Cellular hypersensitivity to gluten derived peptides in coeliac disease.

Wheat gluten derived antigens have been tested for their ability to inhibit the migration of leucocytes from healthy subjects and patients with coeliac disease. Three preparations of a water soluble fraction (Frazer's fraction III, FIII) of partial peptic tryptic digests of wheat gluten had different effects in a direct (one stage) assay. Subfractions B and B2 caused migration inhibition of leucocytes from patients with treated coeliac disease but not of leucocytes from healthy volunteers or patients with Crohn's disease or ulcerative colitis. This migration inhibition seems to be specific for gluten fractions because maize zein fraction B, beta-lactoglobulin and ovalbumin did not cause it. The sensitivity of coeliac leucocytes to fraction B is not related to factors present in coeliac serum as the migration of leucocytes from healthy individuals preincubated with coeliac sera was not inhibited. Puromycin diminished inhibition by fraction B, which was active at 1.2 micrograms/ml in an indirect (two stage) migration inhibition assay; this is consistent with a process involving elaboration of lymphokine(s). More highly purified fractions of B2, P1-P4 were prepared by reverse phase high performance liquid chromatography (HPLC) and showed differing potency in direct and indirect assays, with P4 being the most active fraction. Inhibition of migration by gluten derived peptides appears to result from the release of lymphokine by leucocytes specifically from coeliac patients

Carnitine as a possible adjunct in parenteral feeding.

Carnitine is necessary for the transport of fatty acids across the inner mitochondrial membrane, and depletion in response to Intralipid infusion has previously been demonstrated. This study investigates whether orally administered L-carnitine increases tolerance to a lipid load given intravenously. Eight patients with active inflammatory bowel disease, being treated with intravenous prednisolone, were studied. Intralipid was infused on two occasions. Triglycerides and ketone bodies rose in a reproducible manner. Carnitine did not influence these changes. Carnitine excretion rose after an oral dose indicating that carnitine was absorbed, but carnitine excretion was increased in the steroid-treated individuals and rose after oral prednisolone in two healthy subjects. It is concluded that under the conditions of this study oral carnitine is without demonstrable effect on the handling of an intravenous lipid load