Evaluation of CD 4 and CD25 in hepatitis C virus patients with Graves and non-Graves diseases

Introduction: Graves' disease (GD), a kind of hyperthyroidism, an autoimmune thyroid disease is frequent in patients infected with HCV and the standard interferon-based treatment is related with high increase of the immune- mediated thyroid damageAim: The study aimed to determine the correlatio...

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Hauptverfasser: Al-ziadi, Abdullah Turki Abd, Mezher, Musa Nima, Darweesh, Mayyada F.
Format: Tagungsbericht
Sprache:eng
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Zusammenfassung:Introduction: Graves' disease (GD), a kind of hyperthyroidism, an autoimmune thyroid disease is frequent in patients infected with HCV and the standard interferon-based treatment is related with high increase of the immune- mediated thyroid damageAim: The study aimed to determine the correlation between CD4, CD25 and progression of GD Methods: A case-control study included 94 patients attending to endocrine and diabetic center in AL-Najaf province with group of 30 healthy individual as control. All patients classified into three groups based on the results of blood test for TPO-Ab, TSHR -Ab and infected or non- infected with HCV. Viral load were detected by Real-Time PCR, T4, T3, TSH, TSH R.Ab. and TPO.Ab. measured by using enzyme linked fluorescent assay (ELFA) technique. HCV, CD4 and CD25 level were measured by enzyme-linked immunosorbent assay (ELISA).Results: A positive TSHR and HCV was identified in 50 patients, 22 patients with positive TSHR and HCV negative, 22 patients with negative TSHR and HCV positive. The results revealed presence of HCV RNA in 72 (61.9%) with viral loads ranging from (26 × 102 -283 × 104)IU/ml and the male was recorded highest mean viral load, also this study shows levels of both CD4 and CD25 was increased in patient with Graves' disease and positive HCV.Conclusion: The present study concluded that the high concentration of inflammatory cytokines CD4. And CD25 play crucial role in pathogenesis of HCV that lead to GD and associated with an autoimmune thyroid disease
ISSN:0094-243X
1551-7616
DOI:10.1063/5.0029107