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Biomedical subjects

F Maloof

Publications and source records attributed to F Maloof.

At least 91 records · Page 5Linked to original sources
PubMed1974

Metabolic clearance and production rates of human thyrotropin.

Metabolic clearance (MCR) and production rates (PR) of human thyrotropin (hTSH) were determined by the constant infusion to equilibrium method 57 times in 55 patients. 16 control patients had a mean hTSH MCR of 50.7 ml/min. The mean hTSH MCR was significantly (P < 0.02) higher in 19 euthyroid men (51.6 ml/min) than in 12 euthyroid women (43.0 ml/min), but this apparent sex difference disappeared when the MCR were corrected for surface area, 25.8 (men) versus 25.2 ml/min per m(2) (women). Hypothyroid patients had significantly (P < 0.005) lower hTSH MCR (30.9 ml/min), and hyperthyroid patients had significantly (P < 0.05) higher hTSH MCR (60.9 ml/min) than controls. The hTSH MCR in patients with "decreased thyroid reserve" (40.9 ml/min), hyperfunctioning thyroid nodule (53.8 ml/min), and "empty sella syndrome" (46.6 ml/min) were not significantly different from controls. The mean hTSH PR in controls (104.3 mU/day) was significantly (P < 0.005) different from that in patients with "decreased thyroid reserve" (956 mU/day), hypothyroidism (4,440 mU/day), hyperthyroidism (< 43.9 mU/day) and a hyperfunctioning thyroid nodule (< 38.7 mU/day). In primary hypothyroidism intravenous triiodothyronine therapy (50 mug/day) for 10 days decreased the hTSH PR (from 4,244 to 2,461 mU/day) before changes in the hTSH MCR (from 33.1 to 33.7 mU/day) were observed. These studies have demonstrated that changes in the serum concentration of hTSH are mainly due to altered pituitary hTSH secretion with only a minor contribution from the change in hTSH MCR.

Adult↗
PubMed1973

Partial target organ resistance to thyroid hormone.

An 8-year old boy with a small goiter, normal basal metabolic rate (BMR), and elevated serum thyroid hormone levels (thyroxine [T(4)] 19.5 mug per 100 ml, free T(4) 4 ng per 100 ml, triiodothyronine [T(3)] 505 ng per 100 ml) was studied. He had measurable serum thyroid-stimulating hormone (TSH) levels (average 5.5 muU per ml), and the thyroxine-binding proteins, hearing, and epiphyseal structures were normal. There was no parental consanguinity nor were there thyroid abnormalities either in the parents or six siblings.Methimazole, 50 mg daily, depressed thyroxine synthesis (T(4) 10.5, free T(4) 2.5) and caused a rise in TSH to 11 muU per ml. After discontinuation of treatment, TSH declined to 4.2 muU per ml and chemical hyperthyroidism returned (T(4) 21.0 mug per 100 ml, free T(4) 4.2, and total T(3) 475 ng per 100 ml, radioactive iodine [RAI] uptake 68%), but studies of BMR and insensible water loss showed the patient to be clinically euthyroid. Thyrotropin-releasing hormone (TRH), 200 mug i.v., caused a brisk rise in TSH to 28 muU per ml, with T(4) rising to 28 mug per 100 ml, free T(4) to 5.6, and T(3) to 730 ng per 100 ml, thus indicating that the pituitary-thyroid system was intact and that the patient's TSH was biologically active. The unusual sensitivity of the pituitary cells to TRH in spite of the markedly elevated serum thyroid hormone levels also suggested that the pituitary was insensitive to suppression by T(3) or T(4). Serum dilution studies gave immunochemical evidence that this patient's TSH was normal. Neither propranolol, 60 mg, chlorpromazine, 30 mg, nor prednisone, 15 mg daily, influenced thyroid indices. Steroid treatment, however, suppressed the pituitary response to TRH, T(3) in doses increased over a period of 12 days to as much as 150 mug daily caused a rise in serum T(3) to above 800 ng per 100 ml, a decline of T(4) to euthyroid levels (T(4) 9.5 mug per 100 ml, free T(4) 1.6 ng per 100 ml), suppression of the RAI uptake from 68% to 35%, and marked blunting of the responses to TRH, but the BMR and insensible water loss remained normal. The data suggest that the patient's disorder is due to partial resistance to thyroid hormone.

Child↗
PubMed1973

Suppression of pituitary TSH secretion in the patient with a hyperfunctioning thyroid nodule.

10 patients with a single hyperfunctioning thyroid nodule each were studied for pituitary thyrotropin (TSH) suppression. They were judged to be euthyroid on clinical grounds. The total thyroxine (T(4)D), free thyroxine (FT(4)), total triiodothyronine (T(3)D), and free triiodothyronine (FT(3)) were normal in most of the patients. Incorporation of (131)I into the hyperfunctioning thyroid nodules was not suppressed by the administration of physiological doses of T(3). Basal serum TSH concentrations were undetectable (<0.5 - 1.0 muU/ml) in all patients. The metabolic clearance of TSH in one patient before and after excision of the thyroid nodule was unchanged (40 vs. 42 ml/min) whereas the calculated production rate was undetectable before the operation (<29 mU/day) and normal after (103 mU/day). These data, in one patient, suggest that the undetectable concentration of TSH in these patients is a result of suppressed TSH secretion rather than accelerated TSH clearance. In eight patients, basal serum TSH concentrations failed to increase after the intravenous administration of 200 mug of thyrotropin-releasing hormone (TRH); minimal increases in serum TSH concentrations were observed in two patients. The suppression of TSH was evident despite "normal" concentrations of circulating thyroid hormones. The observation that normal serum concentrations of T(4)D, FT(4), T(3)D, and FT(3) may be associated with undetectable basal serum TSH concentrations and suppressed TSH response to TRH was also found in four hypothyroid patients given increasing doses of L-thyroxine and sequential TRH stimulation tests.

Administration, Oral↗