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Biomedical subjects

R Manna

Publications and source records attributed to R Manna.

At least 91 records · Page 5Linked to original sources
PubMed1979

Early insulin and glucagon response to subsequent pulses of arginine, glucose, and tolbutamide in normal man.

To determine the dynamics of insulin and of glucagon secretion in response to several sequential stimuli administered shortly after an arginine pulse (5 g), 20 nonobese, apparently healthy volunteers were given arginine (5 g), glucose (5 g), and tolbutamide (1 g) by rapid intravenous injection. The early insulin and glucagon area 0-8 min was studied. At the intervals and with the dosages used in this study, different stimuli with and without prestimulation with arginine did not lead to changes in early secretion of insulin. There was no exhaustion of the pool of insulin released after multiple sequential pulses. These results suggest a pattern in which stimulation induces a rapid release of insulin and activates the interchange between the stored and labile insulin pool; the 8-min interval is sufficient for the rapid return of the two compartments to a state of equilibrium. Also for glucagon, subsequent different stimuli did not exhaust glucagon release; nevertheless, glucagon is immediately suppressed by a submaximal glucose pulse.

Adolescent↗
PubMed1979

GH secretion in open-angle glaucoma.

Open-angle glaucoma is frequently observed in patients with acromegaly suggesting that the somatotropic hormone might facilitate a condition of glaucoma. The open-angle glaucoma patients studied, displayed higher plasma human growth hormone (HGH) levels than control subjects 60 min (30.3 +/- 1.7 against 16.8 +/- 2.7 ng/ml; p less than 0.001) and 90 min (19.0 +/- 1.9 against 9.3 +/- 1.2 ng/ml; p less than 0.001) after intravenous administration of arginine (25 g in 30 min). The authors support the hypothesis that the increased plasma HGH level may interfere with the regulation of ocular pressure by modifying the flow of aqueous humor from the eyeball via changes in the sclero-corneal trabecular meshwork; these changes are also found in diabetic subjects. The interplay between HGH and changes of carbohydrate metabolism (frequently occurring in glaucomatous patients) may be at the root of the variations of intraocular pressure in open-angle glaucoma.

Arginine↗
PubMed1979

Gastrin response to insulin in patients with cirrhosis of the liver.

Fasting gastrinemia in cirrhotics (48.35 +/- 2.77 pg/ml) was higher than in normal controls (32.93 +/- 0.75 pg/ml; P less than 0.001). After insulin-induced hypoglycemia, the mean increase of gastrin above basal level was 42.29 +/- 1.92 pg/ml in controls and 10.85 +/- 5.05 pg/ml in cirrhosis (P less than 0.001). BAO was 2.53 +/- 0.36 mEq/h in controls and 0.42 +/- 0.004 mEq/h in cirrhotics (P less than 0.001). After i.v. insulin, TAO was 8.42 +/- 0.72 mEq/h in controls and 3.06 +/- 0.26 mEq/h in cirrhotics (P less than 0.001). The authors suggest that the lack of an adequate gastrin and acid response to the hypoglycemic stimulus in cirrhotics might be accounted for by a decreased insulin sensitivity.

Adult↗
PubMed1979

Serum gastrin in portal and peripheral veins after arginine in man.

Immunoreactive serum gastrin from portal and peripheral veins was determined in five controls and in five cirrhotic patients with indwelling portal catheters in basal conditions, during and after 30 min arginine infusion, in order to assess whether the human liver is involved in gastrin metabolism. A significant difference was found between portal and peripheral gastrin concentrations in controls at 0, 60 and 90 min; no significant differences were found in cirrhotics. Our findings support the hypothesis of an at least partial breakdown of endogenous gastrin in the human liver.

Adult↗
PubMed1976

[Changes in plasma insulin and growth hormone after intravenous glucagon in hepatic cirrhosis].

Decreased increases in blood sugar by comparison with control subjects was noted in patients with cirrhosis of the liver after i.v. administration of 1 mg glucagon. Insulin secretion was similar to that observed in the controls. Basal GH values were higher in the liver patients, whereas after glucagon they displayed a gradual and progressive increase with a peak at 60'. No significant differences in GH pattern were noted in the two groups, however.

Adult↗
PubMed1976

[GH secretion after L-dopa administration in hepatic cirrhosis].

A 500 mg L-Dopa administration in normal and cirrhotic subjects does not determinate a significant varation of plasma glucose and insulin level, while a peak plasma GH level in both cirrhotic and normal subjects occurred at 90' with a significantly greates values in cirrhotics. It is doubtful to affirm that a high plasma GH level is the only one factor which responsable of glucose intolerance in cirrhotic subjects, when there are many others factors contribute to it in synergic way. In order to elucidate the hypothesis on possible pathogenetic mechanism it is discussed some of our own experience and observations.

Adult↗
PubMed1976

[Plasma insulin and GH during oral glucose load in liver cirrhosis].

Blood sugar, insulin and GH values were examined in two groups of cirrhosis of the liver patients, with and without ascites, after the administration of 100 g glucose per os. No significant differences between the two groups were observed. Insulin values were higher than those in the controls, with a pattern similar to that noted in subjects with chemical diabetes. GH values were higher than in normal subjects and secretion was not suppressed.

Adult↗
PubMedDate not supplied

Effect of somatostatin (SRIF) on plasma glucose and insulin response to glucagon in liver cirrhosis.

The present study was performed in order to evaluate the plasma glucose pattern in cirrhotic patients who, in the course of a continuous somatostatin infusion (500 microgram/h), were given pulses of glucagon (1 mg i.v.). In normal as well as in cirrhotic subjects somatostatin infusion provoked a marked reduction of the IRI plasma level and this was uninfluenced by subsequent glucagon administration. The rise in plasma glucose level in response to i.v. glucagon administration during somatostatin infusion was less marked in cirrhotics compared to normal subjects. This can be attributed to a variety of factors such as reduced number of liver cells or quantitative or qualitative changes of the liver cell glucagon receptors. Glucagon does not seem to contribute to the pathogenesis of carbohydrate intolerance in liver cirrhosis.

Adult↗
PubMedDate not supplied

Decreased insulin binding to red blood cells in liver cirrhosis.

eleven male cirrhotic subjects, all with impaired glucose tolerance (IGT), were studied. Insulin binding to circulating erythrocytes was evaluated. The specific bound fraction was decreased compared to normals (5.95 +/-0.76 vs 7.08 +/- 0.84%; p less than 0.005). An negative correlation was found between fasting insulin and bound fraction (r = -0.68; p less than 0.05). We suggest that serum insulin may be chronically augmented as a consequence of liver damage. This induces a down-regulation of insulin receptors that is responsible for insulin resistance and at least in part for the impairment of glucose tolerance.

Erythrocytes↗
PubMedDate not supplied

Thromboxane production in diabetes mellitus.

A correlation between increased platelet adhesiveness and aggregation and the development of angiopathy in diabetes mellitus can be made. Thromboxane produced by platelets represents a potent platelet aggregation factor. We studied the platelet TXB2 production during blood coagulation in carefully selected patients with type II diabetes mellitus in good metabolic control and the results were correlated with the presence or absence of microangiopathy, fasting blood glucose levels, type of therapy, age, duration of diabetes and the most important hematochemical parameters. No statistically significant differences were found between serum TXB2 concentrations in diabetic patients and control subjects, in diabetics with or without microangiopathy and in diabetics on insulin therapy or on oral hypoglycemic agents. We did not observe any correlation between TXB2 production and age, duration of diabetes, sex, basal blood glucose levels, total and HDL-cholesterol, triglycerides, blood creatinine and blood electrolytes. The thromboxane production may be a not important factor for determining the increased platelet aggregation which is at the origin of the angiopathy in diabetes mellitus.

Adult↗
PubMedDate not supplied

Nicotinamide increases C-peptide secretion in patients with recent onset type 1 diabetes.

Nicotinamide, a poly-(ADP-ribose) synthetase inhibitor, has been shown in animal models to induce islet B-cell regeneration. An open controlled trial was therefore carried out for 1 year in 36 patients with recent onset (less than 4 weeks symptoms) Type 1 diabetes. Twenty-three patients were treated with nicotinamide (200 mg daily) in addition to insulin, and 13 control patients were treated with insulin alone. Metabolic and immunological variables at entry were similar in the two groups. A significant increase of stimulated plasma C-peptide levels compared to diagnosis was observed only in the nicotinamide treated group (1.4 +/- 0.3 (+/- SE) micrograms l-1 at diagnosis vs 2.4 +/- 0.4 at 6 months, p less than 0.04; and 3.0 +/- 0.5 at 1 year, p less than 0.01). Patients receiving nicotinamide had lower glycosylated haemoglobin levels at 6 months and 1 year compared to the control group (p less than 0.04 and p less than 0.03, respectively) although insulin dose was lower. Small doses of nicotinamide may be successful in improving metabolic control in recent onset Type 1 diabetes, probably by increasing residual islet B-cell function.

Adolescent↗
PubMedDate not supplied

Insulin adsorption to three-liter ethylen vinyl acetate bags during 24-hour infusion.

Insulin adsorption to ethylen vinyl acetate, 3-liter bags injected with 10 insulin units, during 24-hr infusion has been studied. Three different infusions systems (A, B, and C) were tested and eight bags for each system were used. An elevated insulin adsorption resulted in each system. The maximal insulin recovery, expressed as percentage of the original theoretical 3333 microIU/ml insulin concentration, was 19.54% (at time 6), 20.93% (at time 4), and 16.95% (at time 22) for system A, B, and C, respectively. "Dismissed insulin amount" after 24-hr infusion was 1590 +/- 279.5 microIU, 1505.8 +/- 430.5 microIU, and 1253.3 +/- 369.8 microIU for system A, B, and C, respectively. Comparison of insulin concentration values at different times revealed significant differences only at time 18 (if compared with times 0,2.4,6,8,12,14,16) ant at time 20 (if compared with time 4,6,8,10) for system A, and at time 4 (if compared with time 12,14,16,18,20,22,24) for system B. We conclude that a constant but low insulin delivery can be achieved using 3-liter EVA systems and a 24-hr infusion.

Adsorption↗
PubMedDate not supplied

Cryoglobulinemia: a true internistic disease?

Cryoglobulinemia is a clinical condition characterised by the presence of circulating globulins that precipitate at a temperature lower than 37 degrees Celsius and re-dissolve with warming. We can distinguish 3 different types of cryoglobulinemia, according to their immunochemical characteristics. Cryoglobulinemia can be associated with infectious, inflammatory or neoplastic disease. Cryoglobulinemia type II can be associated with chronic HCV-hepatitis. Clinically, cryoglobulinemias cause hyperviscosity-related symptoms or lesions by immunocomplex deposition (cryoglobulinemic vasculitis). Many organs and systems can be involved, from the skin to the joints, from the central nervous system to the kidney. Diagnosis requires a careful clinical and physical evaluation and the demonstration of circulating cryoglobulins by cryoprecipitation and immunoelectrophoresis. The therapeutic goals are the treatment of the underlying diseases and the complication and prevention of progression/relapse. It is obvious that this disorder can involve different specialists, but the internist plays a central role: he identifies the disease and the associated condition, he treats the underlying disorder and refers the patient to the specialists for the organ-specific manifestations.

Animals↗
PubMedDate not supplied

Association of myasthenia gravis and antisynthetase syndrome: a case report.

Myasthenia gravis is a chronic disease of neuromuscular transmission caused by loss of acetylcholine receptors. It can be found in association with other autoimmune disorders. We report the case of a 47-yr-old woman affected by Myasthenia gravis who complained of fever, progressive weakness of proximal limb muscle, arthritis and Raynauds phenomenon and dyspnea. Chest X-rays and CT scan showed an interstitial lung disease; laboratory data indicated an inflammatory picture and increased serum muscle enzymes. Evaluation for infectious, metabolic, iatrogenic and neoplastic aetiologies was unrevealing. The patients clinical condition together with positive results on antisynthetase antibody assay lead to the diagnosis of antisynthetase syndrome. To our knowledge, this is the first report on the association of Myasthenia gravis with antisynthetase syndrome.

Anti-Inflammatory Agents↗
PubMedDate not supplied

Normalisation of high CA 19-9 values in autoimmune hepatitis after steroidal treatment.

Carbohydrate 19-9 antigen (CA 19-9) is considered a specific marker of pancreatobiliary adenocarcinomas, but slight increase of its levels can be found in several non-malignant diseases of the liver, such as autoimmune hepatitis. We describe a case of marked CA 19-9 elevation (up to 898.0 U/ml) in a patient with autoimmune hepatitis. Laboratory and instrumental examinations excluded malignant diseases. Immunohistochemical analysis for CA 19-9 and MIB-1, performed on liver biopsy, showed reactivity in inflammatory areas, in particular in bile ductule cells and hepatocytes in ductular metaplasia, suggesting that these cells could be involved in CA 19-9 serum levels increase. After steroids, the clinical picture improved and all the laboratory parameters normalised.

Alkaline Phosphatase↗