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“Serrated polyps” is the term used for epithelial lesions of the colon and rectum that have a “sawtooth” pattern on the polyp's surface and crypt epithelium. The so-called serrated pathway describes the progression of sessile serrated adenomas and traditional serrated adenomas to colorectal cancer. Said pathway is well recognized as an alternative mechanism of carcinogenesis and accounts for 15-30% of the cases of colorectal cancer. It also explains a large number of the cases of interval colorectal cancer. Thus, due to their usually aggressive and uncertain behavior, serrated polyps are of the utmost importance in colorectal cancer screening. Our aim was to review the history, current nomenclature, pathophysiology, morphology, treatment, and surveillance of serrated polyps. Resumen: «Pólipos serrados» es el término utilizado para describir lesiones epiteliales del colon y recto que demuestran un patrón de «dientes de sierra» de la superficie y epitelio de las criptas. La llamada vía serrada describe la progresión de adenomas serrados sésiles y adenomas serrados tradicionales a cáncer colorrectal. Esta vía está bien reconocida como un mecanismo de carcinogénesis alternativo, el cual representa el 15-30% de los casos de cáncer colorrectal, explicando además una proporción significativa de los casos de cáncer colorrectal de intervalo. Por tal motivo, debido a su comportamiento incierto y usualmente agresivo, los pólipos serrados son un tema de suma relevancia en el cribado de cáncer colorrectal. Nuestro objetivo fue revisar la historia, nomenclatura actual, fisiopatología, características morfológicas, tratamiento y vigilancia de los pólipos serrados.

Introduction: Angiodysplasias are responsible of 50% of small bowel bleeding. An endoscopic method that allows measuring its severity is not available. Aims: The aim of the study was to validate a new endoscopic score with VCE to measure the severity of small bowel angiodysplasias (SBAD). Methods: Four endoscopists independently reviewed VCE videos of 22 patients with SBAD. The score graded 3 variables: A – extent of lesions: E1, located in one half of the intestine and E2, in both halves; B – number of lesions: N1, 10 lesions; C – probability of bleeding: P1, pale red spots; P2, bright red spots; P3, bleeding stigmata; and P4, active bleeding. Capsule Endoscopy Small Bowel Angiodysplasia Activity Index (CESBAI) was calculated as follows: E × 1 + N × 2 + P × 3. Interobserver variability was analyzed by Spearman’s correlation and agreement Kappa statistic tests. Results: The mean CESBAI scores by observers were O1= 11.6 ± 4.1; O2 = 11.3 ± 4.8; O3 = 11.1 ± 4.9; and O4 = 11.8 ± 4.2 (p > 0.05). Spearman’s correlation values of CESBAI between every 2 observers were from 0.61 to 0.94 (p < 0.001) with a global correlation of 0.73 among all observers. Kappa values of CESBAI between every 2 observers ranged from 0.42 to 0.87 (p < 0.001) with a global agreement of 0.57 among all observers. All evaluators stated that the method was easy to use. Conclusions: CESBAI is a reliable and reproducible score. Nevertheless, these results must be validated in other studies with larger population before assessing its power for predicting bleeding recurrence.

More than 30 million persons worldwide take nonsteroidal anti-inflammatory drugs (NSAIDs) on a daily basis, and annual consumption is increasing. In addition to their analgesic and anti-inflammatory properties, NSAIDs also produce well-known gastrointestinal adverse events. There is no consensus in Mexico on the diagnosis, treatment, and prevention of NSAID-induced gastropathy and enteropathy, and so the Asociación Mexicana de Gastroenterología brought together a group of experts to establish useful recommendations for the medical community. Thirty-three recommendations were formulated in the present consensus, highlighting the fact that the risk for NSAID-induced gastrointestinal toxicity varies according to the drug employed and its pharmacokinetics, which should be taken into account at the time of prescription. The risk factors for gastroduodenal complications due to NSAIDs are: a history of peptic ulcer, age above 65 years, high doses of NSAIDs, Helicobacter pylori infection, and the presence of severe comorbidities. The symptoms and gastroduodenal damage induced by NSAIDs vary, ranging from an asymptomatic course to the presentation of iron-deficiency anemia, bleeding, stricture, and perforation. Capsule endoscopy and enteroscopy are direct diagnostic methods in NSAID enteropathy. Regarding prevention, the minimum dose of an NSAID needed to achieve the desired effect, administered for the shortest period of time, is the recommendation. Finally, proton pump inhibitors are the gold standard for the prophylaxis and treatment of gastroduodenal effects, but they are not useful in enteropathy. Resumen: Más de 30 millones de personas consumen diariamente antiinflamatorios no esteroideos (AINE) en el mundo, y este consumo se ve incrementado anualmente. Aunque los AINE poseen propiedades analgésicas y antiinflamatorias, sus eventos adversos gastrointestinales son bien reconocidos. En nuestro país no existía un consenso respecto al diagnóstico, tratamiento y prevención de la gastropatía y la enteropatía por AINE, por lo que la Asociación Mexicana de Gastroenterología reunió a un grupo de expertos para establecer recomendaciones de utilidad para la comunidad médica. En este consenso se emitieron 33 recomendaciones. El consenso destaca que el riesgo de toxicidad gastrointestinal de los AINE varía según el fármaco empleado y su farmacocinética, lo cual debe ser considerado al momento de su prescripción. Los factores de riesgo de complicación gastroduodenal por AINE son: antecedente de úlcera péptica, edad mayor a 65 años, dosis altas del AINE, infección por Helicobacter pylori (H.pylori), y presencia de comorbilidades graves. Los síntomas y el daño gastroduodenal inducido por AINE son variables ya que puede cursar asintomático o manifestarse como anemia por deficiencia de hierro, hemorragia, estenosis y perforación. La cápsula endoscópica y la enteroscopia son métodos diagnósticos directos en la enteropatía por AINE. Respecto a la prevención, se recomienda prescribir la dosis mínima necesaria de un AINE para obtener el efecto deseado y durante el menor tiempo. Finalmente, los inhibidores de la bomba de protones (IBP) representan el estándar de oro para la profilaxis y tratamiento de los efectos gastroduodenales, mas no son útiles en la enteropatía.

Resumen: Más de 30 millones de personas consumen diariamente antiinflamatorios no esteroideos (AINE) en el mundo y este consumo se ve incrementado año tras año. Aunque los AINE poseen propiedades analgésicas y antiinflamatorias, sus eventos adversos gastrointestinales son bien reconocidos. En nuestro país no existía un consenso respecto al diagnóstico, tratamiento y prevención de la gastropatía y la enteropatía por AINE, por lo que la Asociación Mexicana de Gastroenterología reunió a un grupo de expertos para establecer recomendaciones de utilidad para la comunidad médica. En este consenso se emitieron 33 recomendaciones. El consenso destaca que el riesgo de toxicidad gastrointestinal de los AINE varía según el fármaco empleado y su farmacocinética, lo cual debe ser considerado al momento de su prescripción. Los factores de riesgo de complicación gastroduodenal por AINE son: antecedente de úlcera péptica, edad mayor de 65 años, dosis altas del AINE, infección por Helicobacter pylori y presencia de comorbilidades graves. Los síntomas y el daño gastroduodenal inducido por AINE son variables, ya que puede cursar asintomático o manifestarse como anemia por deficiencia de hierro, hemorragia, estenosis y perforación. La cápsula endoscópica y la enteroscopia son métodos diagnósticos directos en la enteropatía por AINE. Respecto a la prevención, se recomienda prescribir la dosis mínima necesaria de un AINE para obtener el efecto deseado y durante el menor tiempo. Por último, los inhibidores de la bomba de protones representan el estándar de oro para la profilaxis y tratamiento de los efectos gastroduodenales, mas no son útiles en la enteropatía. Abstract: More than 30 million persons worldwide take nonsteroidal anti-inflammatory drugs (NSAIDs) on a daily basis, and annual consumption is increasing. In addition to their analgesic and anti-inflammatory properties, NSAIDs also produce well-known gastrointestinal adverse events. There is no consensus in Mexico on the diagnosis, treatment, and prevention of NSAID-induced gastropathy and enteropathy, and so the Asociación Mexicana de Gastroenterología brought together a group of experts to establish useful recommendations for the medical community. Thirty-three recommendations were formulated in the present consensus, highlighting the fact that the risk for NSAID-induced gastrointestinal toxicity varies according to the drug employed and its pharmacokinetics, which should be taken into account at the time of prescription. The risk factors for gastroduodenal complications due to NSAIDs are: a history of peptic ulcer, age above 65 years, high doses of NSAIDs, Helicobacter pylori infection, and the presence of severe comorbidities. The symptoms and gastroduodenal damage induced by NSAIDs vary, ranging from an asymptomatic course to the presentation of iron-deficiency anemia, bleeding, stricture, and perforation. Capsule endoscopy and enteroscopy are direct diagnostic methods in NSAID enteropathy. Regarding prevention, the minimum dose of an NSAID needed to achieve the desired effect, administered for the shortest period of time, is the recommendation. Finally, proton pump inhibitors are the gold standard for the prophylaxis and treatment of gastroduodenal effects, but they are not useful in enteropathy. Palabras clave: Gastropatía, Enteropatía, Antiinflamatorio, No Esteroideo, Úlcera, México, Keywords: Gastropathy, Enteropathy, Anti-inflammatory, Nonsteroidal, Ulcer, Mexico

We present the case of a 37-year-old female with abdominal pain in the epigastrium radiating to the right flank of a month of evolution. On physical examination, the epigastric mass was palpated, firm and painless. Computed tomography (CT) showed a cystic tumor in the body and tail of the pancreas with solid areas and defined borders (12 x 10 cm), which displaced structures. Endoscopic ultrasound (EUS)-guided fine needle biopsy was performed, with a cytology consistent with solid pseudopapillary tumor (SPT). Subsequently, a distal pancreatectomy with tumor resection and nodal dissection were performed. Cytology reported discohesive cells, some arranged around capillaries, with small nuclei with clefts, CK7 negative and β-catenin positive. After four years of follow-up, there is no evidence of recurrence.

Acute cholangitis is a life-threatening infection, and several features are associated with a worse prognosis if prompt treatment is not started. Eighty-six subjects with acute cholangitis were included in a retrospective analysis. Patients had a median age of 53 years (range: 34.5 to 70 years) and 55 (64.0 %) were female. Of the entire cohort, 16 patients had a history of diabetes mellitus. Regarding acute cholangitis severity, 17 (19.8 %) cases were classified as severe, 41 (47.7 %) as moderate, and 28 (32.6 %) as mild.

Severe acute respiratory syndrome coronavirus 2 infection is the cause of coronavirus disease 2019 (COVID-19), which predominantly affects the respiratory system; it also causes systemic and multi-organic disease. Liver damage is among the main extrapulmonary manifestations. COVID-19-associated liver injury is defined as any liver damage occurring during the disease course and treatment of COVID-19 in patients with or without pre-existing liver disease, and occurs in approximately one in five patients. Abnormal liver test results have been associated with a more severe course of COVID-19 and other complications, including death. Mechanisms linking COVID-19 to liver injury are diverse. Particular consideration should be made for patients with pre-existing liver disease, such as metabolic dysfunction-associated fatty liver disease, chronic liver disease due to viral or autoimmune disease, liver transplant carriers, or cirrhosis, given the risk for more severe outcomes. This manuscript summarizes the current lines of evidence on COVID-19-associated liver injury regarding pathophysiology, clinical significance, and management in both patients with or without pre-existing liver disease, to facilitate clinicians' access to updated information and patient care. Finally, we mention the ideas and recommendations to be considered for future research.

We present the case of a 63-year-old woman with obscure gastrointestinal bleeding (OGIB) due to jejunal cavernous hemangioma diagnosed by video capsule endoscopy (VCE), contrast enhanced computed tomography (CECT) and CT angiography, who was successfully treated with surgical resection. Small bowel cavernous hemangioma is a rare cause of OGIB, most commonly presenting as an iron-deficiency anemia. Two decades ago, the preoperative diagnosis was quite difficult. Currently, the use of VCE and device assisted enteroscopy (DAE) allow detection of the lesion. Biopsy is not recommended due to the risks of uncontrolled bleeding. The use of CECT and CT angiography may be useful for demonstrate the vascular nature of the lesion, and define localization, number and extension of the lesion preoperatively in order to improve surgical results as was observed in our patient. Surgery is the most frequent treatment, notwithstanding, endoscopic resection of lesions has been recently reported. However, the experience is small and there are serious limitations of this technique.

The prevalence of overt diabetes mellitus (DM) in liver cirrhosis is about 30%. However, DM or impaired glucose tolerance can be observed in 90% after an oral glucose tolerance test in patients with normal fasting plasma glucose. Type 2 DM may produce cirrhosis, whereas DM may be a complication of cirrhosis. The latter is known as «hepatogenous diabetes». Overt and subclinical DM is associated with liver complications and death in cirrhotic patients. Treating diabetes is difficult in cirrhotic patients because of the metabolic impairments due to liver disease and because the most appropriate pharmacologic treatment has not been defined. It is also unknown if glycemic control with hypoglycemic agents has any impact on the course of the liver disease.

Aims. To define the prevalence and clinical characteristics of glucose metabolism disorders (GMD) in patients with compensated liver cirrhosis (LC). Material and methods. Fasting plasma glucose (FPG) levels were measured to 130 patients with clinically stable LC. Oral glucose tolerance tests (OGTT) and fasting plasma insulin determinations were performed to patients with normal FPG. Insulin resistance (IR) was calculated with HOMA2-IR index. GMD were classified according to FPG and OGTT tests results and to the chronologic relation between diagnosis of diabetes mellitus (DM) and LC as follows: type-2 DM (T2DM), hepatogenous diabetes (HD) and impaired glucose tolerance. Patients from all groups were compared. Results. The prevalence of GMD were as follows: T2DM in 25 patients (19.2%, 95% CI 12.5-25.9), HD in 28 (21.5%, 95% CI 14.5-28.5) and IGT in 36 (38.5%, 95% CI 30.1-46.7). The total of patients with GMD was 79.2% (95% CI 72.3-86.1). In 41% of cases GMD were subclinical and 48.7% of patients had IR. Patients with T2DM had a higher number of variables with significant differences compared with the other groups (more marked compared to the patients without GMD). The only differences between the patients with T2DM and HD were hypercreatininemia: 1.14 ± 0.53 vs. 0.84 ± 0.22 mg/dL (p = 0.005) and family history of DM: 8 (32%) vs. 2 (7%) (p = 0.02). Conclusion. Almost 80% of patients with compensated LC had GMD. Half of them were subclinical. The patients with T2DM had marked clinical differences compared to patients from the other groups, particularly renal impairment.

Multiple biliary hamartomas are rare benign malformations of the intrahepatic bile ducts first described by von Meyenburg in 1918. They originate from embryonic bile ducts that fail to involute. These are generally asymptomatic and usually encountered as an incidental finding at imaging, laparotomy or autopsy.

Diabetes developed as a complication of cirrhosis is known as «hepatogenous diabetes» (HD). Around 30% to 60% of cirrhotic patients suffer from this metabolic disorder. Insulin resistance in muscular, hepatic and adipose tissues as well as hyperinsulinemia, seem to be pathophysiologic bases for HD. An impaired response of the islet β-cells of the pancreas and the hepatic insulin resistance are also contributing factors. Diabetes develops when defective oxidative and nonoxidative muscle glucose metabolism develops. Non-alcoholic fatty liver disease (NAFLD), alcoholic cirrhosis, chronic hepatitis C (CHC), and hemochromatosis are more frequently associated with HD. HD in early cirrhosis stages may be sub clinical. Only insulin resistance and glucose intolerance may be observed. As liver disease advances, diabetes becomes clinically manifest, therefore HD may be considered as a marker for liver function deterioration. HD is clinically different from that of type 2 DM since it is less frequently associated with microangiopathy and patients suffer complications of cirrhosis more frequently as well as increased mortality. Insulin resistance and HD associate to a decrease in the sustained response to antiviral therapy and an increased progression of fibrosis in patients with CHC. Diabetes treatment is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs that are frequently prescribed to these patients. This paper will review current concepts in relation to the pathopysiolo-gy, the impact on the clinical outcome of cirrhosis, and the therapy of HD. Finally, the role of HD as a risk factor for the occurrence and exacerbation of hepatocel-lular carcinoma (HCC) will also be reviewed.

AIM: To determine if subclinical abnormal glucose tolerance (SAGT) has influence on survival of non-diabetic patients with liver cirrhosis. METHODS: In total, 100 patients with compensated liver cirrhosis and normal fasting plasma glucose were included. Fasting plasma insulin (FPI) levels were measured, and oral glucose tolerance test (OGTT) was performed. According to OGTT results two groups of patients were formed: those with normal glucose tolerance (NGT) and those with SAGT. Patients were followed every three months. The mean follow-up was 932 d (range of 180-1925). Survival was analyzed by the Kaplan-Meyer method, and predictive factors of death were analyzed using the Cox proportional hazard regression model. RESULTS: Of the included patients, 30 showed NGT and 70 SAGT. Groups were significantly different only in age, INR, FPI and HOMA2-IR. Patients with SAGT showed lower 5-year cumulated survival than NGT patients (31.7% vs 71.6%, P = 0.02). Differences in survival were significant only after 3 years of follow-up. SAGT, Child-Pugh B, and high Child-Pugh and Model for End-Stage Liver Disease (MELD) scores were independent predictors of death. The causes of death in 90.3% of cases were due to complications related to liver disease. CONCLUSION: SAGT was associated with lower survival. SAGT, Child-Pugh B, and high Child-Pugh and MELD scores were independent negative predictors of survival.

Background. Clinical and endoscopic features of cirrhotic patients with nonvariceal upper gastrointestinal bleeding (NVUGIB) have been rarely reported and clinical outcomes and predictors of mortality have not been evaluated. Aims. 1) To describe the clinical features; 2) To define the clinical outcomes; and 3) To identify the predictors of in-hospital mortality of cirrhotic patients with NVUGIB. Methods. One hundred sixty cirrhotic patients with NVUGIB were prospectively studied. Clinical features, endoscopic findings, clinical outcomes and in-hospital mortality rate were studied. Predictors of death were identified by means of univariate and multiple logistic regression analysis. Results. The mean age was 56.5 ± 14.4, male gender prevailed. Alcohol was the most frequent etiology. Hemodynamic instability was reported in 29.4%. Mean serum hemoglobin was 9.5 ± 3.3 g/dL and blood transfusions were required in 59.4%. Gastroduodenal ulcers were the most frequent source of bleeding (50.6%). In endoscopy “high-risk” bleeding stigmata (HRBS) at the ulcer base were found in 53.1%. All patients with HRBS received endoscopic treatment. Rebleeding occurred in 3 patients (1.9%) and mortality was of 13.8%. By univariate analysis: Cryptogenic etiology, BUN, hypoalbuminemia, active bleeding at ulcer base, and endoscopic treatment were predictors of mortality. However, only cryptogenic etiology, hypoalbuminemia and active bleeding at ulcer base were independent predictors of death in multivariate analysis. Conclusions. Gastroduodenal ulcers as a source of NVUGIB are frequent in cirrhotic patients. They were severe; half of them had HRBS, and required frequently endoscopic treatment. In-hospital mortality of these patients seemed to be greater than that of non-cirrhotic patients, and it was significantly related to cryptogenic etiology of cirrhosis, renal dysfunction, severe hepatic failure, and active bleeding ulcers on admission to the hospital.

OBJECTIVE to determine the independent predictors of in-hospital death of Hispanic patients with nonvariceal upper gastrointestinal bleeding (NVUGB). EXPERIMENTAL DESIGN prospective and observational trial. PATIENTS in a period between 2000 and 2009, all patients with NVUGB admitted to our hospital were studied. Demographical and clinical characteristics, endoscopic findings and laboratory tests were evaluated χ² and Mann-Whitney U analyses were per-formed for comparisons, and binary logistic regression was employed to identify independent predictors of in-hospital mortality. RESULTS 1,067 patients were included, 65% male with a mean age of 58.8 years. Mean number of comorbidities per patient was 1.6 ± 0.76. The most frequent cause of bleeding were gastric and duodenal ulcers (55.4%); 278 patients (25.8%) received endoscopic treatment of which 69.1% had combined therapy. Rebleeding occurred in 36 patients (3.4%) of which 50% died. In-hospital mortality was 10.2%, of which only 3.1% was associated to bleeding. When comparing causes of death among patients with and without comorbidities, only hypovolemic shock was found significative (48.3 vs. 25%; p = 0.020). Binary logistic regression found that the number of comorbidities, Rockall scale score; serum albumin < 2.6 g/dL on admission; rebleeding and length of hospital stay were independent risk factors of in-hospital mortality. CONCLUSION the number of comorbidities, the Rockall scales core, an albumin level < 2.6 g/dL, the presence of rebleeding and hospital stay were predictors of in-hospital mortality in patients with NVUGB.

Introduction Diabetic myonecrosis was first reported by Angervall and Stener in 1965. In its classical clinical expression, it affects type 1 diabetes mellitus patients with long-standing poor metabolic control and advanced chronic microvascular complications. A sudden-onset of severe pain in the region of the involved muscle, usually the quadriceps, is the typical clinical manifestation. Magnetic resonance imaging (MRI) confirms the clinical diagnosis; in some cases of diagnostic uncertainty, a muscle biopsy may be required. Case Presentation We present the case of a 38 year-old Hispanic male from Mexico, with alcohol-induced hepatic cirrhosis (Child-Pugh C/MELD 45) and type 2 diabetes mellitus admitted to the emergency room due to hepatic encephalopathy with intense pain and an increase in volume of the left thigh. MRI showed edema and inflammatory changes of the quadriceps muscle with a hyperintense signal on T2-weighted images; in addition, there was a subacute hematoma. Conclusion To the best of our knowledge, this is the first case of diabetic myonecrosis associated with and complicated by advanced hepatic cirrhosis reported in the literature.

About 30% of patients with cirrhosis have diabetes mellitus (DM). Nowadays, it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease. DM, which develops as a complication of cirrhosis, is known as "hepatogenous diabetes". Insulin resistance in muscular and adipose tissues and hyperinsulinemia seem to be the pathophysiologic bases of diabetes in liver disease. An impaired response of the islet beta-cells of the pancreas and hepatic insulin resistance are also contributory factors. Non-alcoholic fatty liver disease, alcoholic cirrhosis, chronic hepatitis C (CHC) and hemochromatosis are more frequently associated with DM. Insulin resistance increases the failure of the response to treatment in patients with CHC and enhances progression of fibrosis. DM in cirrhotic patients may be subclinical. Hepatogenous diabetes is clinically different from that of type 2 DM, since it is less frequently associated with microangiopathy and patients more frequently suffer complications of cirrhosis. DM increases the mortality of cirrhotic patients. Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs. This manuscript will review evidence that exists in relation to: type 2 DM alone or as part of the metabolic syndrome in the development of liver disease; factors involved in the genesis of hepatogenous diabetes; the impact of DM on the clinical outcome of liver disease; the management of DM in cirrhotic patients and the role of DM as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma.

Background and Aims: To define if there is an imbalance in plasma levels of some proinflammatory, fibrogenic and antifibrogenic cytokines of patients with liver cirrhosis (LC) and impaired glucose tolerance (IGT) or Diabetes Mellitus (DM) . Methods: We studied 54 patients with compensated LC who had normal fasting plasma glucose (FPG) levels. An oral glucose tolerance test (OGTT) was carried out:18 patients were normal, 18 had IGT, and 18 had DM. Plasma levels of the following cytokines were measured: TNF-α, Soluble Tumor Necrosis Factor Receptor 1 (sTNF-R1), Leptin, TGF-β1, and Hepatocyte Growth Factor (HGF). Also, fasting plasma insulin (FPI) levels were measured and HOMA2-IR was calculated. Results were compared with those of a control group of 18 patients without liver disease or DM. Data were expressed as medians and interquartile ranges. Intergroup comparison was performed using non parametric tests. Results:. Patients with IGT and DM had significantly higher sTNF-R1 (p = 0.0043 and 0.0045 respectively) (Figure 1) and significantly lower TGF-β1 (p = 0.001 and 0.001 respectively) (Figure 2) compared to controls. Leptin , HGF, and TNF-α showed no significant differences among cirrhotic patient and controls. Correlations between sTNF-R1 and HOMA2-IR and between leptin and HOMA2-IR were found. Conclusions: IGT and DM were associated to an imbalance of sTNF-R1 and TGFβ1 in cirrhotic patients. At the same time sTNF-R1and leptin correlated with IR. These findings may suggest that sTNF-R1 might be implicated in the development of DM or in the deterioration of liver function in cirrhotic patients with DM.