The antithyroid arthritis syndrome reviewed.
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Biomedical subjects
Publications and source records attributed to M S Shapiro.
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Hypothalamic pituitary function was studied in 13 patients with myasthenia gravis. Gonadotropin, TSH, and prolactin dynamics were investigated using conventional provocative stimuli. No consistent abnormality was found in either gonadotropin or prolactin release. Abnormal TSH responses to TRH administration was present in six of the 13 patients in association with normal free thyroxine indices and the absence of antithyroid antibodies. This latter observation is relevant when the association of myasthenia gravis with hyperthyroidism, thyroiditis and hypothyroidism is considered.
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A patient with chronic Gaucher's disease is described who developed glomerulopathy 24 years after splenectomy terminating in renal failure. The pathological changes of this very rare complication of Gaucher's disease are described. The few similar cases reported in the literature are reviewed and the possible pathogenetic pathways discussed.
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After debridement of the entire corneal epithelium, epithelial cells of conjunctival origin cover the exposed corneal surface. Four to five weeks later, these cells undergo a morphologic transformation to normal-appearing corneal epithelium. To study this transformation the entire corneal epithelium was removed from rabbits with the use of n-heptanol, after which the histologic appearance of and the number of goblet cells in the regenerated epithelium were noted. Five stages of transformation were seen. Immediately after healing, the epithelium consisted of one to two squamous cell layers with no goblet cells apparent at the light microscope level (stage 1). In the following weeks goblet cells appeared at the limbal edge of the cornea (stage 2), reached a uniform distribution across the cornea (stage 3), and subsequently receded toward the limbus (stage 4), leaving an epithelium with normal corneal morphologic appearance (stage 5). To see if there was an ongoing centripetal cell migration from the conjunctiva across the cornea after initial healing, the central corneal epithelium was isolated from the periphery by a ring of glue. Such isolation resulted in a thinning of the central epithelium and a thickening of the peripheral epithelium. These studies suggest that (1) the transformation into corneal epithelium lags behind defect closure by 4 to 5 weeks, (2) goblet cells do not initially migrate as recognizable cells, and (3) there is a continuous centripetal cell motion even after the initial defect closure is accomplished.
A male with pseudohypoparathyroidism presented with several hormonal abnormalities. He was clinically euthyroid with no palpable goiter, His serum T4, total T3, T3 Sephadex retention, and 131I uptake were normal. However, elevated basal TSH levels and exaggerated TSH responses to TRH which normalized during the administration of thyroid extract suggested reduced thyroidal reserve. Despite these finding the 131I uptake increased after exogeneous TSH, and the T3 level rose after TRH. Basal testosterone levels and response to hCG were normal however, gonadotropins were elevated and there was an exaggerated response after LRH treatment. Both LH and FSH levels were suppressed by testosterone propionate. The patient demonstrated intermittent basal hyperprolactinemia and impaired PRL responsiveness after metolopramide, chlorpromazine, and insulin administration. There was, however, an intact response to TRH. Basal PRL, TSH, and LH levels decreased after the administration of L-dopa and bromocriptine. Although the precise mechanism underlying these finding is unknown, the elevated basal levels of TSH, LH, and FSH and the exaggerated responses to their respective releasing hormones suggest the presence of partial degree of end-organ resistance to these pituitary trophic hormones. Together with the resistance to PTH, this may imply a common defect, presumably at a postreceptor level. However, hyporesponsiveness of PRL to metoclopramide and chlorpromazine and normal responsiveness to TRH suggest that an abnormality of dopamine tone also exists in pseudohypoparathyroidism.
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A 63-year-old man developed an asymptomatic pleural effusion following the administration of 500 gm of procainamide hydrochloride over a six-month period. The diagnosis was initially suggested by the finding of lupus erythematosus cells in the pleural fluid. Lupus erythematosus cells and antinuclear antibodies appeared in the blood two months later and remained for a period of six months. The diagnosis was corroborated by the presence of antibodies to denatured DNA, but not to native DNA.
The clinical effectiveness of beclomethasone dipropionate (BDP) aerosol and adrenal function after withdrawal of oral corticosteroid therapy were evaluated in 32 severely steroid-dependent asthmatic patients. Twenty-four of 28 patients were able to discontinue oral glucocorticosteroid therapy, while four failed to do so. Ventilatory studies showed no substantial changes at the end of six months' BDP treatment. In 24 patients, adrenal insufficiency was present before BDP therapy was started. In 20 of those patients, the response of cosyntropin returned to normal two months after discontinuation of systemic steroid treatment and administration of BDP.
Diagnostic and therapeutic problems in a patient with ectopic ACTH syndrome caused by a malignant bronchial adenoma are discussed. Persistent Cushing's syndrome was present following apparent total adrenalectomy, but radioactive scanning with 131I-19-iodocholesterol showed the presence of residual adrenal tissue in the right suprarenal bed. Amelioration of the hypercortisolism occurred after removal of the bronchial adenoma. A paradoxical elevation of adrenocortical activity followed administration of dexamethasone and data are presented which suggest that periodic secretion of ACTH accounted for this phenomenon.
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