Biomedical subjects

R Ripa

Publications and source records attributed to R Ripa.

At least 19 recordsLinked to original sources

PubMed1995

Zinc and the elderly.

It is frequent in the elderly a zinc deficit, for many causes, which frequently occur in old age. Mineral deficit cause humoral and cellular immunity depression, with large increase of susceptibility to infections and increase of morbidity and mortality; besides it increases the proteinic malnutrition so frequent in old people. This condition is particularly presented in surgical patients and in patients undergoing total parenteral nutrition, when not specifically zinc supplemented. The evaluation of plasmatic zinc for diagnostic aims is scarcely significant, because hypoproteinemia (above all, hypoalbuminemia) is constantly present in old people: more useful and important is the leucocytic mineral evaluation, particularly in polymorphonuclear neutrophils. The average of recommended daily allowance of zinc is 15 mg for elderly people.

Aged↗

PubMed1995

[Zinc and diabetes mellitus].

In patients with type 1 and 2 diabetes was frequently found: low blood zinc levels, high zincuria, severe and ubiquitous cellular depletion of zinc, increased basal and after loading blood mineral clearance, and hyperglycaemia due to the reduction of pancreatic insulin secretion and to the reduced biological action of the hormone on liver, as a consequence of chronic zinc deficit. Strong endocellular zinc depletion in diabetics; low insulin secretion; insulin biological action decrease for zinc deficit; IG-I concentration decrease, that happens in this condition; insulin and IGF-I resistance; insulin and IGF-I receptors depletion in diabetics: are strong arguments for zinc pharmacological supplementation, in gastric protective formulation, to avoid gastroenteric problems.

Diabetes Mellitus, Type 1↗

PubMed1994

[Zinc and atherosclerosis].

The relationship between zinc and atherosclerosis is reviewed. Administration of strong doses of the mineral can turn out atherogenic through three mechanisms: 1. Through the alterations of the lipidic arrangement: decrease of HDL, increase of total cholesterol and LDL cholesterol (action promoted by the induced hypocupremia). 2. Through the alterations of the vasal wall, in consequence of the biochemical modifications of the basic substance (again, through secondary hypocupremia). 3. Through the increased platelet aggregation which seems to be produced by strong doses of zinc. In addition to these harmful actions, the antioxidative action, typical of zinc, must be stressed, which prevents oxidation of LDL and consequently stops the main mechanism of atherogenesis. Besides, the mineral restricts and nullifies the loss of metallothionein in zinc, produced by free radicals and subsequent functional alterations. Moreover, the calcium antagonist action of zinc must be considered: it blocks calcium and its several favorable actions on atherogenesis. In consideration of these last aspects, the rule of zinc, in suitable doses, could be considered as basic in the context of a strategy of prophylaxis and therapy of the atherosclerosis process.

Adult↗

PubMed1994

[Zinc and arterial pressure].

There are complex relations between zinc and arterial pressure. The mineral, which enters in the composition of zinc-enzyme "angiotensin-converting-enzyme" (ACE), takes part in arterial pressure regulation also through influences on others hormonal systems, which carry on many complex actions on circulation (glucocorticoids, catecholamines). It is frequent to find in hypertensive subjects low levels of plasmatic zinc (and high of cadmium): in "essential" hypertensive patients, particularly, it would be present a primary genetic defect leading, through transmembrane desregulation of ionic pumps, to high intracellular zinc and, secondarily, to high intracellular calcium. On the other hand, the same hypertensive process causes zinc and copper metabolism modifications, with an increase in zinc tissue concentration (opposite behaviour of copper). Moreover the plasmatic zinc reduction causes a proportional decrease of plasmatic and tissue ACE activity and arterial hypotension: zinc administration, in vitro and in vivo, clearly increases ACE action, with normalization of altered parameters due to zinc deficit.

Blood Pressure↗

PubMed1978