AimsThe aim of this work is to identify the medicines which interact with the herbal remedy St John's wort (SJW), and the mechanisms responsible. Methods A systematic review of all the available evidence, including worldwide published literature and spontaneous case reports provided by healthcare professionals and regulatory authorities within Europe has been undertaken. Results A number of clinically significant interactions have been identified with prescribed medicines including warfarin, phenprocoumon, cyclosporin, HIV protease inhibitors, theophylline, digoxin and oral contraceptives resulting in a decrease in concentration or effect of the medicines. These interactions are probably due to the induction of cytochrome P450 isoenzymes CYP3A4, CYP2C9, CYP1A2 and the transport protein P-glycoprotein by constituent(s) in SJW. The degree of induction is unpredictable due to factors such as the variable quality and quantity of constituent(s) in SJW preparations. In addition, possible pharmacodynamic interactions with selective serotonin re-uptake inhibitors and serotonin (5-HT 1d ) receptoragonists such as triptans used to treat migraine were identified. These interactions are associated with an increased risk of adverse reactions. Conclusions In Sweden and the UK the potential risks to patients were judged to be significant and therefore information about the interactions was provided to health care professionals and patients. The product information of the licensed medicines involved has been amended to reflect these newly identified interactions and SJW preparations have been voluntarily labelled with appropriate warnings.
In a previous screening study, 16% of patients with psoriasis had IgA and/or IgG antibodies to gliadin (AGA). The aim of the present study was to evaluate the effect of a gluten-free diet (GFD) in 33 AGA-positive and six AGA-negative psoriasis patients. Of the 33 AGA-positive patients, two had IgA antibodies to endomysium (EmA) and 15 an increased number of lymphocytes in the duodenal epithelium, but in some this increase was slight. Two patients had villous atrophy. A 3-month period on a GFD was followed by 3 months on the patient's ordinary diet. The severity of psoriasis was evaluated with the psoriasis area and severity index (PASI). The examining dermatologists were unaware of the EmA and duodenal biopsy results throughout the study. Thirty of the 33 patients with AGA completed the GFD period, after which they showed a highly significant decrease in mean PASI. This included a significant decrease in the 16 AGA-positive patients with normal routine histology in duodenal biopsy specimens. The AGA-negative patients were not improved. After GFD, the AGA values were lower in 82% of those who improved. There was a highly significant decrease in serum eosinophil cationic protein in patients with elevated AGA. When the ordinary diet was resumed, the psoriasis deteriorated in 18 of the 30 patients with AGA who had completed the GFD period. In conclusion, psoriasis patients with raised AGA might improve on a GFD even if they have no EmA or if the increase in duodenal intraepithelial lymphocytes is slight or seemingly absent.
An increased risk of attempted suicide was apparent up to six months after the end of treatment with isotretinoin, which motivates a close monitoring of patients for suicidal behaviour for up to a year after treatment has ended. However, the risk of attempted suicide was already rising before treatment, so an additional risk due to the isotretinoin treatment cannot be established. As patients with a history of suicide attempts before treatment made new attempts to a lesser extent than did patients who started such behaviour in connection with treatment, patients with severe acne should not automatically have isotretinoin treatment withheld because of a history of attempted suicide.
It was recently observed that in six patients with psoriasis and one with palmoplantar pustulosis, with newly discovered gluten intolerance, a gluten-free diet had a remarkable effect on the skin lesions. This prompted us to undertake a screening investigation to discover whether increased levels of serum antibodies to gliadin are more common in patients with psoriasis than in healthy persons. IgA and IgG antibodies to gliadin (IgA AGA and IgG AGA) were quantified by a micro-ELISA method. Out of 302 patients with psoriasis, 16% (18 females, 31 males) showed serum IgA AGA levels above the 90th percentile value (51 u/ml) of the reference group. This tendency was even more marked when the proportion of patients with values > 70 u/ml was compared with the corresponding proportion of 99 reference subjects. Thus, 3% of the reference subjects but 7.9% of the patients had values > 70 u/ml. The corresponding figures for men were 1.6% and 8.9%, respectively. Men with psoriasis had a significantly higher mean IgA AGA than the male reference group. The means based on logarithmic values of the individual IgA AGA values were significantly higher in the psoriatic groups than in the reference groups. Although the mean level of IgG AGA was not increased in the psoriasis group, there was a correlation between the values for IgA AGA and IgG AGA. The serum concentrations of IgG, IgA and IgM were also measured. In the male patients, the mean IgA value was significantly increased. Women in whom IgA AGA was elevated also showed a significantly increased mean IgA.(ABSTRACT TRUNCATED AT 250 WORDS)
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