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Biomedical subjects

G Tamburrano

Publications and source records attributed to G Tamburrano.

At least 91 records · Page 5Linked to original sources
PubMed1983

Circulating anti-insulin receptor antibodies in a patient suffering from lupus nephritis and hypoinsulinemic hypoglycaemia.

A 46-year-old female patient suffering from Lupus Nephritis came to our attention in 1981 for severe recurrent hypoglycaemia; she was obliged to eat every 5-7 hr to maintain glucose values not below 1.3-1.6 mM. All known causes of hypoglycaemia were excluded by performing selective angiography of the pancreas and skull, chest and abdominal computerized tomography, as well as stimulation and suppression tests. Oral glucose tolerance, tolbutamide and intravenous insulin (0.4 U/Kg b.w.) tests demonstrated that the patient was highly insulin resistant; furthermore, studies on the patient's red blood cells suggested that her insulin receptors were completely unable to bind insulin. Studies carried out to reveal the reason for this binding inhibition demonstrated that red blood cells from normal subjects as well as adipocytes from normal rats incubated with the patient's serum did not bind insulin (50% inhibition occurring at about 1:30 serum dilution). Insulin binding inhibitors were found in the fraction of the serum precipitated by ammonium sulphate. The serum cleared of IgG fraction was unable to affect insulin binding. These data demonstrate that the serum from the female patient investigated contained anti-insulin receptor antibodies blocking the binding of insulin to its receptors. Plasmapheresis improved the patient's metabolic status. The clinical picture would suggest that recurrent hypoglycaemia was caused by anti-insulin receptor antibodies acting as insulin on target cells.

Autoantibodies↗
PubMed1982

Plasma levels of glucagon-like polypeptides in gastrectomized patients transformed from Billroth II into Billroth I.

An oral glucose tolerance test (OGTT) has been performed in a group of patients with partial gastrectomy before and after transforming the anastomosis from Billroth type II (B II) into Billroth type I (B I). Glucose tolerance was normal in both groups. The statistically significant differences in blood glucose (BG) values observed at 30 min between B I and normals and at 30, 60 and 90 min between B II and normals occur without concomitant changes in insulin (IRI) plasma levels. In the course of the test a marked rise (statistically significant from 30 to 180 min) in glucagon-like immunoreactants (GLI) plasma levels was noted in B II patients and has been attributed to the rapid intestinal transit. Otherwise, the restoration of duodenal passage induced a clear decrease of GLI levels which returned to normal values. Increased immunoreactive glucagon (IRG) plasma levels in B II group do not seem to be due to cross-reactivity with GLI. The raised BG levels occurring in B II cannot be attributed either to a reduced insulin secretion or to an increase in biologically active components of glucagon.

Blood Glucose↗
PubMed1980

Arginine does not influence insulin binding on circulating monocytes.

Glucose ingestion, food intake or acute exercise produced rapid variations in insulin binding on monocytes. Insulin seems to play a minor or any role in this phenomenon in contrast pancreatic glucagon might be involved since it usually rises when an increase in insulin receptor affinity has been observed. To investigate the role of pancreatic glucagon we have studied the effect of arginine infusion on monocyte insulin receptor in five normal subjects. Results indicate that the aminoacid employed does not induce any change in insulin receptor affinity and concentration suggesting that the simultaneous increase in plasma insulin and pancreatic glucagon levels does not exert any action.

Adult↗
PubMed1979

[The insulinomas].

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Adenoma, Islet Cell↗
PubMed1979

Gastric carcinoma associated with severe hypoglycemia sensitive to diazoxide.

A case of carcinoma of the stomach associated with severe hypoglycemia is reported. Diagnosis of insulinoma was excluded on the basis of history as well as laboratory tests. Postmortem examination revealed widespread small metastases to various organs; no metastasis was found in the pancreas; the histology of this gland did not show any pathological finding. No impairment in pituitary, thyroid, adrenal and liver function was detected. Fasting blood sugar ranged from 18 to 56 mg/100 ml. An oral glucose tolerance test showed a diabetic pattern with low insulin. Tolbutamide, glucagon and glucose injected i.v. gave only a moderate rise in plasma insulin levels; plasma glucagon response to arginine was subnormal. The determination of NSILA-s and gastrin in the serum of this patient gave normal values. Diazoxide infusion induced an increase in blood glucose and subsequent treatment with diazoxide relieved hypoglycemia for some months. The occasional detection of an islet cell antibody by immunofluorescence in this case is not easily understandable, but it might partly account for the carbohydrate intolerance. An impairment in gluconeogenesis dependent upon some substrate deficiency might account for the hypoglycemia in this patient.

Adenocarcinoma↗
PubMed1976

Effects of alcohol on growth hormone secretion in acromegaly.

In 3 normal subjects and in 4 acromegalic patients pretreatment with an alcohol infusion for 4 hours at a constant rate reduced the GH response to Arginine, when comparison was made with pretreatment with saline. The reduction in acromegalics was more marked and sustained than in normals. Though it is likely that the effect of alcohol is exerted on hypothalamic centers, a direct influence on the pituitary cannot be excluded.

Acromegaly↗
PubMed1976

Alcohol hypoglycemia: hormonal changes.

Changes in hormonal (insulin, glucagon, cortisol and growth hormone), glucose and FFA levels in blood were studied in four young, normal subjects during, and following, alcohol infusion after 12 hours' fasting. Similar studies were made during and after saline infusions in the same subjects after a comparable period of fasting. At the end of the infusions of alcohol or saline an arginine test was performed in order to compare insular and pituitary responses. The same investigations were performed in another three young, healthy subjects after 36 hours' fasting. A chronic alcoholic suffering from hypoglycemia was studied after a 12 hours' fast when he was first seen and again nine months after alcohol withdrawal. The results are in keeping with the hypothesis that alcohol has a priming effect on islet alpha and beta cells when there is no substrate defect. When glycogen stores are exhausted hypoglycemia ensues. An adrenergic reaction supervenes and consequently FFA, cortisol and glucagon rise to high levels. The growth-hormone response to an arginine stimulus was lower after alcohol than after saline in all subjects. In the chronic alcoholic patient the plasma growth-hormone response was initially very poor to all of the stimuli, but after nine months' alcohol withdrawal pituitary activity had returned to normal.

Adult↗