Journal of Ecophysiology and Occupational Health

Amit Kumar ¹, Md Arshad ², Ajai Singh ³, Asif Jafri ⁴, Sabir Ali ⁵, Manish Yadav ⁵, Suchit Swaroop ¹

Affiliations
1 Experimental and Public Health Laboratory, Department of Zoology, University of Lucknow, Lucknow – 226007, IN
2 Molecular Endocrinology Lab, Department of Zoology, University of Lucknow, Lucknow-226007, IN
3 Department of Orthopaedics, King George Medical University, Lucknow – 226003, IN
4 Molecular Endocrinology Lab, Department of Zoology, University of Lucknow, Lucknow – 226007, IN
5 Department of Orthopedics, King George Medical University, Lucknow – 226003, IN

Abstract

Osteoarthritis (OA) is considered as multifactorial disorder characterized by erosion of articular cartilage, tightening of joint space, subchondral bone remodelling and internal synovial inflammation. OA reduces joint function progressively as a person gets older. The most important group of the cytokines or chemokines are pre-dominantly involving in the early progression of the disease includes IL-1, IL-6, IL-18 and TNF-a, etc. IL-1 family of cytokines are known to be strongest stimulus for progressive synthesis of Matrix Metallo Proteinases (MMPs). Large number of immune cells, chondrocytes and endothelial cells potentially secrete IL-1 with diverse effect on number of diseases. This review highlights the association of IL-1 family cytokine in OA.

Keywords

Cytokine, IL-1 Family, Mode of Action, Osteoarthritis.

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Amit Kumar ¹, Md Arshad ², Ajai Singh ³, Habiba Khan ², Suchit Swaroop ¹

Affiliations
1 Department of Zoology, Experimental and Public Health Laboratory, University of Lucknow, Lucknow − 226007, IN
2 Department of Zoology, Molecular Endocrinology Lab, University of Lucknow, Lucknow − 226007, IN
3 Department of Orthopaedics, King George Medical University, Lucknow − 226003, IN

Abstract

Osteo-Arthritis (OA) is a disease of joints affecting the normal functions of joint and causes physical disability. Many factors are responsible for development of osteoarthritis including over age, obesity, gender, drug abuse, over load on joints and genetic factors. OA causes health problems and impairs the quality of life with increased economic burden across the world. Apart from the pro-inflammatory role of cytokine Interleukin-1 (IL-1) in osteoarthritis, Tumor necrosis factor-alpha (TNF-α) is also involved in the progression of osteoarthritis. Members of TNF family are secreted from lymphocytes and natural killer cells but in OA patients it is also secreted from chondrocyte cells to influence the catabolic processes in Extra Cellular Matrix (ECM) by inducing the activity of matrix metaloproteinases (MMPs). In promoter region, most of the Single nucleotide polymorphisms (SNPs) of TNF-α located on -863, -857, -308, and -238. These SNPs are involved in various diseases including OA, rheumatoid Arthritis, systemic lupus erythematosus etc. Significance association of SNP -G308A of the TNF-α gene in OA has been observed in various studies. Aim of this mini review is to conclude the fundamental roles of TNF-α cytokine in patients with OA.

Keywords

Cytokine, Gene Variants, Osteoarthritis, Pathophysiology, TNF-α.

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Amar Deep ¹, Ajay Kumar ², Sumit Rungta ³, Suchit Swaroop ¹

Affiliations
1 Experimental and Public Health Laboratory, Department of Zoology, University of Lucknow, Lucknow – 226007, Uttar Pradesh, IN
2 Department of Medicine, King George’s Medical University, Lucknow – 226003, Uttar Pradesh, IN
3 Department of Medical Gastroenterology, King George’s Medical University, Lucknow – 226003, Uttar Pradesh, IN

Abstract

Background and Aims: The goal of Hepatitis C Virus infection treatment is to remove the virus, to avoid advancement of Hepatitis C Virus (HCV) infection and progression of related disease such as liver cirrhosis and hepatocellular carcinoma and to achieve End of Treatment Response (ETR) with 12-week therapy and Sustained Virological Response (SVR) at post-treatment week 12 (SVR-12), which is defined as undetectable HCV RNA at 12 weeks post ETR. In the Compassionate Use Program (CUP) in Europe, Sofosbuvir (SOF) and Daclatasvir (DCV) were used in all genotypes and achieved SVR-12. Aims: Our aim is to compare the efficacy and effectiveness of Sofosbuvir and Daclatasvir in the treatment of HCV infection in the patients who could not afford for the investigating of HCVGenotype and to those in whom genotyping was done. Methods: Group 1 includes ten patients, given Sofosbuvir and Daclatasvir without genotype and group 2 includes nine patients, given Sofosbuvir and Daclatasvir with genotype. The patient group selection was done using a randomized table generated by using excel. All the patients in the groups completed the twelve weeks treatment with twelve weeks and twenty-four weeks of follow up. All the nineteen patients were given Sofosbuvir and Daclatasvir for twelve weeks and the endpoint of therapy was marked by undetectable HCV-RNA in blood by ETR-12 (end of treatment response), Sustained Virological Response at post-treatment week 12 (SVR-12) and Sustained Virological Response at post-treatment week 24 (SVR- 24). Results: Quantitative HCV-RNA (IU/ml) by RT-PCR was undetectable in all the patients in both groups at the end of treatment (ETR-12) and SVR-12- and SVR-24-weeks follow-up after completion of treatment i.e. Sofosbuvir and Daclatasvir has 100% ETR-12, SVR-12 and SVR-24 in both the groups. Conclusion: If patients do not investigate for genotype and use the Sofosbuvir and Daclatasvir in HCV infected patients, there is no effect on outcome ETR. This will reduce the risk of late stage complications such as liver cirrhosis and hepatocellular carcinoma and will also leads to the economic benefits such as no extra burden on patients.

Keywords

Cirrhosis, End of Treatment Response (ETR), Hepatocellular Carcinoma (HCC), Sofosbuvir and Daclatasvir (SOF+DCV), Steatosis, Sustained Virological Response (SVR).

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