Publications by authors named "Wirestrand L"

Objectives: Knowledge of the societal costs of psoriasis is limited. This study estimated the cost of care, psoriasis area and severity index (PASI), and quality of life in a defined patient population in Sweden.

Methods: A prevalence-based prospective recruitment of patients visiting two Swedish dermatology clinics between September and December 2009 was performed, collecting resource utilization for health care contacts, treatment, travelling, and productivity loss during 1 month.

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Background: The neonatal lupus syndrome can be present as congenital heart block (CHB) or as neonatal lupus erythematosus (NLE), both seldom passively acquired autoimmune diseases. CHB starts around week 20 of pregnancy and is a lifelong event, whereas NLE is self limiting and usually starts at the 6th week of the child's age-the maximum recorded up to week 20.

Case Report: An asymptomatic mother with primary Sjogren's syndrome and anti-SSA/Ro52, anti-SSA/Ro60, and anti-SSB/La autoantibodies is described who, at gestational week 23 during her first pregnancy, was diagnosed as having a male fetus with CHB due to third degree atrioventricular block.

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Using a protocol for induction of photoallergy in the mouse after systemic administration, quinine was shown to be just as potent a photosensitizer as its d-isomer, quinidine. The dose-response curves for the two isomers followed a similar course both for induction and elicitation. Cross-reaction experiments, where induction and challenge were performed with different isomers, indicated that quinine and quinidine cross-react.

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Groups of female albino mice were photosensitized and photochallenged to quinine using protocols for either systemic or epicutaneous administration. Compared with control groups, statistically significant inflammatory reactions, measured as wet weight increase in ear tissue, could be obtained both with systemic and epicutaneous administration. Topically induced photoallergy to quinine could be elicited not only by topical, but also by intraperitoneal administration of the drug, and vice versa.

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Photoallergy to systemically administered quinidine was induced in the mouse, and the minimal time for sensitization as well as the duration of the allergy were studied. When groups of female albino mice, pretreated with cyclophosphamide, were exposed to quinidine 100 mg/kg i.p.

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Photoallergic dermatitis was induced in the mouse following the systemic administration of quinidine in combination with UVB and UVA. The reaction was recorded as ear wet weight, ear thickness and tail wet weight. Statistical calculations showed ear wet weight to be the most sensitive evaluation technique.

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Clinical photoreactions have been reported for quinine and quinidine after systemic and topical administration. We have investigated the phototoxic properties of these two quinoline methanol isomers in vitro using the Candida albicans inhibition test and photohemolysis, and in vivo with the mouse tail phototoxicity test. Both isomers were phototoxic in the hemolysis model, quinine being the more potent compound.

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Using the mouse, photoallergy to the antiarrhythmic agent quinidine could be induced following systemic administration. After pretreatment with cyclophosphamide 150 mg/kg, groups of 5-10 mice were injected i.p.

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The urinary excretion of the eumelanin metabolite 6-hydroxy-5-methoxyindole-2-carboxylic acid and the pheomelanin metabolite 5-S-cysteinyldopa was followed during PUVA treatment for 6 weeks. They showed similar excretion patterns, with the highest values within 1-2 wk.

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Pregnant women and women taking oral contraceptives show urinary excretion values of 5-S-cysteinyldopa and of 6-hydroxy-5-methoxyindole-2-carboxylic acid in the same range as nonpregnant women not taking oral contraceptives. The excretion of these melanoma markers can therefore be used in in the biochemical diagnosis of metastatic melanoma in pregnancy and in women taking oral contraceptives.

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The urine of an albino woman contained small quantities of 5-S-cysteinyldopa; 6-hydroxy-5-methoxyindole-2-carboxylic acid, a melanin precursor metabolite, was lacking. The 5-S-cysteinyldopa excretion observed may reflect non-specific oxidation of dopa. Two other albino patients showed normal values for the excretion of 5-S-cysteinyldopa and of 6-hydroxy-5-methoxyindole-2-carboxylic acid.

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The urinary excretion of 2 melanocyte metabolites was studied in normal people of different skin type. The sulphur-free indole derivative 6-hydroxy-5-methoxyindole-2-carboxylic acid was excreted in larger quantities by people with genetically dark skin, whereas the excretion of 5-S-cysteinyldopa was not related to pigment type. No correlation between 5-S-cysteinyldopa and 6-hydroxy-5-methoxyindole-2-carboxylic acid excretion emerged.

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