ABSTRACT
Objective: To investigate Blastocystis' etiologic role and association with gastrointestinal symptomatology in acute and chronic urticaria patients and to identify Blastocystis subtypes responsible for urticaria. Methods: The study included urticaria patients and healthy individuals that presented to our polyclinic between June 2015 and May 2017. The participants were assigned into Group I (137 patients), subdivided into acute (72) and chronic urticaria patients (65), and Group ? (129 control individuals). Blastocystis presence was investigated by native-Lugol examination, trichrome staining, PCR using sequence tagged site primers, and DNA sequencing analysis. The phylogenetic tree was constructed. Results: The native-Lugol and trichrome staining methods revealed that 16 patients (16/133, 12.0%) had Blastocystis-positive stool samples, of which seven samples (7/133, 5.3%) belonged acute and nine (9/133, 6.8%) to chronic urticaria patients. Concerning Blastocystis subtypes, of the acute urticaria patients, three had subtype 1 (ST1), one had ST2, and three had ST3. Of the chronic urticaria patients, one had ST1 and eight had ST3. Blastocystis positivity was detected in two control individuals (2/123, 1.6%), both being ST3. All subtypes identified by PCR were confirmed by the sequencing analysis. The acute and chronic urticaria groups showed no statistically significant differences for Blastocystis positivity (P=0.60) and subtype distribution (P=0.15). A statistically significant difference was found between the urticaria patients and the controls for Blastocystis positivity (P<0.01), but not for subtype distribution (P=0.67) or for Blastocystis presence and gastrointestinal complaints. Conclusions: This study on Blastocystis subtype distribution among Turkish urticaria patients showed results consistent with the literature. It was concluded that Blastocystis should be kept in mind in patients with urticaria.
ABSTRACT
BACKGROUND: High asymmetrical dimethylarginine (ADMA) levels have been associated with endothelial dysfunction and contribute to the development of several diseases. However, data on the relationship between hepatitis B virus (HBV) and ADMA are limited. The aim of our study was to explore the relationship between ADMA and HBV by comparing the ADMA levels in patients with chronic active hepatitis B (CHB), inactive HBV carriers (carriers), and healthy volunteers (controls). METHODS: The participants were divided into three groups: 90 patients with CHB, 90 HBV carriers, and 90 controls. Serum ADMA levels were quantified using an ELISA kit (Cusabio, Wuhan, China). The data were analyzed using an ANOVA or the Kruskal-Wallis test as appropriate, with P<0.05 considered significant. RESULTS: Serum ADMA levels were significantly higher in patients with CHB (228.35±91.10 ng/mL) than in HBV carriers (207.80±75.80 ng/mL) and controls (207.61±89.10 ng/mL) (P=0.049). The clinical scores of the patients were positively correlated with ADMA levels. CONCLUSIONS: The elevated serum ADMA levels in patients with CHB confirm that HBV plays a role in vasculitis. Further investigation of the mechanisms contributing to the high levels of ADMA in CHB may contribute toward development of new treatment modalities.