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Biomedical subjects

V Di Piazza

Publications and source records attributed to V Di Piazza.

At least 19 recordsLinked to original sources
PubMed1992

[Hyperostotic spondylopathy and diabetes mellitus].

The Authors evaluated the prevalence of hyperostosis of the spine in 31 diabetic patients and in a control group of 32 non-diabetics. All of them underwent X-ray examination of the spine in the posteroanterior and lateral projections. Radiological signs of the disease were detected in 10 diabetics (32.25%) and in only 2 non-diabetics (6.25%). There was no statistical difference in the prevalence of the disease between insulin dependent and non-insulin dependent patients, between males and females. The Authors reviewed recent papers published on this subject and conclude that there is no clear explanation for this pathological process to occur. The hypothesis of increased GH secretion in diabetic patients did not find enough evidence but the disease is probably due to an abnormal synthesis of mucopolysaccharides.

Adolescent↗
PubMed1992

[Cryptogenetic liver cirrhosis with hypobetalipoproteinemia. Typing of the HLA histocompatibility system].

One hundred and forty-six patients with chronic liver disease have been studied. Some of them (15) showed a clinical picture characterized by cryptogenetic liver cirrhosis associated with hypotriglyceridemia and hypobetalipoproteinemia. These patients had compensated cirrhosis and no history of alcohol abuse; they did not suffer major illness in the past and had no signs of portosystemic encephalopathy. The pathogenetic mechanism of this association and the possible role of genetic factors are discussed. The HLA system has been studied and the A2 antigen found with high frequency, raising the possibility that patients with this syndrome may represent a particular subgroup among these with liver cirrhosis.

Female↗
PubMed1989

[Is serotonin implicated in the pathogenesis of the alcohol abstinence syndrome?].

5-Hydroxyindoleacetic acid (5-HIAA), the main metabolite of 5-hydroxytryptamine or serotonin, excreted in the urine over a 24 hour period was systematically measured in 35 patients with alcohol withdrawal syndrome (AWS). The level of excreted urinary 5-HIAA ac. was high in only a few patients. The pathogenic mechanisms involved are discussed and though the role of serotonin in the pathogenesis of AWS seems of secondary importance, some 5-hydroxytryptamine methyl analogues may have a major role in the pathogenesis of hallucinations caused by alcohol withdrawal.

Adult↗
PubMed1985

[Changes in the circadian rhythm of urinary cyclic adenosine monophosphate during the alcoholic withdrawal syndrome and related neurobiological correlations].

Urinary cyclic adenosine monophosphate (AMP-c) was measured morning and evening in 35 patients with alcohol withdrawal syndrome (AWS). 65% of the patients revealed a higher night time than day time concentration of AMP-c in the urine, reflecting increased sympathetic adrenergic activity. The circadian rhythm was lost in 88.55% of the 35 patients. The pathogenic factors and mechanisms involved in AWS are discussed and the contribution of sympathetic adrenergic hyperactivity to the onset of the withdrawal syndrome with its concomitant depression of the cholinergic and GABAergic systems is emphasised. Finally it is suggested that insomnia and the loss of REM sleep may also contribute to the onset of the condition.

Adult↗
PubMed1985

[Prolactin in chronic alcoholic liver diseases with and without gynecomastia].

The Authors, after having examined the factors responsible for the hyperprolactinemia in the cirrhotic, confirm the lack of a relationship between the increase in the prolactinic reserve and gynecomastia and between the amount of the prolactinic reserve and the degree of liver disorder. While hyperestrinism and the false transmitters lost most of their pathogenetic importance, other factors such as GABA, the Serotonin and the VIP, offered a new pathogenetic prospective. The prolactin reserve was studied in 63 patients affected by cirrhosis and in 25 affected by fibrosis and hepatic fibrosteatosis, pointing out an increase in the prolactin reserve in 61% of cirrhotic patients and an absence of pathological reports in patients affected by fibrotic hepatopathies. These data confirm the low pathogenetic responsability to be strictly ascribed to ethanol and the preminent role of liver cirrhosis and portal hypertension in the prolactin turnover.

Fatty Liver, Alcoholic↗
PubMed1984

[Prolactin in the alcohol withdrawal syndrome. Role of the dopaminergic system].

The basal prolactinemia and the prolactinic reserve were investigated in 30 chronic alcoholics, during the alcohol withdrawal syndrome. In 80% of these patients, the prolactinic reserve was extremely low, while in 16,66% of them was normal or near the lowest limits, recognizing in the exaggerated dopaminergic central activity the responsible pathogenetic mechanism. The dopaminergic hyperactivity fits into a general context of the sympathetic-adrenergic hypertonia, which notoriously plays a primary pathogenetic role in the pathogenesis of the alcohol withdrawal syndrome. In 5 patients with an inhibited prolactin response, a normalization of the prolactin reserve was registered in a test (the same methoclopramide test) carried out after 2-3 months of abstinence from alcoholic beverages, as an evidence of the normalization of the central dopaminergic activity and of a dopaminergic hyperactivity during the alcohol withdrawal syndrome.

Adult↗
PubMed1984

[Cyclic adenosine monophosphate (3'5' cAMP) in the alcohol withdrawal syndrome. Clinico-pathogenetic perspectives].

The cyclic adenosine monophosphate (AMP-c) excreted in the urine over a 24 hour period was systematically measured in 40 patients suffering from alcohol withdrawal syndrome (AWS) in varying degrees from slight to delirium tremens. In almost all patients the level of excreted AMP-c was high bul returned to normal when the clinical picture together with arterial pressure and cardiac frequency, was normalised. This shows the primary importance of the central sympathetic-adrenergic system in the pathogenesis of AWS and the value of monitoring urinary AMP-c excretion during the syndrome.

Adult↗