Complete Resolution Of Skin Lesions Research Articles

Periorale Dermatitis im Kindesalter - Klinik, Ätiopathogenese und Therapie unter Berücksichtigung eigener Erfahrungen mit dem Einsatz von 20 %iger Azelainsäure-Creme

Perioral dermatitis, a common skin disease in young women, has been rarely reported in children. In this study, 8 children aged 3 - 12 (main 7.5) years suffering from perioral dermatitis for 3 - 7 (main 4.9) months were evaluated. The disease had developed in typical distribution and morphology, with perinasal and periocular lesions along with classical perioral lesions being present. In all patients low- to high-potency topical glucocorticosteroids had been used in the face prior to the onset of disease. Atopy was found in half of the patients. Allergological, bacteriological and mycological examinations did not reveal any pathological results. Demodex mites could not be demonstrated by skin surface biopsies. Patients were treated with 20 % azelaic acid cream which was topically applied twice daily on all affected areas. Treatment led to complete resolution of skin lesions after 4 - 8 (mean 5.6) weeks in all patients. Transient exacerbation of skin condition with a peak between the 2 nd and 6 th day of treatment could be observed in 3 patients, but no additional internal medication was necessary. Side-effects of 20 % azelaic acid cream were registered in 6 patients and were predominantly present in the first two weeks of treatment. Most patients felt short-standing burning sensation immediately after topical application. Side-effects were minimal and became more rare with ongoing treatment. No recurrences were seen within a follow-up period of 2 - 8 (mean 4.6) months. The results of this study are encouraging and should be confirmed by further placebo-controlled studies in larger patient groups.

Phase II Study of Low-Dose Decitabine for the Front-Line Treatment of Older Patients with Acute Myeloid Leukemia (AML).

Decitabine (Dacogen™) was recently approved for the treatment of patients with myelodysplastic syndromes (MDS). Response in MDS is associated with reversal of the hypermethylated phenotype of silenced genes. The prevalence of hypermethylated genes contributing to AML progression, coupled with the challenges involved in the treatment of AML in the elderly, is a basis for exploring the activity of decitabine in this patient population. The objective of this phase II trial was to estimate the rate of morphologic complete response (CR) in patients with AML. To be eligible for the study, patients had to be at least 60 years old with newly diagnosed, untreated AML with intermediate- or poor-risk cytogenetics, and they could not be candidates for standard induction chemotherapy. Decitabine was given at a dose of 20 mg/m2 over 1 hour for 5 consecutive days every 4 weeks. At the time of the analysis, 27 patients were enrolled in the trial (14 men, 13 women; median age = 69 years, range = 61–87) and received at least 1 cycle of treatment (median = 4, range = 1–10). Seventeen patients (63%) received 3 or more cycles of treatment. Seven of 27 patients (26%) responded, 2 patients (7%) with a morphologic CR, 1 patient (4%) with a complete cytogenetic response (CRc), and 4 patients (15%) with a morphologic CR with incomplete blood count recovery (CRi) according to AML response criteria (Cheson, JCO 2003). In addition to these defined responses, 11 other patients demonstrated clinical benefit by achieving stable disease, with 4 of these patients having a >25% reduction in bone marrow blasts. Median time to response was 3 treatment cycles. Of the 13 patients with a prior history of MDS, 6 patients had a response (CR, CRc, or CRi, 46%). Two of 2 patients with leukemia cutis exhibited complete resolution of skin lesions and responded (CR or CRi). Eight patients discontinued treatment prior to receiving 3 cycles because of death, progressive disease, or patient decision. All patients were evaluated for safety. Besides myelosuppression, the most commonly reported adverse events considered related to decitabine treatment were fatigue, nausea, febrile neutropenia, vomiting, and asthenia. Decitabine given daily for 5 days showed activity in patients with newly diagnosed AML, with a toxicity profile that was manageable in this older patient population. The results to date are comparable to those from previous studies in AML patients using a variety of decitabine schedules, which have reported CR rates from 14% to 33% (Blood 2004; 103:1635, Blood 2005; 106:527a, Cancer 2006; 106:1794). Updated response and adverse event data will be available at the time of presentation.

Paraneoplastic pemphigus resembling linear IgA bullous dermatosis

A 69-year-old Chinese man presented in 2001 with a blistering eruption over the upper and lower limbs associated with oral ulceration for 1 month. He had stage IIIA follicular small cell cleaved non-Hodgkin's lymphoma diagnosed 5 years previously, and had received several lines of palliative chemotherapy, including two courses of chlorambucil, six cycles of cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP), and two four-cycle courses of rituximab, with disease stabilization at the time of presentation. Examination revealed erythematous, annular plaques with raised, urticarial borders studded with tense bullae and vesicles over the thighs. Some lesions were arciform and annular, with vesicles arranged in a ring at the border (Fig. 1). There was involvement of the feet with desquamation at the tips of the toes (Fig. 2). Severe erosions with hemorrhagic crusts on the lips, tongue, and buccal mucosa were seen. Herpes simplex virus serology was negative. A biopsy specimen from a vesicle on the left thigh showed suprabasal acantholysis (Fig. 3), some apoptotic keratinocytes (Fig. 4), satellite cell necrosis in the epidermis, and a superficial perivascular infiltrate of lymphocytes and eosinophils. Direct immunofluorescence showed intercellular immunoglobulin G (IgG) and C3 within the epidermis and along the basement membrane zone. Indirect immunofluorescence on monkey esophagus was positive for anti-intercellular antibody at a titre of 1/160 and positive on rat bladder at a titre of 1/80. A presumptive diagnosis of paraneoplastic pemphigus was made. This was later confirmed by the presence of antibodies against envoplakin (210 kDa), periplakin (190 kDa), and desmoglein 1 on immunoprecipitation studies. He was started on prednisolone 60 mg/day (1 mg/kg/day), with complete resolution of skin lesions within 1 week, but persistence of oral ulcers. Cyclophosphamide was added at a low dose of 1 mg/kg/day as he had baseline leukopenia. Cyclosporine was later added to a maximum of 4 mg/kg/day with only mild improvement of the oral lesions. He declined rituximab therapy. He died 2 months later from fulminant pneumonia.

Severe Eczematous Skin Reaction After High-Dose Intravenous Immunoglobulin Infusion

High-dose intravenous immunoglobulins (IVIGs) are increasingly used to treat inflammatory and/or autoimmune disorders. In dermatology, they provide therapeutic benefit in Kawasaki disease and certain cases of dermatomyositis. While most adverse effects following IVIG treatment are not severe, occasionally more severe adverse effects occur, including anaphylactic reactions and acute, usually transient, renal failure. We report 4 cases of a characteristic severe extensive eczematous reaction that occurred approximately 10 days after IVIG infusion for polyradiculoneuritis. In all cases, onset was characterized by dyshidrotic lesions on the palms, rapidly followed by pruriginous maculopapular lesions involving the whole body. All patients were treated with topical and/or systemic steroids, and complete resolution of skin lesions was observed within 1 month. To date, 33 cases of cutaneous rash following IVIG infusion have been reported in the literature, mostly in neurology journals, and the features are identical to those reported herein. Severe eczematous skin reaction with a characteristic initial localization to the palms and/or soles that then extends to the rest of the body is a rare but characteristic adverse effect of high-dose IVIG therapy. Although the precise mechanism of this cutaneous eruption remains to be elucidated, its occurrence within days of IVIG infusion, its characteristic distribution at onset, and its clinical course should be recognized by dermatologists.

Corticosteroid therapy of zoster-associated pain

Lack of exact clinical studies on effects of corticosteroids in therapy and prevention of herpes zoster-related pain, elicited many controversies in the past. The aim of our study was to estimate effects of prednisone on frequency, intensity and duration of postherpetic neuralgia. 68 immunocompetent herpes zoster patients, 8-90 years of age (37 females and 31 males, mean age 55.7 years) were enrolled for study; 30 patients were treated with acyclovir (5 x 800 mg daily for a 7-day period) and prednisone (initial daily dose 60 mg, tapering over 14 days), and the control group of 38 patients with acyclovir only. Patients were clinically followed up for 3 months after complete resolution of skin lesions. Chi-square test was used in statistical data analysis. The difference regarding incidence of postherpetic neuralgia in acyclovir/prednisone group and acyclovir group (although slightly less in the former one) was not significant. Duration of postherpetic neuralgia over 3 months was similar in both groups. Mild postherpetic pain was more common in the acyclovir/prednisone group (44.4%) than in the acyclovir group (28.6%); however, statistical validation requires more patients to be studied. Results of our study didn't confirm efficiency of prednisone regarding occurrence and characteristics of postherpetic neuralgia. Failure of prednisone therapy may be partly contributed to advanced age of patients and delayed onset of therapy. Use of corticosteroids in zoster patients gives neither reliable protection from appearance of postherpetic neuralgia, nor shortens its duration. Further investigations are necessary to estimate their effects on postherpetic pain.

Subacute Cutaneous Lupus Erythematosus Induced by Nifedipine

Background: Subacute cutaneous lupus erythematosus (SCLE) has been reported to be associated with the use of several drugs, including thiazides, terbinafine, and, rarely, calcium channel blockers. Objective: A case of SCLE induced by nifedipine is presented. Methods and Results: A 48-year-old white woman developed a papulosquamous and annular eruption in sun-exposed areas during the summer. The patient was taking nifedipine for essential hypertension for four years. Serology showed the presence of antinuclear and anti-Ro/SSA as well as antihistone antibodies. Histopathologic and immunopathologic (granular IgM deposits at the dermoepidermal junction) findings confirmed the diagnosis of SCLE. Nifedipine discontinuation led to rapid improvement with almost complete resolution of skin lesions in one month in the absence of active treatment. Reduction of antinuclear, anti-Ro/SSA, and antihistone antibody levels was documented after six months. Conclusion: Nifedipine can cause SCLE after a long period of administration. Antihistone antibodies may be associated with drug-induced SCLE.

Thymic origin of abnormal lymphoid cells in Sézary syndrome.

A patient with a 5-year history of pruritus and progressive and generalized erythroderma was found to have abnormal lymphocytes in the peripheral blood and mononuclear dermal infiltrate, all of which are features consistent with those described in Sézary syndrome. Systemic chemotherapy produced an almost complete resolution of skin lesions and pruritus. Serial studies on the abnormal cells included responses to phytohemagglutinin, cytogenetics, and immunofluorescence tests for identification of B or T lymphocytes. The abnormal cells demonstrated hyperdiploidy; the ratio of B to T cells fell whenever abnormal lymphocytes appeared in the peripheral blood, and returned to normal when abnormal cells disappeared from circulation. Lymphocytes separated from a skin nodule labeled as T cells. We conclude that the abnormal lymphocytes in this patient are of thymic origin.

Retinoic acid in the treatment of lichen planus.

Five patients with lichen planus were treated with retinoic acid, and all 5 patients showed almost complete resolution of skin lesions within 1 month. In 4 of the cases treatment started 2–3 months after the beginning of the disease. With retinoic acid by mouth, relief of pruritus and flattening of papules was achieved leaving only residual pigmentation. Hyperkeratotic lesions improved only when retinoic acid was applied topically. The effects of treatment on the duration of the disease are discussed.