Background and Purpose-The mechanisms of ischemic stroke in young adults are poorly understood. During the last years, several studies suggested a role for genetic factors predisposing to thrombophilia and for moderate hyperhomocysteinemia in this setting. Methods-We evaluated in 132 consecutive patients (66 males, 66 females; meanϮSD age, 38.4Ϯ11.7 years; meanϮSD age at first event, 34.8Ϯ10.9 years; range, 6 months to 50 years) referred to our center between January 1997 and December 1999 for a history of young adult ischemic stroke (age at first event, Ͻ51 years) the prevalence of factor V (FV) Leiden, prothrombin (FII) G20210A, and C677T and 5,10-methylenetetrahydrofolate reductase (MTHFR) gene mutations and fasting serum total homocysteine levels.

Background-Severe hyperhomocysteinemia due to cystathionine ␤-synthase deficiency (C␤SD) is associated with early atherothrombotic vascular disease. Homocysteine may exert its effects by promoting oxidative damage. In the present study, we investigated whether in vivo formation of 8-iso-prostaglandin (PG) F 2␣ , a platelet-active product of arachidonic acid peroxidation, is enhanced in C␤SD and whether it correlates with in vivo platelet activation, as reflected by thromboxane (TX) metabolite excretion. Methods and Results-Urine and blood samples were obtained from patients with homozygous C␤SD (nϭ13) and age-matched healthy subjects. Urinary 8-iso-PGF 2␣ excretion was significantly higher in C␤SD patients than in control subjects (640Ϯ384 versus 213Ϯ43 pg/mg creatinine; Pϭ0.0015) and correlated with plasma homocysteine (ϭ0.398, Pϭ0.0076). Similarly, urinary 11-dehydro-TXB 2 excretion was enhanced in C␤SD (1166Ϯ415 versus 324Ϯ72 pg/mg creatinine; Pϭ0.0015) and correlated with urinary 8-iso-PGF 2␣ (ϭ0.362, Pϭ0.0153). Vitamin E supplementation (600 mg/d for 2 weeks) was associated with a statistically significant increase in its plasma levels (from 16.6Ϯ4.6 to 40.4Ϯ8.7 mol/L, Pϭ0.0002) and with reductions in 8-iso-PGF 2␣ (from 790Ϯ159 to 559Ϯ111 pg/mg creatinine, Pϭ0.018) and 11-dehydro-TXB 2 (from 1273Ϯ383 to 913Ϯ336 pg/mg creatinine, Pϭ0.028). A statistically significant inverse correlation was found between urinary 8-iso-PGF 2␣ and plasma vitamin E levels (ϭϪ0.745, Pϭ0.0135). Conclusions-The results of the present study suggest that enhanced peroxidation of arachidonic acid to form bioactive F 2 -isoprostanes may represent an important mechanism linking hyperhomocysteinemia and platelet activation in C␤SD patients. Moreover, they provide a rationale for dose-finding studies of vitamin E supplementation in this setting.

Background: we have observed the effect of insomnia treatment in clinical and prognostic differences of patients admitted for COVID-19 pneumonia in respiratory sub-intensive units that were administered a prolonged-release melatonin 2 mg (PRM 2 mg) therapy versus a group of patients out of therapy. Materials and Methods: We evaluated 40 patients on prolonged-release melatonin 2 mg (PRM 2 mg) therapy versus a control group of 40 patients out of therapy. Results: patients in the PRM 2 mg group had a shorter duration of therapy with non-invasive ventilation (5.2 ± 3.0 vs. 12.5 ± 4.2; p < 0.001), with a shorter stay in sub-intensive care (12.3 ± 3.2 vs. 20.1 ± 6.1; p < 0.001), and, therefore, a shorter overall duration of hospitalization (31.3 ± 6.8 vs. 34.3 ± 6.9 p = 0.03). In addition, a lower incidence of delirium was found (2.2 ± 1.1 vs. 3.3 ± 1.3; p < 0.001). Conclusions: A significant increase in sleep hours and a reduction in delirium episodes occurs in hospitalized insomniac patients treated with PRM 2 mg, compared to untreated patients. Based on these preliminary results, we can assume that there are benefits of prolonged-release melatonin 2 mg in COVID-19 therapy.

No abstract