Effects of tomatoes on the lipid profile.

PURPOSE: The Mediterranean diet has been reported to reduce cardiovascular mortality and morbidity considerably. Tomatoes and lycopene are considered potent antioxidants. Our purpose was to study the effects of a tomatoe-rich diet on the lipid profile following 300g daily of tomatoes for one month. METHODS: Plasma concentrations of triglyceride, total cholesterol, HDL-cholesterol, LDL-cholesterol and VLDL-cholesterol were determined in 98 apparently healthy volunteers (mean age 45.5+/-14.1 yr) before and after one month of follow-up. Fifty volunteers (34 women and 16 men) ate tomatoes 300g daily and 48 volunteers (32 women and 16 men) continued their regular diet without eating tomatoes for a month. RESULTS: In the regular diet group, there were no changes in the lipid profile: triglyceride level (169.6+/-156.8 vs. 147.6+/-93.4mg/dl; P=0.33), total cholesterol level (198.3+/-41.2mg/dl vs. 204.2+/-70.9mg/dl; P=0.23), HDL-cholesterol level (50.6+/-12.2mg/dl vs. 47.6+/-10.8mg/dl; P=0.79), and LDL-cholesterol level (122.7+/-39.4mg/dl vs. 120.2+/-32.2mg/dl; P=0.24) before and after the 1 month offollow-up. In the tomato-rich diet group: triglyceride level 170.8+/-85.4mg/dl to 167.4+/-99.4mg/ dl (P=0.98), total cholesterol level 207.5+/-44.3mg/ dl to 204.1+/-45.1mg/dl (P=0.68), HDL-cholesterol level 46.1+/-10.6mg/dl to 53.4+/-13.3mg/dl (P=0.03), and LDL-cholesterol level 127.7+/-41.8mg/dl to 119.1+/-41.7mg/dl (P=0.57). CONCLUSION: We found that tomatoes'-rich diet (300g daily for one month) increased HDL-cholesterol level significantly by 15.2%.

The stroke trial - can we predict clinical outcome of patients with ischemic stroke by measuring soluble cell adhesion molecules (CAM)?

BACKGROUND: Several studies have found that an increased concentration of haemostatic or inflammation markers was associated with worse prognosis in vascular disease. The inflammatory components in ischemic stroke are of current interest, and there is some experimental evidence that they may be linked. HYPOTHESIS: The study was performed to determine the association between the neurological clinical outcome and levels of cell adhesion molecules in the first four days of hospitalization in patients with acute ischemic event. METHODS: This prospective, pilot, case-controlled study examined the association between the clinical outcome and inflammatory markers within the first few days of hospitalization. The neurological evaluation was performed using the NIH score on admission and four days later, and levels of cell adhesion molecules were measured by ELISA methods on admission and four days later. RESULTS: Twenty three patients with an acute cerebral event (mean age 71 +/- 15 y, 12 women and 11 men) were examined neurologically on admission and four days later. Among 19 patients who improved, there was a significant decrease in the NIH neurological scale, from 3.8 +/- 3.2 to 1.3 +/- 1.8 (p = 0.01), which was accompanied by a significant decrease in the cell adhesion molecules that were measured (E-selectin, ICAM-1 and VCAM-1). Of the four patients who did not improve, their mean clinical NIH score was 10 +/- 4.6 and worsened or remained unchanged after four days of follow-up. In this group, we could not demonstrate a significant change in levels of cell adhesion molecules between days one and four. CONCLUSIONS: Patients who improved clinically within the first four days of hospitalization demonstrated a remarkable inhibition of all three cell adhesion molecules that were measured (E-selectin, ICAM-1, and VCAM-1). Patients who did not improve had more severe cerebral infarcts, a higher NIH score on admission (10 +/- 4.6), and no change was observed in levels of cell adhesion molecules during the follow-up period. Measuring cell adhesion molecule levels may predict objectively the clinical outcome in hospitalized patients with acute ischemic stroke.

Varicella zoster infection and pulmonary complications.

A 34-year-old immunocompetent man with varicella zoster (VZ) infection developed deep vein thrombosis and pulmonary embolism after suffering severe pneumonitis. He recovered after treatment with acyclovir, high-dose steroids, and ventilatory support. The endothelial damage could be a direct link between VZ pneumonitis and pulmonary emboli.

Coumadin-induced hepatitis.

The diagnosis of "coumadin-induced hepatitis" is compatible with the time relationship between the start of the drug and the onset of hepatopathy, the rapid improvement following discontinuation of the drug, recurrence of liver dysfunction after re-exposure to the drug and liver histology. Although liver damage induced by coumadin derivatives is rare, it is important to be aware of the hepatotoxic potential of these drugs, which, in most cases, mimic the clinical presentation of viral hepatitis.