Biomedical subjects
Publications and source records attributed to U Kabadi.
Explore the source record for details and available documents.
We previously demonstrated that hyperglucagonemia may be responsible for thyroid hormone alterations noted in some nonthyroidal illnesses. Since TSH secretion is also known to be altered in many subjects with several nonthyroidal illnesses, we assessed the influence of sustained hyperglucagonemia on TSH secretory pattern in 5 anesthetized dogs. Serum TSH concentrations were determined after a 16-h fast and again at intervals of 15 min during sustained hyperglucagonemia (515-645 pg/mL) induced by iv bolus administration of glucagon 0.1 mg followed by a continuous glucagon infusion 3 ng/kg/min for 3 h. TRH (200 micrograms) was administered iv at 60 min to assess the influence of sustained hyperglucagonemia on the hypothalamic pituitary thyrotroph axis during the study. A control study was also conducted using normal saline instead of glucagon, and both studies were performed in a randomized sequence. Basal TSH levels were not significantly different during both studies. However, serum TSH declined significantly during sustained hyperglucagonemia prior to TRH administration (delta TSH, pre-TRH, -0.86 +/- 0.24 vs 0.02 +/- 0.07 ng/mL for normal saline, p < 0.01). Furthermore, TSH response to iv TRH administration was significantly blunted during glucagon infusion alone as expressed by both the absolute rise (delta TSH, post-TRH, 1.1 +/- 0.5 vs 5.9 +/- 1.7 ng/ml for normal saline, p < 0.01) as well as an integrated response over a 2-h period (sigma TSH, post-TRH, 4.0 +/- 1.1 vs 11.7 +/- 3.5 ng/min/mL, p < 0.001). Therefore, this study demonstrates that sustained hyperglucagonemia inhibits basal TSH secretion as well as TSH response to iv TRH administration, a TSH secretory pattern similar to that noted at the peak of many nonthyroidal illnesses.
Radioiodine therapy has become a cornerstone of treatment of hyperthyroidism. However, the timing of its administration varies between 1) the time of initial diagnosis with concurrent therapy with beta adrenergic blocking drugs or 2) following induction of euthyroidism with thioamide, Propylthiouracil or Methimazole. This study assessed 24-HR 131I uptake values and the thyroid scan in 24 subjects with hyperthyroidism at the time of diagnosis and again after attaining the euthyroid state with Propylthiouracil or Methimazole. Propylthiouracil of Methimazole was withdrawn seven days prior to the second 24-HR 131I uptake and scan. In all subjects, as a group, 24-HR 131I uptake increased following antithyroid therapy as compared to the time of initial of diagnosis [76 + 5% Vs. 54 + 4%; p < 0.01]. The thyroid gland size decreased in nine of twenty-four subjects, but remained unchanged in the remaining subjects. Since 24-HR 131I uptake and the gland size are the major factors influencing the therapeutic radioiodine dosage, it is possible that initial therapy with thioamide drugs may reduce the therapeutic dose of 131I in subjects with hyperthyroidism belonging to both groups, i.e., Graves' disease and Multinodular toxic goiter by inducing a rise in 24-HR 131I uptake. Furthermore, the shrinkage of thyroid glands may further decrease the radioiodine dosage in patients with Graves' disease.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Adrenomyeloneuropathy is a syndrome comprising spastic paraparesis, polyneuropathy, primary adrenocortical insufficiency and variable hypogonadism. We describe a 32 year old man who presented with contractures, peripheral neuropathy, primary adrenocortical insufficiency adn secondary hypogonadism. Abnormal responses of growth hormone, gonadotropins, prolactin and thyrotropin to provocative stimuli were found, without radiographic evidence of a pituitary or hypothalamic lesion. Almost complete recovery from the neurologic abnormalities occurred with glucocorticoid replacement therapy. The clinical features of this patient support a diagnosis of adrenomyeloneuropathy. The hypothalamic-pituitary dysfunction extends the clinical features of this patient support a diagnosis of adrenomyeloneuropathy. The hypothalamic-pituitary dysfunction extends the clinical spectrum of this disease. Remission of the paraparesis coincident with glucocorticoid replacement has not been reported previously.
Explore the source record for details and available documents.
An 8-week double-blind, multicenter, parallel study compared the safety and efficacy of topical capsaicin and oral amitriptyline in patients with painful diabetic neuropathy involving the feet. Two hundred thirty-five patients were randomized to treatment with either capsaicin cream or amitriptyline capsules. Capsaicin-treated patients received inactive capsules, and amitriptyline-treated patients applied vehicle cream. A visual analogue scale of pain intensity and measurements of interference by pain with functional activities were recorded at onset and at 2-week intervals. A visual analogue scale of pain relief and physicians' global evaluation assessed changes in pain status from baseline. Topical capsaicin and oral amitriptyline produced equal and statistically significant improvements in pain over the course of the study. By the end of week 8, 76% of patients in each group experienced less pain, with a mean reduction in intensity of more than 40%. By the end of the study, the interference with daily activities by pain had diminished significantly (P = .001) in both groups, including improvements in sleeping and walking. No systemic side effects were observed in patients treated with topical capsaicin. Most patients receiving amitriptyline experienced at least one systemic side effect, ranging from somnolence (46%) to neuromuscular (23%) and cardiovascular (9%) adverse effects. Topically applied capsaicin is an equally effective but considerably safer alternative to amitriptyline for relief of the pain of diabetic neuropathy.