Human recombinant lactoferrin is ineffective in the treatment of human Helicobacter pylori infection.

BACKGROUND: Lactoferrin, a multifunctional glycoprotein, is known to have anti-microbial actions. Bovine lactoferrin and recombinant human lactoferrin have been shown to inhibit Helicobacter pylori, and more recently recombinant human lactoferrin was found to significantly increase the eradication rate of H. pylori when added to standard triple therapy. AIM: To determine the efficacy, safety and tolerability of recombinant human lactoferrin as a therapy in suppressing or eliminating H. pylori infection in subjects with minimal upper gastrointestinal symptoms who have not previously been treated. SUBJECTS AND METHODS: Nine healthy subjects with minimal upper gastrointestinal symptoms and a positive urea breath test were recruited. None of the volunteers had previously been treated for H. pylori. Subjects received 5 x 1.0 g human recombinant lactoferrin daily for 5 or 14 days. Breath tests were repeated during therapy and shortly after to check for eradication. The safety and tolerability of the drug were assessed by physical examination, by monitoring adverse events, and clinical laboratory evaluation. RESULTS: No conversion of the urea breath test from positive to negative was observed and there was no consistent change in urea breath test count to indicate a possible suppression of H. pylori. CONCLUSION: Lactoferrin, given as a single agent, does not eradicate H. pylori infection.

Investigations into the haemorheological significance of postprandial and fasting hypertriglyceridaemia.

Two study designs were conceived to evaluate the rheological significance of hypertriglyceridaemia. We first investigated the course of serum- (SV) and plasma viscosity (PV) and erythrocyte aggregation in serum (SEA) and plasma (PEA) of healthy normolipidaemic individuals over 4 h after a fatty rich meal, in native material and after removal of triglyceride rich lipoproteins by centrifugation. Secondly, blood from patients with untreated hypertriglyceridaemia was investigated under fasting conditions. PEA and SEA increased in parallel with postprandial triglycerides (+135 mg dl-1), but the effect on PEA was more pronounced (+0.8 abs% increase; 2 h after the meal) as compared to SEA (+0.4 abs% increase). PV and SV increased in parallel to the same extent (+0.05 mPas). In the triglyceride poor infranatant no significant changes occurred. In fasting plasma PEA and PV were significantly lower (1.1 abs% and PV 0.04 mPas respectively) in infranatant than in native plasma, while only small differences in triglyceride (mostly VLDL) were observed. This phenomenon was barely detectable in serum samples. We conclude that triglyceride rich lipoproteins have a profound influence on haemorheological parameters, and that fibrinogen in particular, potentiates the effect of large fasting VLDL on plasma viscosity and erythrocyte aggregation.