The treatment of uraemic osteopathy.
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Biomedical subjects
Publications and source records attributed to K Schaefer.
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The pathogenesis of ocular allergy involves multiple mechanisms, which lead to mast cell degranulation and the release of chemical mediators. Mast cell mediators that have been implicated in allergic ocular disease include histamine, eosinophil chemotactic factors, eosinophil granule major basic protein, platelet-activating factor, prostaglandin D2, and several other less well-defined preformed or newly synthesized mediators. The release of these chemical mediators ultimately results in conjunctival vasodilation, increased vascular permeability, leukocyte chemotaxis, and, rarely, ocular surface destruction. Current therapy of ocular allergy involves elimination of the offending allergen, modulation of the immune system, and pharmacologic inhibition of the chemical mediators. The purpose of this article is to provide a better understanding of the pathogenesis and current therapy of ocular allergic disorders and to review the central role of the mast cell and chemical mediators involved in ocular allergy.
Because of their effect on the immune response, especially in patients with chronic or acute renal failure, factor D (FD) and the immunosuppressive complement fragment Ba are substances which may be important for the immunological status. Since they cannot be eliminated by conventional Cuprophan hemodialysis because of their high molecular weight (24,000 and 33,000 D, respectively), the effect of hemofiltration (HF) on the plasma concentration of both components was tested. It was shown that plasma levels of FD can be lowered by 43.5% during an HF treatment and the plasma concentration of Ba by 30.6%. Moreover, the two substances could be detected in the hemofiltrate. Up to 75 mg FD and up to 37 mg Ba could be eliminated per treatment, depending on the plasma concentrations and the filtration volume. A convective method such as chronic HF is therefore clearly superior to diffusive methods of blood purification when substances with such a high molecular weight have to be eliminated. It has still to be established whether the elimination of FD and Ba by chronic intermittent HF results in a sustained improvement in the immunological status of patients treated in this way.
Hemodialysis (HD) hypotension is frequently encountered during conventional acetate HD. Recently it has been suggested that monocytes that adhere to the dialysis membrane are also stimulated by endotoxins diffusing from the dialysate side. Stimulated monocytes, however, release interleukin-1, which mediates fever and hypotension through its action on the cyclo-oxygenase cascade. To prevent this endotoxin-induced stimulation of monocytes, a hemofilter with a polyamide membrane (FH 88, Gambro, Lund, Sweden, cut-off 20,000 daltons, surface area 2.0 m2) was interposed between the dialysate outlet of the HD machine and the dialyzer. The data obtained clearly show that the filtered dialysate was always pyrogen-free when tested with a limulus-amebocyte-lysate assay. In addition, in 80% of cases no bacteria were detected after the sterilizing filter. Almost no febrile episodes were observed when sterile dialysate was used.