Drug-induced psoriasis: clinical perspectives.

Exposure to certain drugs can elicit an induction or exacerbation of psoriasis. Although well-conducted systematic studies on drug-related psoriasis are mostly lacking, traditionally strong associations have been documented for beta-blockers, lithium, antimalarial drugs such as (hydroxy)chloroquine, interferons, imiquimod, and terbinafine. More recently, new associations have been reported for monoclonal antibody- and small-molecule-based targeted therapies used for oncological and immunological indications, such as tumor necrosis factor-alpha antagonists and anti-programmed cell death protein 1 immune checkpoint inhibitors. Recognizing potential drug-related psoriasis is of clinical relevance to allow an optimal management of psoriasis. However, in clinical practice, identifying medication-related exacerbations and induction of psoriasis can be challenging. The clinical and histopathological features of drug-provoked psoriasis may differ little from that of "classical" nondrug-related forms of psoriasis. In addition, the latency period between start of the medication and onset of psoriasis can be significantly long for some drugs. Assessment of the Naranjo adverse drug reaction probability scale could be used as a practical tool to better differentiate drug-related psoriasis. The first step in the management of drug-related psoriasis is cessation and replacement of the offending drug when deemed clinically possible. However, the induced psoriasis skin lesions may persist after treatment withdrawal. Additional skin-directed treatment options for drug-related psoriasis follows the conventional psoriasis treatment guidelines and includes topical steroids and vitamin D analogs, ultraviolet phototherapy, systemic treatments, such as acitretin, methotrexate, and fumaric acid esters, and biological treatments.

The Association between Atopic Disorders and Keloids: A Case-control Study.

BACKGROUND: Keloids and atopic disorders share common inducing and maintaining inflammatory pathways that are characterized by T-helper cell 2 cytokines. AIMS AND OBJECTIVES: The objective of this study was to test for associations between keloids and atopic eczema, asthma and hay fever. MATERIALS AND METHODS: This was a case-control study with 131 patients diagnosed with keloids at our dermatology outpatient clinic between 2000 and 2012. Controls were 258 partners of keloid or sarcoidosis patients. Patient who reported life time prevalences of atopic eczema, asthma and hay fever were assessed using a questionnaire based on The European Community Respiratory Health Survey (ECRHS) and The International Study of Asthma and Allergies in Children (ISAAC). RESULTS: The prevalence of asthma was lower in keloid patients (19/131 vs. 20/258, P = 0.035), as was being diagnosed with asthma by a physician (18/131 vs. 19/258, P = 0.039) and using inhalators for asthma (13/131 vs. 7/258, P = 0.02). After adjusting for age and non-European descent the odds ratio for having a keloid was (adjusted OR = 4.44; 95% CI 1.59-12.40) in asthmatics using inhalators. There were no clear and consistent associations found for keloids with atopic eczema or with hay fever. CONCLUSION: In conclusion, our study shows that keloids may be strongly associated with atopic asthma. Atopic eczema and hay fever do not seem to be correlated with keloid. Further studies are warranted to assess the validity of atopic asthma as a risk factor for the development of keloid scars.

Cidofovir gel as treatment of follicular spicules in multiple myeloma.

IMPORTANCE: The cause of follicular spicules in multiple myeloma (MM) is not known. OBSERVATIONS: We present a case of follicular spicules in a patient with MM, which is very reminiscent of trichodysplasia spinulosa caused by a polyomavirus. No trichodysplasia spinulosa-associated polyomavirus could be isolated from the skin lesions; however, the spicules were positive for Merkel cell carcinoma virus, which is also a polyomavirus. CONCLUSIONS AND RELEVANCE: Follicular spicules in MM are probably not caused by the trichodysplasia spinulosa-associated virus. Merkel cell polyomavirus could contribute to the origin of this dermatosis.

Prevalence of atopic diseases in patients with sarcoidosis.

It remains unclear whether atopy is associated with the occurrence of sarcoidosis or affects its severity. The purpose of this study was to compare the lifetime prevalence of atopic eczema, asthma, and hay fever in sarcoidosis patients with controls and to assess whether atopy influences the severity of sarcoidosis. The prevalence of atopic disorders assessed with a validated postal questionnaire in sarcoidosis patients with pulmonary, uveitis, and cutaneous sarcoidosis was compared with that of their domestic partners in a case-control study. The serological parameters, the pulmonary function tests, and the high-resolution computed tomography (HRCT) scans of atopic and nonatopic sarcoidosis patients were compared in a nested cohort. Multivariate logistic regression models were used to calculate the odds ratios (ORs) and the 95% confidence intervals (CIs). Two hundred twenty-five sarcoidosis patients and 177 controls were included. The prevalences of atopic eczema, asthma, and hay fever were comparable between patients and controls (12.4% versus 12.4%, 5.3% versus 5.6%, and 16.9% versus 15.8%, respectively). After adjusting for gender and ethnicity, those with sarcoidosis and a history of atopic eczema were significantly less likely to have uveitis (OR, 0.30; 95% CI, 0.13-0.71). Within the sarcoidosis cohort, the distributions of serological markers, the lung function tests, and the HRCT scans were similar between atopic and nonatopic patients. Atopy is not associated with the occurrence of sarcoidosis, but atopic eczema may decrease the likelihood of eye involvement.

Human IgE(+) B cells are derived from T cell-dependent and T cell-independent pathways.

BACKGROUND: The prevalence of IgE-mediated diseases has been increasing worldwide, yet IgE-expressing B cells are poorly characterized, mainly because of their scarcity and low membrane IgE levels. OBJECTIVE: We sought to study the immunobiology of human IgE-expressing B cells in healthy subjects and patients with allergic disease. METHODS: We used a stepwise approach for flow cytometric detection and purification of human IgE-expressing B cells in control subjects, CD40 ligand-deficient patients, and patients with atopic dermatitis. Molecular analysis of replication histories, somatic hypermutation (SHM), and immunoglobulin class-switching was performed. RESULTS: Using multicolor flow cytometry, we reliably detected IgE-expressing plasma cells and 2 IgE-expressing memory B-cell subsets. These IgE-expressing cells showed molecular and phenotypic signs of antigen responses. The replication history and SHM levels of IgE(+) plasma cells and CD27(+)IgE(+) memory B cells fitted with a germinal center (GC)-dependent pathway, often through an IgG intermediate, as evidenced from Sγ remnants in Sµ-Sε switch regions. CD27(-)IgE(+) cells showed limited proliferation and SHM and were present in CD40 ligand-deficient patients, indicating a GC-independent origin. Patients with atopic dermatitis had normal numbers of blood IgE(+) plasma cells and CD27(+)IgE(+) memory B cells but increased numbers of CD27(-)IgE(+) memory B cells with high SHM loads compared with those seen in healthy control subjects and patients with psoriasis. CONCLUSIONS: We delineated GC-dependent and GC-independent IgE(+) B-cell responses in healthy subjects and indicated involvement of the GC-independent pathway in a human IgE-mediated disease. These findings provide new insights into the pathogenesis of IgE-mediated diseases and might contribute to accurate monitoring of IgE(+) B cells in patients with severe disease undergoing anti-IgE treatment.

[A man with a painful and swollen ankle]. / Een man met een pijnlijke, gezwollen enkel.

A 58-year-old male patient was referred to the dermatologist because of swelling and pain of his left ankle. Radiodiagnostic imaging revealed an osteodestructive tumor which after biopsy proved to be a chondrosarcoma. Malignancy should be in the differential diagnosis of chronic one-sided edema.

Atopic dermatitis is not a protective factor for melanoma but asthma may be.

BACKGROUND: There is evidence from cohort studies for an inverse association between atopic dermatitis and asthma and cutaneous melanoma. However, these studies have been too heterogeneous and did not show statistically significant results. Also, this association has not been compared to traditional melanoma risk factors. OBJECTIVES: To test for associations between history of atopic disorders and melanoma life-time prevalence, and for associations between atopic disorders and melanoma prognosis. METHODS: Validated questionnaires from the European Community Respiratory Health Survey and International Study of Asthma and Allergies in Children protocol on life-time prevalence of atopic disorders were sent to 280 patients with histopathologically confirmed melanoma. The control group consisted of their spouses. The skin phototype was also assessed using a validated questionnaire. RESULTS: One hundred and eighty-four melanoma patients and 169 controls responded to the questionnaire. The life-time prevalence of atopic dermatitis and hayfever was not different in melanoma patients (8.7 % vs. 8.2, p = 0.890 and 15.2 vs. 18.3 %, p = 0.432, respectively). Asthma was non-significantly lower in melanoma patients (3.8 vs. 8.2 %, p = 0.075). Atopic melanoma patients did not differ from non-atopic patients in terms of Breslow thickness, metastases and second melanomas. CONCLUSION: Atopic dermatitis is not a protective factor in cutaneous melanoma but a history of asthma may be.

Prevalence of cutaneous adverse events associated with long-term disease-modifying therapy and their impact on health-related quality of life in patients with multiple sclerosis: a cross-sectional study.

BACKGROUND: Glatiramer acetate (GA) and interferon-beta (IFN-ß) are disease-modifying therapies (DMTs) for multiple sclerosis that are administered through subcutaneous (SC) or intramuscular (IM) injections. Skin reactions associated with DMTs are common and may influence patient's health-related quality of life (QoL). We aimed to determine the prevalence of cutaneous adverse events associated with long-term DMT use, and to assess the impact of cutaneous adverse events on QoL. METHODS: A cross-sectional study among patients with multiple sclerosis who had been treated with their first DMT for at least 2 years. Cutaneous events were assessed from photographs of injection-sites by dermatologists blinded for DMT. Generic and dermatology-specific health-related QoL were assessed using validated patient-reported questionnaires. RESULTS: A total of 229 patients were enrolled, of whom 156 (68%) had at least one skin reaction. The prevalence of cutaneous adverse events was higher for SC DMTs (75-82%) compared to IM DMT (41%) (P < 0.001). Erythema and lipoatrophy were the most common skin reactions, observed in 156 (68%) and 45 (20%) patients, respectively. Dermatology-specific, but not generic, QoL was significantly lower among patients with skin reactions compared to those without. CONCLUSIONS: The prevalence of cutaneous adverse events was high in long-term DMT-treatment. Patients with cutaneous adverse events had a lower perceived dermatology-specific QoL.

Decreased prevalence of atopic features in patients with psoriatic arthritis, but not in psoriasis vulgaris.

BACKGROUND: The prevalence of atopic disorders is reduced in patients with various autoinflammatory diseases but, to our knowledge, this association has not been studied in psoriasis vulgaris or psoriatic arthritis (PSA). OBJECTIVE: Prevalence of hay fever, asthma, and sensitization to common aeroallergens was compared in patients with psoriasis vulgaris to patients with PSA and control subjects; we also investigated whether atopy influences the arthritis activity and severity scores in patients with PSA. METHODS: In a cross-sectional cohort study design, the differences in patient-reported lifetime prevalence of atopic disorders and serum IgE directed against common aeroallergens were compared. The effect of atopy on arthritis severity was assessed using the 28-joint Disease Activity Score and Health Assessment Questionnaire. Logistic regression models were used to calculate crude and adjusted odds ratios with 95% confidence intervals (CI) for presence of atopy. RESULTS: A total of 168 patients with PSA, 133 patients with psoriasis vulgaris, and 147 control subjects were included. The lifetime prevalence of hay fever did not differ across groups. Patients with PSA were less likely to have had asthma than control subjects (adjusted odds ratio 0.20; 95% CI 0.04-0.92) and they were less likely to be sensitized (adjusted odds ratio 0.50; 95% CI 0.25-0.99). Health Assessment Questionnaire-visual analog scales for pain and for patient global score were significantly reduced by sensitization to common aeroallergens (beta-coefficients -0.54 [95% CI -0.84 to -0.25] and -18.4 [95% CI -28.5 to -8.25], respectively.) LIMITATIONS: This was a cross-sectional, small-numbered study. CONCLUSION: Atopy may protect against development of PSA and diminish its severity.

Non-melanoma skin cancer: the hygiene hypothesis.

Protection against ultra violet radiation-induced DNA-damage in the skin is not only provided by the pigmentary system. The epidermal barrier consisting of stratum corneum keratinocytes, filaggrin and other proteins is an additional component of the UV-shield. Disruption of the epidermal barrier through frequent body cleansing with soaps and cosmetics may increase the risk of non-melanoma skin cancer.

[A neonate with a skin defect]. / Een neonaat met een huiddefect.

A male neonate was born with a defect of the skin and subcutaneous tissue on the back. The pregnancy started as a gemelli pregnancy but in the 12th week 1 fetus deceased. The diagnosis of truncal aplasia cutis was made.

Itch pathophysiology may differ among ethnic groups.

The prevalence of itch is higher in individuals with darker skin types. In this paper, we review the systems involved in the physiology of itch and how they may differ across the races. Current data point out that the differences may be explained by barrier function, mast cell physiology, and itch receptor polymorphisms.