In the present cross sectional study, we aimed to ascertain the relative associations of GST genotypes with GST activity variations and also with the risk to DMT2 predisposition among men and women separately. Clinical samples obtained from 244 DMT2 cases (120 Males and 124 Females) and 228 controls (117 Males and 111 Females) belonging to Asian Indian ethnicity were used to test for glycemic index, lipid profile, GST activity and GST genotypes. The frequencies of single and combinations of GST genotypes were statistically examined for their association with DMT2 risk among both study groups. The GST activity is significantly lowered in DMT2 group compared to controls (p = < 0.001). This reduction is found to be subjective to single and combinations of GST genotypes among diabetic patients. The frequency distribution for single, double and triple combinations of genotypes of GSTT1, GSTM1 and GSTP1 showed the varying degrees of association with DMT2 risk from 0.5 to 5.6-fold among male and female patients (for all associations, p value was <0.05). Interestingly, GST activity was lowered in both male and female patients with single or combinational genotypes of GSTM1 (Null), GSTT1 (Null), and P1 (V/V) (for all associations, p value was = <0.0001). The reduced anti-oxidant capacity among diabetic patients with certain GST genotypes may have some important implications for disease diagnosis and therapy.

The CYP2C8 and CYP2C9 are two major isoforms of the cytochrome P450 enzyme family, which is involved in drug response, detoxification, and disease development. This study describes the differential distribution of amino acid substitution variants of CYP2C8 (*2-I269F & *3-R139K) and CYP2C9 (*2-C144R & *3-L359A) genes in 234 type 2 diabetes mellitus (T2DM) patients and 218 healthy controls from Andhra Pradesh, South India. Single locus genotype analysis has revealed that homozygous recessive genotypes of 2C8*2-TT (P ≤ .03), 2C9*2-TT (P ≤ .02), and heterozygous 2C9*3-AC (P ≤ .006) are seen to be increasingly present in the case group, indicating a significant level of their association with diabetes in Andhra population. The statistical significance of these recessive genotypes has persisted even under their corresponding allelic forms (P ≤ .01). Genotype association results were further examined by computational protein structure and stability analysis to assess the deleteriousness of the amino acid changes. The mutant CYP 2C8 and 2C9 (both *2 and *3) proteins showed structural drifts at both amino acid residue (range 0.43Å-0.77Å), and polypeptide chain levels (range 0.68Å-1.81Å) compared to their wild-type counterparts. Furthermore, the free energy value differences (range -0.915 to -1.38 Kcal/mol) between mutant and native protein structures suggests the deleterious and destabilizing potential of amino acid substitution polymorphisms of CYP genes. The present study confirms the variable distribution of CYP2C8 (*2 and *3) and CYP2C9 (*2 and *3) allelic polymorphisms among South Indian diabetic populations and further warrants the serious attention of CYP gene family, as a putative locus for disease risk assessment and therapy.

Sweet syndrome is an acute febrile neutrophilic dermatosis first described by Robert Douglas Sweet in 1964. Sweet syndrome presents in three clinical settings: classical (or idiopathic), malignancy-associated, and drug-induced. It has been associated with hematopoietic malignancies and myelodysplastic disorders. A-28-years married woman presented to us with chief complaints of Fever and Multiple swellings over the body since 2 months. At presentation she has Pallor; venous hum present. Multiple, tender, erythematous subcutaneous swellings, firm in consistency noted in both forearms. Skin over the swellings is pinchable; superficial skin is normal. Sweet syndrome can occasionally cause an intense systemic response involving the lungs, liver and musculoskeletal system. The skin lesions in Sweet syndrome typically start as erythematous papules, plaques, and nodules. The lesions can take on pseudovesicular or pseudopustular appearance, and sometimes fully formed vesicles or pustules develop. The lesions can be subcutaneous mimicking erythema nodosum which can’t be differentiated unless a biopsy is taken. Because the diagnosis of Sweet syndrome can be challenging, particularly when associated with other connective tissue disorders such as SLE, a set of diagnostic criteria were proposed initially by Su and Liu and then revised by Von den Driesch. The diagnosis is based upon the presence of two major and two of the four minor criteria. Concurrent Sweet syndrome and SLE are exceedingly rare. Twelve patients with both Sweet syndrome and systemic lupus erythematosus (SLE) have been previously reported. We report a case of sweet syndrome associated with SLE diagnosed in our hospital. In our patient, diagnostic criteria are satisfied for Sweet syndrome as well as for SLE (ACR criteria-patient had polyarthralgia, anemia, thrombocytopenia, ANA and Ds DNA positive. Four out of 11 are fulfilled for SLE). Patient responded to corticosteroids.

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