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Prevalence of diabetes mellitus Type 2 in patients with chronic hepatitis c virus infection.

INTRODUCTION: Hepatitis C virus (HCV) infection is one of the main causes of chronic liver disease worldwide.[2] The long-term hepatic impact of chronic HCV infection is highly variable, with pathological conditions ranging from minimal hepatic changes to chronic hepatitis, extensive fibrosis and cirrhosis with or without hepatocellular carcinoma (HCC).[3]

Although HCV mainly targets the liver, it has become interestingly evident that HCV can induce damage of many organs. Cacoub et al.[4] reported that 38% of patients with HCV would manifest at least one extrahepatic manifestation during the illness. Extrahepatic (EH) manifestations associated with HCV infection include endocrinological manifestations such as diabetes mellitus (DM)[5] and thyroiditis,[6] rheumatologic manifestations such as arthralgias, arthritis[7] and cutaneous manifestations like essential mixed cryoglobulinemia, porphyrea cutanea tarda, lichen planus, sjogren syndrome,[8] and others like glomerulonephritis[9] and metabolic syndrome.[10]

Diabetes Mellitus Type 2 is a major public health problem worldwide as people become more obese and live a more sedentary lifestyle.[11] This is in agreement with studies on T2D in non-infected individuals as well as patients infected with HCV genotypes. The following risk factors are strongly associated with Diabetes Mellitus Type 2: family history, body fat distribution, age, sex, smoking, and physical activity.[12] Several studies from different parts of the world have found that 13% to 33% of patients with chronic HCV have associated diabetes, mostly type 2 DM.[13]

Various pathogenic mechanisms have been studied for the diabetogenic action of HCV. Honeyman et al. found that HCV could trigger an immune reaction against the (P-cells by molecular mimicry, because HCV shares regional amino acid homology with GAD autoantibody (GADA), one of the main islet cell antigens.[14] Direct damage to beta cells of pancreas is the another proposed mechanism. Laskus et al.[15] documented the presence of HCV-RNA in the pancreas acinar cells and in the epithelial cells of the pancreatic duct. Mendler MH et al speculated that iron stores are the link between HCV infection and diabetes,[16] while hepatic steatosis may also contribute to HCV-associated diabetes by impairing the insulin's ability to lower hepatic glucose production and favoring liver fibrosis.[17]

This association between HCV infection and diabetes was for the first time made by Allison et al. in 1994 and was formally tested by a retrospective review of 100 consecutive adult patients with cirrhosis undergoing assessment for liver transplantation. Of the 34 patients with hepatitis C virusrelated cirrhosis, 17 (50%) had diabetes mellitus, in contrast to just six (9%) of the 66 patients with cirrhosis unrelated to hepatitis C virus (chi2 = 19.1, p < 0.0001) with an odds ratio for hepatitis C virus by diabetes mellitus status 10.0 (95% confidence interval 3.4 to 29.3).[18]

In an another Egyptian case control study by Eman I Elhawary et al. 289 HCV patients older than 18 were selected as cases. Also, 289 healthy controls were included. Out of 289 HCV cases, 40 (13.84%) were diabetic. Out of 289 healthy controls, 12 (4.15%) were diabetic.[19] Similarly in a study by Chehadeh et al.[20] study population consisted of 181 HCV positive cases and 170 HCV negative controls. The prevalence of type 2 diabetes among the cases was 39.8%.

Given the high spreads of Metabolic Syndrome and Chronic Hepatitis C, the chances of coexistence of these two conditions in a single patient are elevated. Nevertheless, this overlap is not simply coincidental, but many experimental[21] and clinical[22] studies have suggested how HCV infection itself seems to be able to perturb glucose homeostasis, leading to hepatic and extrahepatic Insulin resistance. The association of hepatitis C infection and diabetes is present, in fact, even before the onset of cirrhosis[23,24] and diabetes does not associate with other viral conditions such as hepatitis B.[25] The high prevalence of diabetes in HCV-infected patients, and its occurrence at early stages of hepatic disease, suggest that screening for glucose abnormalities should be indicated in these patients.

The correlation is not unidirectional as chronic HCV infection is able to influence glucose and lipid metabolism and thus to perturb the metabolic homeostasis of the host leading to extrahepatic consequences. On the other hand the risk of progression from chronic HCV infection to cirrhosis and its clinical outcomes is highly variable and hyperglycemia, is believed to accelerate disease progression and to impact the likelihood of sustained virological response (SVR) after pegylated interferon/ribavirin therapy.[26]

The rationale behind this study is to find out the prevalence of type 2 diabetes in those patients who have chronic hepatitis C virus infection in comparison to general population and to establish the co-relation between stage of infection and type 2 diabetes mellitus in the seropositive HCV patients.

MATERIALS AND METHODS: In this study, a total of 50 ELISA positive chronic hepatitis C patients aged more than 18 years attending the OPD/ Indoor of SGRDIMSAR for routine health checkup formed the case group. An equal number of age and sex matched patients with normal liver function tests, no serological evidence of HCV served as the control group.

After taking relevant history and consent of the patient, fasting and random blood sugar levels were done as a screening tool to diagnose Diabetes Mellitus. Patients already diagnosed diabetics whether or not on therapy were also included in the study.

According to the American Diabetes Association criteria27 patients were assigned a diagnosis of Diabetes Mellitus if;

1. HBA1C>=6.5% or,

2. fasting plasma glucose greater than 126 mg/dl; fasting is defined as no calorie intake for at least 8 hours, or

3. 2-h plasma glucose>=200mg/dL (11.1mmol/L) during an OGTT. The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.

4. In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose >=200 mg/dL (11.1 mmol/L).

The diagnosis of HCV infection was made if patients were positive for anti-HCV antibody by second/third generation microparticle enzyme immunoassay test. Serological analysis for the detection of anti-HCV antibodies was carried out using accurate rapid immunochromatographic kits. Positive cases were later confirmed by using third generation ELISA kit (EliscanATM HCV by Diagnova) for the qualitative determination of antibodies to Hepatitis C Virus in human serum or plasma.

All patients were subjected to detailed history taking including demographic data(age, sex, family history of diabetes, history of alcohol intake), clinical examination and laboratory examination which included haemoglobin level, fasting and post prandial blood glucose, liver profile, serum proteins, glycosylated haemoglobin and ultrasound abdomen.

RESULTS: Of the 100 patients included in the study, 54% were females and 46% were males. 74% patients were from rural area while 26% belonged to urban area. 50 patients were HCV seropositive and served as cases. The remaining 50 were HCV seronegative and served as controls.

a) CASES AND CONTROLS: The comparison between cases and the controls showed that the mean age of cases was 49.88 + 13.709 years while the mean age of controls was 50.74 + 14.267 years which was higher than the cases but the difference was not statistically significant (p = 0.7592). The mean BMI of cases was 24.5592 + 2.736 kg/ [m.sup.2] and 40 % (20 out of 50) of the cases had BMI > 25 kg/ [m.sup.2] while the mean BMI of the controls was 23.3546 + 2.997 kg/[m.sup.2] and only 24 % (12 out of 50) controls had BMI > 25 kg/[m.sup.2]. The difference of the mean BMI among the cases and controls was statistically significant (p = 0.0384)

52% (n= 26) of the cases were anaemic while only 38% (n= 19) controls were found to have anaemia. This difference was not found to be statistically significant (p= 0.16). The mean Hb of cases was 9.738+ 2.442 gm% while the mean Hb of the controls was 10.12 + 2.108 gm %. The difference of means was not statistically significant (p= 0.4045). 22 % (11 out of 50) of the cases were found to have thrombocytopenia which was statistically significantly higher than the control group (1 out of 50); (p= 0.004).

58 % (29 out of 50) of the cases had hypoalbuminemia (Serum albumin <3 gm/dl) as compared to 34 % (17 out of 50) of the controls. Statistically the difference was significant (p= 0.016). The mean serum albumin of the cases (3.056 + 0.8054) was significantly lower than the controls (3.43 + 0.9237); (p= 0.0334).

18% (n= 9) of the cases were found to have prolonged prothrombin time as compared to the 2% (n=1) of the controls and this difference is statistically significant (p= 0.008). The difference in the mean value of PT prolongation (in seconds) between the cases and control group was also statistically significant (p=0.003).

The thrombocytopenia, hypoalbuminemia and the prolongation of Prothrombin time could be explained by the underlying liver parenchymal injury in patients with chronic hepatitis C virus infection.

The prevalence of diabetes mellitus among the cases was 50% (25 out of 50) while the prevalence among the controls was 30 % (15 out of 50). The difference was statistically significant higher (p=0.041).

Among the cases it was found that the prevalence of diabetes increased with increasing severity of the underlying liver disease. 40.9% in the HCV seropositive patients without cirrhosis had diabetes mellitus which was higher than the percentage of diabetics in the HCV seronegative control group (15 out of 50; 30 %). 57.1 % of the HCV seropositive patients with cirrhosis had diabetes mellitus. Further among those having cirrhosis, 6 belonged to Child Pugh Class-A out of which 50% (n=3) had diabetes and 22 belonged to Child Pugh Class-B out of which 59.1% (n=13) were diabetic. This strengthens the relationship of increasing degrees of liver damage being associated with increasing risk of developing diabetes mellitus in these HCV infected patients.

b) HCV SEROPOSITIVE DIABETICS AND HCV SEROPOSITIVE NON-DIABETICS: Among the HCV seropositive group, diabetics had the mean age of 55.12+10.414 years while the mean age of non-diabetics was 44.64+14.767 years. The difference was found to be statistically significant (p = 0.0056). Among the diabetics, 60% (n= 15) of the patients had BMI > 25kg/[m.sup.2] while 40 % (n=10) had BMI <25kg/[m.sup.2]. Among the non-diabetics, 20% (n= 5) of the patients had BMI > 25kg/[m.sup.2] while 80% (n=20) had BMI <25kg/[m.sup.2]. The difference was found to be statistically significant (p = 0.004).

Hypoalbuminemia was present in 68% (n=17) of the diabetics in comparison of 48% (n=12) of the non-diabetics (p=0.152). The mean serum albumin in the diabetics was 3.832 + 0.8335 gm/dl while in the non-diabetics, it was 3.28 + 0.7286 g/dl. The difference is statistically significant (p = 0.0481).

Similarly higher percentage of diabetics (24%) had prolonged prothrombin time than the non-diabetics (12%) but the results were statistically not significant (p=0.27).

Diabetics cases were more prone to have cirrhosis than the non-diabetic HCV cases. Cirrhosis was present in 64% (n=16) of the diabetic patients in comparison to 48% (n=12) of the nondiabetics. The difference was not statistically significant (p=0.25).

c) HCV SEROPOSITIVE DIABETICS AND NON-HCV DIABETICS: Further comparison was made between HCV seropositive diabetics and the non-HCV diabetics and we found that the mean age of HCV diabetics (55.12+10.414 years) was comparable to the mean age of diabetic controls (57.2+9.578 years) and thus not statistically significant (p = 0.53). Females represented 64% of the diabetic HCV cases and 60% of the diabetic non-HCV controls. This could be due to the higher percentage of females enrolled in our study.

The HCV diabetics had significantly higher percentage of patients with thrombocytopenia (p=0.04), hypoalbuminemia (p=0.033) and prolonged Prothrombin time (p=0.04) than the non-HCV diabetics which can be explained by the underlying liver parenchymal injury in the HCV group. As for the comparison of glycemic control between the two groups, the mean HBA1c of the HCV diabetics was 8.1+ 2.084 which was lower than that of the non-HCV diabetics (9.093 + 2.195; p = 0.16). This shows that HCV diabetics had better glycemic control than non-HCV diabetics but the result is not statistically significant and may be because of various confounding factors and warrants further investigation.

DISCUSSION: Diabetes mellitus is a unique extrahepatic manifestation of chronic hepatitis C virus infection. The link between the HCV and diabetes was first reported by Allison et al. in 1994.[1] Based on case-control studies, the prevalence of DM had been reported in 21% to 50% (a two- to ten-fold increase in prevalence) of patients with chronic HCV infection, which was significantly higher than that in the general population or among patients with other forms of liver diseases.[28] In our study the prevalence of Diabetes Mellitus in HCV positive patients was found to be 50% as compared to 30% in the HCV negative controls. In the Egyptian case-control study by Elhawary et al. 13.84% (40 out of 289) HCV cases had diabetes mellitus as compared to 4.15% (12 out of 289) of the HCV negative controls.[19] Similarly in a study by Chehadeh et al.[20] study population consisted of 181 HCV positive cases and 170 HCV negative controls. The prevalence of type 2 diabetes among the cases was 39.8%. Even higher prevalence of diabetes mellitus was found in the HCV positive patients when the study sample was taken from the transplant recepients. Al-Dosary et al found 40% subjects to be diabetic among HCV seropositive liver transplant recepients.[21] Similarly in a study in USA by Baid et al the prevalence of diabetes among HCV positive cases was 70 % (33 out of 44) as compared to 37% in the HCV negative controls.[21] Differences in the criteria employed in the diagnosis of DM, source of controls, case definition, sample size and underlying target population may explain much of this observed variability among the studies.

SOCIODEMOGRAPHIC CHARACTERISTICS OF THE CASES AND CONTROLS: We found that HCV seropositive diabetics were older and more obese than the HCV seropositive non-diabetics. The mean age of HCV diabetics was higher than the mean age of HCV non-diabetics which is similar to the findings of Egyptian study by Elhawary et al.[19] where the mean age of HCV seropositive diabetic cases was 48.1+9.2 years and that of non-diabetic cases was 40.7+10.4 years. (Statistically significant difference, p = 0.001). In the study by Rouabhia S et al 47.6 % of the HCV seropositive diabetics had BMI > 25kg/[m.sup.2] while in the HCV positive non-diabetics 7.6% had BMI >25kg/[m.sup.2] and the difference was statistically significant[30]

Diabetes was more prevalent in females than the males which could be due to higher number of females enrolled in the study. Also diabetes was more prevalent in the urban as compared to the rural population which can be explained by the more sedentary lifestyle and lack of physical activity among the urban population.

LIVER STATUS: We found that the prevalence of Diabetes Mellitus was 40.9 % in the HCV positive patients without evidence of liver cirrhosis. It was 50 % in patients with cirrhosis belonging to CPC-A and was 59.1% in those belonging to CPC-B. Thus the prevalence of diabetes mellitus increases with the increasing severity of the liver injury. Knobler et al. evaluated a group of 45 patients with chronic HCV infection in whom cirrhosis had been carefully excluded. 90 patients without HCV infection served as controls. Higher prevalence of type 2 diabetes was found in patients infected with HCV (33%) as compared to the HCV seronegative controls (5.6%).[24] Further findings are also in consistence with the Southeast Asian study by Memon S et al., where out of the total number of the participants (n= 361); 211(58.4%) had cirrhosis, while 150(41.6%) were non-cirrhotic HCV seropositives. The study found that 81(38.4%) had diabetes in the group with cirrhosis as compared to 33(22%) in the group without cirrhosis.[31] Rouabhia S et al. also found that prevalence of DM increased progressively and significantly with the fibrosis stage from 14.3% in stage F0 to 32.8% in F2 and 62.5% in stage F4. [30]

HEMATOLOGICAL PARAMETERS: Blood picture did not differ significantly between the 2 HCV groups. Anaemia was present in 64% (n= 16) of the diabetic patients while it was present in only 40 % (n= 10) of the non-diabetic patients. But the difference was statistically not significant (p= 0.089). Similarly thrombocytopenia was present in 24% (n=6) of the diabetic patients as compared to 16 % (n=4) of the non-diabetic patients (statistically not significant; p=0.48). In our study we found that HCV seropositive patients with diabetes had significantly lower values of mean serum albumin and significantly higher prolongation of prothrombin time as compared to the HCV seropositive patients without diabetes. Memon S et al also found the similar results with mean serum albumin in HCV positive diabetics to be 3.22+ 0.71 and in HCV positive non-diabetics to be 3.44 + 0.68 (statistically significant difference, p= 0.004).[31]

Our study did not show increased levels of transaminases (SGOT and SGPT) and serum bilirubin in the diabetic group as compared to the non-diabetic group. In contrast, the study by Elhawary et al. abnormal high ALT, high bilirubin values were more frequently seen among diabetic cases as compared to non-diabetic cases.[19]

HCV DIABETIC CASES VS NON-HCV DIABETIC CONTROLS: The comparison of HCV diabetics and the non-HCV diabetics showed no significant difference in age, gender variation and BMI. The former had significant higher percentage of patients with thrombocytopenia (p=0.04), hypoalbuminemia (p=0.033) and prolonged Prothrombin time (p=0.04) which can be explained by the underlying liver disease. El-kafrawy et al. also did not find any significant difference between hemoglobin of patients in two groups i.e. HCV positive with diabetes and HCV negative with diabetes but the mean platelet count of the first group (172.2+52.6) was significantly lower than the second group (253.1+57.38); (p = 0.001). The study by El-kafrawy et al. also showed similar results for hypoalbuminemia and prolonged prothrombin time.[32]

CONCLUSION: In our study we found that the patients with chronic hepatitis C virus infection had a higher prevalence of Diabetes Mellitus than the controls. The risk of type 2 diabetes increases further if the HCV seropositive patient has cirrhosis. The presence of diabetes was found to effect the severity of liver parenchymal disease in the HCV seropositive patients as is evident from the markers of liver parenchymal injury which were markedly deranged in the HCV positive patients with diabetes as compared to both HCV positive patients without diabetes and HCV negative patients with diabetes. Advancing age and increased weight are important predictors of type 2 diabetes in HCV seropositive patients. It is necessary to screen earlier for the presence of type 2 diabetes mellitus and thus prevent development of comorbid complications and mortality through timely intervention.

DOI: 10.14260/jemds/2015/166

REFERENCES:

[1.] Allison ME, Wreghitt T, Palmer CR, Alexander GJ. Evidence for a link between hepatitis C virus infection and diabetes mellitus in a cirrhotic population. J Hepatol 1994; 21: 1135-1139.

[2.] Lavanchy D. The global burden of hepatitis C. Liver Int 2009; 29: 74-81.

[3.] European Association for the Study of the Liver (EASL). Clinical Practice Guidelines: Management of Hepatitis C Virus Infection. J Hepatol 2011; 55: 245-264.

[4.] Cacoub P, Renou C, Rosenthal E, Cohen P, Loury I: EH manifestations associated with HCV infection. A prospective multicenter study of 321 patients. Medicine [Baltimore] 2000, 79: 4756.

[5.] Mehta SH, Brancati FL, Sulkowski MS, Strathdee S, Szklo M, Thomas DL: Prevalence of type 2 diabetes mellitus among persons with hepatitis C virus infection in the United States. Ann Intern Med 2000, 133: 592-599.

[6.] Antonelli A, Ferri C, Fallahi P, Ferrari SM, Ghinoi A, Rotondi M, Ferrannini E: Thyroid disorders in chronic hepatitis C virus infection. Thyroid 2006, 16 (6): 563-72.

[7.] Sanzone AM, Begue RE: Hepatitis C and arthritis: an update. Infect Dis Clin North Am 2006, 20 (4): 877-89.

[8.] El-Serag H, Hampel H, Yeh C, Rabeneck L: EH manifestations of hepatitis C among U.S. male veterans. Hepatology 2002, 36: 1439-45.

[9.] Ozkok A, Yildiz A. Hepatitis C virus associated glomerulopathies. World Journal of Gastroenterology : WJG 2014; 20 (24): 7544-7554.

[10.] Kawaguchi Y, Mizuta T. Interaction between hepatitis C virus and metabolic syndrome. World Journal of Gastroenterology: WJG 2014; 20 (11): 2888-2901.

[11.] Zimmet P, Alberti KG, Shaw J: Global and societal implications of the diabetes epidemic. Nature 2001, 414: 782-7.

[12.] Meisinger C, Thorand B, Schneider A, Stieber J, Doring A, Lowel H: Sex differences in risk factors for incident type 2 diabetes mellitus: the MONICA Augsburg cohort study. Arch Intern Med 2002, 14; 162 (1): 82-9.

[13.] Chehadeh W, Abdella N, Ben-Nakhi A, Al-Arouj M, Al-Nakib W: Risk factors for the development of diabetes mellitus in chronic hepatitis C virus genotype 4 infection. J Gastroenterol Hepatol 2009, 24 (1): 42-8.

[14.] Honeyman MC, Stone NL, Harrison LC: T-cell epitopes in type 1 diabetes autoantigen tyrosine phosphatase IA2: potential for mimicry with rotavirus and other envirommental agents. Mol Med 4: 231-239, 1998.

[15.] Laskus T, Radkowski M, Wang LF, Vargas H, Rakela J: Search for hepatitis C virus extrahepatic replication sites in patients with acquired immunodeficiency syndrome: specific detection of negative-strand viral RNA in various tissues. Hepatology 28: 1398-1401, 1998.

[16.] Mendler MH, Turlin B, Moirand R, Jouanolle AM, Sapey T, Guyader D, Le Gall JY, Brissot P, David V, Deugnier Y: Insulin resistance-associated hepatic iron overload.,1999. Gastroenterology 117: 1155-1163.

[17.] Castera L, Chouteau P, Hezode C, Zafrani ES, Dhumeaux D, Pawlotsky JM: Hepatitis C virusinduced hepatocellular steatosis. 2005, Am J Gastroenterol 100: 711-715.

[18.] Allison ME, Wreghitt T, Palmer CR, Alexander GJ. Evidence for a link between hepatitis C virus infection and diabetes mellitus in a cirrhotic population. J Hepatol. 1994 Dec; 21 (6): 1135-9.

[19.] E. I. Elhawary, G. F.Mahmoud, M. A. El-Daly, F. A.Mekky, G. G. Esmat, and M. Abdel-Hamid, "Association of HCV with diabetes mellitus: an Egyptian case-control study," Virology Journal, 2011, vol. 8, article 367.

[20.] Chehadeh W, Abdella N, Ben-Nakhi A, Al-Arouj M, Al-Nakib W: Risk factors for the development of diabetes mellitus in chronic hepatitis C virus genotype 4 infection. J Gastroenterol Hepatol 2009, 24 (1): 42-8.

[21.] Mhatre, Ashwini, Jan Mary Hale Risser, Charles Erwin Ford, and Xianglin L. Du. The Association between Diabetes and Hepatitis C: A Systematic Review of Epidemiological Evidence. 2008. Masters Abstracts International. 47-02.

[22.] Y. Shintani, H. Fujie, H. Miyoshi et al., "Hepatitis C virus infection and diabetes: direct involvement of the virus in the development of insulin resistance," Gastroenterology, 2004, vol. 126, no. 3, pp. 840-848.

[23.] R. Moucari, T. Asselah, D. Cazals-Hatem et al., "Insulin resistance in chronic hepatitis C: association with genotypes 1 and 4, serum HCV RNA level, and liver fibrosis," Gastroenterology, 2008, vol. 134, no. 2, pp. 416-423.

[24.] Knobler H, Schihmanter R, Zifroni A, Fenakel G, Schattner A. Increased risk of type 2 diabetes in noncirrhotic patients with chronic hepatitis C virus infection. Mayo Clin Proc 2000; 75: 355359.

[25.] Maeno T, Okumura A, Ishikawa T, Kato K, Sakakibara F, Sato K, Ayada M, Hotta N, Tagaya T, Fukuzawa Y, Kakumu S. Mechanisms of increased insulin resistance in non-cirrhotic patients with chronic hepatitis C virus infection. J Gastroenterol Hepatol 2003; 18: 1358-1363.

[26.] Fraser GM, Harman I, Meller N, Niv Y, Porath A. Diabetes mellitus is associated with chronic hepatitis C but not chronic hepatitis B infection. Isr J Med Sci 1996; 32: 526-530.

[27.] E. Bugianesi, F. Salamone, and F. Negro, The interaction of metabolic factors with HCV infection: does it matter? Journal of Hepatology, vol. 56, supplement 1, pp. S56-S65, 2012.

[28.] American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2012; 35 (Suppl 1): S64-S71.

[29.] Negro F, Alaei M: Hepatitis C virus and type 2 diabetes. World J Gastroenterol 2009, 15 (13): 1537-1547.

[30.] Rouabhia S, Malek R, Bounecer H, Dekaken A, Bendali Amor F, Sadelaoud M, Benouar A:Prevalence of type 2 diabetes in Algerian patients with hepatitis C virus infection.World J Gastroenterol 2010, 16 (27): 3427-3431.

[31.] Memon MS, Arain ZI, Naz F, Zaki M, Kumar S, Burney AA. Prevalence of type 2 diabetes mellitus in hepatitis C virus infected population: a Southeast Asian study. J Diabetes Res. 2013; 2013: 539361.

[32.] Nabil El-Kafrawy, Moustafa El-Najjar, Alaa Dawood and Osama Al-Belehy, Relationship between chronic HCV infection and diabetic microvascular complications in Egyptian patients, Life Science Journal, 2011; 8 (4): 344-350.

Ranjeet Kaur (1), Gurinder Mohan (2), Narotam Bhalla (3), Baldeep Kaur (4)

AUTHORS:

(1). Ranjeet Kaur

(2). Gurinder Mohan

(3). Narotam Bhalla

(4). Baldeep Kaur

PARTICULARS OF CONTRIBUTORS:

(1.) Associate Professor, Department of Medicine, Sri Guru Ramdas Institute of Medical Sciences and Research, Sri Amritsar, Punjab.

(2.) Professor & Head, Department of Medicine, Sri Guru Ramdas Institute of Medical Sciences and Research, Sri Amritsar, Punjab.

(3.) Professor, Department of Medicine, Sri Guru Ramdas Institute of Medical Sciences and Research, Sri Amritsar, Punjab.

(4.) Junior Resident, Department of Medicine, Sri Guru Ramdas Institute of Medical Sciences and Research, Sri Amritsar, Punjab.

NAME ADDRESS EMAIL ID OF THE CORRESPONDING AUTHOR:

Dr. Baldeep Kaur, Room No. 10, Flat No. 4, A-Block, P. G. Hostel, SGRDIMSAR, Vallah, Amritsar.

E-mail: bsandhu_@yahoo.com

Date of Submission: 17/12/2014.

Date of Peer Review: 18/12/2014.

Date of Acceptance: 13/01/2015.

Date of Publishing: 21/01/2015.
Table 1: Comparison of variables among cases and controls in
study population

Parameter           Values               Cases   Controls   P value

Age-years           <40                    8        8        1.00
                    [greater than or      42        42
                    equal to]40

Gender              Female                27        27       1.00
                    Male                  23        23

Residence           Urban                 15        11       0.362
                    Rural                 35        39

Anaemia (gm%)       Hb<10gm%              26        19       0.16
                    Hb>=10gm%             24        31

Thrombocytopenia    PLATELETS<= 1lakh/    11        1        0.002
(lakhs/ cumm)       cumm

                    PLATELETS> 1 lakh/    39        49
                    cumm

Hypoalbuminemia     SERUM ALBUMIN <=3     29        17       0.016
(gms/dl)
                    SERUM ALBUMIN >3      21        33

PT prolongation     >=3 sec                9        1        0.008
(seconds)           <3 sec                41        49

BMI kg/m2           >=25 kg/m2            20        13       0.137
                    <25 kg/m2             30        37

Family history of   Yes                   15        15       1.00
diabetes            No                    35        35

Marital Status      Married               46        47       0.69
                    Unmarried              4        3

Diabetes            Yes                   25        15       0.041
                    No                    25        35

Ultrasound status   Cirrhosis             28        0          0
of liver            No cirrhosis          22        50

Table 2: Comparison of variables among the
'HCV seropositive diabetic' and 'HCV seropositive non-diabetic'
groups

                                         HCV Cases

                                                      Non
Parameter            Value               Diabetic   Diabetic   P value

Age-years            <40                    1          7        0.021
                     [greater than or       24         18
                     equal to]40

Gender               Female                 16         11       0.156
                     Male                   9          14

Residence            Urban                  10         5        0.123
                     Rural                  15         20

Anaemia (gm %)       <10gm%                 16         10       0.089
                     >10gm%                 9          15

Thrombocytopenia     Platelet < 1 lakh      7          4        0.306
(per cumm)           Platelet > 1 lakh      18         21

T Bilirubin--mg/dl   > 1.5 mg/dl            2          7        0.066
                     <=1.5 mg/dl            23         18

SGOT- U/L            > 74                   6          11       0.136
                     <=74                   19         14

SGPT- U/L            >130                   2          2          1
                     <=130                  23         23

Hypoalbuminemia      S.Albumin <=3          17         12       0.152
(gm/dl)              S.Albumin >3           8          13

PT prolongation      >=3secs                6          3        0.27
(secs)               <3secs                 19         22

Liver status         Cirrhosis              17         12       0.152
                     No cirrhosis           8          13

BMI--kg/m2            >=25 kg/m2             15         5        0.004
                     <25 kg/m2              10         20

Family history of    Yes                    9          6        0.355
diabetes             No                     16         19

Table 3: Comparison of variables between
'HCV seropositive diabetics' and 'HCV seronegative diabetics'

                                                    Diabetes Cases

                                                HCV            HCV
Parameter             Value                 Seropositive   Seronegative

Age--years             <40                        1              0

                      [greater than or           24             15
                      equal to]40

Gender                Female                     16             9

                      Male                       9              6

Residence             Urban                      10             4

                      Rural                      15             11

Anaemia--gm%          <10gm%                     16             7

                      >=10gm%                    9              8

Thrombocytopenia      Platelet <= 1 lakh         7              0
(per cumm)
                      Platelet > 1 lakh          18             15

T Bilirubin- mg/dl    > 1.5 mg/dl                2              0

                      <=1.5 mg/dl                23             15

SGOT- U/L             > 74                       6              0

                      <=74                       19             15

SGPT- U/L             >130                       2              0

                      <=130                      23             15

Hypoalbuminemia-      S.Albumin <=3              17             5
gm/dl
                      S. Albumin >3              8              10

PT prolongation--     >=3 secs                   6              0
secs
                      <3 secs                    19             15

Liver status          Cirrhosis                  17             0

                      No cirrhosis               8              15

BMI--kg/m2             >=25 kg/m2                 15             6

                      <25 kg/m2                  10             9

Family history of     Yes                        9              8
diabetes
                      No                         16             7

                                            Diabetes
                                             Cases

                                               P
Parameter             Value                  value

Age--years             <40                    0.433

                      [greater than or
                      equal to]40

Gender                Female                  0.8

                      Male

Residence             Urban                  0.392

                      Rural

Anaemia--gm%          <10gm%                 0.283

                      >=10gm%

Thrombocytopenia      Platelet <= 1 lakh     0.024
(per cumm)
                      Platelet > 1 lakh

T Bilirubin- mg/dl    > 1.5 mg/dl            0.261

                      <=1.5 mg/dl

SGOT- U/L             > 74                    0.04

                      <=74

SGPT- U/L             >130                   0.261

                      <=130

Hypoalbuminemia-      S.Albumin <=3          0.033
gm/dl
                      S. Albumin >3

PT prolongation--     >=3 secs                0.04
secs
                      <3 secs

Liver status          Cirrhosis                0

                      No cirrhosis

BMI--kg/m2             >=25 kg/m2              0.22

                      <25 kg/m2

Family history of     Yes                    0.283
diabetes
                      No

Graph 1: Showing comparison of the prevalence of
Diabetes mellitus type 2 among the cases and the control

COMPARISON OF DIABETES MELLITUS TYPE 2

            DIABETICS  NON-DIABETICS

CASES           50          50
CONTROLS        30          70

Note: Table made from bar graph.

Graph 2: Showing the comparison of the prevalence of Diabetes
Mellitus among various groups according the severity of liver
parenchymal injury among the HCV seropositive patients

                          DIABETICS   NON-DIABETICS

HCV positive
  without cirrhosis         40.9          59.1
HCV positive A              50            50
CPC-HCV positive CPC-A      59            41

Note: Table made from bar graph.
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Article Details
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Title Annotation:ORIGINAL ARTICLE
Author:Kaur, Ranjeet; Mohan, Gurinder; Bhalla, Narotam; Kaur, Baldeep
Publication:Journal of Evolution of Medical and Dental Sciences
Article Type:Clinical report
Date:Jan 22, 2015
Words:5041
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