No abstract

In Africa, the use of traditional herbal remedy is widespread. Acute renal failure (ARF) is one of the most serious complications. The use of herbal remedies (mostly orally) accounts for nearly 35% of all cases of acute renal failure in Africa. Development of renal failure following herbal vaginal pessary is rarely reported. In November 2003, a 35-year-old Nigerian female who is a petty trader and a primary school leaver with three children (all males) presented to us in the renal unit with oliguric ARF induced by herbal vaginal pessary. She had sought this alternative medicine in an attempt to have a female child as all her three children are males. Her condition was managed accordingly and required three sessions of hemodialysis. She started diuresing on the eighth day of admission. This case presentation highlights the potential tragedies of herbal preparation, of note, that herbal vaginal pessaries are as deleterious as the oral preparations, and that the dilemma of ignorance is still prevalent in our society.

The results of this preliminary investigation suggest that MI contains active compounds with an anti-inflammatory activity. However, more detailed studies using additional models are necessary to further characterise the effects of MI in inflammatory disorders.

Background: Low-dose aspirin can cause gastric and duodenal ulceration, hereafter called peptic ulcer disease (PUD). Predisposition is thought to be related to clinical and genetic factors; our aim was to identify genetic risk factors associated with aspirin-induced PUD. Methods: Patients (n=1478) were recruited from 15 UK hospitals. Cases (n=505) were defined as patients with endoscopically confirmed PUD within 2 weeks of using aspirin and non-aspirin Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). They were compared to two control groups: patients with endoscopically confirmed PUD without any history of NSAID use within 3 months of diagnosis (n=495), and patients with no PUD on endoscopy (n=478). A genome-wide association study (GWAS) of aspirin-induced cases (n=247) was compared to 476 controls. The results were validated by replication in another 84 cases and 162 controls. Findings: The GWAS identified one variant, rs12678747 (p=1¢65£10 À7 ) located in the last intron of EYA1 on chromosome 8. The association was replicated in another sample of 84 PUD patients receiving aspirin (p=0¢002). Meta-analysis of discovery and replication cohort data for rs12678747, yielded a genome-wide significant association (p=3¢12£10 À11 ; OR=2¢03; 95% CI 1¢65-2¢50). Expression of EYA1 was lower at the gastric ulcer edge when compared with the antrum. Interpretation: Genetic variation in an intron of the EYA1 gene increases the risk of endoscopically confirmed aspirin-induced PUD. Reduced EYA1 expression in the upper gastrointestinal epithelium may modulate risk, but the functional basis of this association will need mechanistic evaluation.