Psoriasis in childhood and adolescence: evaluation of demographic and clinical features

BACKGROUND: The present study was aimed to define the gender ratio, familial occurrence, age of onset, precipitating factors, clinical types, nail and joint involvement of psoriasis in childhood and adolescence in Turkey. METHODS: A total of 61 children with psoriasis under 18 years old were evaluated retrospectively, for age, gender, age of disease onset, family history, concomitant disease, the clinical type of psoriasis, clinical localization, nail and joint involvement and treatment modalities. RESULTS: Of the patients, 23 (37.70%) were boys and 38 (62.30%) were girls. Mean age was 9.28 +/- 4.02 years in girls and 11.18 +/- 3.85 years in boys (9.96 +/- 4.03 years in all children). Mean age at the onset of the disease was 6.81 +/- 4.11 years in girls and 7.03 +/- 4.28 years in boys (6.89 +/- 4.14 years in all patients). In 14 (23%) cases, a positive family history was detected. The most frequent probable triggering factors were upper respiratory tract infections (14.8%) and positive throat culture for A group ss-hemolytic streptococcus (21.3%). Frequency of emotional stress and psychiatric morbidity were 54% and 9.8%, respectively. The most frequent localizations at onset were trunk (44.3%), extremities (54.0%), and scalp (36.0%). Three children (4.9%) had a history of dissemination from psoriatic diaper rash. In total, 51 (83.6%) patients presented with psoriasis vulgaris, eight (13.1%) with generalized pustular psoriasis, and the remaining two (3.3%) with erythrodermic psoriasis. CONCLUSION: The incidence of psoriasis among dermatological patients in childhood and adolescence was 3.8%. The disease tends to appear earlier in girls than boys. The authors suggested that stress and upper respiratory infections are the most important triggering factors in childhood and adolescence psoriasis.     

Does prophylactic sotalol and magnesium decrease the incidence of atrial fibrillation following coronary artery bypass surgery: a propensity-matched analysis

Background  

Atrial fibrillation can occur in up to 40% of patients undergoing coronary surgery.     

Genetic association studies of interleukin-13 receptor alpha1 subunit gene polymorphisms in asthma and atopy.

Interleukin (IL)-13 plays a central role in asthma pathogenesis by binding to the IL-13 receptor, which is a heterodimer composed of the IL-13 receptor alpha1 subunit (IL-13Ralpha1) and IL-4Ralpha. The genetic diversity at the IL-13Ralpha1 gene (IL13RA1) locus on chromosome Xq24 was characterised and the association of identified polymorphisms with asthma and atopy phenotypes examined. The promoter and coding region of IL13RA1 were screened for common genetic variants, and polymorphisms found were genotyped in a large cohort of 341 asthmatic Caucasian families (each containing at least two asthmatic siblings) and 182 nonasthmatic control subjects. Genetic association was determined using case-control and transmission disequilibrium test analyses. Two common polymorphisms were identified, a newly found thymidine (T) to guanine (G) transition of nucleotide -281 (-281T>G) single nucleotide polymorphism in the IL13RA1 promoter and the previously described 1365A>G variant in the IL13RA1 proximal 3' untranslated region. No significant association of either -281T>G or 1365A>G with risk of asthma or atopy phenotypes was found, apart from a suggestive association between the IL13RA1 -281T/1365A haplotype and raised total serum immunoglobulin E levels in adult female asthmatics. These findings indicate that the interleukin-13 receptor alpha1 subunit gene -281T>G and 1365A>G polymorphisms do not contribute to asthma susceptibility or severity, although the interleukin-13 receptor alpha1 subunit gene locus might be involved in the control of immunoglobulin E production.     

Clonazepam in the long-term treatment of patients with unipolar depression, bipolar and schizoaffective disorder.

The value of a long-term treatment with clonazepam in the prophylaxis of affective disorder is discussed controversially in the scientific literature. Altogether there are only a few reports on the use of this compound as a mood stabilizer, most of them describing patients suffering from bipolar affective disorder. The aim of this investigation was to evaluate clonazepam as a phase prophylactic medication in affective disorder. We conducted a retrospective chart review in 34 out-patients of our lithium clinic (15 suffering from unipolar depression, 15 from bipolar disorder, four from schizoaffective disorder), who had been treated with clonazepam as a long-term medication. Clonazepam was either given as monotherapy, or as in the case of lithium non-responders, as adjunctive therapy. Patients with unipolar depression had significantly (P=0.026) less depressive episodes after initiation of treatment with clonazepam. Patients with bipolar disorder did not benefit from this therapy. Neither manic/hypomanic phases nor depressive episodes were reduced in this group of patients. Interestingly, clonazepam also reduced affective phases in our four schizoaffective patients on a trend level. Our results indicate that patients with unipolar depression may benefit from a maintenance treatment with clonazepam. Due to methodological limitations our results need to be replicated in controlled double-blind randomized clinical trials.