Documentation on Palaprin (aloxiprin). Aloxiprin is an aluminium-aspirin complex that dissociates i

Fråga: Documentation on Palaprin (aloxiprin). Aloxiprin is an aluminium-aspirin complex that dissociates in the gastrointestinal tract. Is it better than pure ASA, for chronic treatment (e.g. rheumatic arthritis)? Can there be an interaction, aspirin inhibiting and aluminium stimulating prostaglandin synthesis?

Sammanfattning: The clinical relevance of mucosal protective drugs against aspirin and other NSAID-induced damage in humans needs to be further studied. A pharmacodynamic interaction between aluminium and aspirin on prostaglandin synthesis is improbable. Aloxiprin is an obsolete aspirin preparation that lacks modern clinical documentation.

Svar: Aspirin can damage the gastric mucosa by several mechanisms including: alterations in the back diffusion of hydrogen ions, interference with prostaglandin synthesis, reductions in mucus and bicarbonate secretion, decreases in gastric cellular energy (ATP) and cell turnover rates and platelet dysfunction. Antacids act by decreasing the concentration of intragastric hydrogenion. There is no evidence that regular antacid ingestion can prevent the salicylate induced gastrointestinal damage. "Partial protection against aspirin-induced or other NSAID-induced gastric mucosal damage has been demonstrated by sucralfate, certain prostaglandins, omeprazole and histamine (H2) receptor antagonists" (1). Aloxiprin appeared to be associated with less GI hemorrhage than plain aspirin according to a 1962 reference (2,3).

In rheumatic patients with ulcer or upper gastrointestinal complications while on long term aspirin therapy the use of an enteric coated aspirin formulation or regular aspirin together with one or more cytoprotective agents including H2-receptor antagonists, sucralfate and antacids is recommended (1,4,5).

There is no evidence that aluminium or oxyaluminium hydroxide affect endogenous prostaglandin metabolism. Sucralfate, a complex salt formed from the sulfated disacharide (sucrose) and polyaluminium hydroxide have been shown to stimulate locally PGE2 and 6-keto PGF1-alfa formation (6-9). A direct effect on the activity of mucosal cyclo oxygenase has been proposed (7) but the mechanism remains undetermined. 1 Ivey KJ: Mechanisms of nonsteroidal anti-inflammatory drug-induced gastric damage. Actions of therapeutic agents. Am J Med 1988; 84(suppl 2A): 41-48 2 Martindale, The extra pharmacopoeia. 1982; 28th ed: 3 Wood PHN, Harvey-Smith EA, Dixon AJ: Salicylates and gastrointestinal bleeding. Acetylsalicylic acid and aspirin derivatives. Br Med J 1962; I: 669-675 4 Robinson DR: Management of gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs during the therapy of rheumatic diseases. Am J Med 1988; 84(suppl 2A): 1-4 5 Ivarsson LE: Antacids and H2-receptor antagonists in the prophylaxis and treatment of erosive gastritis: clinical aspects. Scand J Gastroenterol 1984; 19(suppl 105): 86-89 6 Konturek SJ, Kwiecien N, Obtulowicz W, Kopp B, Oleksy J: Double blind controlled study on the effect of sucralfate on gastric prostaglandin formation and microbleeding in normal and aspirin treated man. Gut 1986; 27: 1450-1456 7 Crampton JR, Gibbons LC, Rees W: Effects of sucralfate on gastroduodenal bicarbonate secretion and prostaglandin E2 metabolism. Am J Med 1987; 83(suppl 3B): 14-18 8 Coleman JC, Lacz JP, Browne RK, Drees DT: Effects of sucralfate or mild irritants on experimental gastritis and prostaglandin production. Am J Med 1987; 83(suppl 3B): 24-30 9 Stern AI, Ward F, Hartley G: Protective effect of sucralfate against aspirin-induced damage to the human gastric mucosa. Am J Med 1987; 83(suppl 3B): 83-85