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Biomedical subjects

S E Inzucchi

Publications and source records attributed to S E Inzucchi.

10 recordsLinked to original sources
PubMed1998

Efficacy and metabolic effects of metformin and troglitazone in type II diabetes mellitus.

BACKGROUND: Combination therapy is logical for patients with non-insulin-dependent (type 2) diabetes mellitus, because they often have poor responses to single-drug therapy. We studied the efficacy and physiologic effects of metformin and troglitazone alone and in combination in patients with type 2 diabetes. METHODS: We randomly assigned 29 patients to receive either metformin or troglitazone for three months, after which they were given both drugs for another three months. Plasma glucose concentrations during fasting and postprandially and glycosylated hemoglobin values were measured periodically during both treatments. Endogenous glucose production and peripheral glucose disposal were measured at base line and after three and six months. RESULTS: During metformin therapy, fasting and postprandial plasma glucose concentrations decreased by 20 percent (58 mg per deciliter [3.2 mmol per liter], P<0.001) and 25 percent (87 mg per deciliter [4.8 mmol per liter], P<0.001), respectively. The corresponding decreases during troglitazone therapy were 20 percent (54 mg per deciliter [2.9 mmol per liter], P=0.01) and 25 percent (83 mg per deciliter [4.6 mmol per liter], P<0.001). Endogenous glucose production decreased during metformin therapy by a mean of 19 percent (P=0.001), whereas it was unchanged by troglitazone therapy (P=0.04 for the comparison between groups). The mean rate of glucose disposal increased by 54 percent during troglitazone therapy (P=0.006) and 13 percent during metformin therapy (P= 0.03 for the comparison within the group and between groups). In combination, metformin and troglitazone further lowered fasting and postprandial plasma glucose concentrations by 18 percent (41 mg per deciliter [2.3 mmol per liter], P=0.001) and 21 percent (54 mg per deciliter [3.0 mmol per liter], P<0.001), respectively, and the mean glycosylated hemoglobin value decreased 1.2 percentage points. CONCLUSIONS: Metformin and troglitazone have equal and additive beneficial effects on glycemic control in patients with type 2 diabetes. Metformin acts primarily by decreasing endogenous glucose production, and troglitazone by increasing the rate of peripheral glucose disposal.

Administration, Oral↗
PubMed1998

Ectopic thymic carcinoid masquerading as a thyroid nodule.

A 26-year old woman presented with a thyroid nodule. Ultrasound and scintigraphy confirmed the presence of a 3.5-cm non-functioning mass in the left lobe. A fine needle aspiration demonstrated unusual, malignant-appearing cells, and thyroidectomy was performed. At gross pathological sectioning, the lesion was clearly attached to, but not part of, the thyroid. Microscopic features indicated an atypical carcinoid arising in a cervical remnant of the thymus. This appears to be the first case of ectopic thymic carcinoid presenting as a thyroid nodule.

Adult↗
PubMed1997

Growth hormone in adults: indications and implications.

Adults with hypopituitarism and documented growth hormone deficiency are now eligible for replacement therapy. What are the guidelines for diagnosis and treatment? More broadly, what are the implications for other adults with hyposomatotropism-namely, the elderly? And is there a therapeutic role for the hormone in patients with disease states such as osteoporosis, heart failure, and acute catabolic illness?

Adult↗
PubMed1996

Parathyroid hormone (PTH)-related protein(1-36) is equipotent to PTH(1-34) in humans.

Humoral hypercalcemia of malignancy (HHM) results from the production of PTH-related protein (PTHrP) by human tumors. One previous study has reported the results of human (h) PTHrP(1-34) infusion into humans. In that report, hPTHrP(1-34) was found to be qualitatively similar to but 3- to 10-fold less potent than hPTH(1-34). Because hPTHrP(1-36) and not hPTH(1-34) is likely to be the actual amino-terminal secretory form of PTHrP, and because this previously reported lack of potency was unexpected, we repeated these studies using hPTHrP(1-36) and compared the results with those obtained with hPTH(1-34). Healthy subjects (n = 30) were infused over 6 h with either vehicle alone, hPTH(1-34) at a dose of 8 pmol/kg.h, or hPTHrP(1-36) at doses of 8 or 80 pmol/kg.h. Both hPTH(1-34) and hPTHrP(1-36) caused an increase in serum ionized calcium, a decrease in serum phosphorus, an increase in the fractional excretion of phosphorus, a decrease in the tubular maximum for phosphorus, an increase in nephrogenous cAMP excretion, and suppression of endogenous PTH(1-84). Unlike events observed in HHM, hPTHrP(1-36) induced an increase in plasma 1,25-dihydroxyvitamin D2. In addition, fractional excretion of calcium was reduced by both hPTH(1-34) and hPTHrP(1-36). In their actions on serum calcium, renal calcium and phosphorus handling, and nephrogenous cAMP excretion, hPTHrP(1-36) and hPTH(1-34) appeared equivalent in potency. These studies indicate that short-term infusion of hPTHrP(1-36) into humans reproduces most but not all of the features of HHM. In contrast to the reported findings with hPTHrP(1-34), we found the potency of hPTHrP(1-36) to be comparable with that of hPTH(1-34) in vivo in humans. In addition, unlike the situation in HHM, hPTHrP(1-36) produces an increment in plasma 1,25-dihydroxyvitamin D2. Finally, hPTHrP(1-36) has been shown for the first time to have anticalciuric effects in humans. This would suggest that, in addition to osteoclastic bone resorption, tubular reabsorbtion of calcium by hPTHrP may contribute to the hypercalcemia in patients with HHM.

Adult↗
PubMed1994

Clinical review 61: Effects of growth hormone on human bone biology.

GH has considerable importance in the normal development and growth of bone. An additional role in the maintenance of the adult skeleton is suggested by the alterations in bone mineral density observed in states of deficient or excess GH secretion and in the bone formation response to GH replacement in GHD patients. Deficiency in the secretion of GH is also observed, with increasing and striking frequency after middle-age despite the lack of any defined pituitary disease or injury. Although a causal relationship between hyposomatotropism and osteopenia in normal elderly patients is hypothetical, intriguing therapeutic questions are raised. Preliminary trials of hGH in osteoporosis have not resulted in increases in BMD, but such studies suffer from methodological limitations, chief of which is the failure to account for the GH/IGF-I status of their subjects. Osteopenic patients with the lowest IGF-I levels may need to be assessed independently. The utility of hGH may be in preventing the senile component of osteoporosis, which appears to result mainly from defective bone formation. Such studies will require appropriate patient selection, longer treatment periods, and more sensitive measures of bone density. Combination and/or coherence therapy with other agents, particularly those that attenuate bone resorption, may also prove useful.

Bone Development↗