Thai Journal of Gastroenterology

fever. Vomiting may be provoked by antimalarial drug treatment. While diarrhea has been reported from some parts

of the world, it appears to be uncommon in others. Although malabsorption of amino acids, sugars, fats, chloroquine

and quinine have been documented, in most studies the absorption of oral antimalarials in uncomplicated malaria has

been normal in even the most seriously ill patients. In the acute phase of severe falciparum malaria, patients show the

greatly reduced absorption of those sugars that rely on mediated mechanisms and unmediated diffusion. Absorption

returns to normal in convalescence. Gastric emptying is normal in uncomplicated falciparum malaria. Biopsies of

the gut show parasite sequestration in the vascular bed which presumably interferes with the process of absorption.

Gastrointestinal permeability is increased during severe and uncomplicated falciparum malaria but reverts to normal

in convalescence. Endotoxemia may also originate in the gut. Gram-negative bacteria or endotoxin may shift from

the gut lumen; the normal hepatic clearance mechanisms may fail.

Hyperbilirubinemia is attributable to intravascular hemolysis of parasitized erythrocytes and to hepatic dysfunction

and possibly to an element of microangiopathic hemolysis associated with disseminated intravascular coagulation.

Impairment of hepatic function is common in severe malaria. Unfortunately, assessment of ùliver functionû

by measurement of blood concentrations of bilirubin and liver-related enzymes is notoriously imprecise, particularly

in the presence of coexisting hemolysis, Jaundice is more common in adults with severe malaria than in children. The

measurable consequences of hepatic dysfunction are coagulation abnormalities resulting from failure of clotting factor

syntheses, hypoalbuminemia, and reduced metabolic clearance of many substances, including alanine, lactate, and

antimalarial drugs. The biotransformation of drugs, particularly those metabolized by hepatic microsomal enzymes,

is reduced in proportion to disease severity. Hepatic blood flow is reduced during acute malaria and is significantly

lower in severe malaria than in uncomplicated malaria; it returns to normal during convalescence. Hepatic microsomal

metabolism is also apparently slow in severe falciparum malaria but reverts to normal in convalescence. Liver

metabolic function does not appear to be significantly affected in uncomplicated malaria.