[Relationship between EPA or EPA/AA and arteriosclerosis in elderly patients over 80 years old].

AIM: Fish oil is associated with decreased arteriosclerosis, cardiovascular disease and the prevention of cellular aging. Most studies of n-3 PUFA (polyunsaturated fatty acid) have been conducted in patients under 80 years of age, and there are few studies of subjects ≥80 years of age. This study investigated the relationship between eicosapentaenoic acid (EPA) or arachidonic acid (AA) and arteriosclerosis in elderly patients ≥80 years of age. METHOD: We enrolled 150 patients ≥80 years of age (average, 85±4 years) not taking EPA that presented or were admitted to our hospital. Their EPA or AA levels were measured to investigate the relationship between EPA or EPA/AA and cardiovascular disease or cerebrovascular disease. In addition, we investigated whether the ratio of EPA/AA was associated with estimated glomerular filtration rate (eGFR). RESULTS: The mean EPA level was 55.9±34.5 µg/dL, the mean AA level was 145.1±45.4 µg/dL and the mean EPA/AA was 0.40±0.24 (mean±SD). There were no significant differences between the EPA/AA and EPA values in patients with cardiovascular disease and those in patients without cardiovascular disease. Moreover, there were no significant differences between the EPA/AA and EPA values in patients with cerebrovascular disease and those in patients without cerebrovascular disease. There were no statistically significant correlations between EPA/AA or EPA and eGFR. CONCLUSION: Individuals may achieve a peak value of EPA or EPA/AA in their 70s and there is little change in those levels in patients aged over 80. No relationship was identified between EPA/AA and arteriosclerosis in subjects aged over 80 compared with those under 80 years of age.

Hypertensive encephalopathy in patients with chronic renal failure caused by stopping antihypertensive agents: a report of two cases.

We herein report two cases of patients with chronic kidney disease who developed hypertensive encephalopathy, which occurred after a sudden discontinuance of antihypertensive agents. Both patients underwent care at our hospital after experiencing neurological abnormalities. In both patients, magnetic resonance imaging (MRI) revealed edema in the cerebral white matter and cortices, basal ganglia, brainstem, and cerebellum. Though recently the number of reports about hypertensive encephalopathy has decreased, we describe two case reports and also review the pertinent literature.

Comparison of the effect of lipophilic and hydrophilic statins on serum adiponectin levels in patients with mild hypertension and dyslipidemia: Kinki Adiponectin Interventional (KAI) Study.

The plasma level of adiponectin, which is known as an anti-atherogenic adipocytokine, correlates inversely with the progression of atherosclerosis. An increase in the serum adiponectin level has been reported after the administration of hydrophilic pravastatin, but not after the administration of lipophilic statins thus far. We investigated whether hydrophilic pravastatin acts distinctly from simvastatin, which has the highest lipophilicity, on the favorable effect on adiponectin in dyslipidemic patients. A total of 27 dyslipidemic patients with mild hypertension were enrolled in this study. The patients were initially treated with simvastatin 10 mg/day for six months or more (mean 7.1 months), and then were switched to pravastatin 20 mg/day. The serum adiponectin, cholesterol fractionated components, and C-reactive protein (CRP) were evaluated after six-month intervals. Switching from simvastatin to pravastatin caused little change in the low-density lipoprotein cholesterol levels (103 mg/dl to 104 mg/dl, p = 0.782) and blood pressure (133/70 mmHg to 132/69 mmHg), while the serum adiponectin level significantly increased (11.9 mug/ml to 13.1 mug/ml, p = 0.009, respectively), and the serum CRP significantly decreased (0.078 mg/dl to 0.062 mg/dl, p = 0.040, respectively). Hydrophilic pravastatin increased the serum adiponectin level and decreased the CRP after switching from lipophilic simvastatin in the absence of any difference in the low-density lipoprotein cholesterol level and blood pressure. It remains possible, however, that this difference was due not only to pharmacologic lipophilicity, but also to some other specific characteristics such as the formula of statins, the subject characteristics, race, body size, high-density lipoprotein cholesterol, etc.