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Biomedical subjects

J Guillon

Publications and source records attributed to J Guillon.

At least 37 records · Page 2Linked to original sources
PubMed1983

[Not Available].

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Greek World↗
PubMed1981

Pituitary function in idiopathic haemochromatosis: hormonal study in 36 male patients.

Thirty-six male patients with idiopathic haemochromatosis were subjected to measurements of basal plasma values of testosterone, LH and FSH and to an LRH test. Nineteen were also subjected to basal plasma determinations of T3, T4, cortisol, TSH and prolactin and to a TRH test. In 11 cases GH values were measured before, during and after an arginine infusion. Seventeen patients were found to hae low levels of testosterone, LH and FSH, and no gonadotrophin responses to LRH. Seventeen others had normal levels of these three hormones, with normal responses to LRH. The two remaining patients had normal testosterone values but very increased gonadotrophin values: a fact which remains unexplained. Basal levels of prolactin, GH, T3, T4, and TSH were normal: cortisol levels were either normal or increased in cases of poorly controlled diabetes. Prolactin responses to TRH were always normal. TSH responses to TRH were impaired in 2 cases, and GH responses to arginine in 3 cases. Considering that other factors may be involved in the few impairments found in TSH and GH stimulations, it is concluded that the only indisputable pituitary insufficiency in about half of the cases of idiopathic haemochromatosis is gonadotrophic.

Adult↗
PubMed1980

Adrenocortical function in idiopathic haemochromatosis.

In idiopathic haemochromatosis, excessive iron deposits include adrenal cortex, and mainly the zona glomerulosa. In this view, we measured basal and post-stimulative values of plasma cortisol, aldosterone and renin activity (RA) in two groups of patients: 1) 9 normal-salt repleted subjects (NSR) who were subjected to iv ACTH and furosemide tests, 2) 10 patients who were subjected to chronic salt depletion (CSD), to iv ACTH and furosemide tests. The results were compared with two groups of 7 healthy volunteers (NSR and CSD). In the patients, basal cortisol values were either normal or increased in cases of poorly controlled diabetes (21 +/- 2.1 microgram/100 ml, P < 0.01) and cortisol increase after ACTH injection was normal (to 43.3 +/- 4.3 microgram/100 ml). In the 9 NSR patients, basal aldosterone (7.75 +/- 1.5 ng/100 ml) and RA (1.55 +/- 0.27 ng/ml/h) values were normal; aldosterone and RA rose after furosemide injection: these increases were similar in these patients (respectively to: 13.5 +/- 2.2 ng/100 ml and 4.3 +/- 0.6 ng/ml/h) and in the 7 NSR controls. In the 10 CSD patients, basal aldosterone and RA values were always increased (26.5 +/- 3.2 ng/100 ml and 8.5 +/- 2.3 ng/ml/h) as much as in the 7 CSD controls. After ACTH administration, aldosterone values (26.1 +/- 4 in NSR patients, 54 +/- 8 ng/100 ml in CSD patients) were the same as in the two control groups. This study suggests that there is no adrenocortical deficiency in idiopathic haemochromatosis, in spite of excessive iron deposits in the adrenal cortex.

Adrenal Cortex↗
PubMed1979

[Plasma hormonal pattern of the late diabetic pregnancy (author's transl)].

Plasma estradiol, estriol, progesterone, H.C.S. and cortisol were measured (RIA methods) every two days, in 20 diabetic pregnancies (classes B, C or D of White), between the 33th week and the delivery, and were compared with normal pregnancies. Estriol was always normal, and progesterone values were at the upper limit of the normal range; estradiol, H.C.S. and cortisol were normal or elevated, with mean values significantly higher than controls. E2 and/or progesterone dramatically decreased in 5 cases before birth, just as the urinary measurements. In this study, the insulin requirements were not correlated with these plasma hormone values. Besides pathogenic hypothesis )glycemic control of H.C.S. and cortisol--abnormalities of metabolic pathways of estrogens ?), this work informs the inferred hormonal deficiency in diabetic placenta. Also, it is unable to determine the practical usefulness of these plasma measurements in the management of diabetic pregnancy.

Adult↗
PubMed1978

[Hormone and metabolic profile in diabetic hyperosomolar coma. Plasma insulin response to intravenous tolbutamide (author's transl)].

Fifteen patients with non-ketotic hyperosmolar diabetic coma were investigated and compared with ketoacidotic patients. Basal plasma insulin levels were low in all patients (14.8 +/- 1.0 micronU/ml in hyperosmolar coma, 11.0 +/- 1.3 in keto-acidosis), but insulin level increased after intravenous tolbutamide (between 30 and 105 micronU/ml) in eight hyperosmolar comas. Insulin showed no increase in seven hyperosmolar comas and in none of the ketoacidotic patients. In hyperosmolar coma plasma free fatty acids (1710 +/- 197 micronEq/1), triglycerides (3,4 +/- 0,4 g/1) and cortisol levels (49,7 +/- 9,0 microgram/100 ml) were increased, must as in keto-acidosis. Growth hormone (1,7 +/- 0,1 ng/ml) was normal, unlike the case in keto-acidosis. Plasma lactate concentrations were elevated and account for the frequent mild acidosis found in hyperosmolar coma. In spite of the low peripheral "insulin/glycemia ratio", the positive response to tolbutamide in half of the hyperosmolar cases suggests a less complete pancreatic deficiency than in keto-acidosis. The plasma high free fatty acid and triglyceride levels suggest that the lack of ketosis is not due to inhibition of lipolysis but could be a consequence of inhibition of hepatic ketogenesis.

Adult↗
PubMed1976

[Adrenal scintigraphy using 131 I-19-iodocholesterol. Value in the exploration of Cushing's syndrome].

On the basis of 7 cases representing the essential types of aetiology of Cushing's syndrome, it is possible to define the value, limitations and role of adrenal scintigraphy using 131I-19-iodocholesterol in the diagnostic investigation of hypercortisolism. The essential value of the investigation is morphological rather than functional drome. Thus adrenal scintigraphy has the same role in diagnostic investigation as various radiological procedures such as pneumoperitoneum and angiography. The latter, however, are technically difficult and fraught with risk, in contrast to the isotopic examination. The principle limitations of the method are not dosimetric but lie in the relative difficulty of interpretation of the documents obtained.

Adrenal Gland Neoplasms↗
PubMed1975

[Diabetes mellitus secondary to liver diseases. A review (author's transl)].

Diabetes mellitus is more frequently found in pateints with hepatic cirrhosis (about 10%) than in subjects without liver disease. Cirrhosis has been the main subject of interest in this respect. Very few studies have been made in viral hepatitis or steatosis. In about 40% of cases, the diabetes is identified before the cirrhosis. More often (in about 60% of cases) the diabetes is discovered at the same time as or after the finding of cirrhosis. This "post-cirrhosis diabetes" shows no clinical peculiarity. In about 80% of patients with liver cirrhosis when fasting blood glucose is normal, abnormalities of carbohydrate metabolism are to be found by the oral glucose tolerance test. Approximately 50% show an abnormal response to intravenous glucose and 30% to intravenous tolbutamide. The "mechanism" of these metabolic abnormalities in liver cirrhosis is unknown. The following abnormalities are observed: 1) With similar glycaemic response to a glucose challenge, plasma insulin levels are higher than in patients without liver disease, suggesting insulin unresponsiveness. Resistance to exogenous insulin can be demonstrated. 2) Plasma free fatty acid levels are often elevated. 3) Plasma growth hormone levels are often raised. 4) Plasma glucagon levels are high when porto-caval shunting is present. 5) Potassium is often depleted. These metabolic abnormalities, in association with porto-caval shunting and hepatocyte insufficiency may explain the insulin resistance which characterises liver cirrhosis, and the diabetes which it may precipitate in predisposed persons.

Diabetes Mellitus↗