No abstract

In a previous study (1) we observed that patients suffering frm primary hyperlipoproteinemia (PHLP) presented a decreased ree blood cell deformability when compared with a normolipemic healt~ control group. This increased rigidity could not be attributed te the increased cholesterol in the red blood cell membrane whicl these patients showed, because there was no statistically signifi· cant correlation between the two parameters. Moreover, the increased rigidity could not be attributed to either hematimetric 0] morphological changes in the erythrocytes. Among PHLP, primar~ hypertriglyceridemias (PHTG) frequently show alterations in thE hydrocarbon metabolism. Another of the causes of decreased red cell deformability is thE increase in glycosylated hemoglobin (HbA1C) (2). In order to fine out whether the increased erythrocyte rigidity observed in PHTG if related to the HbA,c level, we have studied the rigidity inde: (RI), using the Hanss Hemorheometre (3) and the HbA,c level in 2: patients belonging to six families affected by PHTG. Table I shows the values of serum lipids, glucose, HbAlc, leucocyte count, remanent leucocyte count in the 8% RBC suspensiol and RI. Table 1 Rigidity index (RI), plasmatic lipids (TG, CHOL), glucose, HbA,c leucocytes (Leuc) and remanent leucocytes (Rem Leuc) in the 8% RBI suspension in primary hypertriglyceridemia (PHTG) and in the con· trol group (CG). PHTG CG TG mgldl 548 + 775* 96 ± 32 CHOL mgldl 204 ± 42 ns 215 ± 35 Glucose mgldl 99 ± 12 ns 90 + 18 HbA,c % 4.95 ± 0.36 ns 4.80 ± 0.36 RI 9.16 ± 1. 0* 8.23 + 0.8 Leuc x 10 9 II 7.0 ± 2.0 ns 6.5 ± 2.3 Rem Leuc x 10 9 II 0.20 ± 0.05 ns 0.18 ± 0.2 ns: not significant; * p

Gout is a form of inflammatory arthritis characterized by sharp pain and severe swelling that often causes severe physical disability. Gout is caused by the chronic elevation of uric acid levels in the blood and is known as the disease of kings due to its strong association with a diet rich in fructose and beer. Recent studies suggest that a high uric acid concentration is the result of a dynamical process that highlights the interactions between leptin production, insulin resistance, low muscle mass and a diet rich in fructose. Once individuals develop hyperuricemia, reach a high uric acid concentration in excess of 7 mg/dL for men and 6 mg/dL for women, they become susceptible to developing gout. We propose a novel dynamic system to analyze and determine the connections between a diet involving different levels of fructose (in both adult men and women in the U.S.) and the concentration of uric acid in the blood. Our model simulations suggest that adult males under a diet containing levels of fructose stimulating a 0.5 uric acid growth rate, could develop hyperuricemia after around 10,000 days, while it only takes women about 5000 days with a diet stimulating a 0.4 growth rate.