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Biomedical subjects

M Maccario

Publications and source records attributed to M Maccario.

At least 127 records · Page 7Linked to original sources
PubMed1989

Chronic treatment with pirenzepine decreases growth hormone secretion in insulin-dependent diabetes mellitus.

We and others previously reported that nocturnal GH secretion in patients with insulin-dependent diabetes mellitus is blunted by acute cholinergic muscarinic blockade with pirenzepine. In this study, we investigated whether this inhibitory effect on GH secretion persists during chronic pirenzepine administration, and if pirenzepine administration affects glycemic control. Nocturnal GH secretion was studied from 2300-0800 h before and after one month of pirenzepine administration (100 mg/day, orally, given at 2300 h) in 13 diabetic patients receiving their usual insulin treatment. GH secretion (GH area under curve) was blunted after pirenzepine administration [mean, 877 +/- 215 (+/- SE) vs. 1407 +/- 311 micrograms/L.min; P less than 0.002]. During pirenzepine administration, hemoglobin A1c significantly decreased (P less than 0.02), and 4 of the 13 patients had lower daily insulin requirements (5-23 U/day), but there was no significant change for the group as a whole. These results indicate that the inhibitory effect of pirenzepine on GH secretion persists when pirenzepine is given chronically and that pirenzepine seems to improve the metabolic control of the patients.

Adult↗
PubMed1989

Transient global amnesia, epilepsy, and migraine: diagnostic comparisons and distinctions.

Transient global amnesia, epilepsy, and migraine are three common neurologic disorders likely to be encountered by military physicians. These three entities share many clinical, electroencephalographic, and pathophysiologic characteristics. We report a patient who exemplifies the indistinct boundaries among these conditions and whose response to treatment supports the use of anticonvulsants for selected patients who have recalcitrant migraine.

Aged↗
PubMed1987

[Aorto-coronary bypass and defibrination after thrombolysis during the acute phase of myocardial infarct].

Coronary bypass was carried out in four patients who have received an intracoronary streptokinase infusion for acute myocardial infarction. Indications for emergency operation were a myocardial ischaemia time of less than 4 h and a slow flow in the reopened artery despite percutaneous transluminal coronary angioplasty. Two patients were in cardiogenic shock treated by inotropic drugs and intra-aortic balloon pump. In all cases, the level of fibrinogen was less than 1 g X l-1. During the operation, the fibrinolysis was stopped by the intravenous injection of aprotinine (3,000,000 U X 2) and tranexamic acid (15 mg X kg-1), the coagulation factors used by the fibrinolysis being replaced by fibrinogen (1 g per litre of blood volume) and fresh plasma (6 to 8 packs in function of the haemodynamic state). Patient heparinization was as usual (300 IU X kg-1). At the end of the cardiopulmonary bypass, after injection of protamine, clotting quality was good and the fibrinogen level was more than 1 g X l-1. In the postoperative period, blood loss was of little importance. Coagulation troubles due to therapeutic fibrinolysis were reversible. It was possible to return quickly the patient's coagulation state to normal, and so carry out emergency coronary arterial surgery in a defibrinated patient. The indications for surgery depended on cardiogenic factors only.

Angioplasty, Balloon↗
PubMed1986

Pathophysiological doses of glucagon cause a transient increase of the hepatic vein potassium concentration in man.

In order to evaluate whether glucagon-induced hyperkalemia is due to mobilization of potassium from the splanchnic region, we measured potassium changes in the hepatic veins following a glucagon injection into the ascending aorta. Twenty-seven subjects undergoing routine cardiac catheterization for diagnostic purposes were studied. Hepatic venous and aortic blood samples were withdrawn simultaneously under basal condition and 30, 60, 120, 180, 300, 600 s after a bolus injection of either saline, glucagon (100 ng/kg body weight) or glucagon +somatostatin (100 micrograms). After the intra-aortic injection, plasma glucagon in the hepatic veins reached levels comparable to those observed under pathophysiological conditions. Plasma potassium increased promptly with a peak at 60 s (delta max: 0.79 +/- 0.12 mmol/l, mean +/- SEM; p less than 0.01). The glucose increment peaked at 300 s (delta max: 2.36 +/- 0.20 mmol/l, mean +/- SEM; p less than 0.01). Potassium increment was potentiated by the addition of somatostatin, despite the abolition of insulin and C-peptide rises (potassium delta max: 0.56 +/- 0.10 mmol/l; p less than 0.05). In conclusion, these data demonstrate that glucagon induces a transient mobilization of potassium from the splanchnic region in man. This effect of glucagon on potassium is not antagonized by glucagon-induced insulin secretion.

Adult↗
PubMed1983

A sibship with neuroaxonal dystrophy and renal tubular acidosis: a new syndrome?

The clinical and pathological features of three siblings from nonconsanguineous parents are described. Two of the children died at 6 1/2 and 7 months of age of a central nervous system disorder characterized by severe behavioral retardation, hypotonia, and pyramidal tract signs. The third child, now 8 years old, has global mental retardation, inability to talk, marked tremors, and gait disturbances. All children exhibited inability to concentrate or acidify the urine, with growth delay partially corrected in the living child by alkali therapy. Computed tomographic scans revealed hyperdense lesions in the thalamus of one of the siblings and more striking hyperdensity of the basal ganglia in the eldest child. Findings at postmortem examination in two children, and by renal and sural nerve biopsy in the third, include swollen axons in the internal capsule and peripheral nerves, and neurons with iron-staining deposits, gliosis, and macrophages containing lipofuscin pigments in the brain. The renal findings include material positive for periodic acid-Schiff and hyperdense granular deposits in renal tubules.

Acidosis, Renal Tubular↗
PubMed1982

Development dysphasia and electroencephalographic abnormalities.

Seven patients, six boys and one girl, ranging in age from 2 years 7 months to 5 years 6 months at first contact, presented with severe language delay and dysphasic errors. They were found to have markedly abnormal EEGs despite the fact that only two of the children had had febrile seizures. The EEG abnormalities consisted to spike-wave or sharp wave discharges in focal or bilateral synchronous fashion, and were not affected by anticonvulsants. The children had normal motor development and no dysmorphic features. Results of neurological examinations were normal. CT and isotope scans were unrevealing. Intelligence, measured by a non-verbal scale, was normal. The authors suggest that an electrophysiological disturbance was the underlying cause of both the language deficits and the EEG abnormalities. The remarkably frequent occurrence of postmaturity (five of the seven cases) suggests that perinatal events may be an etiological factor.

Aphasia↗