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Biomedical subjects

G Mecca

Publications and source records attributed to G Mecca.

At least 55 records · Page 3Linked to original sources
PubMed1980

Reduced umbilical and placental vascular prostacyclin in severe pre-eclampsia.

Prostacyclin production was significantly depressed in foetal and placental vascular tissues from five patients with severe pre-eclampsia in comparison to vascular tissues from women with uncomplicated pregnancy. Such an abnormality may be responsible for a reduced blood flow and defective fetal nutrition thus playing a major role in the pathogenesis of this syndrome.

Adolescent↗
PubMed1980

Haemolytic uraemic syndrome: report of a case and new pathogenetic concepts.

Haemolytic uraemic syndrome (HUS) is a severe clinical condition characterised by thrombocytopenia, microangiopathic haemolytic anaemia and renal impairment [1]. At histological examination hyaline microthrombi occluding terminal arterioles and capillaries are generally found. Other syndromes share major clinical and histological diagnostic criteria with HUS. In particular, there is no method at present which clearly differentiates HUS from thrombotic thrombocytopenic purpura (TTP) [2]. We propose therefore the term thrombotic microangiopathy (TMA) to discuss both syndromes. The pathogenesis of TMA is unclear and many forms of therapy have been attempted without definitive proof of efficacy. The recently reported [3] successful results with exchange transfusion and plasma infusion represented a consistent advance in the management of these diseases. The beneficial effect of these procedures was attributed to replacement of an unknown 'missing' factor in plasma. This finding generated recent observations possibly relevant in understanding the pathogenesis of these diseases.

Adult↗
PubMed1980

Carnitine balance in hemodialyzed patients.

1-Carnitine was assayed before and after dialysis in plasma, dialyzate and muscle of four patients undergoing hemodialysis. The findings suggest that plasma carnitine losses occurring during hemodialysis may be at the expense of the carnitine present in extracellular fluid. Carnitine concentrations in muscle of hemodialyzed patients and controls did not differ significantly. Chronic carnitine administration did prevent plasma carnitine from falling below base levels, but did not affect muscle concentration.

Adult↗
PubMed1979

Plasmapheresis in the treatment of acute renal failure in multiple myeloma.

Three patients with multiple myeloma and severe acute renal failure were treated by repeated plasmapheresis. Recovery of renal function was observed in all. The pathogenetic role of light chains and the possible mechanisms responsible for renal damage are discussed. It is suggested that the removal of light chains by plasmapheresis may be of therapeutic value in this condition.

Acute Kidney Injury↗
PubMed1979

Prostacyclin and human foetal circulation.

Tissues from human umbilical cord arteries and placental veins generated much greater prostacyclin activity than vessels from normal adults. High prostacyclin generation could contribute to maintaining the low peripheral vascular resistance typical of foetal circulation in which blood pressure is low despite very high cardiac output.

Adolescent↗
PubMed1979

Bleeding in renal failure: a possible role of vascular prostacyclin (PGI2).

Specimens of venous tissues from a group of 25 patients with chronic uremia and 7 patients with acute renal failure generated significantly higher PGI2-like (platelet aggregation inhibiting) activity than venous tissues from 30 normal subjects. After repeated washings, when this activity could barely be detected in the controls, pronounced inhibitory activity was still evident in samples containing venous tissues from uremic patients. Both prolonged bleeding times and increased PGI2-like activity returned to normal in 4 acute uremic patients on restoration of their renal function. These findings may be relevant to the pathogenesis of bleeding in renal failure.

Acute Kidney Injury↗
PubMed1979

Treatment of the hemolytic uremic syndrome with plasma.

Two patients with the hemolytic uremic syndrome were treated with plasma exchange an infusion: in both cases, the reduced platelet count reverted to normal values and the microangiopathic anemia ceased within a few days. Systemic blood pressure and requirement for antihypertensive drug therapy were also markedly reduced following treatment with plasma. Venousprostacyclin (antiplatelet aggregating) activity was undetectable in both patients before but was restored after treatment with plasma. The plasma samples collected before, but not those collected at various intervals after replacement therapy, had decreased capacity to stimulate prostacyclin activity in rat aortic rings. It is suggested that in patients with the hemolytic uremic syndrome or with other clinical conditions which can be included under this rubric (such as thrombotic thrombocytopenic purpura) a plasma factor is lacking which stimulates prostacyclin activity. Plasma would supply such a missing factor, thus representing a rational treatment for some of the life-threatening manifestations (thrombocytopenia, hemolytic anemia, hypertension) of this severe syndrome.

Antihypertensive Agents↗