Printer Friendly

CORRELATION BETWEEN SERUM ASCITES ALBUMIN GRADIENT (SAAG) AND ESOPHAGEAL VARICES IN PATIENTS HAVING CHRONIC LIVER DISEASE.

Byline: Nabeela Iqbal, Syed Khalid Shah and Shamima Hanif

Keywords: Chronic liver disease, Esophageal varices, SAAG, Upper GI endoscopy.

INTRODUCTION

Chronic liver disease is one of the common diseases prevailing in South Asia. The increasing prevalence needs to be evaluated and updated for hepatitis B and C, the main causative agents for chronic liver disease, as increasing number people are being affected by this dangerous disease. The overall burden of Hepatitis B and C associated chronic liver disease has also increased in Pakistan1.

HBV and HCV are the most important etiologies of chronic liver disease leading to cirrhosis. Patients with cirrhosis are eventually confronted with the development of esophageal varices due to portal hypertension and esophageal variceal bleeding is the most common and potentially lethal complication of liver cirrhosis, occurring at an incidence of 30-40% and carrying a mortality of rate of 30-50%. Two third of survivors will bleed again within a period of six months if not treated with prophylactic beta blockers or endoscopic therapy. Those receiving such therapy are less likely to bleed and that is why screening such patientsfor esophageal varices by periodic endoscopy is recommended, which can have cost implications2,3.

Several retrospective studies have shownthat SAAG and serum albumin as probable noninvasive biochemical markers of esophageal varices in cirrhotic patients and SAAG has been concluded an indirect biochemical marker in detecting the occurrence and grades of esophageal varices as a n endoscopic parameter of portal hypertension. The SAAG is simple and minimally invasive technique which has a validity rate of 90% in detecting ascites due to portal hypertension1,4.

SAAG is an excellent biochemical parameter in differentiating ascites due to portal hypertension from other causes of ascites and ascites with high SAAG is indirectly associated with the presence of esophageal varices in cirrhotic patients2,5.

A serum ascites albumin gradient (SAAG) value >1.1g/dl, means that the cause of ascites is most likely to be portal hypertension; this is usually in the setting of cirrhosis. When the gradient <1.1g/dl,the work up for infectious or malignant causes of ascites should be done6.

Patients with cirrhosis often are subjected to screening endoscopy for varices so that prophylactic therapy and/or follow up can be planned. Routine endoscopic screening of all cirrhotic patients with or without varices carries health service cost implications. In a province like Baluchistan it might be cost effective to identify those patients who would benefit most from routine screening. In order to reduce the increasing burden that endoscopy units will have to bear, the present study is not only going to help in improving cost effectiveness of routine endoscopy but also optimizing prophylactic therapy in the form of beta blockers by the clinicians. The study will allowthe use of SAAG as a prior indicator, although indirect, which would help in estimating the complications of portal hypertension in the form of esophageal varices. Thus keeping away from needless interference and avoiding the risk of bleeding, infections and other complications during screening endoscopy.

Table-I: Analysis of age of study population.

###Minimum###Maximum###Mean###Std. Deviation

Age###20###75###44.86###12.319

Table-II: Analysis of various variables of study population.

###Minimum###Maximum###Mean###Std. Deviation

SAAG###0.60###4.60###1.905###0.7955

Variceal grade###1###4###3.075###1.040

PATIENTS AND METHODS

This cross sectional study was conducted in the medical unit 3 of Sandeman Provincial Hospital Quetta from October 2015 to April 2016. In this study 80 cirrhotic patients were included. The subjects were chosen by non-probability consecutive sampling, all having chronic liver disease with ascites visiting Medical OPD and emergency department of SPH Quetta fulfilling the inclusion criteria which included classical findings of chronic liver disease on clinical examination, deranged liver biochemistry and ultrasonography findings consistent with cirrhosis of liver. Exclusion criteria incorporated all those patients having ascites due to etiologies other than cirrhosis like congestive heart failure, abdominal tuberculosis, hepatocellular carcinoma, renal failure, intra-abdominal malignancy. The criteria were strictly followed to control the confounder and bias in the study. Informed consent was taken from the patients before including them in the study.

The study was conducted after taking approval from ethical review committee of the institute. The whole study protocol was described to the patient so that confidence could be gained. The attendant of the patient accompanied him/her at all times in regard with ethical issue. Female patients were provided full privacy during the procedure. The information of the patient was kept confidential. Patients were subjected to laboratory investigations i.e, complete blood count, liver function tests, serum albumin, prothrombin time and viral profile (HBsAg, anti HCV), diagnostic tap of the ascitic fluid under aseptic measures, ascitic fluid analysis: cell type, cell count, sugar and ascitic albumin. Serum ascitic-albumin gradient was calculated. Abdominal ultrasound was done to look for altered echo texture of liver parenchyma, ascites, size of the portal vein and splenomegaly.

Upper GI endoscopy of all patients was performed in med unit III SPH Quetta, by a consultant gastroenterologist, again after a written consent by the patient. Patients werepre medicated with intravenous Hyoscine and Xylocain spray as a topical anesthetic and evaluated for the occurrence and grades of esophageal varices.

Observer was blinded to SAAG value at the time of endoscopy to avoid bias of the results. The correlation between SAAG value and esophageal varices (occurrence and grades) was examined to determine the applicability of the method to Baluchistan population. Basic demographic information, SAAG value and endoscopic findings were recorded on a predesigned proforma (Annex-I).

Statistical Package for the Social Sciences (SPSS) for Windows version 17.0 was used for the purpose of statistical testing of data. Descriptive statistics: frequencies and percentages were computed for categorical variables like gender, level of SAAG and grade of esophageal varices. Mean and standard deviation were used to estimate quantitative variables like age. Pearson Correlation Coefficient was used to measure the linear correlation between SAAG and grade of esophageal varices. It gave a result of -1 to +1, where +1 is total positive correlation, 0 is no correlation, -1 is total negative correlation. Effect modifier was controlled through stratification of age and gender to see the effect of these variables on outcome variable.

RESULTS

Eighty patients fulfilling the inclusion criteria were enrolled in this study.

There were 56 (70%) males and 24 (30%) females (fig-1). The mean +- standard deviation age of study population was 44.86 +- 12.319 years (table-I).

On analysis of age group it was observed that 40 (50%) patients were less than 40 years of age, 73 (91.25%) patients had SAAG value above 1.1 mg/dl (table-II).

Positive correlation of SAAG with variceal grade was observed (table-III).

Stratification of age and gender is mentioned in tables III through X.

DISCUSSION

Ascites, defined as accumulation of fluid in the peritoneal cavity, might be an association of several diseases. Ascites in patients, due to any disease, poses issues in diagnosis and therapy7-9. Biochemical, microbiological and cytological analysis of ascitic fluid is very important and mainstay for differential diagnosis among the diseases causing ascites. Conservatively, ascites has been categorized as being either transudative or exudative, based upon the ascitic fluid total protein concentration10,11, the ascitic fluid to serum ratio of total protein12,13, or the ascitic fluid to serum ratio of lactic dehydrogenase14.

Despite the presence of these mentioned parameters, none are effective in distinguishing the types of ascitic fluid but the serum-ascites albumin concentration gradient (SAAG) has been declared superior, in comparison with the exudatetransudate concept in distinguishing by several studies. The classification has a validity rate of 90% or more in detecting the ascites as a complication of portal hypertension15-17.

The classification of ascitic fluids according to the absence or presence of portal hypertension (PHTN) has been made possible owing to the high precision and minimal invasiveness of SAAG7,16-23. It is repeatedly highlighted in the literature that the SAAG is an indirect indicator of PHTN1,16,17,19-23 and that a direct relationship probably exists between SAAG and different PHTN measurements such as the portal pressure gradient1, net portal pressure19,20 or corrected portal pressure17. These quantifications can be procured only by invasive measures, which are associated with cost implications and hence not feasible in most centers in the resources strained countries. Esophageal varices have proven to be an endoscopic parameter of portal hypertension in cirrhotic patients. The indirect way to assess the presence PHTN is by detection of esophageal varices (EV).

A number of potential modalities exist to assess the status of EV including barium radiography, ultrasonography and upper gastro-intestinal endoscopy. The upper gastrointestinal endoscopy is currently the best reliable procedure available to diagnose presence of EV and hence, PHTN24. The quantification of the portal pressure gradient (PP-GRAD) and the portal pressure (PP), as demonstrated by previous research, have been deemed most appropriate hemodynamic variables for assessing the growth of PHTN and its complications in the form of esophageal varices20-24. The SAAG has been found having correlation with different PHTN measurements, such as PP-GRAD, net portal pressure19-20, or corrected portal pressure. In 1990, Kajani et al24 investigated the correlation in patients with alcoholic liver disease and with cirrhosis due to other causes seperately16.

In this study, a correlation was found between SAAG and either portal pressure or esophageal varices in patients with cirrhosis due to alcohol abuse. But in the patients with non-alcoholic cirrhosis, no correlation was found between SAAG and portal pressure, while the correlation between SAAG and the grade of varices was found to be weaker. Despite these controversial results and discrepancies, the SAAG owes an ability to indicate the existence or absence of PHTN with an accuracy of 96.7%7-9,16,23. This test possess an accuracy despite of ascitic fluid infection, diuresis, therapeutic paracentesis, albumin infusion, and etiology of liver diseases7-9. In a study performed by Hoefs et al. in 1983, which showed that an excellent correlation exists between portal hypertension and SAAG25.

In this study, a numeric formula was established for the first time between portal hypertension and SAAG. While it was established in this formula that p<0.05, the numeric formula was as follows: PP-GRAD=7.08 X (SAAG+3.62).

In this study a clear cut correlation between SAAG levels and the growth of esophageal varices in patients having cirrhosis due to chronic liver disease was found. Patients having a high SAAG were the ones only found with esophageal varices thus establishing a high probability of finding EV in patients with higher values SAAG.

Table-III: Analysis of corelation of saag with variceal grade.

###SAAG###Variceal Grade

###Pearson Correlation###1###0.631**

SAAG###Sig. (2-tailed)###0.000

###N###80###80

###Pearson Correlation###0.631**###1

Variceal Grade###Sig. (2-tailed)###0.000

###N###80###80

Table-IV: Analysis of data with age stratification.

###Age Group###SAAG###Variceal Grade

###Pearson Correlation###1###0.665**

###SAAG###Sig. (2-tailed)###0.000

###N###40###40

<30

###Pearson Correlation###0.065**###1

###Variceal Grade###Sig. (2-tailed)###0.000

###N###40###40

###Pearson Correlation###1###0.605**

###SAAG###Sig. (2-tailed)###0.000

###30 and###N###40###40

###Above###Pearson Correlation###0.605**###1

###Variceal Grade###Sig. (2-tailed)###0.000

###N###40###40

Table-V: Analysis of data with gender stratification.

###Gender###SAAG###Variceal Grade

###Pearson Correlation###1###0.592**

###SAAG###Sig. (2-tailed)###0.000

###N###56###56

###Male

###Pearson Correlation###0.592**###1

###Variceal Grade###Sig. (2-tailed)###0.000

###N###56###56

###Pearson Correlation###1###0.731**

###SAAG###Sig. (2-tailed)###0.000

###N###24###24

###Female

###Pearson Correlation###0.731*###1

###Variceal Grade###Sig. (2-tailed)###0.000

###N###24###24

Further more our study shows that grades of esophageal varices were significantly related with the degree (p<0.01) of SAAG with a Pearson relationship of r=0.55 (p1.5g/dl. Thai J Gastroenterol 2011; 12:47-51.

3. Khan H, Iman N, Hypoalbuminemia: a marker of esophageal varices in cirrhosis due to hepatitis B and C. Rawal Med J 2009; 34: 98-101.

4. Gurubacharya DL, Mathura KC, Karki DB. Correlation between serum ascites gradient and endoscopic parameters of portal hypertension. Kathmandu Univ Med J 2005; 3(4): 327-33.

5. Jaffri MSA, Shaikh AA, Jaffri MH, Khushk A, Shah MA, Munir SM. Diagnostic sensitivity and specificity of serum-ascites albumin gradient in patients with ascites. J Liaquat Univ Med Health Sci 2009; 8(3): 196-200.

6. Longo DL, Fauci AS, Jameson JL, Kasper DL, Braunwald E, Loscalzo J. Abdominal swelling and ascites. Harrison's principles of internal medicine. 18th ed. New York: McGraw-Hill; 2012. p. 330-3.abraldes

7. Abraldes JG, Bureau C, Stefanescu H. Anticipate Investigators. Noninvasive tools and risk of clinically significant portal hypertension and varices in compensated cirrhosis: The "Anticipate" study. Hepatology 2016; 64: 2173-84.

8. Sarangapani A, Shanmugam C, Kalyanasundaram M, Rangachari B, Thangavelu P, subbarayan JK. Non invasive prediction of large esophageal varices in chronic liver disease patients. Saudi J Gastroenterol 2010; 16: 38-42.

9. Berzigotti A, Seijo S, Arena U. Elastography, spleen size, and platelet count. indentify portal hypertension in patients with compensated cirrhosis. Gastroenterology 2013; 144: 102-111.

10. Franchis R. Expanding consensus in portal hypertension. J Hepatol 2015; 63: 743-52.

11. European Association for the study of the Liver, Asociacion Latinoamerica para el Estudio del Higado. EASL-ALEH clinical practice guidelines: non invasive tests for evaluation of liver diseaseseverity and prognosis. J Hepatol 2015; 63: 237-64.

12. Bosch J, Groszmann RJ, Shah VH. Evolution in the understanding of pathophysiological basisof portal hypertension: how changes in paradigm are leading to successful new treatments. J Heaptol 2015; 62(S1): S121-S130.

13. Sinagra E, Perricone G, D' Amico M. Systemic review with metaanalysis: the haemodynamic effects of carvedilol compared with propranololfor portal hypertension in cirrhosis. Aliment Pharnacol Ther 2014; 39: 557-68.

14. Berzigotti A, Bosch J. Pharmacological mangement of portal hyper-tension. Clin Liver Dis 2014; 18: 303-17.

15. Mohanti A, Tate JP, Garcia-Tsao G. Statins are associated with decreased risk of decompensationand death in veterans with hepatitis C-related compensated cirrhosis. Gastroenterology 2016; 150: 430-40.

16. Gracia Tsao G, Fuchs M, Shifmann ML. Emricasan (IDN-6556) administered orallu fot 28 dayslowers portal pressure in patients with compensated cirrhosis and severe portal hypertension. AASLD. Hepatology 2015; 62(6 Suppl): 1379-99.

17. McCarty TR, Njei B. Self expanding metal stents for acute refractory variceal bleeding: a systemic review and meta-analysis. Dig Endosc 2016; 28(5): 539-47.

18. Puente A, Hernandez-Gea V, Graupera I. Drugs plus ligation to prevent rebleeding in cirrhosis: an updated systemic review. Liver Int 2014; 34: 823-33.

19. Gracia Tsao G, Bosch J. Varices and variceal hemorhage in cirrhosis: a new view of an old problem. Clin Gastroenterol Hepatol 2015; 13: 2109-17.

20. Demirel U, Karincaoglu M, Harputluoglu M, Ates M, Seckin Y, Yildirim B, et al. Two findings of portal hypertension: evaluation of correlation between serum-ascites albumin gradient and esophageal varices in non-alcoholic cirrhosis. Turk J Gastroenterol 2003; 14: 219-22.

21. Torres E, Barros P, Calmet F. Correlation between serum-ascites albumin concentration gradient and endoscopic parameters of portal hypertension. Am J Gastroenterol 1998; 93: 2172-8.

22. Masroor M, Qamar R, Ahmed I, Danish S, Sattar A, Imran K, et al. Do we always need Endoscopy to predict varices. Med Channel 2007; 13: 55-8.

23. Holster IL, Tjwa ETTL, Moelker A. Covered transjugular intra-hepatic portosystemic shunt versus endoscopic therapy +beta blocker for prevention of variceal rebleeding. Hepatology 2016; 63: 581-89.

24. Kajani MA, Yoo YK, Alexender JA. Serum ascites albumin gradient in nonalcoholic liver disease. Dig Dis Sci 1990; 35: 33-7.

25. Hoefs JC. Serum protein concentration and portal pressure determine the ascites fluid protein concentrationin patients with chronic liver disease. J Lab Clin Med 1983; 102: 260-73.
COPYRIGHT 2019 Knowledge Bylanes
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2019 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Publication:Pakistan Armed Forces Medical Journal
Date:Apr 30, 2019
Words:2828
Previous Article:A COMPARATIVE STUDY OF DYSLIPIDAEMIA IN DIABETIC PATIENTS WITH AND WITHOUT NEUROPATHY.
Next Article:CHANGES IN THE LEVEL AND FACTORS AFFECTING STUDENTS' MOTIVATION IN THE FIRST 6 MONTHS OF DENTAL EDUCATION AT DENTAL COLLEGES.
Topics:

Terms of use | Privacy policy | Copyright © 2020 Farlex, Inc. | Feedback | For webmasters