Objectives:To identify risk factors other than genetic for severe carbamazepine-induced mucocutaneous reactions, that is, SJS, TEN, and exfoliative dermatitis (ED).Materials and Methods:We did a case-control study using data from the Swedish national database of spontaneously reported adverse drug reactions (ADRs). We selected all patients who had been reported from January 1, 1965 to March 31, 2010 as having experienced SJS (n = 78), TEN (n = 6), or ED (n = 8), and assessed as at least possibly related to carbamazepine. We also included diagnoses possibly representative of early signs of these serious conditions, that is, erythema multiforme (EM, n = 34) and scaly rash (n = 13). We compared data on demographics, drug treatment, and clinical features for these patients (cases, n = 139) with those from patients who had experienced any other type of ADR from carbamazepine during the same time period (controls, n = 887).Results:After adjustment for multiple comparisons, alcohol abuse was statistically significantly more common among cases than controls (34.5% vs 8.7%, odds ratio 5.5 [95% confidence interval 3.6-8.4], P = 3.14 × 10-14 ). The same was seen for SJS and EM individually.Conclusion:Alcohol abuse is a possible risk factor for serious carbamazepine-induced mucocutaneous reactions.
The immunosuppressant drug azathioprine is associated with a 4% risk of acute pancreatitis in patients with inflammatory bowel disease (IBD). Studies have demonstrated an increased risk in carriers of HLA-DQA1*02:01 and HLA-DRB1*07:01. We investigated whether these human leukocyte antigen (HLA) types were associated with azathioprine-induced pancreatitis also in Swedish patients with IBD, and whether the type of disease affected the association. Nineteen individuals with IBD who developed acute pancreatitis after initiation of azathioprine were genotyped and compared with a population control cohort (n = 4891) and a control group matched for disease (n = 81). HLA-DQA1*02:01 and HLA-DRB1*07:01 were in full linkage disequilibrium, and were significantly associated with acute pancreatitis both when cases were compared with population controls (OR 3.97 [95% CI 1.57-9.97], p = 0.0035) and matched controls (OR 3.55 [95% CI 1.23-10.98], p = 0.0275). In a disease-specific analysis, the correlation was positive in patients with Crohn's disease versus matched controls (OR 9.27 [95% CI 1.86-46.19], p = 0.0066), but not in those with ulcerative colitis versus matched controls (OR 0.69 [95% CI 0.07-6.74], p = 0.749). In patients with Crohn's disease, we estimated the conditional risk of carriers of HLA-DQA1*02:01-HLA-DRB1*07:01 to 7.3%, and the conditional risk of a non-carrier to 2.2%. We conclude that HLA-DQA1*02:01-HLA-DRB1*07:01 is a marker for increased risk of acute pancreatitis in individuals of Swedish genetic origin, treated with azathioprine for Crohn's disease. Study Highlights WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC?HLA-DQA1*02:01 and HLA-DRB1*07:01 have been shown to increase the risk of acute pancreatitis in individuals with inflammatory bowel disease (IBD) treated with azathioprine. WHAT QUESTION DID THIS STUDY ADDRESS?It is unknown whether this risk also applies to patients of Swedish origin and if the risk differs depending on type of IBD.
The aim of this study was to estimate the changes of autofluorescence and sensitized fluorescence under the effect of cosmetics. We used a method of fluorescence spectroscopy in vivo and examined the mouse skin covering the tumour. Analysis of fluorescence spectral changes was made after differentiation of the cosmetics according to its effects: i) inducing temporary changes of skin autofluorescence after absorbtion into skin (lipsticks, face powders, body lotions, mascaras); ii) permanently changing the fluorescence of the skin (collagen containing products). Cosmetics have been shown to be optically active and capable to alter the fluorescence of exogenously accumulated photosensitizers and endogenous tissue fluorophores.
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