| Abstract|| |
Tuberculous peritonitis is a common form of abdominal tuberculosis and is frequently associated with liver disease. Diagnosis of this disease presents a diagnostic dilemma and the presence of liver cirrhosis further confounds the clinical picture. Moreover, the co-existence of these two diseases casts doubt on the validity of various diagnostic tests available. The interpretation of tests of ascitic fluid analysis becomes questionable despite the fact that peritoneal tuberculosis and liver disease cause ascites to develop through separate mechanisms. In addition, the treatment of tuberculosis mandates a better understanding of the co-existent disease in view of the potential hepatotoxicity of anti-tuberculous medication. This review aims to address the prevalence of coexistent liver disease in patients with tuberculous peritonitis, the diagnostic difficulties posed by such and the various treatment approaches to be adopted.
Keywords: Tuberculous peritonitis, peritoneal tuberculosis, cirrhosis, liver disease, treatment
|How to cite this article:|
Sanai FM. The liver in tuberculous peritonitis. Saudi J Gastroenterol 2006;12:93-4
Peritoneum and its reflections are common sites oftuberculous involvement of the abdomen and it comprises of31-58% of cases of abdominal tuberculosis,.
An abnormally high prevalence of this disease is found inpatients with underlying alcoholic liver disease (ALD). In astudy by Shakil et al, 90% of cases with mixed tuberculousperitonitis (TBP) and cirrhosis were related to ALD. However,occurrence of this disease in non-alcoholic cirrhotics is notunusual. Reports originating from the western world suggestthat the coexistence of cirrhosis with TBP occurs in 62%,while those originating from developing nations suggestlower coexistence rates of up to 13%,.
Malnutrition frequently develops in cirrhotic patients andis more prominent in patients with ALD due to a numberof reasons. Previous studies have documented the poorernutritional health of patients with ALD compared to nonalcoholics. Additionally, these patients demonstratecutaneous anergy to a variety of antigens, suggesting impairedT cell-dependent functions, and this immune defect is againmore commonly seen in ALD compared to cirrhosis from othercauses. Therefore, it is likely that an interaction betweenimmunological dysfunction and malnutrition produces thehigher prevalence of TBP in patients with cirrhosis.
An enlarged liver or a spleen is uncommon in TBP, butfrequently seen in those with underlying liver disease andlikely reflects underlying portal hypertension. Presence ofhepatosplenomegaly rather than a shrunken liver is consistentwith the observation that alcohol is a common etiology for theunderlying liver disease of these patients  . It must also beborne in mind that concomitant tuberculous involvement ofthe liver may also result in hepatomegaly  .
The prothrombin time may be prolonged especially in thesetting of underlying liver disease. Lymphocytic predominanceof the ascitic fluid analysis is typical of TBP. However, this isby no means pathognomonic since a misleading lymphocyticpredominance may be created in portal-hypertensive ascitesat the end of diuresis or immediately after antibiotic therapy.As such, the presence or absence of lymphomonocytic ascitesis not a reliable marker of tuberculosis, while its existencemay serve as a reasonable indicator for further investigations.Ascitic fluid total protein (AFTP) levels greater than 25 g/Lis seen in almost all patients with isolated TBP but the testshould be interpreted with caution when TBP complicatescirrhosis which causes a significant reduction of sensitivity(42 to 70%) ,. Furthermore, AFTP greater than 25 g/L isseen in nephrogenous ascites, cirrhosis, cardiac ascites andperitoneal carcinomatosis.
A low serum-ascites albumin gradient (≤ 11 g/L) is seen in100% of patients with TBP  . However, the sensitivity fallsto 29-88% when TBP complicates chronic liver disease,.Similarly, adenosine deaminase (ADA) activity in the asciticfluid has overall sensitivity and specificity levels over 90%for the diagnosis of TBP. But, Hillebrand et al reported amuch lower sensitivity of 59% and postulated that their lowersensitivity may have been related to the higher incidence ofcirrhosis in their group of patients. These observations werecountered by Burgess et al when they evaluated cirrhoticpatients with TBP in their study and reported a sensitivity of94%, a figure that was consistent with other studies.
Delay in treatment initiation can lead to significantmortality. Chow et al reported an overall mortality of 35%in patients with TBP, while in the subset of patients withunderlying cirrhosis it was up to 73%. A major concern inthe treatment of TBP is the hepatotoxicity of anti-tuberculousdrugs in view of the high ratio of co-existing cirrhosis.Asymptomatic elevation of aspartate transaminase (AST)occurs uncommonly with the standard 4-drug regimen fortuberculosis. According to recent recommendations by theAmerican Thoracic Society, Centers for Disease Control, andInfectious Disease Society of America, in such situations drugtherapy need not be altered but the frequency of clinical andlaboratory monitoring should be increased. Stoppage oftreatment is recommended if AST is elevated five folds; orthree folds in the presence of symptoms . An increase inbilirubin or alkaline phosphatase is also considered serious.Attempts to restart treatment should be made when ASTvalues are less than two folds increased and the preferreddrug to be introduced first is rifampicin (RIF), followed byisoniazid (INH) and pyrazinamide (PZA) a week apart. ASTelevations may occur from tuberculous involvement of theliver, while in others, as previously discussed, there may be apre-existing liver disease.
The treatment of TBP in patients with background liverdisease is problematic. The likelihood of drug-induced hepatitismay be greater. Also, the implications of hepatotoxicity forpatients with cirrhosis are potentially serious. One study ofpatients with tuberculosis and underlying liver disease usedINH, RIF, ethambutol (EMB) and ofloxacin for 2 monthsfollowed by INH and RIF for 10 months and found 0%hepatotoxicity, while the control cohort utilizing a standardregimen developed hepatotoxicity in 26% . Treatmentrecommendations include any of the following regimens insuch a scenario  :
1) RIF, PZA and EMB for 6 months.
2) INH, RIF, EMB for 2 months followed by INH and RIF for another 7 months.
3) RIF, EMB, a fluoroquinolone, cycloserine/injectible agents for 12-18 months.
4) EMB, streptomycin, a fluoroquinolone and another second line oral drug.
| References|| |
|1.||Al Karawi MA, Mohamed AE, Yasawy MI, Graham DY, Shariq S, Ahmed AM, et al. Protean manifestations of gastrointestinal tuberculosis: report on 130 patients. J Clin Gastroenterol 1995; 20:225-32. [PUBMED] |
|2.||Radhika S, Rajwanshi A, Kochhar R, Kochhar S, Dey P, Roy P. Abdominal tuberculosis: diagnosis by fine needle aspiration cytology. Acta Cytol 1993;37:73-8. |
|3.||Shakil AO, Korula J, Kanel GC, Murray NGB, Reynolds TB. Diagnostic features of tuberculous peritonitis in the absence and presence of chronic liver disease: a case control study. Am J Med 1996;100:179-85. |
|4.||Al Muneef M, Memish Z, Al Mahmoud S, Al Sadoon S, Bannatyne R, Khan Y. Tuberculosis in the belly: a review of forty-six cases involving the gastrointestinal tract and peritoneum. Scand J Gastroenterol 2001;5:528-32. |
|5.||Mimica M. The usefulness and limitations of laparoscopy in the diagnosis of tuberculous peritonitis. Endoscopy 1992;24:588-91. [PUBMED] |
|6.||Caly WR, Strauss E, Carrilho FJ, Laudanna AA. Different degrees of malnutrition and immunological alterations according to the aetiology of cirrhosis: a prospective and sequential study. Nutrition J 2003;2:10. [PUBMED] |
|7.||Schirren CA, Jung MC, Diepolder H, Hoffmann R, Riethmuller G, Pape GR. Analysis of T cell activation pathways in patients with liver cirrhosis, impaired delayed hypersensitivity and other T cell-dependent functions. Clin Exp Immunol 1997; 108:144-50. [PUBMED] |
|8.||Sanai FM, Bzeizi KI. Systematic review: tuberculous peritonitis - presenting features, diagnostic strategies and treatment. Aliment Pharmacol Ther 2005; 22:685-700. [PUBMED] |
|9.||Hillebrand DJ, Runyon BA, Yasmineh WG, Rynders GP. Ascitic fluid adenosine deaminase insensitivity in detecting tuberculous peritonitis in the United States. Hepatology 1996:24;1408-12. [PUBMED] |
|10.||Burgess LJ, Swanepoel CG, Taljaard JJF. The use of adenosine deaminase as a diagnostic tool for peritoneal tuberculosis. Tuberculosis 2001;81:243-48. |
|11.||Chow KM, Chow VCY, Hung LCT, Wong SM, Szeto CC. Tuberculous peritonitis-associated mortality is high among patients waiting for the results of mycobacterial culture of ascitic fluid samples. Clin Infect Dis 2002;35:409-13. |
|12.||American Thoracic Society/ Centers for Disease Control and Prevention/ Infectious Disease Society of America: treatment of tuberculosis. Am J Respir Crit Care Med 2003;167:603-62. |
|13.||Saigal S, Agarwal SR, Nandeesh HP, Sarin SK. Safety of an ofloxacinbased antitubercular regimen for the treatment of tuberculosis in patients with underlying chronic liver disease: a preliminary report. J Gastroenterol hepatol 2001;16:1028-32. [PUBMED] |
Faisal M Sanai
Hepatology division (A41) Department of Medicine, Armed Forces Hospital, PO Box 7897, Riyadh 11159
Source of Support: None, Conflict of Interest: None