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Biomedical subjects

E Melzi

Publications and source records attributed to E Melzi.

5 recordsLinked to original sources
PubMed1992

Lupus anticoagulant: interference with in vivo prostaglandin production and with platelet sensitivity to prostacyclin.

The hypothesis has been made that inhibition of prostacyclin (PG12) production may play a role in the pathogenesis of thrombosis in patients with the lupus anticoagulant (LA), but so far no evidence of reduced PG12 levels in vivo has been produced. We have tested the plasma levels of PG12 and thromboxane A2 (TXA2) and the platelet sensitivity to PG12 in 14 patients with and without LA and in 14 healthy controls. No significant difference in the prostanoid basal levels was detected among the groups; however, in some patients PG12 increments seemed to parallel the clinical course of the disease. Platelet sensitivity to exogenous PG12 was significantly enhanced in the LA + patients and correlated with PG12 values. We suggest that in these subjects additional factors, other than reduced PG12, may predispose to thrombosis.

Adult↗
PubMed1989

Relevance of prostaglandins in true menstrual migraine.

Eighteen patients suffering from true menstrual migraine and 12 control subjects were studied. We evaluated in different phases of the menstrual cycle and during the migraine crisis the peripheral plasma concentrations of 6-keto-PGF1 alpha (the stable metabolite of PGI2), thromboxane B2 (the stable metabolite of thromboxane A2), PGF2 alpha and PGE2. The mean values of 6-keto-PGF1 alpha in menstrual migraine sufferers are lower than in normal women throughout the whole cycle. The difference between the trends observed in the two groups is statistically significant (p less than 0.05). The plasma levels of TXB2 and of PGF2 alpha are similar in the two groups investigated, both in basal conditions and during the attack. The plasma concentrations of PGE2 are slightly lower in migraineurs in basal conditions than in normals. However, during the crisis they increase significantly (p less than 0.05). In conclusion, among all the parameters considered, PGE2 seems to play the most important role during the pain phase of the attack. The results of the present study suggest that a deficit of PGI2, one of the most important protecting agents against ischemia, might be a typical feature of menstrual migraine and might cause in these patients a vascular hypersensitivity to different ischemic stimuli.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Menstrual migraine: a possible pathogenic implication of platelet function.

It has been suggested that migraine is a blood disorder caused by a primary abnormality of platelet behaviour. We have studied in different phases of the cycle of 11 healthy normal women and 13 patients suffering from menstrual migraine: 1. The platelet aggregation induced in vitro by ADP, collagen and ristocetin; 2. The platelet sensitivity to prostacyclin (PSP); 3. The platelet content of 5-hydroxytryptimine (5-HT); 4. The possible correlation between these parameters and the plasma concentration of progesterone. The results demonstrate that in patients with menstrual migraine the platelet response to various aggregating agents is not modified compared to the controls, whereas there is a different response of the PSP to the modulating effect of plasma progesterone. Moreover, in the same patients the platelets have an increased capability of accumulating 5-HT during the perimenstrual phase of the cycle. This suggests that platelet dysfunction may play a role in the pathogenesis of menstrual migraine.

Adenosine Diphosphate↗