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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 5  |  Issue : 1  |  Page : 24-27

A follow-up study on adult patients with cirrhosis recruited in an open cohort from the hills of Himachal Pradesh


1 Department of Gastroenterology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India
2 Department of Medicine, Dr. Rajendra Prasad Government Medical College, Tanda, Kangra, Himachal Pradesh, India
3 Department of Medicine, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India
4 Department of Physiology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India

Date of Web Publication13-Jan-2016

Correspondence Address:
Sujeet Raina
C-15, Type-V Quarters, Dr. Rajendra Prasad Government Medical College Campus, Tanda, Kangra - 176 001, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-344X.173879

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  Abstract 

Aim: Cirrhosis is an important cause of morbidity and mortality in India. Global burden of diseases study estimated 1 million deaths due to liver cirrhosis in the year 2010 and out of which one-fifth occurred in India alone. The purpose of this study was to assess the clinical profile of cirrhosis in adults in a Tertiary Care Hospital in the Northern hilly state of Western Himalayas. Materials and Methods: A hospital-based prospective study was conducted in a Tertiary Care Center of Himachal Pradesh, located in the North of India from June 1, 2012 to May 31, 2013. In all 178 patients who were proved of cirrhosis on the basis of history, physical examination, biochemistry, and radiology and of age >18 years were included in the study. All the patients were closely followed for a maximum of 1 year after recruitment. Results: In this study, most of the patients were from age group 40 to 59 years (64.6%), and mean age was 51.2 ± 8.9 years. Most common cause for cirrhosis was alcohol which constituted 62.9% of total cases. Majority of patients (61.8%) presented to our hospital in Child-Turcotte-Pugh (CTP) Class C. Most common complication of cirrhosis at presentation was ascites which was present in 89.8% of the patients. One year mortality in CTP Class B was 23.2% and in CTP Class C was 55.5%. Conclusion: The study identified alcohol as the leading cause of cirrhosis affecting people in the state and most of the patients presented to the hospital in an advanced stage of cirrhosis.

Keywords: Ascites, cirrhosis, Himachal Pradesh, varices, Western Himalayas


How to cite this article:
Sharma B, Raina S, Marwah R, Sharma N, Kaushik M, Kaushal S. A follow-up study on adult patients with cirrhosis recruited in an open cohort from the hills of Himachal Pradesh. Int J Health Allied Sci 2016;5:24-7

How to cite this URL:
Sharma B, Raina S, Marwah R, Sharma N, Kaushik M, Kaushal S. A follow-up study on adult patients with cirrhosis recruited in an open cohort from the hills of Himachal Pradesh. Int J Health Allied Sci [serial online] 2016 [cited 2024 Mar 28];5:24-7. Available from: https://www.ijhas.in/text.asp?2016/5/1/24/173879


  Introduction Top


The high mortality of end-stage liver disease is a global public health problem. In India, mortality due to liver cirrhosis increased from 77,741 in 1980 to 188,575 in 2010. One-fifth of global liver cirrhosis deaths in 2010 occurred in India alone.[1] In 2012, as per the WHO age-standardized death rates due to liver cirrhosis in India among males and females are 39.5 and 19.6, respectively, out of which alcohol attributable fractions constitute 62.9% and 33.2%, respectively.[2] Although many prognostic models have been proposed in the last two decades to predict mortality in cirrhosis, the Child-Turcotte-Pugh (CTP) score is by far the most largely used both in clinical practice and in clinical research.[3] One-year survival rates for patients with CTP A, B, and C cirrhosis are 100, 80, and 45%, respectively.[4] Hepatic encephalopathy develops in 50–70% of patients with cirrhosis and its occurrence is an indicator of a poor prognosis, with projected 1- and 3-year survival rates of 42% and 23%, respectively, without liver transplantation.[5] Epidemiological data on the clinical profile, natural course, and survival is insufficient and has not yet been reported from Himachal Pradesh so far. Therefore, this study was planned and conducted in a Tertiary Care Hospital providing gastroenterology services in Himachal Pradesh, India, located in Western Himalayas.


  Materials and Methods Top


This prospective study was conducted in a Tertiary Care Center of Himachal Pradesh. The patients were recruited from June 1, 2012 to May 31, 2013. All indoor patients where the diagnosis of cirrhosis was established on the basis of history, physical examination, biochemistry, virological markers, serology, upper gastrointestinal (GI) endoscopy, radiology (at least one clinical symptom or sign of hepatocellular failure and one symptom or sign of portal hypertension along with ultrasound evidence of liver cirrhosis) and of age >18 years were included in the study. Patients on immunosuppressant drugs and unwilling to participate in the study were excluded. A questionnaire regarding risk factors was included in detailed history which included: Detailed alcohol history including amount and duration of alcohol intake, blood transfusion, surgery, needle prick, tattoo, and high-risk behavior. A detailed examination was performed in every case, and clinical presentation was recorded. Complete hemogram, liver function tests, renal function tests, blood glucose, virologic markers such as hepatitis B surface antigen (HBsAg) and antihepatitis C virus (HCV) antibody by immunochromatographic rapid card test was done in each patient.

Ascitic fluid biochemistry and cytology were performed in every patient with ascites. Serological markers such as antinuclear antibodies, antibody against liver-kidney-microsomes, antismooth muscle antibodies, and immunoglobulin A tissue transglutaminase antibody were done on the basis of clinical profile and if indicated. Serum ceruloplasmin, urinary copper levels, and slit lamp examination for Kayser–Flesher ring was done if indicated. All obese patients in whom other etiology of cirrhosis was ruled out were placed under nonalcoholic steatohepatitis (NASH) as a possible cause for cirrhosis. Ultrasound abdomen was done in all patients followed by computed tomography (CT) if the ultrasound was inconclusive or there was evidence of hepatocellular carcinoma (HCC). Upper GI endoscopy was performed in all patients unless contraindication was present. The severity of cirrhosis was assessed with CTP classification as shown in [Table 1].[3] All the patients were closely followed for a maximum of 1 year after recruitment. Various events such as jaundice, ascites, variceal bleeding, spontaneous bacterial peritonitis (SBP), encephalopathy, and death occurring during follow-up were recorded. The study was approved by the College Ethics Committee.
Table 1: Child-Pugh classification of cirrhosis

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  Results Top


The study included a total number of 178 patients; 124 (69.7%) were males and 54 (30.3%) were females, whereas 78.6% belonged to rural areas and 21.4% were from urban areas. A total of 115 (64.6%) patients were in the age group of 40–59 years. Mean age was 51.2 ± 8.9 years. The age distribution and causes of cirrhosis observed with their frequency are shown in [Figure 1]. CTP classification was done in all patients. One hundred and ten (61.8%) patients presented to our hospital in CTP Class C cirrhosis as shown in [Figure 2]. Upper GI endoscopy showed varices in 154 (86.5%) patients whereas fundal and cardiac varices were uncommon and were present in 3.2% and 1.9% of patients, respectively. Evidence of ascites was present on ultrasonography or CT scan of the abdomen in 89.8% of patients. Hepatic encephalopathy was present in 124 (69.7%) of patients in our study. Forty-eight (27.0%) patients presented with variceal bleed. Thirty-three patients were in CTP Class C cirrhosis. SBP was present in 44 (24.7%) of patients. Thirty-nine were in CTP Class C and five patients were in CTP Class B cirrhosis. While no patient in CTP Class A cirrhosis had SBP. Evidence of HCC was present in three patients. All patients were HBsAg positive. Of the total 178 patients included in our study, 25 patients were readmitted twice, 19 of them were in CTP Class C cirrhosis, and five patients were readmitted thrice, three of them were in CTP Class C cirrhosis in our study. Presentations during readmission were: Jaundice (26%), ascites (29%), SBP (9%), variceal bleed (11%), and hepatic encephalopathy (30%). In our study, 30 (16.8%) patients died during their first admission whereas 148 patients were discharged. All 30 patients were in CTP Class C cirrhosis. The causes of death in were variceal bleed in 13 patients, sepsis in 12 patients and liver failure in seven patients. Two of these patients had variceal bleed as well as evidence of sepsis. During 1 year follow-up, 45 more patients died. Thirty-one (38.7%) belonged to CTP Class C cirrhosis, 13 (23.2%) in CTP Class B cirrhosis, and one (8.3%) in CTP class cirrhosis. Nineteen (12.8%) were lost in follow-up as shown in [Table 2]. One year survival in CTP Class C cirrhosis was 33.6%, 64.2% in CTP Class B cirrhosis, and 91.6% in CTP Class A cirrhosis.
Figure 1: Bar chart showing age distribution and etiology of cirrhosis

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Figure 2: Pie chart showing Child-Turcotte-Pugh classification at admission

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Table 2: Overall mortality during hospitalization and 1-year follow-up

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  Discussion Top


The course of cirrhosis is extremely variable from patient to patient due to several factors, including hepatic synthetic function, the cause of cirrhosis, and the occurrence of liver malignancy. Therefore, establishing a prognosis in a given patient with cirrhosis remains a challenging issue.[6] Cirrhosis mortality has been steadily increasing in India since 1980, as has alcohol consumption, prevalence of hepatitis B and C, and diabetes (a major risk factor for nonalcoholic fatty liver disease).[1] In the present study, only 21 (11.7%) patients belonged to <39 years age which is much below than observed in other studies.[7] The reason is that cirrhosis below the age of 40 years is commonly due to either Wilson's disease, autoimmune hepatitis, inferior vena cava and/or hepatic vein obstruction (Budd–Chiari syndrome), and perinatal or childhood infection with hepatitis B. Only seven patients had cirrhosis due to autoimmune hepatitis, and one patient had Wilson's disease. None of the patients was diagnosed as Budd–Chiari in our study. Alcohol was the leading cause in (62.9%) followed by hepatitis B as the second most common cause (10.1%) for cirrhosis. This is at variance with reports from other parts of India.[8],[9] According to the alcohol  Atlas More Details of India, the prevalence of alcohol use among men in Himachal Pradesh is between 25% and 49%.[10] Liquor consumption is perceived as a part of the social and religious life of the tribal population of Himachal Pradesh.[11] The prevalence of HBV estimated in Himachal Pradesh is 0.536 (confidence interval 0.135–0.937).[12] NASH was the third most common cause of cirrhosis in our study. Metabolic syndrome has emerged as a significant health concern as was observed in the newly diagnosed hypertensive patients in the state reflecting the epidemiological transition experienced in this hilly region.[13] Hepatitis C is not a common cause of cirrhosis in this region possibly because of low prevalence area. A study has shown the relative absence of HCV infection in Shimla.[14] Majority of patients (61.8%) presented to our hospital in CTP Class C. This reflects that most of the patients presented to the hospital in advanced stage of cirrhosis.

Most common complication of cirrhosis at presentation was ascites which was present in 89.8% of the patients. It was followed by varices in 154 (86.5%) patients, hepatic encephalopathy in 124 (69.7%) patients, variceal bleed in 48 (27.0%) patients, and SBP in 44 (24.7%) of patients. Ascites is the major complication of cirrhosis, occurring in 50% of patients over 10 years of follow-up.[15] The presence of gastroesophageal varices correlates with the severity of liver disease. Varices are documented in 40% patients with CTP Class A and in 80% with CTP Class C. Approximately, 30% of patients with esophageal varices will bleed within the 1st year after diagnosis.[16] Overt hepatic encephalopathy occurs in approximately 30–45% of cirrhotic patients.[17],[18] The prevalence of SBP in hospitalized patient ranges between 10% and 67%.[19],[20],[21],[22] Among the patients, mortality during the first admission was 16.9%. All patients were in CTP Class C. This suggests high mortality in patients with the advanced liver disease. Cause of death in our study was variceal bleed in 43.3%, sepsis in 40%, and liver failure in 23.3%patients. A study done by Sarin et al. reported GI bleeding (52%) as a leading cause of death among young cirrhotics followed by terminal liver failure (40%), whereas, in adults, terminal liver failure (63.8%) was a leading cause of death followed by GI bleeding (25.5%).[7] We also followed up patients for a maximum period of 1 year. One patient from CTP Class A cirrhosis and 13 (23.2%) patients from CTP Class B progressed to CTP Class C cirrhosis during the study period.

At follow-up after 1 year, further 45 patients died. Overall mortality was 42.1%. One year survival in CTP Class C cirrhosis was 33.6%, 64.2% in CTP Class B cirrhosis, and 91.6% in CTP Class A cirrhosis.

Our results were similar to the studies done before which have reported 1-year mortality in various CTP class. Expected 1-year survival in CTP Class A, CTP Class B, and CTP Class C is 100%, 80%, and 45%, respectively.[3],[23] In a systematic review of 118 studies, 1-year cumulative survival in CTP Class A was 95%, CTP Class B was 80%, and CTP Class C was 45%.[24]

Limitation of our study was that being a hospital-based study; etiology of cirrhosis observed in our study may not reflect the etiological spectrum of cirrhosis of the state. Second, in our study NASH was considered as a possible cause for cirrhosis in obese patients in whom no other etiology was established. However, liver biopsy was not done in these patients to confirm the diagnosis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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Mokdad AA, Lopez AD, Shahraz S, Lozano R, Mokdad AH, Stanaway J, et al. Liver cirrhosis mortality in 187 countries between 1980 and 2010: A systematic analysis. BMC Med 2014;12:145.  Back to cited text no. 1
    
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Trimukhe R, Rai R, Narayankar SM, Shewale S, Jagtap N, Rai S, et al. Epidemiological spectrum of chronic liver disease in eastern Madhya Pradesh India. J Assoc Physicians India 2011;59:48.  Back to cited text no. 9
    
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Bali R, Gupta R, Chand M, Chauhan JK. Alcoholism – A social evil among the tribals of Kinnaur District of Himachal Pradesh. J Farm Sci 2011;1:137-44.  Back to cited text no. 11
    
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Batham A, Gupta MA, Rastogi P, Garg S, Sreenivas V, Puliyel JM. Calculating prevalence of hepatitis B in India: Using population weights to look for publication bias in conventional meta-analysis. Indian J Pediatr 2009;76:1247-57.  Back to cited text no. 12
    
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Thakur S, Raina S, Thakur S, Negi PC, Verma BS. Prevalence of metabolic syndrome among newly diagnosed hypertensive patients in the hills of Himachal Pradesh, India. Indian J Endocrinol Metab 2013;17:723-6.  Back to cited text no. 13
    
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Ganju SA, Goel A. Hepatitis C virus activity in Shimla - a preliminary report. Indian J Med Microbiol 2001;19:227.  Back to cited text no. 14
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Ginés P, Quintero E, Arroyo V, Terés J, Bruguera M, Rimola A, et al. Compensated cirrhosis: Natural history and prognostic factors. Hepatology 1987;7:122-8.  Back to cited text no. 15
    
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Prasad S, Dhiman RK, Duseja A, Chawla YK, Sharma A, Agarwal R. Lactulose improves cognitive functions and health-related quality of life in patients with cirrhosis who have minimal hepatic encephalopathy. Hepatology 2007;45:549-59.  Back to cited text no. 18
    
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Almdal TP, Skinhøj P. Spontaneous bacterial peritonitis in cirrhosis. Incidence, diagnosis, and prognosis. Scand J Gastroenterol 1987;22:295-300.  Back to cited text no. 19
    
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    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2]


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