Effects of coronavirus disease 2019 on the digestive system and its nutritional implications.

PURPOSE OF REVIEW: There has been a deluge of scientific data since coronavirus disease 2019 (COVID-19) was first reported. The effects of COVID-19 on the digestive system are now increasingly well understood. This article aims to review the current data on the effects of COVID-19 on the digestive system with particular emphasis on preexisting digestive diseases and its implications on nutrition practices. RECENT FINDINGS: Evidence has shown that Severe acute respiratory syndrome coronavirus 2 virus affects the gastrointestinal (GI) tract, pancreas and hepatobiliary system resulting in different GI manifestations. Several preexisting digestive diseases have been investigated. These studies have revealed that these special patient population groups are generally not at an increased risk to contract COVID-19, but are susceptible to develop increasing severity of disease. Aside from medical therapy, optimizing nutritional care has a beneficial role in this group of patients. SUMMARY: GI manifestations of COVID-19 in addition to preexisting digestive diseases have an impact on patient's nutrition. Digestion, absorption and transport of nutrients may be impaired. To date, there are no existing guidelines on the nutritional management of patients for this particular at-risk group. Most nutrition practices are based only on observations and clinical experience. Basic prepandemic nutrition care principles are primarily followed but often individualized based on clinical judgment.

Budd-Chiari syndrome: consensus guidance of the Asian Pacific Association for the study of the liver (APASL).

Budd Chiari syndrome (BCS) is a diverse disease with regard to the site of obstruction, the predisposing thrombophilic disorders and clinical presentation across the Asia-Pacific region. The hepatic vein ostial stenosis and short segment thrombosis are common in some parts of Asia-Pacific region, while membranous obstruction of the vena cava is common in some and complete thrombosis of hepatic veins in others. Prevalence of myeloproliferative neoplasms and other thrombophilic disorders in BCS varies from region to region and with different sites of obstruction. This heterogeneity also raises several issues and dilemmas in evaluation and approach to management of a patient with BCS. The opportunity to recanalize hepatic vein in patients with hepatic vein ostial stenosis or inferior vena cava stenting or pasty among those membranous obstruction of the vena cava is a unique opportunity in the Asia-Pacific region to restore hepatic outflow closely mimicking physiology. In order to address these issues arising out of the diversity as well as the unique features in the region, the Asia Pacific Association for Study of Liver has formulated these guidelines for clinicians.

Gastrointestinal Manifestations of COVID-19: Impact on Nutrition Practices.

Although Coronavirus disease 2019 (COVID-19) is primarily a respiratory disease, growing evidence shows that it can affect the digestive system and present with gastrointestinal (GI) symptoms. Various nutrition societies have recently published their guidelines in context of the pandemic, and several points emphasize the impact of these GI manifestations on nutrition therapy. In patients with COVID-19, the normal intestinal mucosa can be disrupted by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, and this could result in GI symptoms and a compromise in nutrient absorption. Optimization of oral diet is still recommended. However, given the GI effects of COVID-19, a fraction of infected patients have poor appetite and would not be able to meet their nutrition goals with oral diet alone. For this at-risk group, which includes those who are critically ill, enteral nutrition is the preferred route to promote gut integrity and immune function. In carrying this out, nutrition support practices have been revised in such ways to mitigate viral transmission and adapt to the pandemic. All measures in the GI and nutrition care of patients are clustered to limit exposure of healthcare workers. Among patients admitted to intensive care units, a significant barrier is GI intolerance, and it appears to be exacerbated by significant GI involvement specific to the SARS-CoV-2 infection. Nevertheless, several countermeasures can be used to ease side effects. At the end of the spectrum in which intolerance persists, the threshold for switching to parenteral nutrition may need to be lowered.

COVID-19 and its effects on the digestive system and endoscopy practice.

The Coronavirus Disease 2019 (COVID-19) is a respiratory illness caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has been classified as a pandemic by the World Health Organization in March 2020. Several studies have demonstrated that the gastrointestinal (GI) tract is also a potential route. As the pandemic is continuously evolving, and more data are made available, this article highlights the best evidence and practices regarding the effects of the SARS-CoV-2 virus relevant to GI practice. Published clinical studies have supported that SARS-CoV-2 affects the GI tract and the liver. The largest published dataset comprised of 4243 patients and showed a pooled prevalence of GI symptoms at 17.6%. GI symptoms varied and usually preceded pulmonary symptoms by 1-2 days. These include anorexia (26.8%), nausea and vomiting (10.2%), diarrhea (12.5%), and abdominal pain (9.2%). Incidence of liver injury ranges from 15 to 53%. Evidence shows that the severity of COVID-19 infection is compounded by its effects on nutrition, most especially for the critically ill. As such, nutrition societies have recommended optimization of oral diets and oral nutritional supplements followed by early enteral nutrition if nutritional targets are not met, and parenteral nutrition in the distal end of the spectrum. In addition to possible fecal-oral transmission, GI endoscopy procedures, which are considered to be aerosol-generating procedures, contribute to increased risk to GI health-care professionals. Infection prevention measures and guidelines are essential in protecting both patients and personnel.

The 2014 Hepatology Society of the Philippines consensus statements on the diagnosis and treatment of hepatitis C

Hepatitis C virus (HCV) infection is a devastating disease that is increasingly being diagnosed among Filipinos, especially in at-risk populations. There are disease-specific nuances in the evaluation and management of this infection. Furthermore, advances in the field brought about by clinical research are rapidly moulding the way we evaluate and manage HCV patients. Evidently, consensus statements formulated by experts in the field are needed in order to serve as a guide to physicians who see HCV patients in the clinic. With this in mind, the Hepatology Society of the Philippines spearheaded the formation of these statements which aimed to address issues in the diagnosis, evaluation, treatment, and follow-up care of patients with HCV infection.Recommendations on the specific tests to perform in the evaluation of HCV patients before, during and after treatment, and first-line treatment of patients with acute and chronic HCV infection were provided. Treatment algorithms for chronic HCV infection, divided according to viral genotype, were also devised. We acknowledge the limitations brought about by the local inavailability of some drugs/treatment regimens in the local setting at the time of the formulation of these statements. As such, these statements will be revised as soon as new data become locally applicable.  

Genotype-specific interactions of insulin resistance, steatosis, and fibrosis in chronic hepatitis C.

UNLABELLED: The interaction between insulin resistance (IR), steatosis and genotype to fibrosis in chronic hepatitis C virus (HCV) infection has not been comprehensively assessed. We hypothesized that IR is a key mediator for the development of both steatosis and fibrosis in 346 untreated, nondiabetic patients solely infected with either genotype 1 or 3. We examined for genotype-specific interactions between IR, steatosis and fibrosis by performing subgroup analyses. Because cirrhosis is known to cause IR, we repeated the analysis in a cohort of 313 noncirrhotic HCV-infected patients. We confirmed the impact of IR on fibrosis by analysis of 153 lean subjects in whom any effect of steatosis would be minimized. In HCV genotype 3 patients, increased steatosis was linked to high viral load (P = 0.001), and was not associated with fibrosis (P = 0.1). In contrast, body mass index (P = 0.04) and homeostasis model assessment of insulin resistance (HOMA-IR) (P = 0.01) contributed directly to steatosis in HCV genotype 1. HOMA-IR rather than steatosis was independently associated with fibrosis for both HCV genotype 1 (OR, 3.22; P = 0.02) and genotype 3 (OR, 3.17; P = 0.04). Exclusion of cirrhotic subjects did not alter the findings with respect to the greater contribution of IR compared to hepatic steatosis, as a predictor of fibrosis (P = 0.02). Genotype-specific subgroup analyses did not alter this finding. The extent of HOMA-IR remained significantly associated with fibrosis in lean patients, independent of the confounding effect of body mass index on IR (OR, 8.02; P = 0.003). CONCLUSION: IR is a major independent determinant of fibrosis in chronic HCV infection, regardless of the genotype and the severity of liver damage.

Combined percutaneous radiofrequency ablation and ethanol injection for hepatocellular carcinoma in high-risk locations.

OBJECTIVE: The purpose of this study was to investigate whether combining percutaneous ethanol injection (PEI) with radiofrequency ablation in the management of hepatocellular carcinoma (HCC) in high-risk locations improves treatment outcomes. SUBJECTS AND METHODS: We compared the outcome of management of high-risk tumors with PEI and radiofrequency ablation (n = 50) or radiofrequency ablation alone (n = 114) with the outcome of radiofrequency ablation of non-high-risk tumors (n = 44). We also compared the survival rates of patients with and those without high-risk HCC. PEI was performed into the part of the tumor closest to a blood vessel or vital structure before radiofrequency ablation. RESULTS: The study included 142 patients with 208 HCCs managed with radiofrequency ablation. Despite larger tumor sizes (2.8 +/- 1 cm vs 1.9 +/- 0.7 cm vs 2.5 +/- 0.1 cm for the high-risk radiofrequency plus PEI, non-high-risk radiofrequency, and high-risk radiofrequency groups, respectively; p < 0.001), the primary effectiveness rate of high-risk radiofrequency ablation and PEI (92%) was similar to that of non-high-risk radiofrequency ablation (96%). The primary effectiveness rate of high-risk radiofrequency ablation and PEI was slightly higher (p = 0.1) than that of high-risk radiofrequency ablation (85%). The local tumor progression rates (21% vs 33% vs 24% at 18 months) of the three respective groups were not statistically different (p = 0.91). Patients with and those without high-risk tumors had equal survival rates (p = 0.42) after 12 (87% vs 100%) and 24 (77% vs 80%) months of follow-up. Independent predictors of primary effectiveness were a tumor size of 3 cm or less (p = 0.01) and distinct tumor borders (p = 0.009). Indistinct borders (p = 0.033) and non-treatment-naive status of HCC (p = 0.002) were associated with higher local tumor progression rates. The only predictor of survival was complete ablation of all index tumors (p = 0.001). CONCLUSION: The combination of radiofrequency ablation and PEI in the management of HCC in high-risk locations has a slightly higher primary effectiveness rate than does radiofrequency ablation alone. A randomized controlled study is warranted.

Insulin resistance and response to therapy in patients infected with chronic hepatitis C virus genotypes 2 and 3.

BACKGROUND/AIMS: Obesity is associated with impaired treatment responses in chronic hepatitis C. The aim of this study was to determine the relationship between the insulin resistance frequently seen in obese subjects and sustained virological response to anti-viral therapy (SVR) in patients with genotype 2 or 3 infection. METHODS: Eighty-two patients were studied; 59 received interferon/ribavirin while 23 received peg-interferon/ribavirin. RESULTS: The overall SVR was (77%). Patients with a SVR had lower mean serum insulin (10.7+/-0.8 microU/ml vs. 22.2+/-4.9; P = 0.03), fibrosis stage (1.9+/-0.1 vs. 2.7+/-0.3; P = 0.007) and insulin resistance measured by the homeostasis model (HOMA-IR) (2.5+/-0.2 vs. 6.1+/-1.5; P = 0.03). Age, gender, ethnicity, alcohol consumption, treatment regimen, viral load, portal activity and steatosis did not influence the SVR. By linear regression, body mass index (P < 0.001) and fibrosis stage (P < 0.001) were independently associated with HOMA-IR. After adjusting for fibrosis stage, patients with HOMA-IR of < 2 were 6.5 times more likely to achieve SVR than those with HOMA-IR > or = 2. CONCLUSIONS: Even in treatment-responsive genotypes 2 and 3, high HOMA-IR is associated with a reduced response. Improving insulin sensitivity may be a useful adjunct to anti-viral therapy in these individuals.

Treatment of hepatocellular carcinoma using internally cooled electrodes. A prospective comparison of modified automated vs. manual pulsed radiofrequency algorithms.

OBJECTIVES: To compare the effectiveness of modified automated and manual pulsed radiofrequency (RF) algorithms using internally cooled electrodes for hepatocellular carcinoma (HCC). METHODS: Seventy-seven treatment-naive cirrhotic patients with 102 HCC (< or =4 cm) underwent 109 sessions of ultrasound-guided percutaneous RF ablation using a 17-gauge, 20-cm-long, single internally cooled electrode. Patients were assigned alternatively: 40 patients to the modified automated algorithm group and 37 patients to the manual algorithm group. The mean tumor diameters were 2.34 +/- 0.9 and 2.25 +/- 0.7 cm in the automated and manual groups, respectively (p = 0.56). Primary technique effectiveness and local tumor progression were compared between the two groups. RESULTS: More overlapping ablations (n = 112) were required in the manual than in the automated group (n = 82) to achieve similar primary technique effectiveness rates of 96.1 and 94.1%, respectively. After a mean follow-up period of 26.7 +/- 1.1 months, the local tumor progression rates at 12 and 18 months were 4 and 20% in the manual group and 12 and 24% in the modified automated group (p = 0.3). Only tumors >3 cm were independently associated with local tumor progression (odds ratio 1.25; 95% CI 1.06-2.34, p = 0.03). CONCLUSIONS: The manual algorithm requires more overlapping ablations and treatment sessions in order to achieve similar primary technique effectiveness and local tumor progression rates compared with the modified automated algorithm.

Insulin resistance and liver injury in hepatitis C is not associated with virus-specific changes in adipocytokines.

UNLABELLED: The role of tumor necrosis factor alpha, interleukin 6, leptin, and adiponectin in the pathogenesis of hepatitis C virus (HCV)-associated insulin resistance (IR) remains controversial. We tested the hypothesis that these adipocytokines contribute to chronic HCV-associated IR and liver injury by first comparing their serum levels and homeostasis model assessment of insulin resistance (HOMA-IR) in 154 untreated, non-diabetic, HCV-infected male subjects with fibrosis stage 0-2, to that in 75 healthy volunteers matched for age, body mass index (BMI), and waist-hip ratio (WHR). We next examined whether the adipocytokine levels were associated with the extent of hepatic steatosis, portal/periportal inflammation and fibrosis in our total cohort of 240 HCV-infected male subjects. Significantly higher levels of HOMA-IR (2.12 versus 1.63, P = 0.01), TNFalpha (1.28 versus 0.60 pg/ml, P < 0.001) and IL6 (2.42 versus 1.15 pg/ml, P = 0.001) were noted in the HCV cohort compared with healthy controls respectively, but there were no significant differences in leptin and adiponectin concentrations. By multiple linear regression, independent predictors of HOMA-IR included the body mass index, and the serum levels of leptin (positive correlation) and adiponectin (negative correlation), but not that of TNFalpha and IL6. Only TNFalpha levels were correlated with the extent of histological injury (portal/periportal inflammation, P = 0.02). CONCLUSION: Whereas leptin and adiponectin contribute to IR, none of the adipocytokines accounted for the elevated IR in HCV-infected subjects. The adipocytokines were not associated with histological features of chronic HCV infection except for TNFalpha which correlated with portal/periportal inflammation. HCV-associated IR is most likely an adipocytokine-independent effect of the virus to modulate insulin sensitivity.

Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis.

Hepatic steatosis has been associated with fibrosis, but it is unknown whether the latter is independent of the etiology of fat infiltration. We analyzed the relationship between clinical characteristics, insulin resistance (HOMA-R) and histological parameters in 132 patients with "viral" steatosis caused by genotype 3 chronic hepatitis C (CHC-3) and 132 patients with "metabolic" steatosis caused by nonalcoholic fatty liver disease (NAFLD), matched by age, BMI, and degree of liver fat accumulation. Tests of liver function were comparable in the two study populations. The prevalence of features of insulin resistance was higher in NAFLD, as was HOMA-R (P = .008). Logistic regression analysis confirmed that steatosis was associated with a high viral load and low serum cholesterol in CHC-3, and with high aminotransferase, glucose, ferritin and hypertriglyceridemia in NAFLD. At univariate analysis, advanced fibrosis was associated with steatosis in NAFLD, but not in CHC-3. Other parameters related to fibrosis severity were HOMA-R and a low platelet count in CHC-3, and high aminotransferases, HOMA-R, ferritin and low HDL-cholesterol in NAFLD. On multivariate analysis, only low platelet count (OR = 0.78; 95% CI, 0.67-0.92) and HOMA-R (OR = 2.98; 1.13-7.89) were independent predictors of advanced fibrosis in CHC-3. In NAFLD, severe fibrosis was predicted by fat grading (OR = 3.03; 1.41-6.53), ferritin (OR = 1.13; 1.03-1.25) and HOMA-R (OR = 1.16; 1.02-1.31). In conclusion, insulin resistance is an independent predictor of advanced fibrosis in both NAFLD and CHC-3, but the extent of steatosis contributes to advanced disease only in NAFLD. Virus-induced hepatic steatosis as seen in CHC-3 does not contribute significantly to liver fibrosis.

Non-alcoholic fatty liver disease.

This article reviews the nomenclature, clinical and histological basis for a diagnosis of non-alcoholic fatty liver disease or non-alcoholic steatohepatitis, its natural history, pathophysiology and an approach to clinical management.