Journal of Clinical Gastroenterology and Hepatology Open Access

Non-Invasive Predictors of Large Esophageal Varices in Patients with Cirrhosis in Cameroon

Nsenga Djapa Guy Roger^1,2*, Kowo Pierre Mathurin³, Mohamadou Galdima⁴, Ndjitoyap Ndam Antonin Wilson³, Talla Paul³, Ankouane Andoulo Firmin³ and Njoya Oudou^{3 1}Department of Internal Medicine and Specialties, University of Dschang, Cameroon
²Gastroenterology Unit, Internal Medicine Service, Ebolowa Regional Hospital, Cameroon
³Department of Internal Medicine and Specialties, University of Yaoundel, Cameroon
⁴Department of Internal Medicine and Specialties, University of Ngaoundere, Cameroon
^*Correspondence: Nsenga Djapa Guy Roger, Department of Internal Medicine and Specialties, University of Dschang, Cameroon, Email:

Received: 30-Mar-2022, Manuscript No. IPJCGH-22-13411; Editor assigned: 01-Apr-2022, Pre QC No. IPJCGH-22-13411 (PQ); Reviewed: 15-Apr-2022, QC No. IPJCGH-22-13411; Revised: 20-Apr-2022, Manuscript No. IPJCGH-22-13411 (R); Published: 27-Apr-2022, DOI: 10.36648/2575-7733.6.4.20

Introduction

One of the most relevant complications of cirrhosis is the occurrence of portal hypertension which leads to varices within the splanchnic circulation. In this regard, esophageal varices (EV) are a major concern in cirrhotic patients because of the risk of bleeding and related high mortality [1]. The prevalence of EV in newly diagnosed cirrhotic patients is approximately 60%-80% and the 1 year rate of first variceal bleeding is approximately 5% for small EV and 15% for large EV [1,2]. The determination of the presence of EV by upper digestive endoscopy is therefore mandatory in patients with cirrhosis at diagnosis [3]. For long term follow up, guidelines recommend monitoring of cirrhotic patients by routine endoscopy for the detection of the development of EV and to initiate prophylactic measures to prevent the bleeding of EV when they become large [3,4]. Endoscopy is however a costly, invasive, and time consuming procedure [5]. The detection of EV in African patients with cirrhosis is a matter of concern because of the frequent malfunction or unavailability of endoscopy units [6]. This study was conducted to evaluate known noninvasive predictors of esophageal varices in patients with cirrhosis in Cameroon.

Patients and Methods

It was a prospective, cross-sectional study conducted in three university teaching hospitals in Yaounde for a period of 12 months from November 1^st 2013 to October 31^st 2014. All patients underwent a detailed clinical evaluation at inclusion. Patients with evidence of hepatocellular carcinoma and/or portal vein thrombosis on ultrasonography or computer tomography, previous or current treatment with beta blockers, nitrates and diuretics were excluded from the study including those who had received endoscopic treatment for portal hypertension.

Clinical Assessment

Relevant history and physical characteristics including symptoms and signs of liver failure (spider angioma, palmar erythema, jaundice, fetor hepaticus etc.), hepatomegaly, splenomegaly, and abdominal vein collaterals were recorded. Ascites was graded as none, mild (detectable only on ultrasound), moderate (visible moderate symmetrical abdominal distension) or severe (marked abdominal distension) [7]. Hepatic encephalopathy was graded from grade 0 to 4, as per the Conn's grading as [8]:

• Grade 0: Normal neuropsychological functioning

• Grade 1: changes in behavior with minimal change in level of consciousness

• Grade 2: gross disorientation, drowsiness, possibly asterixis, inappropriate behavior

• Grade 3: marked confusion, incoherent speech, sleeping most of the time but arousable to vocal stimuli

• Grade 4: comatose, unresponsive to pain; decorticate or decerebrate posturing.

Biological Assessment

Hematological and biochemical workup included measurement of hemoglobin, total leukocyte count, platelet count, prothrombin time, and serum concentrations of bilirubin (total and conjugated), protein, albumin, alanine aminotransferase and aspartate aminotransferase. For each patient, a modified Child Pugh score was calculated [9].All patients were screened for viral hepatitis. They were considered to be infected with:

• Hepatitis C virus when they tested positive for anti HCV antibodies using a third generation ELISA commercial kit.

• Hepatitis B virus when they tested positive for HBsAg and/ or positive HBcAb with a detectable viral load using a real time polymerase chain reaction assay. Hepatitis B surface antigen was tested using a third generation ELISA test. The test was considered positive when the optical density of the test sample was greater than the threshold. It was considered negative when the optical density of the test sample was lower than the threshold.

• Hepatitis D virus Screening was only requested when there was evidence of hepatitis B infection. Patients were considered infected when they had a positive serology. Commercial total anti-HDV antibody ELISA kits were used to screen for hepatitis D viral infection.

Tests for other causes of cirrhosis (serum ceruloplasmin and slit lamp examination for Wilson’s disease, tests for autoantibodies for autoimmune liver disease, iron studies for hemochromatosis) were practically not carried out in our study.Cirrhosis was said to be related to alcohol when consumption was at least 40 g per day for men and 30 g per day for women.

Ultrasound Doppler

All patients underwent ultrasonography after overnight fast and the following details were recorded: Maximum vertical span of the liver; nodularity of liver surface; spleen size (length of its longest axis); diameter of the portal and splenic veins; and presence of ascites [10].

Endoscopic Evaluation

All patients underwent upper gastrointestinal endoscopy for assessment of esophageal and gastric varices. If esophageal varices were present, they were graded using the North Italian Endoscopic Club as

• Grade 1: small straight varices that can be depressed;

• Grade 2: enlarged tortuous varices occupying less than one third of the lumen; and

• Grade 3: large coil shaped varices occupying more than one third of the lumen [11].

Varices are considered large varices whenever they are either grade 2 or 3.When present, gastric varices were graded following Sarin’s classification [12]. The presence or absence of portal hypertensive gastropathy, gastric and duodenal ulcers were recorded.

Variables

Qualitative variables were gender, cause of cirrhosis, grade of esophageal varices, type of gastric varices, gastric and duodenal ulcers.Quantitative variables were age, Child Pugh score, spleen diameter, portal vein diameter, right liver span, platelet count, serum albumin, serum bilirubin, prothrombin time.

Statistical Analysis

Data was analyzed using the SPSS (version 11 for windows) and Microsoft Excel 2007 softwares. For quantitative variables, means and standard deviations were calculated. For qualitative variables, proportions were calculated with their confidence intervals (CI). Univariate analysis for determining the association of various clinical, laboratory and ultra-sonographic variables with presence of esophageal varices was performed using Pearson’s χ² test. P<0.05 were considered significant, and all variables found significantly associated with the presence of esophageal varices were studied on multivariate analysis to identify independent predictors of the presence of esophageal varices, and the threshold of predictively of large esophageal varices.

Results

A total of 64 patients were enrolled in our study, most of whom were men (with a male to female ratio of 1.78) and a media nage of 54 years old (Figure 1).

Figure 1: Distribution of patients with respect to age.

While hepatitis C-related cirrhosis predominantly affected elderly patients, hepatitis B infected patients were relatively younger (Figure 2). Similarly, while delta hepatitis was mostly with cirrhosis among young patients, risky alcohol consumption predominantly affected the elderly.

Figure 2: Distribution of patients according to the etiology of cirrhosis within the various age groups.

Ascitis was the most relevant clinical finding at inclusion, followed by jaundice. No patient in our study presented with encephlopathy, spinar angiomata or leukonychia. Only 18 patients (28.13%) had compensated cirrhosis at inclusion.

Esophageal varices were present in 48 patients (75%). Nine had gastroesophageal varices, with 77.78 being type I (Table 1).

Table 1: Non-invasive markers and their correlation to esophageal varices.

Bilirubin, portal vein diameter and prothrombin time were not significantly associated with the presence of esophageal varices. All other markers were significantly associated with the presence off esophageafl varfices (Table 1).

A statistically significant correlation was found between the presence of esophageal varices and the platelet count on spleen diameter ratio on one hand (p=0.01) and the right liver span on albumin ration on the other hand (p=0.02).

The predictive values of the various markers were generally low. Spleen diameter, Child Pugh score and right liver span on albumin ratio had the highest sensitivity, specificity, positive and negative predictive values. The area under the receiver operation curve (AUROC) was significant only for the spleen diameter, Child Pugh score and the right liver span on albumin ration (Table 2).

Table 2: Predictivity of large esophageal varices.

Discussion

A total of 64 patients were enrolled in the study. The sex ratio was 1.78 (41 men against 23 women). This male preponderance correlates with most findings both in African and Western studies. It was reported to be 1.88 by Mouliom in 2006 [13]. The median age was 54 years old.

Viral hepatitis accounted for the majority of cases of cirrhosis in our study, as is the case with most African series [13,14-16], contrary to findings in western countries were alcoholic liver diseases and metabolic diseases are more rampant [17]. As a matter of facts, 51.6% (33 patients) had HBV related liver cirrhosis, 46.9% (30 patients) had HCV related cirrhosis and only 14.1% had alcohol related cirrhosis. The mean age at presentation of HBV related cirrhosis was 36.41 years, with a peak within the group of patients aged between 30-39 years. Ankouane et al in a recent study found the mean age of patients with HBV related hepatocellular carcinoma to be 38.5 ± 12.3 years [18]. On the otherhand, the mean age at presentation of HCV related cirrhosis was 66.17%. Likewise, Ankouane et al reported that most patients with hepatitis C virus related hepatocellular carcinoma were beyond age 50 (mean 61.5 years old) [19].

Of the 64 cirrhotic patients enrolled, 46 (71.87%) presented with decompensation. In most studies, cirrhosis is diagnosed at decompensation with ascites being its commonest unveiling mode [13,20-22]. This portrays the long asymptomatic characteristic of this chronic disease. While 20.31% had their cirrhosis revealed by upper gastrointestinal bleeding, 7.81% had it revealed by jaundice. Jaundice was not as frequent a mode of decompensation of cirrhosis in our study compared to findings in similar studies in other parts of Africa [20,23]. Furthermore, none of our patients presented with hepatic encephalopathy. In our study, esophageal varices were present in 48 patients (75%) with 53.15% having large esophageal varices (34 patients). Even higher rates have been reported in other African studies [20,23]. Mouliom reported that 86% of cirrhotic patients had esophageal varices [13]. Gastric varices were present in 9 of our patients (14.01%) and were all gastroesophageal varices, predominantly type 1 (77.78% of all GOV). Mouliom reported a rate of gastric varices of 19.40% [13].

Data on the relationship between Child Pugh score and the risk of EV is somewhat conflicting. One study showed that Child Pugh score was an acceptable predictor of the presence of EV [24], whereas another well designed study suggested that it was not a useful predictor [25-27]. In our study however, 18 patients (28.13%) were Child Pugh A, 31 patients (48.44%) Child Pugh B and 15 patients (23.44%) Child Pugh C. Ascites was the predominant mode of decompensation as earlier mentioned. The relative risk increased from 1.87 to 2.86 as we moved from patients with Child Pugh A to classes B and C respectively (p-values of 0.006 and 0.012). This association has been described by several authors [24,28-31]. Using the linear logistic regression model, patients with a score greater or equal to 8 were significantly at risk of presenting high grade esophageal varfices (Table 2). Furfthermore, Chfifld Pugh score appears fto be an independent predictor of esophageal varices on multivariate analysis.

The mean spleen diameter in patients in our study was 142.86 mm (range: 68 mm to 240 mm). Similar high spleen diameters have been reported by Mouliom in Cameroon and other studies conducted in Sub-Saharan countries [13,29,31]. Spleen diameter greater than 140 mm were 2.37 times more at risk of having esophageal varices (p=0.004). Using the linear logistic regression model, patients with a spleen diameter greater 148.339 mm were significantly at risk of having high grade esophageal varices (p<0.001), with a positive predictive value of 0.75. Splenomegaly in cirrhosis is equally an independent predictor of esophageal varices.

The mean platelet count in our population was 109266 cells/ mm³ (range: 59000 mm³-432000 mm³). There was an inverse correlation between platelet count and the grade of esophageal varices which was found to be statistically significant. Patients with platelet count less than 100000/mm³ were twice at risk of developing esophageal varices (p value=0.013). Patients with platelet count less than or equal to 104117 cells/ mm³ were at risk of presenting with large esophageal varices. However, contrary to findings of other studies, this correlation was not statistically significant (p=0.055).

Though not a marker of portal hypertension, prothrombin level decreases with advanced liver disease (which results in increase portal hypertension). Similarly to what has been reported by Lahmidani in 2015 [32], there was no correlation between prothrombin level and the grade of esophageal varices in our study. The relative risk did not change with a drop in prothrombin level. The mean prothrombin level in our study was 61.21% (range 15%-99%). However a positive correlation has been reported by some authors [33-35].

The mean serum albumin level in our population was 33.20 g/l (range: 20.17 g/l-54 g/l). It appeared to decrease with increasing grade of esophageal varices. As a matter of facts, the relative risk was 2.61 for patients with an albumin level between 28 g/l and 35 g/l, while it was 1.39 for patients with an albumin level less than 28 g/l. This finding has been equally reported by Sarwar et al [36]. A level less or equal to 32.24 g/l in our study had a statistically significant correlation with the presence of large esophageal varices following the linear logistic regression model (p=0.009). However its sensitivity and positive predictive value were low (0.38 and 0.43) with an AUROC less than 0.5.

There was no correlation between bilirubin level and the grade of esophageal varices. Though patients with bilirubin level between 34 and 50 μmol/L were 2.12 times more at risk of presenting esophageal varices, this correlation was not significant (p=0.18). A local study equally found that there was no correlation [13].There was equally no correlation between the portal vein diameter and the presence of esophageal varices in our study (p-value of 0.55 for a cut off of 12 mm). Our mean portal vein diameter was found to be 12.63 mm (range: 8 mm-21 mm). Similar findings have been reported by Wan-dong H et al [37].

The mean platelet count on spleen diameter (PC/SD) ratio in our study was 840.82. This ratio decreased with an increase in the size of esophageal varices using the logistic regression model, and the correlation was statistically significant (p=0.004). This correlation has consistently been reported by several authors [33,38,39-41]. Patients with a ratio less or equal to 736 were significantly at risk of having large esophageal varices, though the sensitivity and positive predictive value were low (0.38 and 0.42). This ratio was also found to be an independent predictor of esophageal varices on multivariate analysis (p=0.001).

The right liver span on albumin ratio has equally been reported as a promising predictive marker of the presence of esophageal varices [38,41]. The mean ratio in our study was 4.4574 and it significantly correlated with the presence and grade of esophageal varices (p=0.017). A ratio greater or equal to 4.8 was significantly predictive of high grade esophageal varices (p=0.006), with a sensitivity of 0.56 and a positive predictive value of 0.76 (AUROC=0.67). This is equally found to be an independent predictor of esophageal varices on multivariate analysis (p=0.02).

Conclusion

Cirrhosis predominantly affects adult male patients, and is mostly associated to chronic viral hepatitis. Child Pugh score, spleen diameter, platelet count on spleen diameter and right liver span on albumin ratios were independent predictors of esophageal varices. Portal vein diameter and bilirubin level were not significantly associated with the presence of esophageal varices. Voluntary screening programs will help diagnose liver disease an early stage and prevent the occurrence

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