One of the drawbacks of the studies of non-juice products such as capsules is that few of the triallists reported how much ‘active’ ingredients (if any) were in the tablets or capsules they used. Until there are more studies of products containing enough of the active ingredient, measured in a standardized way, cranberry products cannot be recommended for preventing UTI. No definitive mechanism of action has been established for cranberry in the prevention or treatment of UTI. However, research suggests that cranberries

Ruxolitinib ic50 prevent bacteria (particularly Escherichia coli) from adhering to uroepithelial cells that line the wall of the bladder. Without adhesion, E. coli cannot cause infection. One of the potential problems in demonstrating effectiveness is that the active ‘ingredient’ in cranberry products (Proanthocyanidin – PAC) is only effective for around 10–12 h. For cranberry juice to be effective, a patient

would need to consume two glasses a day for an indefinite period of time. Furthermore, cranberry juice is calorific, some people find it unpalatable (and incur side effects such as gastrointestinal upset), and is likely to cost a not insubstantial sum. For cranberry juice to be most effective, a patient would need to be committed to the regimen and not have any other contra-indications (e.g. diabetes). At this time, tablets and capsules should not find more be recommended unless they clearly contain the recommended amount of PAC (at least 36 mg/day). All residents of Australia and New Zealand can access The Cochrane Library for free, thanks to funding provided by the Australian and New Zealand Governments. “
“A 51-year-old man with good past health presented with nephrotic syndrome in April 2003, due to idiopathic membranous nephropathy (IMN). He was treated with prednisolone 45 mg daily and mycofenolate mofetil 1000 mg twice daily. However, he developed steroid-induced psychosis, requiring a rapid taper of prednisolone. He achieved partial remission and both medications

were tailed off in 6 months. He had a relapse one month later. He was treated with cyclosporin A (CYC) alone and achieved complete remission. He had a second relapse 2 years later, to which he responded to an increased dose of CYC. Four years later, he had a third relapse. He was put on Rituximab 375 mg/m2 per week for Glycogen branching enzyme 4 weeks. After 3 months, while CYC was tapered to 25 mg twice daily, he developed an erythematous papulopustular eruption over his trunk and limbs with silvery scaling, clinically compatible with pustular psoriasis (Fig. 1). He had no personal or family history of psoriasis. The close temporal relationship made Rituximab a highly suspicious culprit. He was treated with topical steroid. His skin lesions improved gradually. At 18 months after Rituximab therapy, he remained in complete remission from nephrotic syndrome. There is no further relapse of psoriasis. Rituximab is generally well tolerated in patients with IMN.