Search

Background and Aim: Innate immune disarray is a key component in the development and progression of acute on chronic liver failure (ACLF) and predisposition to infections. We evaluated the neutrophil dysfunction and its impact on outcomes in patients with ACLF. Methods: Forty patients with acute decompensation of cirrhosis (10 each of grades 0, 1, 2, and 3 ACLF) and 10 healthy controls were prospectively evaluated for neutrophil immunophenotype (NP), neutrophil phagocytic capacity (NPC), and oxidative burst (OB) in both resting and stimulated conditions. The patients were followed up for 90 days or until death or transplant, whichever was earlier. Results: NP was normal (in %) and NPC (in mean fluorescence intensity [MFI]) was better in controls compared to patients with ACLF (83.74 ± 12.38 vs 63.84 ± 22.98; P = 0.007 and 98.33 ± 130.60 vs 18.73 ± 17.88, P = 0.001, respectively). Resting OB was higher in patients with ACLF compared to controls (97 ± 4.9% vs 91 ± 9%; P = 0.034), but it failed to increase further after stimulation, suggesting an immune exhaustion. NP was normal (in %) and NPC (in MFI) was better in 90‐day survivors compared to nonsurvivors (78 ± 11.9 vs 62.2 ± 24.11, P = 0.02 and 33.3 ± 22.7 vs 16.36 ± 13.3; P = 0.004, respectively). Phenotypically normal neutrophils >71.7% had 78.6% sensitivity and 65.4% specificity with an area under receiver operating curve (AUROC) of 0.70 (95% confidence interval [CI]: 0.55–0.90); P = 0.017, and NPC >17.32. MFI had 71.4% sensitivity and 69.6% specificity with an AUROC of 0.73 (95% CI: 0.54–0.86), P = 0.035, in predicting 90‐day survival. Conclusion: Neutrophils have impaired bactericidal function in patients with ACLF compared to healthy adults. Neutrophil phenotype and phagocytic capacity may be used to predict 90‐day survival in patients with ACLF. [ABSTRACT FROM AUTHOR]

Background and Aim: The aim of this study is to evaluate the epidemiology and impact of bacterial infections at admission in patients with acute decompensation (AD) of cirrhosis. Methods: A cohort with AD of cirrhosis (European Association for the Study of the Liver criteria) admitted at a tertiary center was evaluated between 2013 and 2014 for the presence of bacterial infections at admission. Clinical, demographic, and microbiological data were collected prospectively till death, transplant, or 90 days. Results: Of 179 patients with AD, 102 (56.9%) had bacterial infections at admission. The commonest infections were spontaneous bacterial peritonitis (SBP) (n = 65; 63.7%), spontaneous bacteremia (n = 10; 9.8%), pneumonia (n = 9; 8.8%), urinary tract infection (n = 8; 7.8%), spontaneous bacterial empyema (n = 4; 3.9%), and cellulitis (n = 2; 1.9%). The commonest source was community acquired (n = 85; 83.3%). Serum albumin and sodium levels were lower in infected as compared with non‐infected cohort (P = 0.015; for both). Escherichia coli was the commonest organism isolated from SBP (n = 14; 21.5%), urinary tract infection (n = 5; 45.5%), and bacteremia (n = 3; 20%). There was a trend toward higher 28‐day mortality in infected cohort as compared with non‐infected cohort (48 [52.7%] vs 28 [32%]; P = 0.152). Multidrug‐resistant organisms (MDROs) were isolated in 63% of all culture‐positive infections. The presence of MDRO was an independent predictor of 28‐day mortality. Conclusions: Infections are the leading reason for the occurrence of AD; SBP is the most common infection, and E. coli is the commonest microorganism based on this single‐center study of Indian patients with AD of cirrhosis. There is a high prevalence of MDROs among culture‐positive infections that independently predict 28‐day mortality in AD of cirrhosis. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the efficacy and safety of irreversible electroporation (IRE) in the treatment of unresectable hepatocellular carcinoma (HCC).Materials and Methods: A retrospective study was conducted from September 2014 to June 2017. A total of 21 HCCs in 21 patients with cirrhosis were treated with IRE. There were eight subcapsular or exophytic, ten perivascular and three peribiliary tumors. The median tumor size was 26 mm (range 14-40 mm). The technical success of the procedure was recorded. Median follow-up, median time to local recurrence, median local tumor progression-free survival (PFS) and complications were recorded.Results: Technical success was achieved in all the patients. The median follow-up was 10 months (range 2-30 months). The median time to local recurrence and local tumor PFS were 4 months (range 3-4 months) and 7 months (range 3-30 months), respectively. The tumor-related factor that was significantly associated with local PFS was the size. Maximum tumor diameter < 25 mm was significantly associated with local tumor PFS (p = 0.045). Other parameters including tumor location, segmental portal vein thrombosis, baseline alpha-fetoprotein level and underlying etiology did not affect local tumor PFS. Complications were noted in nine patients and were classified as grades 1 and 2. No procedure-related mortality was encountered.Conclusion: IRE is an effective treatment for ablation of small HCCs. Larger prospective studies with strict selection criteria will establish the safety and efficacy of IRE in the treatment of unresectable HCC in patients who cannot undergo thermal ablation. [ABSTRACT FROM AUTHOR]

Background and aim: Due to a dysregulated immune response, patients with acute-on-chronic liver failure (ACLF) have increased risk of infection and multi organ failure in comparison to compensated cirrhosis. The comparative data on the presence of ‘immune paresis’ in patients with ACLF and decompensated cirrhosis without ACLF is not available. Aim of the present study was to compare the immunological parameters in patients with decompensated cirrhosis with and without ACLF. Methodology: In a prospective study, 76 patients with decompensated cirrhosis with (n = 38) and without (n = 38) ACLF and 10 healthy controls (HC) were evaluated for monocytic human leukocyte antigen–antigen D Related (HLA-DR) expression, mean density of HLA-DR expressed on the surface of these cells, neutrophil oxidative burst (NOB) capacity and serum levels of cytokines (IL-1, IL-6, IL-8, IL10, IL-12, and TNF-α). Results: Patients of decompensated cirrhosis with and without ACLF demonstrated significantly lower mean percentage of monocytes expressing HLA-DR and quantitative increase in the NOB after stimulation with PMA when compared to HC. However there was no difference in mean percentage of monocytes with HLA-DR expression (43.61±26.56% vs. 43.10±20.98%) (p = 0.91), mean density of HLA-DR expression on the surface (30.34±29.32 vs. 41.71±52.13) (p = 0.42) and quantitative increase in NOB after stimulation with PMA (16.55±11.91 vs. 17.24±16.18) (p = 0.47) amongst patients with decompensated cirrhosis with and without ACLF. Patients with ACLF had significantly higher pro-inflammatory and anti-inflammatory cytokines in comparison to patients with decompensated cirrhosis without ACLF. Conclusion: Patients with decompensated cirrhosis demonstrate a component of immune-paresis, however there is similar impairment in HLA–DR expression and NOB capacity in patients with and without ACLF. Both inflammatory and anti-inflammatory cytokines are increased in patients with ACLF in comparison to patients with decompensated cirrhosis without ACLF. [ABSTRACT FROM AUTHOR]

There is a paucity of health policy relevant data for chronic liver disease from India, impeding formulation of an interventional strategy to address the issue. A prospective, multicentric study to delineate the etiology and clinical profile of chronic liver disease in India is reported here. A centrally coordinated and monitored web-based data repository was developed (Feb, 2010 to Jan, 2013) and analyzed. Eleven hospitals from different parts of India participated. Data were uploaded into a web based proforma and monitored by a single centre according to a standardized protocol. 1.28% (n = 266621) of all patients (n = 20701383) attending the eleven participating hospitals of India had liver disease. 65807 (24·68%) were diagnosed for the first time (new cases). Of these, 13014 (19·77%, median age 43 years, 73% males) cases of chronic liver disease were finally analyzed. 33.9% presented with decompensated cirrhosis. Alcoholism (34·3% of 4413) was the commonest cause of cirrhosis while Hepatitis B (33·3%) was predominant cause of chronic liver disease in general and non-cirrhotic chronic liver disease (40·8% out of 8163). There was significant interregional differences (hepatitis C in North, hepatitis B in East and South, alcohol in North-east, Non-alcoholic Fatty Liver Disease in West) in the predominant cause of chronic liver disease. Hepatitis B (46·8% of 438 cases) was the commonest cause of hepatocellular Cancer.11·7% had diabetes. Observations of our study will help guide a contextually relevant liver care policy for India and could serve as a framework for similar endeavor in other developing countries as well. [ABSTRACT FROM AUTHOR]

Background/Aim: This study intends to determine the correlation of a patient's hepatic venous pressure gradient (HVPG) measurement with six factors: Child-Turcotte-Pugh (CTP) score, model for end-stage liver disease (MELD) score, presence of ascites, size of varices, presence of variceal bleeding, and an etiology of cirrhosis. The study also aims to identify the predictors of higher HVPG measurements that can indirectly affect the prognosis of cirrhotic patients. Patients and Methods: Thirty patients diagnosed with cirrhosis were enrolled prospectively and each patient's HVPG level was measured by the transjugular catheterization of the right or middle hepatic vein. The wedged hepatic venous pressure (WHVP) and free hepatic venous pressure (FHVP) were measured using a 7F balloon catheter. The HVPG level was calculated as the difference between the WHVP and FHVP measurements. Results: The mean HVPG level was higher in alcoholic than in nonalcoholic cirrhosis (19.5 ± 7.3 vs 15.2 ± 4.5 mm Hg, P = 0.13). The mean HVPG was also higher in bleeders compared with nonbleeders (18.5 ± 5.3 vs 10.7 ± 3.1 mmHg, P = 0.001). Patients with varices had a higher mean HVPG level than those without varices (17.4 ± 5.8 vs 11.7 ± 3.9 mmHg, P = 0.04). The difference among the three categories of varices (small, large, and no varices) was statistically significant (P = 0.03). In addition, the mean HVPG level was higher in patients with ascites than in those without ascites (18.7 ± 4.7 vs 11 ± 5.3 mmHg, P = 0.002), and it was significantly higher in patients in CTP class C (21.8 ± 5.5 mmHg) as compared with those in CTP class B (16.9 ± 2.9 mmHg) and CTP class A (10.5 ± 4.1 mmHg; P ≤ 0.001). Conclusion: HVPG levels were significantly higher in patients in CTP class C as compared with those in CTP classes A and B, thereby indicating that an HVPG measurement correlates with severity of liver disease. A high HVPG level signifies more severe liver disease and can predict the major complications of cirrhosis. [ABSTRACT FROM AUTHOR]

Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion. [ABSTRACT FROM AUTHOR]

OBJECTIVES:Hepatic encephalopathy (HE) represents a spectrum of neurocognitive impairment seen in cirrhotic patients and is considered to be fully reversible with treatment; however, recent evidence suggests otherwise. This longitudinal study was carried out to evaluate the persistence of cognitive impairment in cirrhotics with prior overt HE (OHE) episode despite treatment.METHODS:Of the 213 patients screened, 107 patients who met the eligibility criteria were enrolled and 102 patients completed the study (52 patients without prior OHE episode and 50 patients with prior OHE). All patients underwent psychometric hepatic encephalopathy score (PHES) evaluation at three separate visits (day 1, day 3, and between 30 and 60 days). A one-point improvement in PHES between the first and second evaluation was considered as a measure of learning.RESULTS:Patients with a previous OHE episode showed learning impairment in PHES on repetition on day 3 (P=0.084), whereas patients without a previous OHE episode demonstrated learning effect (P<0.0001) irrespective of whether they had minimal HE (MHE) or not. Univariate analysis demonstrated that Child-Turcotte-Pugh score, lactulose and/or rifaximin therapy, the presence of MHE, and a previous OHE episode were associated with learning impairment. Multivariate analysis demonstrated that only the presence of a previous episode of OHE (adjusted odds ratio 38.398; 95% confidence interval 9.192-160.4; P<0.0001) significantly affected learning.CONCLUSIONS:This study conclusively demonstrated learning impairment in cirrhotic patients with a previous episode of OHE despite normal mental status. Improvement in PHES on repetition may be a measure of learning. [ABSTRACT FROM AUTHOR]

Background/Aims: The role of model for end-stage liver disease (MELD) among Indian patients with cirrhosis is uncertain. We studied and compared MELD with Child-Turcotte-Pugh (CTP) and creatinine-modified-CTP (CrCTP) scores for predicting 1-, 3-, and 6-months mortality. Methods: One-hundred and two patients with cirrhosis were studied. The CrCTP was calculated by adding creatinine score of 0, 2 and 4 with creatinine levels of ≤1.2mg/dL, 1.3–1.8 mg/dL and ≥1.9mg/dL, respectively to CTP score. Survival curves were plotted and receiver operating characteristics (ROC) curves were used to compare the scores. Predictors of mortality were analyzed using Cox proportional hazards model. Results: Scores of CTP, CrCTP, and MELD have excellent diagnostic accuracy for predicting mortality (c-statistics >0.85). The MELD was superior to CTP for predicting 3-months [c-statistic and 95% confidence interval, 0.967 (0.911–0.992) vs 0.884 (0.806–0.939)] and 6-months [0.977 (0.925–0.996) vs 0.908 (0.835–0.956)] mortality (P=0.05), while CrCTP [0.958 (0.899–0.988)] was better than CTP for predicting 3-months mortality (P=0.02). Serum creatinine (hazard ratio 4.43, P<0.0001) is a strong independent predictor of mortality. Conclusion: The MELD accurately predicts mortality in cirrhosis and is better than CTP for predicting the short-term and intermediate-term mortality. Adding serum creatinine to CTP though significantly improves its diagnostic accuracy for short-term mortality; however, it remains lower than MELD alone. [ABSTRACT FROM AUTHOR]

Hepatic encephalopathy (HE) is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Overt HE occurs in approximately 30–45% of cirrhotic patients. Minimal HE (MHE), the mildest form of HE, is characterized by subtle motor and cognitive deficits and impairs health-related quality of life. The Indian National Association for Study of the Liver (INASL) set up a Working Party on MHE in 2008 with a mandate to develop consensus guidelines on various aspects of MHE relevant to clinical practice. Questions related to the definition of MHE, its prevalence, diagnosis, clinical characteristics, pathogenesis, natural history and treatment were addressed by the members of the Working Party. [ABSTRACT FROM AUTHOR]

Background and Aims: Neuropathy in association with chronic liver disease, including cirrhosis, is recognized; however, there are differences in the incidence and type of neuropathy reported. The causal relationship of liver disease to neuropathy has been questioned. This study was designed to evaluate the incidence and character of peripheral neuropathy in patients with liver cirrhosis. The effect of alcohol consumption, severity of liver disease and encephalopathy on the incidence and severity of neuropathy were also studied. Methods: Patients having an identifiable cause of peripheral neuropathy, except alcohol, were excluded from the study. Patients with evidence of vitamin B[sub 12] deficiency or diabetes were also excluded from the study. In this study, 33 patients with liver cirrhosis were evaluated clinically and electrophysiologically to detect any evidence of peripheral neuropathy. Nerve conduction studies were performed in the upper and lower limbs using surface electrodes. These patients also underwent a detailed clinical examination. Results: Clinical signs of peripheral neuropathy were found in seven (21%) patients. Nerve conduction studies were abnormal in 24 (73%) patients. The pattern of involvement was predominantly of an axonal sensory motor polyneuropathy. Neuropathy was found both in patients with alcohol-related and non-alcohol-related cirrhosis. The presence of encephalopathy did not have a significant bearing on the incidence and severity of neuropathy. The neuropathy was also not significantly related to the severity of liver disease. Conclusions: The present study reveals that a significant number of patients with liver cirrhosis show evidence of peripheral neuropathy, which is present regardless of the etiology of cirrhosis, and is subclinical in a majority of these patients. The cause of neuropathy was probably the liver disease itself, as the incidence and severity of neuropathy in the alcohol-related cirrhosis, although higher, was... [ABSTRACT FROM AUTHOR]

Portal hypertension is characterized by an increase in portal pressure (> 10 mmHg) and could be a result of cirrhosis of the liver or of noncirrhotic diseases. When portal hypertension occurs in the absence of liver cirrhosis, noncirrhotic portal hypertension (NCPH) must be considered. The prognosis of this disease is much better than that of cirrhosis. Noncirrhotic diseases are the common cause of portal hypertension in developing countries, especially in Asia. NCPH is a heterogeneous group of diseases that is due to intrahepatic or extrahepatic etiologies. In general, the lesions in NCPH are vascular in nature and can be classified based on the site of resistance to blood flow. In most cases, these disorders can be explained by endothelial cell lesions, intimal thickening, thrombotic obliterations, or scarring of the intrahepatic portal or hepatic venous circulation. Many different conditions can determine NCPH through the association of these various lesions in various degrees. Many clinical manifestations of NCPH result from the secondary effects of portal hypertension. Patients with NCPH present with upper gastrointestinal bleeding, splenomegaly, ascites after gastrointestinal bleeding, features of hypersplenism, growth retardation, and jaundice due to portal hypertensive biliopathy. Other sequelae include hyperdynamic circulation, pulmonary complications, and other effects of portosystemic collateral circulation like portosystemic encephalopathy. At present, pharmacologic and endoscopic treatments are the treatments of choice for portal hypertension. The therapy of all disorders causing NCPH involves the reduction of portal pressure by pharmacotherapy or portosystemic shunting, apart from prevention and treatment of complications of portal hypertension. [ABSTRACT FROM AUTHOR]

Cirrhosis leads to considerable morbidity and mortality, compromises quality of life, and often necessitates assistance in activities of daily living. An informal caregiver bears the psychological burden of coping with the needs of the patient and the knowledge of morbid prognosis of a loved one. This aspect is rarely recognized and almost never addressed in a clinical practice. This cross-sectional study assessed the factors influencing psychological burden of cirrhosis on the caregivers in a predominantly lower-middle socioeconomic class Indian population. Patients underwent psychometric tests [Psychometric Hepatic Encephalopathy Score (PHES)], and questionnaires for quantifying caregiver burden [Perceived Caregiver Burden (PCB) and Zarit Burden Interview (ZBI)] and assessing depression [Beck Depression Inventory (BDI)] and anxiety [Beck Anxiety Inventory (BAI)] were administered. One hundred patients with cirrhosis [70% male, 27% with past hepatic encephalopathy (HE), and 53% with minimal HE] and their caregivers (66% women, 81% spouse, 26.51 years of mean relationship) were evaluated. Caregiver burden scores were higher in patients with previous overt HE than in those without previous overt HE [PCB (74.63 vs. 66.15, P = 0.001), ZBI (27.93 vs. 21.11, P = 0.023), BDI (11.63 vs. 8.96, P = 0.082), and BAI (11.37 vs. 8.12, P = 0.027)]. Similarly, caregivers of patients with minimal HE had higher caregiver burden that those of patients who did not have minimal HE [PCB (70.74 vs. 65.85, P = 0.027), ZBI (26 vs. 19.51, P = 0.015)]. Burden scores correlated well with each other and with liver disease severity scores and negatively correlated with socioeconomic status. Repeated hospital admissions, alcohol as etiology, and lower socioeconomic status were the independent predictors of caregiver burden. Higher perceived burden is common in caregivers of patients with cirrhosis. Repeated hospital admissions, alcoholism, and lower socioeconomic status influence caregiver burden. [ABSTRACT FROM AUTHOR]

Antibiotics and albumin infusion constitute the standard of treatment in patients with decompensated cirrhosis who have spontaneous bacterial peritonitis (SBP). Recent studies have also shown that the use of albumin in patients with advanced liver disease who have infections other than SBP leads to the resolution of acute and chronic liver failure and prevents the development of nosocomial infections. The recommended dose of albumin for these patients is out of reach for many in resource-limited settings like India. The evidence for this recommendation is also scarce. This study aimed to assess the efficacy of a lower dose of albumin infusion in addition to antibiotics on short-term mortality and morbidity in patients with cirrhosis and infections. A prospective, open-label, randomized control study was performed. Consecutive patients with cirrhosis and infections were randomized in a 2:1 ratio into two groups: group A (116) and group B (58) patients. In addition to antibiotics and standard medical therapy, group A was given albumin in a dose of 20 g/day for five days, and group B was given the recommended dose (1.5 g/kg/body weight and 1 g/kg body weight on days one and three, respectively). The primary outcome was in-hospital mortality. Secondary outcomes were improvements in clinical and laboratory parameters. Except for etiology, all the baseline clinical and laboratory variables in both groups were comparable. The in-hospital mortality in groups A and B was (11 [10.67%] vs. 6 [10.09%], (P = 0.965). The duration of hospitalization, 30-day mortality, improvement in shock and sensorium, and absolute improvements in serum creatinine, international normalized ratio (INR), and serum bilirubin were also comparable in both groups. Low-dose albumin infusion in patients with cirrhosis and infections can have the same results as standard-dose albumin and can be used in resource-limited situations. CTRI/2020/03/023794. [Display omitted] [ABSTRACT FROM AUTHOR]

Erectile dysfunction(ED) is common in patients with chronic liver disease(CLD). Although it significantly worsens the quality of life, caregivers and researchers often neglect it. Evaluating the prevalence of ED in patients with CLD, associated factors, and response to therapy with tadalafil, a phosphodiesterase-5 inhibitor. A total of 60 males with Child-Pugh score between 5 and 10 and no overt hepatic encephalopathy were studied. ED was assessed based on the 15-question International Index of Erectile Function (IIEF) questionnaire. Patients were classified as ED+ if score was <25. Patients with ED were given 10 mg of tadalafil for 4 weeks. The mean age was 45.2 he 7.8 years. The mean Child-Turcotte-Pugh (CTP) score was 6.4 sc 1.7, and model for end-stage liver disease (MELD) score was 12.1 sc 4.5. Twenty-seven (45%) patients had compensated cirrhosis, and 45(75%) had alcohol as etiology. Twenty-five (42%) had an IIEF score <25, suggestive of ED. The IIEF score had significant correlation with the presence of ascites(r = −0.27, P 0.04) and serum creatinine (r −0.26, P = 0.05); however, there was no correlation with CTP, MELD, or alcohol as etiology. Among ED group, IIEF scores improved significantly with 4 weeks of tadalafil therapy (15.1 ± 5.6 vs 22.0 ± 3.4, P < 0.001), and 11(44%) had resolution of ED. ED is common in patients with cirrhosis. Tadalafil administration significantly improves ED in these patients. [ABSTRACT FROM AUTHOR]

Tuberculosis remains one of the ‘Captains of the Men of Death’ even today, particularly in the developing world. Its frequency is increased 14-fold in patients with chronic liver diseases (CLD) and liver cirrhosis, more so in those with decompensated disease, probably due to the cirrhosis-associated immune dysfunction syndrome, and case-fatality rates are high. The diagnosis of tuberculosis, particularly the interpretation of the Mantoux test, is also fraught with difficulties in CLD, especially after previous BCG vaccination. However, the greatest challenge in the patient with CLD or liver cirrhosis and tuberculosis is managing their therapy since the best first-line anti-tuberculosis drugs are hepatotoxic and baseline liver function is often deranged. Frequency of hepatotoxicity is increased in those with liver cirrhosis, chronic hepatitis B and chronic hepatitis C, possibly related to increased viral loads and may be decreased following antiviral therapy. If hepatotoxicity develops in those with liver cirrhosis, particularly decompensated cirrhosis, the risk of severe liver failure is markedly increased. Currently, there are no established guidelines for anti-tuberculosis therapy (ATT) in CLD and liver cirrhosis although the need for such guidelines is self-evident. It is proposed that ATT should include no more than 2 hepatotoxic drugs (RIF and INH) in patients with CLD or liver cirrhosis and stable liver function [Child-Turcotte-Pugh (CTP) ≤7], only a single hepatotoxic drug (RIF or INH) in those with advanced liver dysfunction (CTP 8–10) and no hepatotoxic drugs with very advanced liver dysfunction (CTP ≥11). A standard protocol should be followed for monitoring ATT-related hepatotoxicity and for stop rules and reintroduction rules in all these patients, on the lines proposed here. It is hoped that these proposals will introduce uniformity and result in streamlining the management of these difficult patients. [ABSTRACT FROM AUTHOR]