“These findings have implications for vaccination policies aimed at preventing and controlling meningococcal B disease,” the authors wrote.

The research was funded by Princeton University, the National Institutes of Health, and the Department of Homeland Security. Dr. Bai, Dr. Borrow, and Dr. Findlow reported having previously received research funding, unrelated to this study, from GlaxoSmithKline, Novartis, Pfizer, and Sanofi Pasteur. Dr. Johnsen has been reimbursed for travel expenses from Pfizer for a presentation. No other authors had financial disclosures.

One-third of the individuals who received a multicomponent meningococcal B vaccine during an outbreak did not show a protective response against the outbreak strain, though they also did not contract the disease, a study showed.

“This level of seropositivity was lower than expected, given the antigenic similarity between the outbreak strain and the components of the vaccine and given that the Meningococcal Antigen Typing System predicted that 4CMenB would induce responses against the outbreak strain,” Nicole E. Basta, PhD, of the University of Minnesota, Minneapolis, and her associates wrote in the New England Journal of Medicine (2016;375:220-8. doi:10.1056/NEJMoa1514866).

©Steve Mann/thinkstockphotos.com

“Our results indicate that knowledge of [human complement serum bactericidal antibodies] immunity against the vaccine reference strains is not sufficient to predict individual-level immunity against an outbreak strain, even when the strain expresses one or more antigens that are closely related to the vaccine antigens,” the investigators added.

Amidst an outbreak of meningococcal B at Princeton (N.J.) University in the winter of 2013, the Food and Drug Administration allowed use of the meningococcal serogroup B (4CMenB) vaccine before its licensure, in an attempt to control the outbreak. Two strains of meningitis were used in developing this vaccine: 5/99 strain, which was not at all similar to the outbreak strain, and 44/76-SL, which was 96% genetically similar to the outbreak strain.

Among 535 people who completed the study, 499 individuals received two doses of 4CMenB 10 weeks apart, 17 received one dose of the vaccine, and 19 were unvaccinated. When the fully vaccinated individuals were tested for titers 8 weeks after their second dose, two-thirds (66.1%) had low-level seropositivity for the outbreak strain, with a geometric mean titer (GMT) of 7.6. One in five of the unvaccinated people (21.1%) had low seropositivity for the outbreak strain (GMT, 2.8), and 58.8% of the partly vaccinated individuals had seropositivity with a GMT of 5.4.

The researchers then assessed titers for the two strains used in developing 4CMenB in 61 fully vaccinated individuals, all randomly selected from the one-third of fully vaccinated people who did not have a detectable response to the outbreak strain. Most of them (86.9%) were seropositive for the 44/76-SL strain with a GMT of 17.4, and all of them were seropositive for the 5/99 strain, with a considerably larger GMT of 256.3.

Among those fully vaccinated who responded to the outbreak strain with titers above 8, all had seropositivity for 44/76-SL (GMT, 178.8), and 96.7% had seropositivity for the 5/99 strain (GMT, 214.2). Among the 18 unvaccinated individuals, just 1 had very low seropositivity to the 5/99 strain (GMT, 1.2), and 6 of them (33.3%) responded to the 44/76-SL strain (GMT, 3.2).

“These findings have implications for vaccination policies aimed at preventing and controlling meningococcal B disease,” the authors wrote.

The research was funded by Princeton University, the National Institutes of Health, and the Department of Homeland Security. Dr. Bai, Dr. Borrow, and Dr. Findlow reported having previously received research funding, unrelated to this study, from GlaxoSmithKline, Novartis, Pfizer, and Sanofi Pasteur. Dr. Johnsen has been reimbursed for travel expenses from Pfizer for a presentation. No other authors had financial disclosures.

One-third of the individuals who received a multicomponent meningococcal B vaccine during an outbreak did not show a protective response against the outbreak strain, though they also did not contract the disease, a study showed.

“This level of seropositivity was lower than expected, given the antigenic similarity between the outbreak strain and the components of the vaccine and given that the Meningococcal Antigen Typing System predicted that 4CMenB would induce responses against the outbreak strain,” Nicole E. Basta, PhD, of the University of Minnesota, Minneapolis, and her associates wrote in the New England Journal of Medicine (2016;375:220-8. doi:10.1056/NEJMoa1514866).

©Steve Mann/thinkstockphotos.com

“Our results indicate that knowledge of [human complement serum bactericidal antibodies] immunity against the vaccine reference strains is not sufficient to predict individual-level immunity against an outbreak strain, even when the strain expresses one or more antigens that are closely related to the vaccine antigens,” the investigators added.

Amidst an outbreak of meningococcal B at Princeton (N.J.) University in the winter of 2013, the Food and Drug Administration allowed use of the meningococcal serogroup B (4CMenB) vaccine before its licensure, in an attempt to control the outbreak. Two strains of meningitis were used in developing this vaccine: 5/99 strain, which was not at all similar to the outbreak strain, and 44/76-SL, which was 96% genetically similar to the outbreak strain.

Among 535 people who completed the study, 499 individuals received two doses of 4CMenB 10 weeks apart, 17 received one dose of the vaccine, and 19 were unvaccinated. When the fully vaccinated individuals were tested for titers 8 weeks after their second dose, two-thirds (66.1%) had low-level seropositivity for the outbreak strain, with a geometric mean titer (GMT) of 7.6. One in five of the unvaccinated people (21.1%) had low seropositivity for the outbreak strain (GMT, 2.8), and 58.8% of the partly vaccinated individuals had seropositivity with a GMT of 5.4.

The researchers then assessed titers for the two strains used in developing 4CMenB in 61 fully vaccinated individuals, all randomly selected from the one-third of fully vaccinated people who did not have a detectable response to the outbreak strain. Most of them (86.9%) were seropositive for the 44/76-SL strain with a GMT of 17.4, and all of them were seropositive for the 5/99 strain, with a considerably larger GMT of 256.3.

Among those fully vaccinated who responded to the outbreak strain with titers above 8, all had seropositivity for 44/76-SL (GMT, 178.8), and 96.7% had seropositivity for the 5/99 strain (GMT, 214.2). Among the 18 unvaccinated individuals, just 1 had very low seropositivity to the 5/99 strain (GMT, 1.2), and 6 of them (33.3%) responded to the 44/76-SL strain (GMT, 3.2).

“These findings have implications for vaccination policies aimed at preventing and controlling meningococcal B disease,” the authors wrote.

The research was funded by Princeton University, the National Institutes of Health, and the Department of Homeland Security. Dr. Bai, Dr. Borrow, and Dr. Findlow reported having previously received research funding, unrelated to this study, from GlaxoSmithKline, Novartis, Pfizer, and Sanofi Pasteur. Dr. Johnsen has been reimbursed for travel expenses from Pfizer for a presentation. No other authors had financial disclosures.

Acinetobacter baumanii was the most common cause of ventilator-associated pneumonia in ICU patients, and the risk of A. baumannii infection was significantly higher when airways were colonized with Candida species, based on data from 618 adults.

A. baumannii is a frequent cause of ventilator-associated pneumonia (VAP) in ICU patients, but its potential interactions with Candida species have not been well studied, wrote Dr. Xiaojiang Tan of Southern Medical University, Guangzhou, China, and colleagues (Med Mycol. 2016 Aug 1;54[6]:557-66. doi: 10.1093/mmy/myw009). The researchers reviewed data from 264 ICU patients on mechanical ventilation who had Candida species airway colonization and 354 who did not.

Overall, Candida was an independent risk factor for A. baumannii VAP; patients with Candida were significantly more likely than those without Candida to develop A. baumannii (23% vs. 15%). Other independent risk factors for A. baumannii VAP included the use of a central venous catheter and the use of mechanical ventilation for at least 7 days. Among patients on mechanical ventilation for at least 48 hours, Candida airway colonization occurred in 43%, and A. baumannii VAP occurred in 18%.

GrahamColm/Wikimedia Commons

Candida albicans showed an especially strong association with A. baumannii VAP; it was identified in 38% of cases, compared with 21% caused by non-albicans species.

No significant differences in hospital stay or in-hospital mortality were noted between Candida-colonized and noncolonized patients, and antifungal treatment had no apparent impact on the development of A. baumannii VAP, but antifungals were associated with higher in-hospital mortality (53% vs. 39%, P = .037).

The results were limited by the retrospective nature of the study and the use of data from a single center; thus, the relationship between Candida and A. baumannii VAP may not be generalizable, the researchers noted. However, “the strong independent association between the two suggests that Candida spp. growth from the lower respiratory tract in intubated patients could be an important indicator of the risk for VAP, and even that C. albicans airway colonization may play a role in subsequent development of A. baumannii VAP,” they wrote.

The researchers reported having no relevant financial conflicts.

Acinetobacter baumanii was the most common cause of ventilator-associated pneumonia in ICU patients, and the risk of A. baumannii infection was significantly higher when airways were colonized with Candida species, based on data from 618 adults.

A. baumannii is a frequent cause of ventilator-associated pneumonia (VAP) in ICU patients, but its potential interactions with Candida species have not been well studied, wrote Dr. Xiaojiang Tan of Southern Medical University, Guangzhou, China, and colleagues (Med Mycol. 2016 Aug 1;54[6]:557-66. doi: 10.1093/mmy/myw009). The researchers reviewed data from 264 ICU patients on mechanical ventilation who had Candida species airway colonization and 354 who did not.

Overall, Candida was an independent risk factor for A. baumannii VAP; patients with Candida were significantly more likely than those without Candida to develop A. baumannii (23% vs. 15%). Other independent risk factors for A. baumannii VAP included the use of a central venous catheter and the use of mechanical ventilation for at least 7 days. Among patients on mechanical ventilation for at least 48 hours, Candida airway colonization occurred in 43%, and A. baumannii VAP occurred in 18%.

GrahamColm/Wikimedia Commons

Candida albicans showed an especially strong association with A. baumannii VAP; it was identified in 38% of cases, compared with 21% caused by non-albicans species.

No significant differences in hospital stay or in-hospital mortality were noted between Candida-colonized and noncolonized patients, and antifungal treatment had no apparent impact on the development of A. baumannii VAP, but antifungals were associated with higher in-hospital mortality (53% vs. 39%, P = .037).

The results were limited by the retrospective nature of the study and the use of data from a single center; thus, the relationship between Candida and A. baumannii VAP may not be generalizable, the researchers noted. However, “the strong independent association between the two suggests that Candida spp. growth from the lower respiratory tract in intubated patients could be an important indicator of the risk for VAP, and even that C. albicans airway colonization may play a role in subsequent development of A. baumannii VAP,” they wrote.

The researchers reported having no relevant financial conflicts.

Acinetobacter baumanii was the most common cause of ventilator-associated pneumonia in ICU patients, and the risk of A. baumannii infection was significantly higher when airways were colonized with Candida species, based on data from 618 adults.

A. baumannii is a frequent cause of ventilator-associated pneumonia (VAP) in ICU patients, but its potential interactions with Candida species have not been well studied, wrote Dr. Xiaojiang Tan of Southern Medical University, Guangzhou, China, and colleagues (Med Mycol. 2016 Aug 1;54[6]:557-66. doi: 10.1093/mmy/myw009). The researchers reviewed data from 264 ICU patients on mechanical ventilation who had Candida species airway colonization and 354 who did not.

Overall, Candida was an independent risk factor for A. baumannii VAP; patients with Candida were significantly more likely than those without Candida to develop A. baumannii (23% vs. 15%). Other independent risk factors for A. baumannii VAP included the use of a central venous catheter and the use of mechanical ventilation for at least 7 days. Among patients on mechanical ventilation for at least 48 hours, Candida airway colonization occurred in 43%, and A. baumannii VAP occurred in 18%.

GrahamColm/Wikimedia Commons

Candida albicans showed an especially strong association with A. baumannii VAP; it was identified in 38% of cases, compared with 21% caused by non-albicans species.

No significant differences in hospital stay or in-hospital mortality were noted between Candida-colonized and noncolonized patients, and antifungal treatment had no apparent impact on the development of A. baumannii VAP, but antifungals were associated with higher in-hospital mortality (53% vs. 39%, P = .037).

The results were limited by the retrospective nature of the study and the use of data from a single center; thus, the relationship between Candida and A. baumannii VAP may not be generalizable, the researchers noted. However, “the strong independent association between the two suggests that Candida spp. growth from the lower respiratory tract in intubated patients could be an important indicator of the risk for VAP, and even that C. albicans airway colonization may play a role in subsequent development of A. baumannii VAP,” they wrote.

The researchers reported having no relevant financial conflicts.

Thrombus

Image by Andre E.X. Brown

The European Medicines Agency’s Committee for Medicinal Products for Human Use (CHMP) has recommended approval for 2 biosimilars of the low-molecular-weight heparin enoxaparin.

Both of the agents, Inhixa and Thorinane, are intended to prevent and treat thrombosis-related disorders in adults.

The CHMP’s recommendations will be reviewed by the European Commission.

If the recommendations are formally adopted, Inhixa and Thorinane will be approved for use in the European Union as well as Norway, Liechtenstein, and Iceland.

Both Inhixa and Thorinane are indicated for:

• Prophylaxis of venous thromboembolism (VTE), particularly in patients undergoing orthopedic, general, or oncological surgery.
• VTE prophylaxis in patients bedridden due to acute illnesses, including acute heart failure, acute respiratory failure, severe infections, and exacerbation of rheumatic diseases causing immobilization of the patient (applies to strengths of 40 mg/0.4 mL).
• Treatment of deep vein thrombosis, complicated or uncomplicated by pulmonary embolism.
• Treatment of unstable angina and non-Q wave myocardial infarction, in combination with acetylsalicylic acid.
• Treatment of acute ST segment elevation myocardial infarction, including patients who will be treated conservatively or who will later undergo percutaneous coronary angioplasty (applies to strengths of 60 mg/0.6 mL, 80 mg/0.8 mL, and 100 mg/1 mL).
• VTE prevention in the extracorporeal circulation during hemodialysis.

If approved, Inhixa will be available as a solution for injection—2000 IU (20 mg) in 0.2 mL, 4000 IU (40 mg) in 0.4 mL, 6000 IU (60 mg) in 0.6 mL, 8000 IU (80 mg) in 0.8 mL, and 10,000 IU (100 mg) in 1 mL.

And Thorinane will be available as a solution for injection—2000 IU (20 mg) in 0.2 mL, 4000 IU (40 mg) in 0.4 mL, 6000 IU (60 mg) in 0.6 mL, 8000 IU (80 mg) in 0.8 mL, and 10,000 IU (100 mg) in 1 mL.

Inhixa is being developed by Techdow Europe AB, and Thorinane is being developed by Pharmathen S.A.

Thrombus

Image by Andre E.X. Brown

The European Medicines Agency’s Committee for Medicinal Products for Human Use (CHMP) has recommended approval for 2 biosimilars of the low-molecular-weight heparin enoxaparin.

Both of the agents, Inhixa and Thorinane, are intended to prevent and treat thrombosis-related disorders in adults.

The CHMP’s recommendations will be reviewed by the European Commission.

If the recommendations are formally adopted, Inhixa and Thorinane will be approved for use in the European Union as well as Norway, Liechtenstein, and Iceland.

Both Inhixa and Thorinane are indicated for:

• Prophylaxis of venous thromboembolism (VTE), particularly in patients undergoing orthopedic, general, or oncological surgery.
• VTE prophylaxis in patients bedridden due to acute illnesses, including acute heart failure, acute respiratory failure, severe infections, and exacerbation of rheumatic diseases causing immobilization of the patient (applies to strengths of 40 mg/0.4 mL).
• Treatment of deep vein thrombosis, complicated or uncomplicated by pulmonary embolism.
• Treatment of unstable angina and non-Q wave myocardial infarction, in combination with acetylsalicylic acid.
• Treatment of acute ST segment elevation myocardial infarction, including patients who will be treated conservatively or who will later undergo percutaneous coronary angioplasty (applies to strengths of 60 mg/0.6 mL, 80 mg/0.8 mL, and 100 mg/1 mL).
• VTE prevention in the extracorporeal circulation during hemodialysis.

If approved, Inhixa will be available as a solution for injection—2000 IU (20 mg) in 0.2 mL, 4000 IU (40 mg) in 0.4 mL, 6000 IU (60 mg) in 0.6 mL, 8000 IU (80 mg) in 0.8 mL, and 10,000 IU (100 mg) in 1 mL.

And Thorinane will be available as a solution for injection—2000 IU (20 mg) in 0.2 mL, 4000 IU (40 mg) in 0.4 mL, 6000 IU (60 mg) in 0.6 mL, 8000 IU (80 mg) in 0.8 mL, and 10,000 IU (100 mg) in 1 mL.

Inhixa is being developed by Techdow Europe AB, and Thorinane is being developed by Pharmathen S.A.

Thrombus

Image by Andre E.X. Brown

The European Medicines Agency’s Committee for Medicinal Products for Human Use (CHMP) has recommended approval for 2 biosimilars of the low-molecular-weight heparin enoxaparin.

Both of the agents, Inhixa and Thorinane, are intended to prevent and treat thrombosis-related disorders in adults.

The CHMP’s recommendations will be reviewed by the European Commission.

If the recommendations are formally adopted, Inhixa and Thorinane will be approved for use in the European Union as well as Norway, Liechtenstein, and Iceland.

Both Inhixa and Thorinane are indicated for:

• Prophylaxis of venous thromboembolism (VTE), particularly in patients undergoing orthopedic, general, or oncological surgery.
• VTE prophylaxis in patients bedridden due to acute illnesses, including acute heart failure, acute respiratory failure, severe infections, and exacerbation of rheumatic diseases causing immobilization of the patient (applies to strengths of 40 mg/0.4 mL).
• Treatment of deep vein thrombosis, complicated or uncomplicated by pulmonary embolism.
• Treatment of unstable angina and non-Q wave myocardial infarction, in combination with acetylsalicylic acid.
• Treatment of acute ST segment elevation myocardial infarction, including patients who will be treated conservatively or who will later undergo percutaneous coronary angioplasty (applies to strengths of 60 mg/0.6 mL, 80 mg/0.8 mL, and 100 mg/1 mL).
• VTE prevention in the extracorporeal circulation during hemodialysis.

If approved, Inhixa will be available as a solution for injection—2000 IU (20 mg) in 0.2 mL, 4000 IU (40 mg) in 0.4 mL, 6000 IU (60 mg) in 0.6 mL, 8000 IU (80 mg) in 0.8 mL, and 10,000 IU (100 mg) in 1 mL.

And Thorinane will be available as a solution for injection—2000 IU (20 mg) in 0.2 mL, 4000 IU (40 mg) in 0.4 mL, 6000 IU (60 mg) in 0.6 mL, 8000 IU (80 mg) in 0.8 mL, and 10,000 IU (100 mg) in 1 mL.

Inhixa is being developed by Techdow Europe AB, and Thorinane is being developed by Pharmathen S.A.