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Research Article | Volume 30 Issue 7 (July, 2025) | Pages 308 - 312
A Study of Clinical and Biochemical Profile in Hepatitis C and its Correlation with HCV RNA Titre for Disease Severity
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1
Senior Resident, Department of General Medicine, Medical College and SSG Hospital, Vadodara
2
Associate Professor, Department of General Medicine, Medical College and SSG Hospital, Vadodara
3
Assistant Professor, Department of Medicine, GRMC Gwalior, M.P.
4
H.O.D of Department, Department of General Medicine, Medical College and SSG Hospital, Vadodara
5
Assistant Professor, Department of General Medicine, Medical College and SSG Hospital, Vadodara.
Under a Creative Commons license
Open Access
Received
June 17, 2025
Revised
July 4, 2025
Accepted
July 25, 2025
Published
July 30, 2025
Abstract

Background & Methods: The aim of the study is to study of clinical and biochemical profile in hepatitis c and its correlation with HCV RNA Titre for disease severity. HCV Antigen positive patient attending inpatient and out-patient of Medicine Department. Results: Correlation between TC and HCV titer. It is not showing statistically significant correlation between TC and HCV titer. (correlation coefficient r =0.3950, p= 0.0106). Correlation between PC and HCV titer. There is no statistically significant correlation found between PC and HCV titer. (correlation coefficient r =-0.1082, p= 0.5009). There was no significant correlation between the HCV RNA LOAD and any biochemical markers in Acute as well as Chronic Hepatis C infection in my study. Conclusion: In our study most of the patients with HCV RNA detected level has no statistically significant correlation with Patient Clinical Profile and Biochemical Profile. Clinical and Biochemical profile has more predictive value than HCV RNA level. So Early Detection and Early treatment with Directly Acting Antiviral agents can improve the patient and prevent it from the further complication.

Keywords
INTRODUCTION

Hepatitis C virus (HCV), which is previously known as a non-A, non-B hepatitis, HCV is a linear, single-strand, positive-sense, 9600-nucleotide RNA virus[1]. Hepatitis C infection is usually acquired through infected syringes and needles, and transfusion of infected blood, Sexual transmission of HCV occurs infrequently in heterosexual couples, it‘s estimated overall prevalence of nearly 3%. Approximately 80% patients with hepatitis C virus develop chronic infection, and progression to cirrhosis occurs in nearly 20% of these subjects[2].

 

Moreover, patients with HCV-related cirrhosis are at an increased risk of developing hepatocellular carcinoma, which is estimated to occur at the rate of 1.5% to 4% per year. In most individuals, liver disease progresses slowly over several decades, but the rate of progression is highly variable. Whereas some patients develop cirrhosis and end-stage liver disease within one to two years of exposure, others may die of old age or an entirely unrelated cause[3].

Although it is mostly unclear why some patients progress more rapidly than others, several factors have been identified as having a role in disease severity. HCV patients co-infected with hepatitis B virus (HBV) have an increased risk of developing cirrhosis and decompensated liver disease as well as hepatocellular carcinoma. Several researches have noted more severe clinical and histological abnormalities in HCV infected chronic alcoholics compared to non-alcoholics with HCV infection[4-5]. Other factors associated with a more rapid course of liver disease include age at acquisition of HCV infection, gender of the patient and presence of immunodeficiency states[6].

 

Several studies have assessed the correlation between serum HCV viral titers and different clinical and laboratory parameters. Several studies demonstrate a statistically significant correlation of aminotransferase values with the histological parameters, and even stronger correlation with AST values with liver damage. Hence the biochemical markers and HCV RNA LOAD are the important predictor for acute and chronic infection also development of liver cirrhosis[7].

MATERIALS AND METHODS

This was a Cross section observational study conducted over 10 months duration between March 2022 to December 2022 in SSG HOSPITAL, Vadodara, Gujarat, India. Ethical committee approval was obtained from The Institutional Ethics Committee for Human Research- PG Research (IECHR-PGR) to carry out this study on 28 February 2022. Once patient met the inclusion criteria, Informed written consent were taken before the enrolment of the patients.

 

Inclusion Criteria:

  1. The patients with HCV antigen positive aged 18 -60 years attending medicine in and out patient department
  2. The patients with HCV RNA viral load detection
  3. Subject who is willing to give consent for the study

 

Exclusion Criteria:

  1. Subjects less than 18 years and more than 60 years of age.
  2. Subjects with liver cirrhosis due to any other cause like non-alcoholic fatty liver disease, auto immune liver cirrhosis, Hepatitis B.
RESULT

Table 1: Socio demographic Details of Patients

 

The age group and gender wise distribution of patients. The age and gender wise distribution of patients are calculated in frequency and percentage. Majority of the patients belong to age group of 51-60 years. Number of patients is same in age group of 18-30 and 41-50 years.

 

Table 2: Symptoms of Patients

 

 

Different symptoms in patients with Hepatitis C infection. Frequency and percent are calculated for each symptoms. Almost 95% percent patients present with anorexia followed by nausea (65%), yellowish discoloration skin (52.50%), vomiting (40.00%). Other symptoms like pedal edema (20%), abdominal distention (15%), Hematemesis (12.50%) present in some patients. Very few patients present with the symptoms like decrease urine output (10%) and altered sensorium (5%).

 

Table 3: Correlation Coefficient of HB and HCV RNA Load

 

Correlation between HB and HCV titer. There is no statistically significant correlation found between HB and HCV titer. (correlation coefficient r =-0.1078, p= 0.50220)

 

Table 4: Correlation Coefficient of TC and HCV RNA Load

 

Correlation between TC and HCV titer. It is not showing statistically significant correlation between TC and HCV titer. (correlation coefficient r =0.3950, p= 0.0106)

Table 5: Correlation Coefficient of PC and HCV RNA Load

 

Correlation between PC and HCV titer. There is no statistically significant correlation found between PC and HCV titer. (correlation coefficient r =-0.1082, p= 0.5009)

DISCUSSION

Hepatitis C virus (HCV) is a blood borne pathogen that is endemic in most parts of the world, with an estimated overall prevalence of nearly 3%. Approximately 80% patients with hepatitis C virus develop chronic infection, and progression to cirrhosis occurs in nearly 20% of these subjects. Several studies have assessed the correlation between serum HCV viral titres and different clinical and laboratory parameters[8].

 

Majority of the patients belong to age group of 51-60 years. Number of patients is same in age group of 18-30 and 41-50 years. We have 53% female and 47% male patients. Percentage of female patients is slightly more than male patients[9].

 

A study was done by Cohen JM et al with aim of finding risk factor for hepatitis C. He found out that Hepatitis was more common in the age group of 40-59 year of age group. Our study findings are also similar to the findings of this study and we have more patients in the age group of 51-60 years and 41-50 years of age group[10]. The same study did not find any association between gender and disease occurrence.

 

A study done by Meda N et al aimed to find out the seroprevalence of hepatitis C virus had revealed that maximum Hepatitis C virus prevalence was present in the age group of 41-49 years of age group.

 

Almost 95% percent patients present with anorexia followed by nausea (65%), yellowish discoloration of skin (52.50%), vomiting (40%). Other symptoms like pedal edema (20%), abdominal distention (15%), Hematemesis (12.50%) present in some patients. Very few patients present with the symptoms like decrease urine output (10%) and altered sensorium (5%). Signs of Hepatitis pallor and icterus were also present in some patients in this study[11]. The symptoms observed in the study were similar to that of standard clinical presentation of Hepatitis C available in literature.

 

In a study done by Alsaran KA et al they had found out that mean Haemoglobin is more among patients diagnosed with Hepatitis C. On the other hand, we were not able to correlate Haemoglobin with the HCV RNA virus[12]. Therefore, it is difficult to comment upon correlation of HCV RNA virus and Haemoglobin

CONCLUSION

In our study most of the patients with HCV RNA detected level has no statistically significant correlation with Patient Clinical Profile and Biochemical Profile. Clinical and Biochemical profile has more predictive value than HCV RNA level. So Early Detection and Early treatment with Directly Acting Antiviral agents can improve the patient and prevent it from the further complication.

REFERENCE
  1. Almazroo OA, Miah MK, Venkataramanan R. Drug Metabolism in the Liver. Clin Liver Dis. 2017 Feb;21(1):1-20.
  2. Stec DE, John K, Trabbic CJ, Luniwal A, Hankins MW, Baum J, Hinds TD. Bilirubin Binding to PPARα Inhibits Lipid Accumulation. PLoS One. 2016;11(4):e0153427. [PMC free article]
  3. Sticova E, Jirsa M. New insights in bilirubin metabolism and their clinical implications. World J Gastroenterol 2013; 19: 6398–6407.
  4. Erlinger S,  Arias  IM,  Dhumeaux    Inherited  disorders  of bilirubin transport and conjugation: new insights into molecular mechanisms and consequences. Gastroenterology 2014; 146: 1625–1638.
  5. Fanali G, di Masi A, Trezza V et al. Human serum albumin: from bench to bedside. Mol Aspects Med 2012; 33: 209–290.
  6. Hartmann M,  Szalai  C,  Saner     Hemostasis  in  liver transplantation: pathophysiology, monitoring, and treatment. World J Gastroenterol 2016; 22: 1541–1550.
  7. Friedman SL: Hepatic stellate cells: protean, multifunctional and enigmatic cells of the liver, Physiol. Rev. 88:125, 2008.
  8. Pawlotsky JM. Virology of hepatitis B and C viruses and antiviral targets. J Hepatol 2006; 44(1 Suppl): S10–S13.
  9. Soi V, Daifi C, Yee J, Adams E. Pathophysiology and Treatment of Hepatitis B and C Infections in Patients With End-Stage Renal Disease. Adv Chronic Kidney Dis. 2019 Jan;26(1):41-50. [PubMed]
  10. Horner SM, Gale M Jr. Intracellular innate immune cascades and interferon defenses that control hepatitis C virus. J Interferon Cytokine Res 2009; 29(9): 489–498.
  11. Hishiki T, Shimizu Y, Ujino S et al. Lipid and lipoprotein components play important roles the egress and infectivity of hepatitis C virions. In: Miyamura T, Lemon SM, Walker CM, Wakita T, eds. Hepatitis C Virus I: Cellular and Molecular Virology. Tokyo: Springer Japan, 2016, pp. 255–272
  12. Rehermann B, Bertoletti A. Immunological aspects of antiviral therapy of chronic hepatitis B virus and hepatitis C virus infections. Hepatology 2015; 61(2): 712–721.
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