Case report: multiagent chemotherapy of Hodgkin's disease associated with red cell aplasia, acquired ichthyosis and anhidrosis.
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Biomedical subjects
Publications and source records attributed to E D Mukhtar.
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Patients with enteric fever confirmed by isolation of Salmonella species from blood culture, were treated with the combination of trimethoprim-sulphamethoxazole (co-trimoxazole). All 133 patients responded well to treatment. The mean defervescence was 2.74 days. No serious side effects were noticed and relapses occurred in the patients during the period of follow up.
Patients with Graves' disease (n = 105) had an increased frequency of HLA-B8 (40%) and a reduced frequency of HLA-B12 (24.8%) when compared with random controls (n = 117; 24.8% and 40.2% respectively). Comparison of patients with their first degree relatives (n = 118) shows the frequency deviations in these antigens to be characteristic of the families from which patients with Graves' disease are drawn, rather than of the disease itself. The haplotypes, identified in eight-six patients and 113 relatives, indicate that the excess of HLA-B8 in patients and their relatives is primarily due to the halpotype 1-8. The relative risk for an HLA-B8 individual of developing Graves' disease is 2.02, whilst the relative risk for an individual of haplotype 1-8 is 4.23. No significant associations were found between the incidence of any HLA antigen or combination thereof and the presence or absence of thyroglobulin and thyroid microsomal antibodies, or antibodies which interact with the TSH receptor.
Triiodothyronine (T3) suppression and thyrotropin-releasing hormone (TRH) tests were used to study thyroid function in 50 patients with thyroid disease. The results of the thyroid function tests were compared with the levels of serum thyroid-stimulating immunoglobulins (TSI) measured by a radio-receptor assay. In euthyroid and hyperthyroid patients, the presence of TSI corresponded with the absence of TSH control of thyroid function. However, in two hypothyroid patients with serum TSI levels readily detectable in the receptor assay, T3 suppression and TRH tests indicated that thyroid function was under TSH control.
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Thyroid-stimulating immunoglobulins (T.S.I.) have been detected in the serum of all patients with untreated Graves' disease, and in these patients the levels of T.S.I. correlated significantly with the early uptake of 131I by the thyroid. The frequency of T.S.I. in patients treated solely by antithyroid drugs, by radioiodine, or by partial thyroidectomy was 53 per cent, 50 per cent, and 17 per cent, respectively. The reduced frequency of T.S.I. in the serum of patients treated by drugs or radioiodine was probably due to spontaneous remission, but in the case of partial thyroidectomy the operation itself clearly had a dramatic effect on the serum-T.S;I. These results accorded well with the reported frequency of thyroid autonomy in similar groups of patients and suggested that thyroid-stimulating immunoglobulins were responsible for hyperthyroidism in Graves' disease.
Thyroid function in health is largely controlled by thyroid-stimulating hormone (TSH) produced by the thyrotroph cells of the anterior pituitary. Alterations of intrathyroidal iodine content may also be involved in autoregulation by the thyroid, particularly in states of iodine deficiency and excess (Ingbar, 1972). During pregnancy placental thyroid-stimulating agents-human chorionic thyrotrophin (HCT) and human molar thyrotrophin (HMT)-are produced. In the common variety of hyperthyroidism, Graves' disease, thyroid function appears to be regulated by thyroid-stimulating immunoglobulins (TSI) (Smith & Hall, 1974a). Human molar thyrotrophin can be produced by trophoblastic tumours in both sexes and thyroid-stimulating factors have been reported to be released by malignant tumours of the gut and by bronchogenic carcinomas, although this is one of the rarest of the ectopic hormone syndromes.