Helicobacter pylori are considered the most common human pathogen colonizing gastric mucosa. Gastritis with or without H. pylori infection is associated with increase in levels of homocysteine and high-sensitivity C-reactive protein (hs-CRP) but a more pronounced increase is noted in gastritis with H. pylori infection. Increasing level of homocysteine, due to decreased absorption of vitamin B12 and folic acid, together with increased CRP levels in gastritis with H. pylori infection may be the earliest event in the process of atherosclerosis and plaque formation. Retrospective study conducted at tertiary care hospital in Mumbai by Department of Biochemistry in association with Department of Surgery. Eighty patients who underwent gastroscopy in view of gastritis were subjected to rapid urease test for diagnosis of H. pylori infection. Vitamin B12, folic acid, homocysteine and hs-CRP were analyzed using chemiluminescence immuno assay. Student’s t-test, Pearson’s correlation and linear regression used for statistical analysis.Patients with H. pylori gastritis had significantly lower levels of vitamin B12 (271.6±101.3 vs 390.6±176.7 pg/mL; P=0.0005), as well as higher levels of homocysteine (17.4±7.4 vs 13.8±7.8 µmol/L; P=0.037) and hs-CRP (2.5±2.9 vs 1.2±1.1 mg/L; P=0.017), than in patients without H. pylori gastritis. However, folic acid showed (8.9±3.2 vs 10.0±3.6 ng/mL; P=0.171) no significant difference.Elevated homocysteine and hs-CRP in H. pylori gastritis may independently induce endothelial dysfunction, leading to cardiovascular pathology.

Background: This study determines the protein carbonyls which cause cellular damage and glutathione, glutathione peroxidase, glutathione reductase act as antioxidants. Materials and Methods:This study was carried out in different categories of pulmonary and extra pulmonary tuberculosis cases of newly sputum culture positive diagnosed pulmonary categorie I (n=100), extra pulmonary patients categorie (n=35) before and after the DOTS treatment of 6 months, categorie II (n=100), categorie III (n=100) and in normal control subjects (n=100). Results:The serum protein carbonyl levels were significantly increased in the pulmonary and extra pulmonary tuberculosis patients. The activities of blood glutathione, glutathione per oxidase, and glutathione reductase were found to be significantly decreased in subjects of all the categories of pulmonary and extra pulmonary tuberculosis. A negative correlation between the carbonyl protein content and glutathione, glutathione peroxidase, and glutathione reductase was seen in pulmonary tuberculosis, p<0.001. Conclusion:Increased antioxidant defense mechanism due to increase oxidative stress in tuberculosis. The changes were reversed after 6 months of antitubercular treatment in patients with a good recovery, but the increase in the oxidative stress was not completely reversed. INTRODUCTIONTuberculosis is a chronic granulomatous disease which is caused by Koch's bacilli, which is called Mycobacterium tuberculosis. The lung is the portal entry of Mycobacterium tuberculosis and it provides a congenial environment for this slowly replicating pathogen. The infection is established in the alveolar macrophages of the distal alveoli [1]. Proteins constitute the major 'working force' for all forms of biological work. The Reactive Oxygen and Nitrogen Species (ROS and RNS) are formed in higher fluxes under pathological conditions. They cause cellular damage due to the oxidation of amino acid residues on proteins, forming protein carbonyls [2] (aldehydes, ketones e.g. Lys, Arg, Pro, Thr). Oxidative stress also increases the protein oxidation [3]. The modification of proteins is initiated mainly by reactions with OH; however, the course of the oxidation process is determined by the availability of O 2 and O 2 -or its protonated form (HO 2 ). Collectively, these reactive oxygen species can lead to oxidation of the amino residue side chains, formation of protein-protein cross-linkages and oxidation of the protein backbone, resulting in protein fragmentation, that transition metal ions substitute for OH and O 2 - [4].Glutathione, which is involved in the transport of amino acids, acts as a coenzyme for enzymes and it protects against oxygen radicals and toxic compounds [5]. Se-dependent GSH peroxidase is capable of utilizing hydrogen peroxide (H 2 0 2 ) and a variety of organic hydroperoxides as substrates. The Se-independent activity is attributed to the isoenzymes of the GSH S-transferases, particularly GSH S-transferass B which acts on the organic hydroperoxides but not on hydrogen pero...

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Objective: Alzheimer's disease (AD) is characterised by progressive cognitive decline due to neurodegeneration. Over activation of the hypothalamic–pituitary–adrenal axis, oxidative stress and inflammation potentially damage the neuronal system, affecting cognition. Aim: This study aimed to assess the relationship between serum cortisol, Interleukin-6 (IL-6) and homocysteine (Hcy) levels in AD. Methods: Case-Control observational study consisting of 71 patients with AD and 70 healthy controls above 60 years of age. Serum samples were analysed for cortisol, IL-6 and Hcy levels using chemiluminescence immunoassay (Immulite 1000) technique. Cognitive functions were measured using the Mini-Mental State Examination (MMSE) Score. AD subjects were categorised based on the modified Kuppuswamy socioeconomic status scale. Statistical evaluation was conducted using SPSS Statistics software. Group data were analysed using a two-tailed Student's t-test, analysis of variance (ANOVA), the Mann–Whitney U test and Pearson's correlation test. Results: Serum cortisol, IL-6 and Hcy levels were significantly increased (p < 0.01) in AD (cortisol: 19.69 ± 8.96 ug/dl; IL-6: 10.27 ± 2.76 pg/ml; Hcy: 23.29 ± 3.81 μmol/l), as compared with the controls (cortisol: 13.37 ± 5.59 ug/dl; IL-6: 3.37 ± 0.79 pg/ml; Hcy: 8.25 ± 2.36 μmol/l). MMSE scores in AD were negatively correlated with cortisol, IL-6 and Hcy levels. Conclusions: Serum cortisol, IL-6 and Hcy levels are independent biomarkers for AD progression. Hypercortisolaemia, hyperhomocysteinemia and inflammation play important roles in AD-related cognitive dysfunction and are interlinked.

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Aims: The aim of this study was to investigate thyroid status in Alzheimer’s Disease (AD) patients and its response to donepezil and vitamin B12 supplement therapy for 6 months. Design: Case-Control Observational study. Place and Duration: Department of Biochemistry, GGMC & Sir J. J. Group of Hospitals, Mumbai, India between March 2017 and July 2019. Methodology: Case-Control study comprised of 71 AD patients and 70 healthy controls above 60 years of age.  Blood serum samples were analyzed for thyroid hormones levels by the chemiluminescence method. AD patients were treated with donepezil (5 mg/day) and vitamin B12 supplement (1.5 mg/day) and thyroid profile was observed at intervals of 3 and 6 months. Statistical evaluation was done by using IMB SPSS statistics version 25. Results: Serum levels of thyroid hormones were low in euthyroid AD patients when compared with controls at the baseline level [T3 (120.64 ± 20.64 vs 127.8 ± 17.29), T4 (7.71 ± 2.34 vs 7.54 ± 1.85), FT3 (1.2 ± 0.13 vs 2.26 ± 0.63) and FT4 (0.79 ± 0.08 vs 1.29 ± 0.27)] except TSH which was increased in AD [TSH (2.71 ± 1.19 vs 2.34 ± 0.65)]. During follow-ups at 3 and 6 months, there was a slight decrease in TSH levels in response to the therapy. Conclusion: The AD patients were euthyroid with low T3, FT3 and FT4 serum levels and high TSH serum levels. Thyroid hormones might play a role as markers for disease progression. Donepezil and vitamin B12 therapy could not benefit restore the normal thyroid functioning in a period of 6 months. Further longitudinal research with larger cohort might help in elucidating thyroid dysfunction in AD and develop novel therapeutic strategies.

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Background: In recent years, progress in Tuberculosis (TB) control and eradication has been threatened by the emergence of drug resistant strains of Mycobacterium tuberculosis (MTB). Several studies describe micronutrient malnutrition in TB. This study focuses on the effect of drug resistance and disease progression on levels of various vitamins.Methods: The case control study comprised of 50 normal healthy human volunteers (Control), 50 newly diagnosed TB patients (CAT I) and 50 TB patients showing multi drug resistance (MDR). Recruited subjects were of both genders in age group of 18- 60 years and from different socioeconomic status. Blood serum samples analysed for levels of Vitamin A, Vitamin D, Vitamin E, Vitamin C, Vitamin B12 and Folic acid by using Spectrophotometer, ELISA and Chemiluminescence instruments. Statistical evaluation was done for correlation among variables.Results: The levels of vitamins in TB patients were significantly reduced when compared with controls. Also, MDR-TB patients showed severe malnourished state in comparison to those who were newly diagnosed for the disease.Conclusions: There is a need to provide vitamin supplements in proper sufficient dosage with anti-TB drugs during treatment, which will help fight against the disease and ensure rapid recovery of the patients.