Biomedical subjects

J M Falko

Publications and source records attributed to J M Falko.

75 records · Page 5Linked to original sources

PubMedDate not supplied

Decreased serum C-peptide/insulin molar ratios after oral glucose ingestion in hyperthyroid patients.

Since C-peptide/immunoreactive insulin (IRI) molar ratios may reflect hepatic extraction of insulin, we measured simultaneous serum glucose, IRI, and C-peptide levels during fasting and 30, 60, 90, 120, and 180 min after 75 g of oral glucose in 10 hyperthyroid patients and 10 age- and weight-matched controls. Mean fasting serum glucose and IRI levels were significantly higher in the hyperthyroid versus control subjects (glucose: 4.9 +/- 0.3 mmol/L versus 4.36 +/- 0.11 mmol/L, P less than 0.01; IRI: 0.10 +/- 0.02 pmol/ml versus 0.05 +/- 0.01 pmol/ml; P less than 0.025). After glucose, mean serum glucose levels were significantly higher in the hyperthyroid versus control subjects at all times studied except for 180 min (P less than 0.01). Mean IRI levels were significantly higher at all times studied including 180 min (P less than 0.01). Mean fasting C-peptide levels were significantly greater in the hyperthyroid patients compared with the controls (1.2 +/- 0.25 pmol/ml versus 0.62 +/- 0.09 pmol/ml; P less than 0.025). After oral glucose, mean C-peptide levels were significantly higher (P less than 0.025) in the hyperthyroid compared with control subjects at 30-60 min but not at 90-180 min. Molar ratios of C-peptide/IRI were significantly lower (P less than 0.05) in the hyperthyroid versus control subjects at all times studied except fasting. In summary, glucose intolerance and hyperinsulinism occur in hyperthyroidism. In addition, C-peptide/IRI molar ratios are reduced after oral glucose ingestion.

Administration, Oral↗

PubMedDate not supplied

Gastric inhibitory polypeptide (GIP) responses after oral glucose ingestion in hyperthyroidism.

Gastric inhibitory polypeptide (GIP) is a gastrointestinal hormone stimulated after oral nutrient ingestion, but not after intravenous nutrient administration. GIP stimulates insulin release in the presence of hyperglycemia and as such is considered a major enteroinsular hormone. Since elevated glucose and insulin levels are found in hyperthyroidism, we compared the GIP responses to oral glucose ingestion in 12 hyperthyroid patients and 10 age-matched controls. Seventy-five grams of oral glucose was ingested after overnight fasting and samples were obtained at 0, 30, 60, 90, 120, and 180 min for serum glucose and immunoreactive insulin (IRI) and GIP (IRGIP). The mean serum glucose levels in hyperthyroid subjects were significantly higher (P less than or equal to 0.05) at every time studied except at 180 min. At 60 min, peak mean glucose was 171 +/- 14 mg/dl versus 128 +/- 7 mg/dl in controls (P less than 0.02). Except for fasting, mean IRI levels were significantly higher (P less than 0.001) in hyperthyroid subjects than in controls at all times studied. At 60 min, IRI rose to a peak of 125 +/- 11 microU/ml in hyperthyroid subjects versus 50 +/- 9 microU/ml in controls (P less than 0.001). Mean fasting, stimulated, and incremental IRGIP levels were slightly higher but not statistically different in the hyperthyroid subjects versus controls. Glucose and IRI responses are exaggerated in hyperthyroidism after oral glucose ingestion. Even though GIP has insulinotropic action, its role in the hyperinsulinism found in hyperthyroid subjects appears to be minimal.

Adult↗

PubMedDate not supplied

Unusual manifestations of cushing's syndrome in a multiple endocrine neoplasia type I kindred.

OBJECTIVE: To describe two unusual cases of Cushing's syndrome in a kindred with multiple endocrine neoplasia type I (MEN I). METHODS: The clinical and laboratory data as well as follow-up course of the two patients are reviewed in detail. RESULTS: Our first patient with a history of MEN I had hypercortisolism and computed tomographic evidence of a right adrenal mass (8.5 by 11 cm) extending into the inferior vena cava as well as multiple pulmonary nodules. He was diagnosed with Cushing's syndrome attributable to metastatic adrenal cancer that progressed despite chemotherapy. He died 2 years later. His son, who was also diagnosed with MEN I, had adrenocorticotropic hormone-dependent Cushing's syndrome. The plasma corticotropin-releasing hormone (CRH) level was high; magnetic resonance imaging showed normal pituitary findings but an islet cell tumor of the pancreas. The islet cell tumor was resected, and the patient's urinary cortisol declined to upper limits of normal. CRH was detected in the tissue, and the patient was thought to have Cushing's syndrome as a result of a CRH-secreting islet cell tumor. One year later, however, his Cushing's syndrome recurred. Inferior petrosal sinus sampling suggested a pituitary source, and the patient underwent transsphenoidal hypophysectomy. Histopathologic examination did not reveal pituitary hyperplasia or microadenoma, but the patient was cured of his Cushing's syndrome. CONCLUSION: Cushing's syndrome is a rare initial manifestation of MEN I. We report two unusual causes of Cushing's syndrome in MEN I--that is, adrenal cancer and a probable CRH-secreting islet cell tumor. The natural history of Cushing's syndrome in MEN I is not known; further studies should be conducted.

Journal Article↗