Acroqueratodermia siríngea acuagénica. Aportación de un nuevo caso / Aquagenic syringeal acrokeratoderma

No disponible

No disponible

Prognostic factors in leukocytoclastic vasculitis: a clinicopathologic study of 160 patients.

OBJECTIVE: To analyze risk factors for systemic involvement and long-term course in leukocytoclastic vasculitis. DESIGN: A clinicopathological study of 160 patients with leukocytoclastic vasculitis followed up for at least 3 years. Univariate and multivariate analysis were conducted by logistic regression methods. SETTING: The Bellvitge Hospital, a referral center in Barcelona, Spain. PATIENTS: One hundred sixty patients with cutaneous leukocytoclastic vasculitis. Patients in the categories cutaneous/systemic vasculitis and acute/chronic cutaneous vasculitis were selected for comparative analysis. MAIN OUTCOME MEASURES: Clinical, laboratory, and histopathological findings. RESULTS: Of 89 females and 71 males, aged 14 to 89 years, systemic involvement was documented in 20% of cases. Perinuclear-staining antineutrophil cytoplasmic autoantibodies were found in 21% of patients and cryoglobulins in 25.4%. Of the patients, 1.9% died of systemic vasculitis. The average duration of cutaneous lesions was 27.9 months. In 67.2%, a cause or associated condition was identified. Of the skin specimens, 59.6% showed vasculitis limited to superficial dermal vessels. Direct immunofluorescence was positive in 84.3% of cases. In the multivariate analysis, paresthesia, fever, and absence of painful lesions were found to be risk factors for systemic involvement. Cryoglobulins, arthralgia, and normal temperature were risk factors for chronic cutaneous disease. CONCLUSION: Our results identify prognostic factors in leukocytoclastic vasculitis and may provide some aid in the management of this heterogeneous group of patients.

Radiographic findings and patterns in multidrug-resistant tuberculosis.

Multidrug-resistant tuberculosis (MDR TB) is prevalent in urban areas with large HIV-positive populations. We retrospectively evaluated the chest radiographs of MDR TB patients at presentation and compared them to patients with drug-sensitive tuberculosis (DS TB). Although the overall radiographic findings and patterns of MDR TB and DS TB were similar, there were significant differences among the MDR TB patients depending on how MDR TB was acquired. Patients who developed MDR TB during an outbreak showed noncavitary consolidations, pleural effusions, and a primary radiographic pattern (70%). On the other hand, patients who acquired MDR TB due to noncompliance with antituberculous therapy often had cavitary consolidations (50%) and generally demonstrated a postprimary radiographic pattern. Cavitation occurred equally in patients with MDR TB who are HIV positive regardless of CD4 cell count. Chest radiographic findings and patterns in MDR TB are most accurately interpreted in conjunction with clinical history, specifically prior TB treatment. Nevertheless, approximately one-third of patients did not show the "expected" radiographic pattern.

Lymphocytic autoimmune hidradenitis, cutaneous leucocytoclastic vasculitis and primary Sjögren's syndrome.

We describe a 60-year-old woman with primary Sjögren's syndrome, mixed cryoglobulinaemia and cutaneous leucocytoclastic vasculitis who developed generalized hypohidrosis with a markedly decreased sweating response to pilocarpine chloride. Skin biopsies demonstrated dense peri-eccrine lymphocytic infiltrates in the lower reticular dermis, with glandular atrophy. From previous studies it is evident that although patients with Sjögren's syndrome commonly have skin dryness, a lymphocytic hidradenitis has been documented only in a few cases. The histological findings in this case support the role of autoimmune hidradenitis in the development of hypohidrosis in Sjögren's syndrome.

Mycobacterium kansasii pulmonary infection in patients with AIDS: spectrum of chest radiographic findings.

PURPOSE: To determine the chest radiographic findings and clinical manifestations of Mycobacterium kansasii pulmonary infection in patients with acquired immunodeficiency syndrome (AIDS). MATERIALS AND METHODS: Criteria for diagnosis included two or more positive cultures from respiratory sources, pulmonary symptoms or fever, and no other identifiable cause of pulmonary disease. Chest radiographs at initial examination and follow-up were evaluated for parenchymal opacities, cavitation, adenopathy, and pleural effusions. Medical records were reviewed for clinical signs and symptoms, CD4 cell count, presence of additional pathogens, and response to antimycobacterial therapy. RESULTS: Of 96 patients, 16 (17%) satisfied all criteria for M kansasii pulmonary infection. The mean CD4 cell count was 24/mm3. Twelve patients (75%) demonstrated alveolar opacities, only three (19%) of which were cavitary. Interstitial opacities (6%) and pleural effusions (12%) were uncommon. Four (25%) patients had thoracic lymphadenopathy, which was the only positive radiographic finding in two patients. Fourteen patients were treated for M kansasii, and 10 (71%) showed clinical and radiographic improvement. CONCLUSION: Patients with AIDS and pulmonary M kansasii frequently demonstrate focal alveolar opacities. Symptomatic patients with pulmonary nontuberculous mycobacteria should be presumptively treated for pulmonary M kansasii until final culture results are available.

Adhesion molecule expression and endothelial cell activation in cutaneous leukocytoclastic vasculitis. An immunohistologic and clinical study in 42 patients.

OBJECTIVES: To investigate the sequential expression of adhesion molecules on endothelium and inflammatory cells in cutaneous leukocytoclastic vasculitis, and the relation of these adhesive molecules with clinical and histologic variables. DESIGN: An immunohistochemical analysis (streptavidin-biotin-peroxidase technique) of 42 vasculitic lesions of up to 96 hours was performed using a panel of monoclonal antibodies specific for different adhesion molecules. Twenty normal skin samples and 3 perilesional specimens served as control samples. A clinical protocol was also performed, and patients were followed up for 1 to 5 years. SETTING: A clinicopathologic research unit of a university hospital. PATIENTS: Forty-two patients, 21 women and 21 men, aged 22 to 79 years, with cutaneous leukocytoclastic vasculitis. INTERVENTIONS: Three skin biopsy specimens of vasculitic lesions from each patient were obtained for histopathologic examination on paraffin, direct immunofluorescence, and immunohistochemical analysis on cryostatic tissue sections. MAIN OUTCOME MEASURES: The histologic characteristics and the immunohistochemical-stained specimens were evaluated by 3 independent investigators, using a semiquantitative method. RESULTS: Increased endothelial expression of very late activation antigen-1, HLA-DR, and intercellular adhesion molecule-1 was observed. The induction of E-selectin expression was more marked in recent lesions (P < .001) and correlated with the proportion of infiltrating neutrophils (P = .03). Endothelial expression of vascular cell adhesion molecule-1 was restricted to developed lesions. Most infiltrating cells were neutrophils expressing Mac-1. In 1 patient, lymphocyte function associated antigen-1 expression was also up-regulated. No significant increase in CD3, CD8, or CD71 immunoreactivity was found. An up-regulation of perivascular cells expressing HLA-DR and vascular cell adhesion molecule-1 was observed in vasculitic lesions. This cellular staining correlated with long-term evolution of the disease (P = .04). CONCLUSIONS: Adhesion molecules are sequentially upregulated in cutaneous leukocytoclastic vasculitis. The results of this study support the possible involvement of E-selectin in mediating recruitment of neutrophils expressing Mac-1.

Changes in T-cell phenotype and adhesion molecules expression in psoriatic lesions after low-dose cyclosporin therapy.

Cyclosporin is a very effective treatment for severe psoriasis, but its exact mechanism of action in this disease is not completely understood. It has been hypothesized that the drug could act through the inhibition of the expression of certain cell adhesion molecules on the keratinocytes prior to the reduction in the number of epidermal inflammatory cells. Several studies have focused on ICAM-1 changes on keratinocytes and endothelial cells after cyclosporin treatment in psoriatic patients but their results have been somewhat contradictory. We examined changes in T-cell markers and adhesion molecules among keratinocytes, endothelial and inflammatory cells after low-dose cyclosporin treatment for severe psoriasis. We performed a histological and immunohistochemical study on psoriatic skin among 10 patients (7 males and 3 females; mean age 37 years) treated with low-dose (2.5 mg/kg/day) cyclosporin, prior to therapy, after 1 month, and after 3 months of treatment. The mean PASI (Psoriasis Area and Severity Index) before treatment was 23 +/- 4, 13 +/- 7 after the first month of therapy, and 8 +/- 2 at the end of the third month of therapy. Pretherapy samples showed a moderate to severe inflammatory infiltrate mainly due to T-lymphocytes expressing a T-cell memory (UCHL-1) and helper/inducer (CD4) phenotype. Most of these cells also expressed HLA-DR and LFA-1 and ICAM-1 antigens. After the treatment, an overall reduction in the degree of epidermal hyperplasia was seen (p = 0.01). The severity of the infiltrate was clearly reduced (p = 0.05), but no significant changes in the phenotype profile were observed. Although slightly reduced, endothelial ICAM-1 expression persisted after cyclosporin therapy. Keratinocyte ICAM-1 expression was uniformly and significantly reduced after 1 month and 3 months of therapy (p = 0.01). These results support the hypothesis that cyclosporin interferes with the expression of keratinocyte adhesion molecules in patients with psoriasis. Servitje O, Bordas X, Serón D, Vidaller A, Moreno A, Curcó N, Sais G, Peyrí J. Changes in T-cell phenotype and adhesion molecules expression in psoriatic lesions after low-dose cyclosporin therapy.