Chronic urticaria (CU) is characterized by the occurrence of wheals lasting for more than 6 weeks. The role of platelet activation in the pathophysiology of this condition has not been clearly studied. We undertook a cross-sectional study among 45 patients with CU and 45 age- and gender-matched healthy controls. The severity of the disease was assessed using the urticaria severity score. The autologous plasma skin test (APST) was done in all cases of CU. The platelet count and indices were estimated by an automated haematological laser optical analyzer. Platelet aggregation and soluble P-selectin levels were estimated in all study participants. It was observed that there was a significantly higher mean platelet volume (MPV) and platelet distribution width (PDW) in patients with CU when compared to controls. Platelet aggregation and soluble P-selectin levels were significantly higher in patients with CU, as compared to controls. Urticaria severity score correlated positively with platelet aggregability and soluble P-selectin levels. APST-positive patients had significantly higher platelet aggregation and higher soluble P-selectin levels, when compared to the APST-negative patients, indicating more platelet activation in the autoimmune group. There is significant platelet activation in patients with CU, especially in those with autoreactivity.

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Our results serve as preliminary evidence for the clinical use of genetic markers as predictors of response to methotrexate in psoriasis. This might aid in the future in the development of a point-of-care testing (POCT) gene chip, to predict optimal treatment response in patients with psoriasis, based on their individual genotypic profile.

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BackgroundThough cardiovascular (CV) risks are reported in first-degree relatives (FDR) of type 2 diabetics, the pathophysiological mechanisms contributing to these risks are not known. We investigated the association of sympathovagal imbalance (SVI) with CV risks in these subjects.Subjects and MethodsBody mass index (BMI), basal heart rate (BHR), blood pressure (BP), rate-pressure product (RPP), spectral indices of heart rate variability (HRV), autonomic function tests, insulin resistance (HOMA-IR), lipid profile, inflammatory markers, oxidative stress (OS) marker, rennin, thyroid profile and serum electrolytes were measured and analyzed in subjects of study group (FDR of type 2 diabetics, n = 72) and control group (subjects with no family history of diabetes, n = 104).ResultsBMI, BP, BHR, HOMA-IR, lipid profile, inflammatory and OS markers, renin, LF-HF (ratio of low-frequency to high-frequency power of HRV, a sensitive marker of SVI) were significantly increased (p<0.0001) in study group compared to the control group. SVI in study group was due to concomitant sympathetic activation and vagal inhibition. There was significant correlation and independent contribution of markers of insulin resistance, dyslipidemia, inflammation and OS to LF-HF ratio. Multiple-regression analysis demonstrated an independent contribution of LF-HF ratio to prehypertension status (standardized beta 0.415, p<0.001) and bivariate logistic-regression showed significant prediction (OR 2.40, CI 1.128–5.326, p = 0.002) of LF-HF ratio of HRV to increased RPP, the marker of CV risk, in study group.ConclusionSVI in FDR of type 2 diabetics occurs due to sympathetic activation and vagal withdrawal. The SVI contributes to prehypertension status and CV risks caused by insulin resistance, dyslipidemia, inflammation and oxidative stress in FDR of type 2 diabetics.