Search PubMed⌕ Search

Biomedical subjects

F Stephan

Publications and source records attributed to F Stephan.

At least 37 records · Page 2Linked to original sources
PubMed1984

Histomorphometric study of the enhancement of renal compensatory hypertrophy by ACTH in the rat.

In the female adult rat, renal compensatory hypertrophy is greatly enhanced by hyperadrenocorticism elicited by the administration of ACTH given at a dose of 18 Y/100 g BW/d for 7 days after uninephrectomy (UN). This renotrophic effect of ACTH is particularly prominent in rats drinking a NaCl solution (9 g/l). In the present experiments, we performed histomorphometrical measurements of the glomerular tuft (GT) and the proximal tubule (PT) in the hypertrophying kidney (HK) remaining 7 days after UN in 10 rats treated with ACTH and 7 control animals. The histologic preparations were examined under light microscopy with the "Kontron" image analyzer. ACTH increased the weight of the HK (1213.8 +/- 20.3 mg versus 1037.3 +/- 13.3, p less than 0.001) and determined an enlargement of the cross sectional area of the GT (12559 +/- 3351.3 mu2 versus 10486 +/- 407.5, p less than 0.01) and of the epithelial area of the PT (1751 +/- 40.8 mu2 versus 1586 +/- 41.5, p less than 0.025). These morphometrical data are consistent with the increased Protein/DNA ratio - a marker of cellular hypertrophy - found in other rats studied under the same experimental conditions. The increased weight gain of the HK elicited by ACTH is related to the hypertrophy of the epithelial cells of the PT and possibly to an enlargement of the glomeruli.

Adrenocorticotropic Hormone↗
PubMed1984

[Bromocriptine and the growth hormone response to thyroliberin in the insulin-dependent diabetic].

The effect of bromocriptine on growth hormone (GH) responses to TRH was studied in 14 insulin-dependent diabetics. The effect of this dopaminomimetic agent was inconstant. In the 6 patients with inadequate responses of GH to TRH, bromocriptine inhibited this response. Inversely, it appeared capable of stimulating a GH response in certain non-responders. The could suggest the existence of disturbances of dopaminergic control of GH secretion in diabetics, but the lack of reproducibility of responses of GH to TRH makes this an uncertain conclusion.

Adolescent↗
PubMed1983

[Asymptomatic thyroid dysfunction. Routine detection using the free thyroxine index].

Free plasma thyroxine index (FT4I) and plasma concentrations of triiodothyronine (T3) were routinely determined on admission in 1862 hospital patients without signs or history of thyroid dysfunction. Total thyroxine (T4) and FT4I values were beyond confidence limits in 16.3% and 7.5% respectively of the patients, whereas T3 values were low in 23%. Among the 84 patients with high FT4I, 31 had clinically unsuspected hyperthyroidism confirmed by the TRH test (T3 increased in 66% of the cases). Among the 46 patients with low FT4I, 14 had demonstrable hypothyroidism (low T3 in 65% of the cases). In this population, the prevalence of proven thyroid dysfunction without clinical symptoms was 1.66% for hyperthyroidism and 0.75% for hypothyroidism. The diagnostic value of normal FT4I was estimated at 50%. The persistence of an abnormal FT4I on a second determination indicated the presence of hyperthyroidism in 72% of patients with high FT4I values and of hypothyroidism in 74% of patients with low FT4I values. In doubtful cases, TSH assays or TRH tests led to the concept of "transient" dysthyroidism, and the potential total prevalence of routinely discovered dysthyroidism could be estimated at 3.54% including 2.47% for hyperthyroidism. The latter occurred in 95% of people older than 50, with a sex ratio of 0.94. The cost of diagnosis for each new case clinically unsuspected hyperthyroidism is 1200 Z, but this could be reduced to 450 Z if only patients over 50 years of age were investigated and if FT4I determinations were replaced by free T4 determinations.

Adult↗
PubMed1983

[Modification of the renotrophic action of adrenal hypercorticism by nutritional factors in uninephrectomized rats].

In the rat renal compensatory hypertrophy (RCH) was enhanced by hyperadrenocorticism induced by the administration of a long acting ACTH at a dose of 18 Y/100 g body weight/d. for 7 d. after uninephrectomy (UN). In the present experiments we compared the differences delta between the weight, the content in protein, RNA and DNA of the left solitary kidney and the same determinations done on the right kidney excised at UN 7 d. earlier. The rats drank freely a isotonic solution of NaCl (G1) or KCl (G2) or glucose (G3, G4). The rats of group G1, G2 and G3 received a standard solid food; the G4 rats ate a K poor diet. About half of the animals were treated with ACTH. RCH occurred in all the rats even when they lost body weight. The gain in weight of the solitary kidney was enhanced in all the rats treated with ACTH but not in the G2 rats loaded with KCl. This renotropic action of hyperadrenocorticism was most prominent in the K depleted G4 rats. The protein/DNA ratio, a marker of cellular hypertrophy, was increased by hyperadrenocorticism in the G1 and D2 rats drinking respectively the NaCl or the KCl solutions. This ratio did not change in the ACTH treated G3 and G4 rats drinking the glucose solution suggesting that, in this experimental condition, cellular hyperplasia and hypertrophy occurred at the same extent. These experiments suggest that, in the uninephrectomized rat, the renotrophic action of ACTH is modulated by nutritional factors. The enhancement of RCH by ACTH may be related to hyperglycemia, hyperinsulinism or altered handling of Na and K by the nephron.

Adrenal Glands↗
PubMed1982

[Serum beta 2 microglobulin assay in diabetes mellitus (author's transl)].

Beta 2 microglobulin (beta 2m) is continuously produced and subsequently almost exclusively eliminated by glomerular filtration (GRF). There is a strong correlation between serum beta 2m and serum creatinine concentrations. Beta 2m assay however seems to enhance diagnostic accuracy of minor decreases in GRF. Serum beta 2m concentrations were assayed in 193 consecutive patients with diabetes mellitus. They correlated well with serum creatinine. Supranormal serum beta 2m concentrations (greater than 2.4 micrograms/lm) were found in 15.5% of patients with normal serum creatinine. Increase in beta 2 m/was related to poor metabolic control of diabetes and correlated positively with glycosylated hemoglobin concentrations. Serum beta 2m concentrations were also related to the duration of recognized diabetes. Serum beta 2m assay allows early detection of GRF disorders in patients with diabetes mellitus. Such disorders may be partly reversible once metabolic control is improved.

Adolescent↗
PubMed1982

[Hormonal adaptation to chronic self-starvation in patients with anorexia nervosa (author's transl)].

An intravenous glucose tolerance test (glucose 0.33 g/kg bodyweight) was performed in 35 women with chronic anorexia nervosa (AN) and in 19 age-matched women of normal weight. Plasma free fatty acids (FFA), immunoreactive insulin (IRI) and growth hormone (GH) levels were measured before and after the test. Although the mean value of glucose disappearance rate K was significantly reduced in the patient group as compared with the control group, K was in fact normal (greater than or equal to 1.10 +/- 10(-2)) in 20 anorectic women (AN 1) and lowered in 15 (AN 2). The basal and post-stimulation IRI levels were decreased in all anorectic women, but particularly in the AN 2 group with impaired glucose tolerance. The glucose load elicited a striking rise in GH in patients of the AN 2 group, a slight increase in those of the AN 1 group and no change in women of the control group. FFA values before the test were high mainly in the AN 2 patients but the difference with reference values did not reach statistical significance owing to the large s.e.m. After the glucose load there was a similar decrease in FFA levels in all three groups, but levels in the AN 2 group remained significantly higher than in the control group. Hyposecretion of IRI and hypersecretion of GH may account for the impaired glucose tolerance observed in all patients of the AN 2 group. Both hormonal changes facilitate neoglucogenesis and lipolysis, thereby providing the energy substrates required for survival of the self-starved subjects. The anorectic women also had low plasma T3 enabling adjustment of the oxidative metabolism to the reduced food supply.

Adolescent↗
PubMed1982

Effect of diabetic control on the level of circulating thyroid hormones.

Basal plasma levels of thyroxine (T4), triiodothyronine (T3) and reverse T3 were determined by radioimmunoassay in 44 control subjects, 44 Type 1 (insulin-dependent) and 39 Type 2 (non insulin-dependent) diabetic patients aged from 15 to 75 years. All were clinically euthyroid. The quality of diabetic control was assessed by the percentage of glycosylated haemoglobin. In both the diabetic groups there was a significant decrease in T3 and a rise in reverse T3 whereas T4 was normal. We found no significant differences between plasma thyroid hormone levels in Type 1 and Type 2 diabetic patients. In the poorly controlled diabetics (glycosylated haemoglobin greater than or equal to 12%), T3 was 90 +/- 5 ng/dl, which differed significantly from the level found in the better controlled patients (106 +/- 5 ng/dl, p less than 0.01). In the diabetic patients without associated illness, a negative linear correlation was found between T3 and glycosylated haemoglobin and a positive correlation between reverse T3/T3 and glycosylated haemoglobin. No correlation between T3 or reverse T3 and fasting blood glucose could be established. In conclusion, many diabetics showed a low T3 syndrome suggesting that there may be an impairment in the extrathyroidal conversion of T4 to T3. This may well be enhanced by a poor diabetic control (glycosylated haemoglobin greater than or equal to 12%).

Adolescent↗
PubMed1982

Enhancement of renal compensatory hypertrophy by hyperadrenocorticism and its modulation by nutritional factors.

Renal compensatory hypertrophy (RCH) is enhanced by ACTH in the uninephrectomized rat. In the present experiments, the kidney weight and its content in protein, RNA and DNA were determined in 48 adult, female rats; 24 had free access to a NaCl solution (9 g/l) and the others to a glucose solution (50 g/l). In each group 12 rats were sacrificed 2 or 7 d. after uninephrectomy (UN). In each subgroup 6 rats were treated with ACTH (18 micrograms/100 g B.W./d) from operation until autopsy. RCH has been evaluated by the arithmetical difference between the data determined in the right control kidney excised at UN and those determined in the left solitary kidney. In all the rats, hyperadrenocorticism increased significantly the weight of the solitary kidney and its content in protein and RNA. There was a significant decrease of the DNA content of the solitary kidney in the rats sacrificed 7 d. post-UN, treated with ACTH and drinking the saline solution. DNA was not affected by ACTH in the 7 other groups suggesting that ACTH favours cellular hypertrophy mainly in the rats drinking the saline solution. The renotrophic action of hyperadrenocorticism may be related to an altered handling of Na+ and K+: there was a positive correlation between the weight gain of the solitary kidney and the urinary excretion of Na+ (r = 0.507, p less than 0.001) and of K+ (r = 0.460, p less than 0.001). Hyperinsulinism was present in all the rats given ACTH; it may act as a growth factor. Hyperglycemia played an important role in former experiments but it was absent in the present studies.

Adrenocorticotropic Hormone↗
PubMed1982

Growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics with or without severe microvascular lesions.

Plasma levels of growth hormone (GH) were determined in fifty-two non obese insulin-dependent diabetics (IDD) and in twenty eight control patients before and after the i.v. administration of 250 micrograms in thyrotropin-releasing hormone (TRH). The mean basal plasma GH level in the IDD was normal. Administration of TRH elicited a rise of GH above 6 ng/ml in 40% of the IDD whereas no elevation occurred in any control subject. The basal and post-stimulative GH levels were similar in diabetics with mild retinopathy and in diabetics without microvascular lesions. The basal and peak plasma GH levels as well as the GH increase after TRH were significantly higher in ten patients with nephropathy and severe retinopathy than in 42 IDD having no detectable renal damage. It is concluded that there is a disturbance of GH secretion in IDD. This abnormality seems to be independent of the short-term glycemic control and appears to be partially related to the presence of severe microvascular lesions. The present results do not prove a causal relationship between the abnormal GH secretion and the development of the diabetic microangiopathy as the pituitary dysfunction could also be a consequence of central microvascular lesions.

Adolescent↗
PubMed1981

[Correlation between renal compensatory hypertrophy and urinary sodium excretion in the ACTH treated rat].

In the rat, renal compensatory hypertrophy (RCH) is enhanced by the administration of ACTH (beta 1-24 corticotrophin) given at a dose of 18 micrograms/100 g. body weight/d. after uninephrectomy. In the rats drinking tap water, the enhancement of RCH by ACTH occurs without any significant change in urinary Na+ excretion. But, in the animals drinking a NaCl solution (9 g/l), ACTH determines a polyuria with hypernatriuria and a more striking increase of RCH positively correlated with the urinary Na+ excretion.

Adrenocorticotropic Hormone↗
PubMed1980

[Metabolic risks of salbutamol in diabetic patients. A study using somatostatin (author's transl)].

Salbutamol-induced diabetic ketoacidosis having recently been reported, the authors have studied the metabolic changes produced by the drug in 6 nondiabetic patients. All patients received a 3-hour infusion of salbutamol (S) 20 z g/minm. On the following day, three of these were given somatostatin (SRIF) 100 mg/hour mixed with S infused at the same rate, whilst the remaining 3 patients received SRIF alone. On the 3rd day, patients of the first sub-group received the same infection of S and SRIF as before plus exogenous glucagon 90 ng/kg/hour. Somatostatin is know to inhibit insulin and glucagon secretion. Exogenous glucagon was given in order to reproduce the metabolic conditions of insulin-deficient diabetes mellitus. Salbutamol alone induced a small rise in blood glucose and insulin, free fatty acids, glycerol and ketonic bodies, but no changes in endogenous glucagon. SRIF alone produced no significant metabolic variations. In the presence of SRIF, all salbutamol-induced metabolic changes were increased. Adding glucagon mainly resulted in high levels of ketonic bodies. All variations correlated with each other. Thus, whilst the hyperglycaemic, lipolytic and ketogenic effects of S in non-diabetic patients are partly masked by insulin hypersecretion, they are enhanced in the absence of insulin and, to an even greater extent, by an excess of glucagon. Diabetic patients treated with salbutamol should therefore be under close surveillance and have their insulin dosage increased.

Adult↗
PubMed1980

[Thyrotoxicosis with low T3 and high reverse T3 levels. 9 cases (author's transl)].

In common forms of hyperthyroidism serum levels of triiodothyronin (T3) are higher than those of thyroxin (T4) and isolated elevations of serum T3 have even been noted. We report 9 cases of proven hyperthyroidism with normal or low levels of T3 and elevated T4 and reverse T3 (rT3). Most out of the patients were more than seventy years old and had associated diseases. Our data show that the low T3 with elevated rT3 syndrome--which has been noted in many metabolic and pathologic conditions--can coexist in hyperthyroidism. They emphasize the lack of diagnostic discrimination of T3 assays in thyroid dysfunction especially in the older patient or one with associated disease.

Adult↗