[Pathogenesis of gouty arthritis]. / Pathogenese der Gicht-Arthritis.

The urate crystal stands in the centre of the pathogenesis of gouty arthritis. External influences, such as changes of temperature and mechanical loads as well as factors, which lead to a short term change of the level of uric acid in the serum, such as alcohol, meals rich in purine, uricosurics and saluretics are, indeed, able to induce an attack of gout, but they are no obligatory prerequisite. The granulocytes are to be regarded as the second important prerequisite of the crystal arthritis. They become effective either via the process of phagocytosis or their cell membrane produces prostaglandins, the formation of which is evoked by electrostatic forces of the crystals. Mediators, such as kinins, Hageman's factor and complement are mainly responsible for the initial pain reaction, vasodilation and leukotaxis, lysosomal enzymes evoke the secondary changes at the joint.

[The effect of glucose substitutes on human uric acid metabolism (author's transl)]. / Wirkung von Glukoseaustauschstoffen auf den Harnsäurestoffwechsel des Menschen

Fructose, sorbitol and xylitol produce a rise in serum uric acid during intravenous injection. This is most pronounced with xylitol. The amount of increase in uric acid depends on the amount given. Irreversible decomposition of preformed adenine nucleotide in the liver is considered most important as a cause. Patients in whom there is already an impairment of the energy output on the part of the liver should not be given fructose or sorbitol and certainly not xylitol intravenously.

Utilization of intravenous maltose.

Ten healthy male subjects received an infusion of 10% maltose solution at a rate of 0.5 g/kg body weight/h for 345 min. Blood maltose levels rose continuously for the first hours; after 285 min a constant level was maintained. Concomitantly increasing maltosuria occurred; the total renal maltose excretion averaged 30.4% of the administered dose. In addition to maltose losses, considerable glucosuria (up to 16% of total carbohydrate excretion) was found. The glucosuria occurred in spite of normal blood glucose levels. Serum insulin did rise during maltose infusion.