[Lipoprotein Lp(a) in patients with chronic renal insufficiency on hemodialysis]. / Lipoproteína Lp(a) en pacientes afectos de insuficiencia renal crónica en hemodiálisis.

An increased concentration of lipoprotein Lp(a) is considered a risk factor for coronary artery disease. In the present study, the plasma levels of Lp(a), total cholesterol, cholesterol bound to high density lipoproteins (C-HDL), and triglycerides (TG) were measured in 50 patients with chronic renal failure treated with hemodialysis (HD). The results were compared with those from a control group constituted by 46 individuals. Hypertriglyceridemia was detected in 34% of the HD patients and in none of the controls (p less than 0.001); also, a significant reduction of C-HDL level was found in the HD group as compared with controls (p less than 0.001). These two results are in agreement with previously reported data. The outstanding result of our study was the higher prevalence of positive Lp(a) (greater than 30 mg/dl) in the HD group as compared with controls (p less than 0.05). As the increase in Lp(a) is a risk factor for coronary artery disease, we suggest that its measurement may be helpful to delineate the serum lipid profile of these patients.

[Tangier disease: study of the first case in Spain]. / Enfermedad de Tangier: estudio del primer caso español.

The clinical, biochemical and pathological studies of the first case of Tangier's disease that, to our knowledge, has been detected in Spain are reported. The patient had all the characteristic features of the disease: hypercholesterolemia with very pronounced reduction of plasmatic high density lipoproteins, splenomegaly, orange yellow tonsils and peripheral neuropathy. In addition, he had pneumonia and pancytopenia. Neurological examination and computed tomography suggested cerebral involvement, not previously reported in this condition. Biopsies demonstrated lipid accumulation in the reticuloendothelial cells of diverse localizations and in Schwann's cells.

Progressing cerebral infarction in relation to plasma glucose in gerbils.

We studied neurologic morbidity and its evolution during hyperglycemia induced immediately after permanent unilateral common carotid artery ligation in Mongolian gerbils. A total of 60 animals were divided into five groups: one experiencing severe hyperglycemia for 1 hour after the onset of ischemia (brief hyperglycemia group, n = 13), a normoglycemic control group for the brief hyperglycemia group (n = 12), a group with severe hyperglycemia for 4 hours after the onset of ischemia (prolonged hyperglycemia group, n = 11), a normoglycemic control group for the prolonged hyperglycemia group (n = 13), and a hyperosmolar normoglycemic control group for the prolonged hyperglycemia group (n = 11). Neurologic morbidity and mortality were higher in the two hyperglycemic groups than in the three normoglycemic control groups. The neurologic deficit progressed according to the duration of severe hyperglycemia. In the three normoglycemic control groups neurologic status stabilized 120 minutes after the onset of ischemia, in the brief hyperglycemia group stabilization occurred at 210 minutes, and in the prolonged hyperglycemia group neurologic deficit progressed for approximately 360 minutes, coinciding with the death of all but one gerbil, in which the neurologic deficit remained stable until death 23 hours after ischemia. We suggest that hyperglycemia is another cause of progressing cerebral infarction.