Prevalence of Liver disorders in Islamabad City
Author's: Sabeen Toor, Sidra Toor, Asfa Ashraf, Saman Alam, Samavia Anwaar, Ayesha Saddiqa, Shahzad Ali, Samra Toor, Ali Muhammad, Shamim Akhter
Corresponding Author: Asfa Ashraf
Corresponding Author Email: email@example.com
Article Type: Short Communication
Published Online: May. 13, 2016
The purpose of this study was to determine the prevalence of liver disorders through liver function enzyme tests (LFTs) in Islamabad. A total of 250 blood samples were screened in Kahuta Research Laboratory (KRL), Islamabad for the presence of liver disorders through liver function enzyme tests (LFTs) viz., alanine aminotransferase (ALT), Total Bilirubin (T.Bil) and alkaline phosphatase (ALP). The results were analyzed by comparing the correlation among ALT, ALP and T. Bilirubin and compiled by comparing elevated level of LF enzymes with respect to age. It has been observed that correlation coefficient between ALT and T. Bilirubin; ALP and T. Bilirubin; ALT and ALP was positive values which indicate that slightly elevation in these enzymes released from hepatocytes cause liver disorders. The level of ALT and ALP abruptly decreased in (1-15 years), and then it gradually increased in age groups 16-30 years, 31-45 years. Their level was much higher in (46-60 years). However the level of T. Bilirubin was higher in children and adults in age groups (1-15 years) and (46-60 years) but it was slightly elevated in age groups (16-30 years) and (31-45 years). It is concluded that elevation of liver enzymes is responsible for liver disorders.
Liver performs its vital functions such as synthesis, storage, recycling and detoxification under normal conditions. There are number of factors involved in the elevation of liver enzymes. Previous studies reported risk factors included parental drug abuse (Marengo, 1993), blood transfusion (Dusheiko, 1990), accidental needle stick (Kiyosawa et al., 1991), ear piercing, bite by human (Abildgaard and Petrsland, 1991), haematophagous arthropods such as mosquito, ticks and bedbugs (Hollinger, 1990), organ recipients (Pereia et al., 1991), obesity (fatty deposits in liver cells) (Fattovich et al., 1997). Urine, saliva and blood samples used to detect sick factor of liver disorder (Dubios et al., 1994). Liver disorders including Hepatitis A, B, C, D, E and G, liver tumors, liver stones, liver cancer and obstructions of bile duct due to stones (Stanley, 1996).
It has been observed that liver diseases also induced by antibiotics such as Nitrofuranation, Amoxicillin, Clavulanic acid, Tetracycline, Isoniazid and Methotrexate used to treat autoimmune disorders and cancer. Disulfiram used to treat alcoholics can also cause liver inflammation (Seng and Katzel, 2001). Numerous medications cause liver inflammation including taking excess amount of Acetaminophen (Schalm et al., 1997). Niacin is used to control elevated blood level of cholesterol, but liver inflammation for this medication is related to the dose taken (Prince et al., 2002).
Liver function enzyme tests (LFTs) including Alanine transaminase (ALT), Aspartate transaminase (AST), Alkaline phosphatase (ALP), Albumin, Total bilirubin (T.BIL), Direct bilirubin and Gamma glutamyl transpeptidase (GGT) tests are used as a marker to determine the status of patient’s liver (Haurigan and Bowling, 2001). Medical treatments for liver disorder include surgery, low sodium diet and water pills (diuretics), anti-inflammatory drugs and liver transplantation (Schalm et al., 1997).
The main objective of this study was to diagnose and determine the prevalence of liver diseases through liver function enzyme tests (LFTs) in Islamabad, Pakistan.
Abildgaard, N., Petrsland, N., 1991. Hepatitis C virus transmitted by tattooing needles. Lancet, 2: 460-2.
Ali, H.M., Bhatti, S., Iqbal, M.N., Ali, S., Ahmad, A., Irfan, M., Muhammad, A., 2015. Mutational analysis of MDM2 gene in hepatocellular carcinoma. Sci. Lett., 3(1):33-36.
Dubois, F., Francios, M., Mrriotte, N., 1997. Serum alanine aminotransferase measurement as a guide to selective testing for hepatitis C during medical checkup. J. Hepatol., 112: 463-72.
Dufour, D.R., Loot, J.A., Nolte, F.S., Gretch, D.R., Koff, R.S., Scoff, B.C., 2001. Diagnosis and monitoring of hepatitis injury. J. Clin. Chem., 46(12): 2027-49.
Dushaiko, G.M., 1990. Progress in hepatitis C research. Lancet, 334: 605-6.
Fattovich, G., Dally, G., Bahr, M.J., 1997. Morbidity and mortality in compensated cirrhosis type C. Gastoenterol., 112: 463-72.
Haurigan, K.J., Bowling, F.G., 2001. Alcoholic liver disease. J. Gastroenterol. Hepatol., 16: 1138-43.
Hollinger, F.B., 1990. Non-A and Non-B hepatitis viruses. J. Virol., 12(7): 1394-98.
Hoofnagle, J.H., Bisceglie, A.M., 1998. The treatment of chronic hepatitis. N. Engl. J. Med., 336(5): 347-55.
Kiyosawa, k., Sodenyma, T., Tanaka, E., 1991. Hepatitis C virus in hospital. Viral Hepatol., 8(4): 256-63.
Loannou, G.N., Boyko, E.J., Lee, S.P., 2006. The prevalence and predictors of elevated serum aminotransferase activity in the United States in 1999-2002. Am. J. Gastroeterol., 101(1): 76-82.
Marengo, R.A., 1993. Hepatitis C as an update. The Doctor, 25(4): 6-8.
Muhammad, A., Farooq, M.U., Iqbal, M.N., Ali, S., Ahmad, A., Irfan, M., 2013. Prevalence of diabetes mellitus type II in patients with hepatitis C and association with other risk factors. Punjab Univ. J. Zool., 28 (2): 69-75.
Pereia, B., Milford, E.L., Krlkman, R.L., 1991. Transmission of hepatitis C virus by organ transplantation. N. Engl. J. Med., 325: 454-60.
Prince, M., Chetwynd, A., Newman, W., Medcalf, J.V., James, O.F.W., 2002. Survival and symptom progression in a geographically based cohort of patients with primary biliary cirrhosis. Gastroenterol., 123: 1044-51.
Schafer, D.F., Sorrell, M.F., 1997. Liver failure. N. Engl. J. Med., 336(16): 1173-74.
Schalm, S.N., Fattovich, G., Bronwer, J.T., 1997. Therapy of hepatitis C patients with cirrhosis. Hepatol., 26(3): 1285-1325.
.Seng, L.T., Katzel, G.M., 2001. How hepatitis C virus counteracts the interferon responses. Virol., 285: 1-12.
Stanley, A.J., Haydon, G.H., Piris, J., 1996. Assessment of liver histology in patients with hepatitis C and normal transaminase levels. Eur. J. Gastroessnterol. Hepatol., 8(9): 869-72.
Tarao, K., Rino, Y., Ohkawa, S., Tamai, S., Miakawa, K., Takakura, H., Endo, O., Yoshitsugu, M., Watanabe, N., Matsuzaki, S., 2002. Close association between high serum alanine aminotransferase levels and multicentric hepatocarcinogenesis in patients with hepatitis C virus-associated cirrhosis. Cancer, 94(6):1787-95.
Get Article Updates