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Cutaneous Alterations (cutaneous + alteration)
Selected AbstractsPresence of Leishmania organisms in specific and non-specific skin lesions in HIV-infected individuals with visceral leishmaniasisINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2002Ricardo J. Bosch MD BackgroundLeishmania coinfection is frequently seen in human immunodeficiency virus (HIV)-infected patients in endemic areas, and from time to time the protozoan is detected in cutaneous biopsies. Objective To establish the characteristics and possible ethiologic role of the presence of Leishmania in these lesions. Methods We studied 12 cutaneous biopsies with Leishmania organisms from nine HIV-infected patients (seven men and two women) with visceral leishmaniasis, diagnosed by bone marrow examination, seen over a period of 9 years. Results Based on clinical characteristics, evolution and response to anti-leishmanial treatment, cutaneous alterations were found to be related to the presence of the protozoan in six cases, whereas in the other six cases it was not considered responsible for the dermatological lesions (dermatofibroma, and lesions of psoriasis, Reiter's syndrome, bacillary angiomatosis, cryptococcosis and oral aphthae). Of note was the high prevalence of specific mucocutaneous manifestations, usually accompanied by intense pruritus, great variability, and a tendency to relapse after treatment stopped. On two occasions, detection of the protozoa in skin biopsies led to the diagnosis of a previously unsuspected visceral leishmaniasis. Conclusions Cutaneous detection of Leishmania is frequent in HIV-infected individuals with visceral leishmaniasis. Sometimes Leishmania is associated with changes attributable to other dermatological processes, and its presence does not imply a causative role. A clear relationship between the systemic process and the therapeutic response is necessary to demonstrate an ethiologic role. [source] A reappraisal of the histologic findings of pigmented pretibial patches of diabetes mellitusJOURNAL OF CUTANEOUS PATHOLOGY, Issue 2 2004Gregory M. Houck Background:, Pigmented pretibial patches (PPPs) are the most common cutaneous alterations in diabetes mellitus, found in up to 50% of diabetic patients. They classically present as flat-topped, dull-red papules on the pretibial areas, later becoming hyperpigmented and atrophic. Little is known regarding the pathogenesis of these lesions, and the histopathologic findings have been regarded as non-specific. Methods:, We investigated the clinical and pathologic attributes of a series of 12 diabetic patients with PPP in an effort to discern any specific histologic attributes compared to normal skin removed from diabetic patients with cutaneous carcinoma. Results:, All cases of PPP showed hyaline microangiopathy, all patients showed extravasated erythrocytes and/or hemosiderin deposits, and 10 patients showed an appreciable number of perivascular plasma cells. The average number of plasma cells per vascular plexus was 2.2. Control specimens removed from five diabetic patients showed hyaline microangiopathy, and three showed extravasated erythrocytes and hemosiderin. One patient showed a single vascular plexus with two plasma cells, p = 0.01. Conclusion:, The presence of increased dermal perivascular plasma cells in the appropriate clinical context might be an important and under-recognized clue for PPP. The pathogenic significance of this finding is unknown. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 62JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003C Briani Thalidomide seems to be effective in the treatment of cutaneous forms of lupus erythematosus refractory to other therapies. Peripheral neuropathy is the most severe side effect, but the incidence of neuropathy and its relation to thalidomide doses are still unclear. We prospectively monitored 12 patients treated with thalidomide for cutaneous lupus erythematosus in order to estimate the occurrence of side effects, particularly peripheral neuropathy. A total of 12 female patients, median age 38,6 years (range 26,56), with subacute or chronic cutaneous lupus erythematosus were considered. The patients were treated with low dose thalidomide (starting dose 100 mg, tapered to 50 mg/day or 50 mg alternative day) for up to 18 months. The average follow-up period was 8,6 months (range 2,18). Prior to, and regularly during treatment patients underwent neurological evaluation and electrophysiological study of at least 8 nerves in the 4 arms (ulnar, median, sural, peroneal nerves). At recruitment, one patient presented a sensory-motor peripheral neuropathy. Of the remaining 11 patients, six did not present electrophysiological evidence of neuropathy, one had a carpal tunnel syndrome and four showed slowing of ulnar nerve velocity at elbow. No patients developed neuropathy neither worsening of electrophysiological parameters during thalidomide treatment. The most common side effect was tremor, always reversible after withdrawing or reducing thalidomide. Paresthesias, somnolence, amenhorrea, constipation were also present. Only one patient had to stop the therapy for the occurrence, 10 days after taking 50 mg of thalidomide, of a severe, stabbing, "zoster-like" thoracic pain, which disappeared upon withdrawal of the drug. Started again on thalidomide, the symptoms reappeared and the patient definitely interrupted the therapy with benefit. All the 11 patients who continued on the therapy presented a significant improvement or remission of the cutaneous alterations. These preliminary data seem to indicate that low dose thalidomide is efficacious and tolerable for cutaneous lupus erythematosus. Peripheral neuropathy seems not to be a major side effect. A longer follow-up and the study of more patients are needed to confirm the results. [source] Cutaneous Markers of Primary Immunodeficiency Diseases in ChildrenPEDIATRIC DERMATOLOGY, Issue 2 2000Angelica Berron-Ruiz M.D. We studied PIDs in a large pediatric hospital, their association with cutaneous alterations, and the importance of cutaneous alterations as diagnostic markers. Among 382,383 pediatric patients, 130 (0.0003%) had a PID: humoral in 27, cellular and combined in 18, phagocytic in 37, and associated with major defects in 45. An average of two cutaneous alterations were present in 90 (69%) patients: infections in 80, eczema-dermatitis in 38, and miscellaneous in 57. In 71 (79%) patients the cutaneous alterations preceded and were the basis for the clinical immunologic diagnosis. Only two PIDs were not associated with cutaneous lesions. [source] Ultrastructural changes induced in cutaneous collagen by ultraviolet-A1 and psoralen plus ultraviolet A therapy in systemic sclerosisTHE JOURNAL OF DERMATOLOGY, Issue 2 2008Noriyuki SAKAKIBARA ABSTRACT In the present study, we examined the ultrastructural alterations in collagen fibrils clinically softened by ultraviolet-A1 (UVA1, 340,400 nm) therapy and psoralen plus long-wave ultraviolet (PUVA) therapy and compared collagen fibril diameters in four patients with systemic sclerosis (SSc). In skin sclerosis, the dermis is compacted from the epidermal layer to the sweat glands, and the collagen bundles are thicker with decreased space between them. We obtained skin specimens before and after UVA1 or PUVA therapy, and compared cutaneous alterations in one diffuse-type patient and one limited-type patient following UVA1 therapy, and in two diffuse-type patients following PUVA treatment. Ultramicroscopic analysis revealed that UVA1 treatment decreased the diameter of the broad collagen fibrils, mainly in the upper reticular layer. PUVA induced similar alterations in the collagen fibrils, extending to the upper and middle reticular layers. PUVA therapy induced alterations in collagen fibril diameter in deeper layers than did UVA1 therapy, which might be related to the direct action of UV light and the depth of the light penetration. In three of four patients, collagen fibril diameter decreased, collagen fibril thickness equalized, and new, thin fibrils developed among the collagen fibrils, suggesting that collagen degradation and synthesis underlie the alterations induced by UVA1 and PUVA phototherapies. [source] | ||||||||||