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Biomedical subjects

M Lecha

Publications and source records attributed to M Lecha.

At least 37 records · Page 2Linked to original sources
PubMed1984

Why do melanomas ulcerate?

Ulceration is an indicator of unfavourable prognosis in malignant melanoma (MM). But why do melanomas ulcerate?. Possible causes of ulceration were investigated in a group of 69 ulcerated and 69 non-ulcerated malignant melanomas. A significant correlation (P less than 0.001) between ulceration and mitotic index was found. In a group of 69 ulcerated malignant melanomas, 49 had over 7, 15 had 4-6, and only 5 had 0-3 mitotic figures per 10 high-power fields. Among 69 non-ulcerated melanomas, 28 had more than 7, 24 had 4-6, and 17 had 0-3 mitotic figures per 10 high-power fields. This study supports the hypothesis that ulceration of melanomas is usually the result of the destruction of the epidermis by the proliferating neoplastic cells or modification of blood supply due to the expansile activity of the tumor. The relationship between ulceration and mitotic activity helps clarify the prognostic significance of ulceration.

Humans↗
PubMed1984

[Early forms of porphyria cutanea tarda. Apropos of 2 cases with a study of familial enzymatic deficiency and definition of the mode of genetic transmission].

The authors report two cases of cutaneous porphyria in children aged 6 and 9 respectively. The clinical and biochemical patterns were similar to those of porphyria cutanea tarda. The manifestations were drug-induced in both cases (by sulfonamides and griseofulvin in the first patient, and by hydantoin and benzodiazepine in the second). The clinical examination and the determination of porphyrins in the relatives showed no abnormalities. However, the study of the erythrocyte uroporphyrinogen decarboxylase showed 50 p. 100 reduced activity in the father and grandfather of the first patient, and in the second case's mother. Treatment with chloroquine (3 mg/kg/week) produced the total remission of both cases with no recurrences in 4 and 2 years respectively.

Carboxy-Lyases↗
PubMed1983

[Cellular immunity in polymorphous light eruption].

Lymphocytic-cell subsets (T total, T helper, T suppressor-cells) have been studied with Monoclonal Antibodies (OKT-3, OKT-4, OKT-8) in 21 patients with Polymorphous light Eruption in inactive phase and have been compared with 13 controls. The results shvon normal cell figures (T total, helper and suppressor). However, when observing the ratio between T helper cells and T suppressor cells, a slight decrease in this ratio is appreciated, which would correspond to a relative increase of suppressor cells. These results are similar to those obtained for the inactive S. L. E. (9).

Humans↗
PubMed1982

Photocontact dermatitis to cobalt salts.

4 patients with chronic photocontact dermatitis were sensitive to cobalt salts. They presented as cases of contact dermatitis from cement or pig fodder with persistent lesions on exposed areas. Only 2 of them had standard patch test positive reactions to chromate and cobalt, but all showed positive photo-patch tests to cobalt. Photo-oxidation tests proved that cobalt salts are photosensitizing. Exposure to cobalt salts was responsible for the patients' chronic actinic dermatitis.

Adult↗
PubMed1982

[Lucio's leprosy].

A case of diffuse lepromatous leprosy with lepra reaction type II-Lucio's phenomenon-in a 24 years old male patient is reported. The histological examination of the necrotic lesions and of the apparently normal skin showed the presence of dense perivascular and perianexial lymphohystiocitic infiltrates with great quantities of bacilli. The first biopsy did not show a picture a leuccocytoclastic vasculitis but only areas of necrosis. The immunofluorescence studies revealed on direct examination complement deposits on vessel walls. The complement levels in blood were lowered and circulating inmunecomplexes were also detected. These data confirm the opinion that Lucio's phenomenon is caused by circulating inmunecomplexes fixed on dermal vessel walls causing skin necrotic lesions.

Adult↗
PubMed1982

[Thalidomide in the treatment of aphthosis and Behçet's disease. 4 years' experience].

The authors summarize their experience in the treatment of recurrent, necrotic and giant mucocutaneous aphthosis (9 cases) and Behçet's disease (9 cases) with Thalidomide during four years. In recurrent mucocutaneous aphthosis the results were very good, with fast disappearance of pain, healing of the ahthae and disappearance or delay of recurrence. The result in Behçet's disease is similar, possibly less, in mucocutaneous lesions. Uveitis also reacts favorably but we can not say that the results were superior to those obtained by other drugs (corticoids, cytostatics immunosuppressives), although its side effects are less. On the other hand it does not appear to have any effect on other symptoms such as arthritis (in which colchicine is active), thromboflebitis or fever. There is not sufficient experience to judge its action on neurological symptoms. The recommended dose is 100 mgr./day for 10 days, a higher dose does not appear to give better results. Patients who have received treatment several times appear to have the same results, but slower. Neurotoxicity has not been observed and the only side effect which has been noted is digestive intolerance in two cases, after which the medication was stopped. The authors consider that Thalidomide, with due precaution, which must be scrupulously determined, is the most active medicament in particularly severe cases with profusion of necrotic aphthae, mutilating and recurring mucocutaneous aphthosis, also being useful in controlling some symptoms of Behçet's disease.

Adolescent↗
PubMed1981

Hepatoerythropoietic porphyria: a new uroporphyrinogen decarboxylase defect or homozygous porphyria cutanea tarda?

Uroporphyrinogen decarboxylase levels were measured in haemolysed whole blood or fibroblasts from 3 unrelated patients with hepatoerythropoietic porphyria (HEP) and in 4 unrelated patients with familial porphyria cutanea tarda, a condition in which the enzyme is defective. In HEP patients enzyme activities were 7% of normal in erythrocytes and 8% of normal in cultured skin fibroblasts. All the features of HEP, including the characteristic accumulation of protoporphyrin in erythrocytes, are secondary to this enzyme defect. The father of 1 HEP patient was heterozygous for the same enzyme defect. He also had uroporphyrinuria and was therefore indistinguishable from patients with subclinical familial porphyria cutanea tarda. It is suggested that patients with HEP are homozygous for the gene that causes porphyria cutanea tarda.

Child↗