Localized dermographism at the site of a fixed drug eruption.
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Biomedical subjects
Publications and source records attributed to M Lomuto.
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NERDS is an eosinophilic disorder recently described by Butterfield and characterized by an association of nodules, eosinophilia, rheumatism, dermatitis and swelling. We describe an additional case, the third, of this new eosinophilic syndrome. The cardinal features included joint and cutaneous manifestations with prominent para-articular nodules and rheumatism, xerosis, recurrent urticarial eruption with angioedema associated with tissue and peripheral blood eosinophilia. A drug-induced (diclofenac) allergic rash and lymphadenopathy appeared during the course of the illness. Persistent leukocytosis with a maximum of 65% of eosinophils, mostly exhibiting the hypodense phenotype (activation index), was always present. During the acute phase of the disease, flow-cytometric analysis of blood and bone marrow revealed proliferation of activated CD4+/OKDR+ T helper cells and CD25+/OKDR+ eosinophils.
Between 1981 and 1991, eleven infants (ranging in age from 2 to 9 months) were hospitalized in our department for evaluation of microscopically verified scabies infestations. Six presented signs of Norwegian scabies. All of the latter infants had been treated (prior to the scabies infestation) for long periods with topical steroids, in most cases for lesions suggestive of atopic dermatitis. We believe that the occurrence of the Norwegian form in these newborns was due to localized steroid-induced suppression of the normal immune response.
BACKGROUND: Our observation of familial cases of fixed drug eruption (FDE) prompted us to consider a genetic predisposition to this disease. OBJECTIVE: Our purpose was to determine whether there is any association between FDE and any of the major histocompatibility complex class I or II alleles. METHODS: HLA class I and II typing was performed by lymphocytotoxicity assay in 36 unrelated patients with FDE. RESULTS: Significantly higher (p < 0.0001) frequencies of the B22 and Cw1 antigens were found in the 36 patients with FDE. CONCLUSION: Our data are the first to suggest a genetic predisposition to FDE.
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Fixed drug eruptions following the use of pyrazolone derivatives occurred in 4 members of the same family: a 12-year-old girl, her grandmother, and two of her great aunts. Although the pathophysiologic events leading to this type of reaction are unknown, these cases of familial occurrence suggest that genetic predisposition might be an important causal factor.
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We describe 2 cases of severe photosensitivity dermatitis following the use of nifedipine for arterial hypertension. In both cases casual rechallenge with nifedipine confirmed that this drug was the causative agent.
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Sacroiliac joint abnormalities were evaluated by computed tomography (CT) in 29 patients with psoriatic arthritis and in 15 with colitic arthritis. CT showed a better sensitivity than conventional X-ray analysis in the evaluation of the articular space alterations in psoriatic and colitic arthritis as well as in detecting erosions and ankylosis of sacroiliac joints in patients with ankylosing spondylitis or psoriatic arthritis. Thus, CT appears a promising tool for the early detection of the pathological changes of sacroiliac joints.
A radiographic study of the hands, using the method of optical enlargement or 'microradioscopy', was carried out on a group of 58 psoriatic patients suffering from different clinical forms of the disease, but without clinical symptoms of arthropathy. A significant statistical incidence for the following lesions was revealed: (a) focal discontinuity and irregularity of the tuft cortical, similar to a nail-stroke; (b) focal lamellar thickening of the periosteum; (c) small intraspongous geodes; (d) increase of the intracortical striae; (e) small juxta-articular erosions. The radiological aspect of the hands, characterized by monolateral and variously combined lesions (with the almost constant presence of the erosions of the tuft cortical) is characteristic, enough to be recognized as a marker of the disease. The authors assume that psoriasis is a systemic disease characterized by accelerated turnover, and that cutaneous and bone lesions represent a different clinical expression of this same biological process.
A significant increase of some HLA antigens (B13, B17) was shown in 122 psoriasis patients, compared to 176 unrelated individuals of the control group. This finding is not completely secondary to an increase in Cw6, supporting the opinion that different loci within the HLA region are responsible for different forms of the disease. Some familial cases of psoriasis suggest a possible involvement of Bw35, despite the fact that the increase of this antigen in a random population was not significant for the corrected value. In this case it seems likely that a gene associated with Bw35 may be responsible for an infectious form of disease. The fact that 32% of our psoriatic patients did not show either B13, B17 or Cw6, indicated that the Is gene could also segregate with an other haplotype. The Is gene is also dominant, with an incomplete penetrance of B17 and Bw35 among relatives.
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