Sticky Platelet Syndrome: An Underrecognized Cause of Graft Dysfunction and Thromboembolic Complications in Renal Transplant Recipients

Sticky platelet syndrome (SPS) leads to hyperaggregabilty of platelets in response to physiologic stimuli. In this report we describe three patients with clinical symptoms of SPS after renal transplantation. The first patient developed an infarction of her transplant kidney with additional, subsequent renal microinfarctions. The second patient suffered multiple strokes and deep vein thrombosis with episodes of pulmonary embolism and ischemic bowel disease due to colonic microinfarctions. The third patient experienced a long episode of unexplained respiratory and graft dysfunction immediately after transplantation until therapy for SPS was initiated, at which point symptoms resolved quickly. Kidney transplant recipients with SPS may be at increased risk of developing thrombosis, given that most immunosuppressive drugs are known to induce either endothelial cell damage or augment platelet aggregation. All patients awaiting renal transplantation should be screened for a history of thrombosis and, if appropriate, tested for SPS. Affected patients should receive dose-adjusted acetylsalicylic acid.     

Das Cinderella-Schuh-Syndrom

The Cinderella shoe syndrome specifies a commonly observed, not yet labeled disproportion of footwear and the morphologic conditions of the wearer. Disproportioned shoes and socks are worn–frequently unconsciously–due to personal reasons, fashion trends, misinformation and wrong advice; they can induce severe foot disorders. The Cinderella shoe syndrome has an important significance within the development, the treatment and the recurrence-prophylaxis of foot disorders, as well as in the assessment of possible reasons for recurrence after foot surgery. To recognize it, to treat individual psychologic reasons, to give support in the choice of footwear, to inform about and to change social reasons are all challenges of the foot surgeon.     

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.     

Congenital dextrocardia complicated by hypertension,coronary artery disease and myocardial infarction

The case record of a seventy-three year old man with congenital dextrocardia and situs inversus viscerum complicated by hypertension, coronary artery disease and myocardial infarction is presented. Electrocardiographic recordings of the limb leads, with and without reversal of the arm lead wires, and of the precordial leads of the V series derived from both right and left chest areas are presented. In this instance the electrocardiographic findings in precordial leads taken over the right chest point to fresh anteroseptal infarction; those leads recorded from the left chest were not informative. This serves to emphasize the fact that precordial leads should be recorded from the right side of the chest rather than the left in order that the exploring precordial electrode may overlie the area of cardiac damage, and thus manifest maximal changes in the electrocardiogram. We agree that the electrocardiogram may best be interpreted by application of the usual criteria to the limb leads taken with the arm lead wires reversed although in this case the limb leads yielded no information of diagnostic significance.