For the sake of patient safety considerations, puncture position could be confirmed endoscopically by transillumination and clear visualization of the indentation prior to puncture needle insertion. The relation of stomach anatomy to the other abdominal organs is of clinical significance to endoscopists, particularly with the advent of PEG. The stomach is commonly described as a “J-shaped” object that sits

in the left upper quadrant of the abdomen. The stomach connects the selleck chemicals llc esophagus at the lower esophageal sphincter, which is fixed in the retroperitoneum region. The duodenum is fixed in position by suspension ligaments, including hepatoduodenal ligament and ligament of Treitz. The stomach is suspended from the dorsal wall of the abdominal cavity. The stomach volume normally ranges from 1.5 to 2 L in adulthood. After overnight fasting, shortly before PEG, the stomach was insufflated with 500–1000 mL of air administered through a nasogastric tube or endoscope to obtain selleck chemical adequate distention of the stomach. The PEG feeding tubes were routinely placed through the abdominal wall to the anterior surface of the stomach. The anterior surface of stomach contacts with adjacent organs varies greatly, depending on the gastric sizes, shapes, and patient’s position. When the stomach is empty, the transverse colon may lie on the front part of stomach. As the stomach

fills, it tends to expand forward and downward in the direction of least resistance. The lowest part of the stomach may reach or be below the region of the umbilicus. Our results showed that the shape, size, and position of the stomach on plain abdominal film should replicate the actual anatomy during PEG.[9] This anatomy shares similar reference of marked puncture points, including: (i) the identical volume

of air insufflated into the stomach, (ii) similar gastric muscular tone of the same patient, (iii) similar supine posture during PEG procedure, and (iv) similar surrounding viscera of the same patient.[9] Using the air insufflation technique may help to guide the site selection prior to the PEG and shorten the PEG procedural time. The traditional location for PEG has been in the left upper quadrant 上海皓元 of the abdomen in the vortex formed by the midline and the left costal margin, regardless of variation in the position of the stomach within the peritoneal cavity.[25] The shape and position can be greatly modified by normal anatomic variation and by extrinsic compression from the surrounding viscera. The actual puncture sites of PEG may be hidden in the thoracic cavity,[9, 11, 13] descend near the umbilicus, or reach the pelvic cavity.[9, 26] The location of the puncture points marked on abdominal films varied greatly. The marked puncture points on the abdominal plain films may lie high under the costal margin (Fig. 3a).

For the sake of patient safety considerations, puncture position could be confirmed endoscopically by transillumination and clear visualization of the indentation prior to puncture needle insertion. The relation of stomach anatomy to the other abdominal organs is of clinical significance to endoscopists, particularly with the advent of PEG. The stomach is commonly described as a “J-shaped” object that sits

in the left upper quadrant of the abdomen. The stomach connects the check details esophagus at the lower esophageal sphincter, which is fixed in the retroperitoneum region. The duodenum is fixed in position by suspension ligaments, including hepatoduodenal ligament and ligament of Treitz. The stomach is suspended from the dorsal wall of the abdominal cavity. The stomach volume normally ranges from 1.5 to 2 L in adulthood. After overnight fasting, shortly before PEG, the stomach was insufflated with 500–1000 mL of air administered through a nasogastric tube or endoscope to obtain Caspase activity assay adequate distention of the stomach. The PEG feeding tubes were routinely placed through the abdominal wall to the anterior surface of the stomach. The anterior surface of stomach contacts with adjacent organs varies greatly, depending on the gastric sizes, shapes, and patient’s position. When the stomach is empty, the transverse colon may lie on the front part of stomach. As the stomach

fills, it tends to expand forward and downward in the direction of least resistance. The lowest part of the stomach may reach or be below the region of the umbilicus. Our results showed that the shape, size, and position of the stomach on plain abdominal film should replicate the actual anatomy during PEG.[9] This anatomy shares similar reference of marked puncture points, including: (i) the identical volume

of air insufflated into the stomach, (ii) similar gastric muscular tone of the same patient, (iii) similar supine posture during PEG procedure, and (iv) similar surrounding viscera of the same patient.[9] Using the air insufflation technique may help to guide the site selection prior to the PEG and shorten the PEG procedural time. The traditional location for PEG has been in the left upper quadrant MCE公司 of the abdomen in the vortex formed by the midline and the left costal margin, regardless of variation in the position of the stomach within the peritoneal cavity.[25] The shape and position can be greatly modified by normal anatomic variation and by extrinsic compression from the surrounding viscera. The actual puncture sites of PEG may be hidden in the thoracic cavity,[9, 11, 13] descend near the umbilicus, or reach the pelvic cavity.[9, 26] The location of the puncture points marked on abdominal films varied greatly. The marked puncture points on the abdominal plain films may lie high under the costal margin (Fig. 3a).

Conclusions: Dietary habits, by increasing the percentage of intestinal Gram-negative endotoxin

producers, may accelerate liver fibrogenesis, introducing dysbiosis as a cofactor contributing to chronic liver injury in NAFLD. (Hepatology 2014;59:1738–1749) “
“Welzel et al.1 found that preexisting metabolic syndrome conferred a statistically significant increase of primary liver cancers that was independent of other risk factors. We suggest that this pathological association may partially be related to the higher body iron stores often found in such patients. A wealth of evidence has established a link between serum ferritin, insulin resistance, and nonalcoholic fatty liver disease (NAFLD). Body iron excess has frequently been found in patients with metabolic R428 solubility dmso syndrome.2 Furthermore, it has been suggested that the relation between serum ferritin and most of metabolic syndrome features might be mediated by the presence of NAFLD at the population-based

level.3 Excessive hepatic iron accumulation in NAFLD can be one of the potential cofactors involved in enhanced oxidative stress, which triggers liver cell necrosis and activation of hepatic stellate cells, both of which lead to fibrosis.4 Indeed, iron depletion by phlebotomy was found to be beneficial in improving insulin resistance in patients with NAFLD and hyperferritinemia.5 On the other hand, it has been shown that individuals with excess total body iron have a higher risk of liver cancer even in the absence of genetic Selleck DAPT hemochromatosis.6 Interestingly, iron depletion therapy with both phlebotomies and a low-iron diet was shown to significantly lower the risk of hepatocellular carcinoma in patients with

chronic hepatitis C.7 Therefore, we hypothesize that iron, metabolic syndrome, NAFLD, and liver cancer may be linked together, and their risk might be modified in parallel by maneuvers that affect either feature. Luca Mascitelli M.D.*, Mark R. Goldstein M.D., FACP†, * Medical Service, Comando Brigata Alpina “Julia”, Udine, Italy, † Fountain Medical Court, Bonita Springs, FL. “
“Background and Aims:  We evaluated the prognosis and associated factors in patients with small hepatocellular carcinoma (HCC; up to 3 nodules, each up to 3cm in diameter) treated with percutaneous 上海皓元医药股份有限公司 radiofrequency ablation (RFA) as first-line treatment. Methods:  Eighty-eight consecutive patients who underwent percutaneous RFA as first-line treatment were enrolled, among whom 70 who had hypervascular HCC nodules which were treated by a combination of transcatheter arterial chemoembolization and RFA. RFA was repeated until an ablative margin was obtained. Results:  The rate of local tumor progression at 1 and 3 years was 4.8% and 4.8%, respectively. The rate of overall survival at 3 and 5 years was 83.0% and 70.

60 ± 0.43 to 1.00 ± 0.36, P < 0.05) was observed 1 month after resection. Patients with consistent CTC7.5 <2 had lower recurrence rates than those with values consistently ≥2 (15.5% versus 87.50%, P < 0.001). EpCAM+ CTCs displayed cancer stem cell biomarkers (CD133 and ABCG2), epithelial-mesenchymal transition, Wnt pathway activation, high tumorigenic potential, and low apoptotic propensity. Conclusion: selleck Stem cell–like phenotypes are observed in EpCAM+ CTCs, and a preoperative CTC7.5 of ≥2 is a novel predictor for tumor recurrence in HCC patients after surgery, especially in patient subgroups with AFP levels of ≤400 ng/mL or low tumor recurrence

risk. EpCAM+ CTCs may serve Proteasome purification as a real-time parameter for monitoring treatment response and a therapeutic target in HCC recurrence. (HEPATOLOGY 2013) Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide, and associated morbidity and mortality rates have escalated in recent years.1 Despite improvements in surveillance and clinical treatment strategies, the prognosis of HCC remains very poor due to high incidence of recurrence and

metastasis.2 Traditional clinicopathological parameters such as tumor morphology, histopathological features, and tumor staging system offer limited information for predicting postoperative recurrence and fail to monitor the therapeutic response in a real-time 上海皓元医药股份有限公司 manner.3 Therefore, it is imperative to develop novel approaches for discriminating high-risk factors of recurrent patients and continuous surveillance of antitumor treatment response. The spread of circulating tumor cells (CTCs) in the blood plays a major role in the initiation of metastases and tumor recurrence after surgery.3 Recent studies have reported that stem cell markers are frequently overexpressed in CTCs of metastatic breast cancer.4 In addition, clinical observations and animal model studies indicate that although thousands of tumor cells disseminate into the circulation, only a small population with stem cell–like properties survives migration

to establish secondary colonies.5, 6 Therefore, CTCs with stem cell properties might be potential sources for cancer relapse and distant metastasis, consistent with the cancer stem cell (CSC) hypothesis.7 AFP, alpha-fetoprotein; AUC, area under the curve; BCLC, Barcelona Clinical Liver Cancer; CI, confidence interval; CK, cytokeratin; CSC, cancer stem cell; CTC, circulating tumor cell; DAPI, 4′,6-diamidino-2-phenylindole; EpCAM+, epithelial cell adhesion molecule–positive; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NOD/SCID, nonobese diabetic/severe combined immunodeficiency; qRT-PCR, quantitative real-time polymerase chain reaction; ROC, receiver operating characteristic; TACE, transcatheter arterial chemoembolization; TTR, time to recurrence.

Achievement of these goals will require ongoing, up-to-date education employing effective strategies. The cost of such programs needs to be prospectively evaluated

in the clinic. I have found the last 40 years of my career in clinical research this website in hepatology to be nothing less than “thrilling.” I hope the same will be so for those who are just starting their careers. This is my last chance to publicly “express my opinion” on medical matters as I retire from medicine to move into a new lifestyle. The author wishes to thank all her patients and colleagues who have helped her enjoy the last 40 plus years so much. The author’s thanks also go to Justus Krabshuis, who provided the graphs he prepared that illustrate the number of RCT reports published on PubMed Medline. “
“The development of end-stage graft disease is suspected Fostamatinib to be partially determined by an individual genetic background. The aim of our study was to determine the prevalence of YKL-40-gene polymorphism in hepatitis C virus (HCV)-positive patients and its impact on the incidence of acute cellular rejection (ACR), graft fibrosis and antiviral treatment response. A total of 149 patients, who underwent

liver transplantation for HCV-induced liver disease, were genotyped for YKL-40 (rs4950928; G/C) by TaqMan Genotyping Assay. The results were correlated with 616 post-transplant graft biopsies regarding inflammation, fibrosis and evidence for ACR. No association of YKL-40-gemotypes was observed regarding mean inflammation grade (P = 0.216) and antiviral treatment outcome (P = 0.733). However, the development of advanced fibrosis (F3-4) was significantly faster in patients with YKL-40-G-allele: t(CC) = 4.6 versus t(CG/GG) = 2.4 years; P = 0.006. Patients with lower fibrosis (F0-2) compared to advanced fibrosis (F3-4) received

significantly 上海皓元医药股份有限公司 more frequent dual immunosuppression (calcineurin inhibitors [CNIs]/mofetile mycophenolate [MMF] vs CNIs; P = 0.003). ACR-occurrence was associated with YKL-40-genotypes (ACR: CC = 60.4%, CG = 25.0% and GG = 14.6% vs non-ACR: CC = 74.2%, CG = 23.8% and GG = 2.0%; P = 0.009) and with gender compatibility between donor and recipient (P = 0.012). Fibrosis progression and ACR-incidence after transplantation for HCV-induced liver disease seem to be under genetic control. The negative impact of G-allele on post-transplant events observed in our study, deserves attention and should be verified in larger liver transplantation-cohorts. “
“Background and Aim:  Transglutaminase 2 (TG2), catalyzing crosslinking between lysine and glutamine residues, is involved in many liver diseases.

OBJECTIVE: To estimate the cost-effectiveness of birth-cohort screening. DESIGN: Cost-effectiveness simulation. DATA SOURCES: National Health and Nutrition Examination Survey, U.S. Census, Medicare reimbursement schedule, and published sources.TARGET POPULATION: Adults born from 1945 through 1965 with 1 or more visits to a primary care provider annually.TIME HORIZON: Lifetime.PERSPECTIVE: Societal, health care.INTERVENTION: One-time antibody test of 1945-1965 birth cohort.OUTCOME MEASURES: Numbers of cases that were identified and treated and that achieved a sustained viral response; liver disease and death from HCV; medical and productivity costs; quality-adjusted

life-years (QALYs); incremental cost-effectiveness ratio (ICER). RESULTS

OF BASE-CASE ANALYSIS: Compared with the status quo, birth-cohort screening identified 808,580 additional cases of chronic HCV infection Selleckchem C59 wnt at a screening cost of $2874 per case identified. Assuming that birth-cohort Fluorouracil in vivo screening was followed by pegylated interferon and ribavirin (PEG-IFN+R) for treated patients, screening increased QALYs by 348,800 and costs by $5.5 billion, for an ICER of $15,700 per QALY gained. Assuming that birth-cohort screening was followed by direct-acting antiviral plus PEG-IFN+R treatment for treated patients, screening increased QALYs by 532,200 and costs by $19.0 billion, for an ICER of $35,700 per QALY saved. RESULTS OF SENSITIVITY ANALYSIS: The ICER of birth-cohort screening was most sensitive to sustained viral response of antiviral therapy, the cost of therapy, the discount rate, and the QALY losses assigned to disease states. LIMITATION: Empirical data on screening and direct-acting antiviral treatment in real-world clinical settings are scarce. CONCLUSION: Birth-cohort screening for HCV in primary care medchemexpress settings was cost-effective. PRIMARY FUNDING SOURCE: Division of Viral Hepatitis, Centers for Disease Control and Prevention. Americans can always be counted on to do the right thing…after they have exhausted all other possibilities. Winston Churchill After all but ignoring screening for hepatitis C virus (HCV) for many years

(not for lack of will, but from lack of funding), the Centers for Disease Control and Prevention (CDC) has recommended universal screening for Baby Boomers.1 In the United States, HCV prevalence is the highest in those born between 1946 and 1970; 1 in 30 Baby Boomers are infected with HCV. The majority acquired hepatitis C decades ago, before it was even identified (1989).2 Even more troubling is that by 2020, at least one third of them will already have progressed to cirrhosis with its apocalyptic effect on health and healthcare costs.3 Up to three quarters of individuals infected with HCV in the United States are unaware of their HCV status.1 The CDC HCV screening recommendations were, until recently, exclusively targeting individuals with high-risk behaviors.

OBJECTIVE: To estimate the cost-effectiveness of birth-cohort screening. DESIGN: Cost-effectiveness simulation. DATA SOURCES: National Health and Nutrition Examination Survey, U.S. Census, Medicare reimbursement schedule, and published sources.TARGET POPULATION: Adults born from 1945 through 1965 with 1 or more visits to a primary care provider annually.TIME HORIZON: Lifetime.PERSPECTIVE: Societal, health care.INTERVENTION: One-time antibody test of 1945-1965 birth cohort.OUTCOME MEASURES: Numbers of cases that were identified and treated and that achieved a sustained viral response; liver disease and death from HCV; medical and productivity costs; quality-adjusted

life-years (QALYs); incremental cost-effectiveness ratio (ICER). RESULTS

OF BASE-CASE ANALYSIS: Compared with the status quo, birth-cohort screening identified 808,580 additional cases of chronic HCV infection buy Afatinib at a screening cost of $2874 per case identified. Assuming that birth-cohort Torin 1 solubility dmso screening was followed by pegylated interferon and ribavirin (PEG-IFN+R) for treated patients, screening increased QALYs by 348,800 and costs by $5.5 billion, for an ICER of $15,700 per QALY gained. Assuming that birth-cohort screening was followed by direct-acting antiviral plus PEG-IFN+R treatment for treated patients, screening increased QALYs by 532,200 and costs by $19.0 billion, for an ICER of $35,700 per QALY saved. RESULTS OF SENSITIVITY ANALYSIS: The ICER of birth-cohort screening was most sensitive to sustained viral response of antiviral therapy, the cost of therapy, the discount rate, and the QALY losses assigned to disease states. LIMITATION: Empirical data on screening and direct-acting antiviral treatment in real-world clinical settings are scarce. CONCLUSION: Birth-cohort screening for HCV in primary care 上海皓元医药股份有限公司 settings was cost-effective. PRIMARY FUNDING SOURCE: Division of Viral Hepatitis, Centers for Disease Control and Prevention. Americans can always be counted on to do the right thing…after they have exhausted all other possibilities. Winston Churchill After all but ignoring screening for hepatitis C virus (HCV) for many years

(not for lack of will, but from lack of funding), the Centers for Disease Control and Prevention (CDC) has recommended universal screening for Baby Boomers.1 In the United States, HCV prevalence is the highest in those born between 1946 and 1970; 1 in 30 Baby Boomers are infected with HCV. The majority acquired hepatitis C decades ago, before it was even identified (1989).2 Even more troubling is that by 2020, at least one third of them will already have progressed to cirrhosis with its apocalyptic effect on health and healthcare costs.3 Up to three quarters of individuals infected with HCV in the United States are unaware of their HCV status.1 The CDC HCV screening recommendations were, until recently, exclusively targeting individuals with high-risk behaviors.

33 Similar to previous studies,34 we propose that changes in the biliary microenvironment may partly explain the effect of GABA on small and large cholangiocytes. Another interesting aspect to consider regards the possible role of GABA receptor antagonists in experimental models and human pathologies. When the liver of BDL rats is deprived of cholinergic (by vagotomy) or adrenergic (by 6-hydroxydopamine) innervation, large cholangiocytes lose their response to cholestasis and undergo apoptosis, reducing cAMP levels and the choleretic response to secretin.35, 36 The damage and loss of

proliferative and secretory functions of cholangiocytes, by vagotomy and 6-OHDA, is prevented by the administration of forskolin, and β1-/β2-adrenergic receptor agonists.35,

36 Because GABA concomitantly damages NSC 683864 concentration large cholangiocytes and induces ductular reaction, we speculate that the administration of GABA receptor antagonists may prevent the damage of large cholangiocytes (sustaining large biliary proliferation and secretion) in the denervated liver. This may be important for the homeostasis of the transplanted (denervated) liver, where ischemic or infectious insults against intrahepatic bile ducts may not be adequately counteracted during the immediate post-transplant period. The finding that the activation of IP3/Ca2+-dependent signaling regulates the differentiation www.selleckchem.com/products/ulixertinib-bvd-523-vrt752271.html of small into large cholangiocytes supports the concept that cross-talk between IP3/Ca2+ and cAMP is important in the regulation

of biliary homeostasis. For example, alpha-1 adrenergic receptor agonists stimulate secretin-stimulated choleresis of BDL rats by Ca2+- and protein kinase C (PKC)α/βII-dependent activation of cAMP signaling.37 Gastrin inhibits cAMP-dependent secretion and hyperplasia in BDL rats by activation of Ca2+-dependent PKCα.38 In support MCE of our findings, activation of the Ca2+/calcineurin/NFAT2 pathway controls smooth muscle cell differentiation.39 Ca2+ ions regulate the differentiation and proliferation of human bone-marrow–derived mesenchymal stem cells.40 In this study, we have identified two signaling molecules (CaMK I and AC8) playing major roles in the differentiation of Ca2+-dependent small into large cholangiocytes. Previous studies in other cells support the concept that CaMK I regulates the expression of AC8.41 In fact, when secretion was induced by forskolin, a general stimulator of AC isoforms, except for AC9 and sAC, administration of calmodulin inhibitors and AC8 small interfering RNA did not cause a significant inhibitory effect.9 AC8 is the only known calmodulin-activated AC in cholangiocytes, whereas AC9 activity is inhibited by calmodulin.

33 Similar to previous studies,34 we propose that changes in the biliary microenvironment may partly explain the effect of GABA on small and large cholangiocytes. Another interesting aspect to consider regards the possible role of GABA receptor antagonists in experimental models and human pathologies. When the liver of BDL rats is deprived of cholinergic (by vagotomy) or adrenergic (by 6-hydroxydopamine) innervation, large cholangiocytes lose their response to cholestasis and undergo apoptosis, reducing cAMP levels and the choleretic response to secretin.35, 36 The damage and loss of

proliferative and secretory functions of cholangiocytes, by vagotomy and 6-OHDA, is prevented by the administration of forskolin, and β1-/β2-adrenergic receptor agonists.35,

36 Because GABA concomitantly damages selleckchem large cholangiocytes and induces ductular reaction, we speculate that the administration of GABA receptor antagonists may prevent the damage of large cholangiocytes (sustaining large biliary proliferation and secretion) in the denervated liver. This may be important for the homeostasis of the transplanted (denervated) liver, where ischemic or infectious insults against intrahepatic bile ducts may not be adequately counteracted during the immediate post-transplant period. The finding that the activation of IP3/Ca2+-dependent signaling regulates the differentiation C59 wnt in vivo of small into large cholangiocytes supports the concept that cross-talk between IP3/Ca2+ and cAMP is important in the regulation

of biliary homeostasis. For example, alpha-1 adrenergic receptor agonists stimulate secretin-stimulated choleresis of BDL rats by Ca2+- and protein kinase C (PKC)α/βII-dependent activation of cAMP signaling.37 Gastrin inhibits cAMP-dependent secretion and hyperplasia in BDL rats by activation of Ca2+-dependent PKCα.38 In support MCE公司 of our findings, activation of the Ca2+/calcineurin/NFAT2 pathway controls smooth muscle cell differentiation.39 Ca2+ ions regulate the differentiation and proliferation of human bone-marrow–derived mesenchymal stem cells.40 In this study, we have identified two signaling molecules (CaMK I and AC8) playing major roles in the differentiation of Ca2+-dependent small into large cholangiocytes. Previous studies in other cells support the concept that CaMK I regulates the expression of AC8.41 In fact, when secretion was induced by forskolin, a general stimulator of AC isoforms, except for AC9 and sAC, administration of calmodulin inhibitors and AC8 small interfering RNA did not cause a significant inhibitory effect.9 AC8 is the only known calmodulin-activated AC in cholangiocytes, whereas AC9 activity is inhibited by calmodulin.

There were no significant MK0683 differences

of TGF-β1 before and after splenectomy. The reason for the chronological changes in TGF-β1 levels after splenectomy is unknown because various factors including platelets may be involved in the production of TGF-β1. We also found a slightly higher number of TGF-β1 positive cells in non-tumor areas in the liver tissue of patients with HCC than in those without. Furthermore, the number of TGF-β1 positive cells significantly increased with the progression of liver fibrosis.[4, 21, 26, 42] In conclusion, splenectomy in cirrhotic patients with hepatitis may be able to improve liver fibrosis, cause beneficial immunological changes and lower the risk of carcinogenesis. It seems necessary to accumulate further cases to establish a convincing conclusion. This study was partially supported by a Health and Labor Sciences Research Grant from the Ministry of Health, Labor and Welfare Japan, regarding Research on Intractable Diseases, Portal Hemodynamic Abnormalities. “
“Background

and Aim:  Antituberculosis drugs, isoniazid and rifampicin, in combination, are known to develop drug-induced hepatotoxicity (DIH). A higher risk of DIH during antituberculosis treatment (ATT) has been reported in the Indian subcontinent compared to its Western counterparts. The role of genetic factors in a higher incidence of ATT hepatotoxicity in the Indian population is still unclear. The present study was aimed at investigating MCE the role of the N-acetyltransferase2 (NAT2) and cytochrome P4502E1 FDA-approved Drug Library order (CYP2E1) gene polymorphisms in ATT hepatotoxicity. Methods:  The study population included 218 pulmonary tuberculosis patients who were started on ATT and followed

up for the occurrence of ATT-induced hepatitis. The genetic polymorphisms of the NAT2 and CYP2E1 genes were studied by polymerase chain reaction–restriction fragment length polymorphism. Results:  The occurrence of DIH was 18.8% (41/218). There was a higher prevalence of NAT2 slow-acetylator genotypes in DIH (70.73%) compared to non-DIH (44.63%; P < 0.05). The frequency of the NAT2*5/*7 and NAT2*6/*7 genotypes was significantly higher in DIH than non-DIH (19.51% vs 6.78%, and 19.51% vs 5.08%). No association of the CYP2E1 RsaI polymorphism could be demonstrated with DIH. However, the DraI C/D genotype of the CYP2E1 gene was mostly prevalent in DIH (85.37%), compared to non-DIH (64.41%) (P < 0.05). Slow-acetylator status and the CYP2E1 C/D or C/C genotype together showed a higher frequency in DIH (65.85%) compared to non-DIH (28.81%) (P < 0.0001). Conclusion:  The study demonstrates for the first time a possible association between the DraI polymorphism of the CYP2E1 gene and the risk of ATT hepatotoxicity.