A Five-Year Followup of Human Seminal Plasma Allergy in an 18-Year-Old Woman

Case reports of women with the rare condition of human seminal plasma allergy have indicated that the condition may be associated with life-threatening anaphylactic reactions in relation to coitus. Few observations, if any, of long-term outcome of the condition are available. The aim of this paper was to present a case diagnosed in an 18-year-old girl who presented with generalized urticaria, nasal congestion and secretion, conjunctivitis, and periorbital and labial oedema 6–8 hours after coitus. During five years of followup the condition improved clinically significantly. Due to intimacy concerns and the low prevalence of the condition robust long term data on the natural course of the condition are difficult to obtain. The present case suggests that in some patients the condition may improve over time

Identification of 5-Hydroxy-6-indolyl-O-sulfate in Urine of Patients with Malignant MelanomaIdentification of 5-Hydroxy-6-indolyl-O-sulfate in Urine of Patients with Malignant Melanoma

It has previously been shown that enzymatically hydrolyzed urine of patients with malignant melanoma contains 5,6-dihydroxyindole (5,6DHI). In this study we describe the elucidation of the entire structure of urinary 5,6DHI-conjugate. Differential hydrolysis of melanotic urine revealed that, in contrast to β-glucuronidase, sulfatase can liberate 5,6DHI from its conjugated form. 5,6DHI-sulfate was synthesized by reacting 5,6DHI with sulfur trioxide trimethylamine complex. Thin-layer chromatography (TLC) documented its close similarity to the Thormählen-positive compound usually entitled “C.” Gas chromatographic-mass spectrometric (GC-MS) analysis of methylated and subsequently hydrolyzed synthetic 5,6DHI-sulfate showed that the synthetic product consisted of a mixture of 5-hydroxy-6- indolyl-O-sulfate and 6-hydroxy-5-indolyl-O-sulfate (with a certain amount of 5,6DHI-disulfate). 5,6DHI-sulfate was purified with use of DEAE-cellulose column chromatography from melanotic urine. Methylation of this conjugate with deuterated dimethylsulfate and subsequent GC-MS analysis of the hydrolyzed product provided evidence that 5,6DHI from melanotic urine was almost exclusively sulfated in position 6. It was concluded (1) that 5,6DHI is excreted as a 6-O-sulfate, and (2) that this compound is consistent with Thormählen-positive compound “C.

Evaluation of coagulation activation after Rhinovirus infection in patients with asthma and healthy control subjects: an observational study

Background Asthma exacerbations are frequently triggered by rhinovirus infections. Both asthma and respiratory tract infection can activate haemostasis. Therefore we hypothesized that experimental rhinovirus-16 infection and asthmatic airway inflammation act in synergy on the haemostatic balance. Methods 28 patients (14 patients with mild allergic asthma and 14 healthy non-allergic controls) were infected with low-dose rhinovirus type 16. Venous plasma and bronchoalveolar lavage fluid (BAL fluid) were obtained before and 6 days after infection to evaluate markers of coagulation activation, thrombin-antithrombin complexes, von Willebrand factor, plasmin-antiplasmin complexes, plasminogen activator inhibitor type-1, endogenous thrombin potential and tissue factor-exposing microparticles by fibrin generation test, in plasma and/or BAL fluid. Data were analysed by nonparametric tests (Wilcoxon, Mann Whitney and Spearman correlation). Results 13 patients with mild asthma (6 females, 19-29 y) and 11 healthy controls (10 females, 19-31 y) had a documented Rhinovirus-16 infection. Rhinovirus-16 challenge resulted in a shortening of the fibrin generation test in BAL fluid of asthma patients (t = -1: 706 s vs. t = 6: 498 s; p = 0.02), but not of controls (t = -1: 693 s vs. t = 6: 636 s; p = 0.65). The fold change in tissue factor-exposing microparticles in BAL fluid inversely correlated with the fold changes in eosinophil cationic protein and myeloperoxidase in BAL fluid after virus infection (r = -0.517 and -0.528 resp., both p = 0.01). Rhinovirus-16 challenge led to increased plasminogen activator inhibitor type-1 levels in plasma in patients with asthma (26.0 ng/mL vs. 11.5 ng/mL in healthy controls, p = 0.04). Rhinovirus-16 load in BAL showed a linear correlation with the fold change in endogenous thrombin potential, plasmin-antiplasmin complexes and plasminogen activator inhibitor type-1. Conclusions Experimental rhinovirus infection induces procoagulant changes in the airways of patients with asthma through increased activity of tissue factor-exposing microparticles. These microparticle-associated procoagulant changes are associated with both neutrophilic and eosinophilic inflammation. Systemic activation of haemostasis increases with Rhinoviral load

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Zorginstellingen werken in toenemende mate samen binnen het publieke domein. Er ontstaan steeds meer samenwerkingsverbanden tussen zorg en onderwijs, arbeidstoeleidingen wonen. In de praktijk blijkt dat in deze samenwerkingsverbanden de kwaliteit van de zorg en de veiligheid van de cliënt niet goed geregeld zijn.Hoe kan dit