[Heparin and lipoprotein(a). Observations during hemodialysis]. / Eparina e lipoproteina(a). Osservazioni in corso di emodialisi.

The effect of heparin (bolus e.v. 5.000 I.U.) on blood levels of Lp(a) and other lipids (triglycerides, -HDL, -LDL and total cholesterol, apo A1, apo B100 and apo A1/apo B100) was studied in 15 patients (8 M and 7 F) with chronic renal failure during hemodialysis. Statistically significant reductions of the basal values were found for Lp(a) and the other lipids in the blood taken before the beginning of dialysis, 30 min' after the heparin bolus. The analysis of third blood sample (at the end of the hemodialysis, one hour after the end of the heparin maintenance infusion) showed a rise of HDL and LDL-lipoproteins over the basal values clearly in relation to reduced heparin and plasmatic fraction of the blood. The values of Lp(a) had not so high increase as consequence of more elevated affinity with heparin and of a possible enhanced metabolic rate via lipoprotein lipase. The authors, in agreement with similar changes of Lp(a) and other lipids previously observed in patients with coronary diseases during bypass surgery in extracorporeal circulation or angioplasty, (interventions requiring generous heparin treatment), believe to have now sufficient data for attributing heparin a causal role for the above mentioned effects. The authors stress the needing of other studies better understand the action to mechanisms of heparin and to evaluate possible future clinical applications of this new interesting Lp(a)-clearing effect.

Salt-losing diarrhoea in idiopathic proctocolitis.

The faecal output of chloride, sodium and potassium was studied in 14 patients with active idiopathic proctocolitis, in an attempt to establish a relationship between faecal electrolyte output and acid-base balance data. 7 patients with ileostomy and 8 healthy volunteers were used as controls. The daily faecal excretion of chloride and sodium in proctocolitis was significantly in excess of normal, whereas that of potassium was within the normal range. From the comparison with the results in patients with ileostomy it is concluded that colitic colon has an impaired capacity to absorb chloride and sodium but retains the ability to secrete potassium. The intestinal loss of chloride in addition to that of sodium and water may be regarded as a salt-losing diarrhoea and may account for the metabolic alkalosis commonly found in proctocolitis.