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Hepatic encephalopathy (HE) is the most common complication, and one of the complicating manifestations of liver disease. Malnutrition is the most common complication of liver failure. Furthermore, it is a prognostic factor (survival rate, length of stay in hospitals and life quality) in cirrhosis patients. The primary concept of HE pathogenesis is intestine-derived nitrogen compounds that affect brain function. Daily protein intake is a key in HE pathogenesis; therefore, HE patients need nutrient intake in addition to medication

Virus Hepatitis B (VHB) eradication still cannot be achieved under current clinical guidelines due to the typical virus life cycle. Four phases of disease in chronic hepatitis B infection have been used as guidance in preparing therapy indications. Virus suppression with a nucleoside analog (NA) is an important part of chronic hepatitis B therapy, but the high post-termination recurrence rate of NA results in an unlimited duration of therapy. Long-term NA therapy results in various problems such as resistance, reduced adherence, side-effects, and economic burden for patients. The latest findings add to the possibility of larger HBsAg seroconversion after the termination of NA therapy. Various guidelines provide guidance on the termination of NA therapy. It is stated that the termination of NA therapy can be performed using strict surveillance methods for individuals who have undergone antiretroviral therapy after which follows HBeAg seroconversion, minimal amount of VHB DNA, non-cirrh osis status, and normal ALT levels

This report concerns a case of esophageal stricture treatment after drinking corrosive substances (strong acid). Esophageal stricture can be caused by a malignancy and non-malignancy, including strong acid. Manifestations of esophageal stricture include swallowing difficulty, particularly solid food, sore throat on swallowing, and history of drinking or ingestion of corrosive substances. The therapeutic principle of esophageal stricture includes maintaining the esophageal mucosa to maintain good esophageal patency, esophageal diameter, minimizing stricture and fibrosis formations, and minimizing mucosal tissue damage

Tuberculosis Peritonitis is a parietal or visceral peritoneal inflammation caused by Mycobacterium tuberculosis bacteria. Pathogenesis Tuberculosis peritonitis is preceded by infection with M. tuberculosis followed by spreading to the peritoneum. This is a report of a young female patient with a major complaint of overall abdominal pain and weight loss accompanied by other non-specific clinical symptoms such as fever, enlargement (ascites), with malnutrition, and a history of the patient's child being treated for tuberculosis lymphadenitis. The investigation showed anemia, erythrocyte sedimentation rate (ESR) and increased CRP, and ascites fluid analysis showed an exudate, ascites glucose ratio with blood < 0.96. Radiological examination of abdominal ultrasound found ascites, with abdominal CT scan examination finding thickening of the intestinal wall, supporting tuberculosis (TB) with bilateral ovarian cyst appearance. Diagnosis of tuberculosis peritonitis is based on histologic tiss ue examination by laparotomy. This laparotomy examination is performed because anamnesis, physical examination, and other support are not able to determine a definitive diagnosis. Furthermore, patients receive Fixed Drug Combination (FDC) therapy consisting of Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol for 2 months, followed by a combination of Rifampicin and Isoniazid for 7-10 months. The prognosis of tuberculosis peritonitis is sufficient if the diagnosis is immediate and patients are adequately treated

Hepatitis C is a disease caused by hepatitis C virus (HCV), which can cause liver cirrhosis and cancer. Chronic hepatitis C infection has extrahepatic manifestations, including thrombocytopenia. Patients with this disease have exhibited varied thrombocytopenia prevalence, with reported prevalence of more than 24%. Thrombocytopenia pathogenesis in chronic hepatitis C infection involves the interaction of various factors, including liver fibrosis, hypersplenism, bone marrow suppression, immune dysfunction and decreased levels and activity of thrombopoietin. Thrombocytopenia affects chronic hepatitis C infection treatment, including adjustment of antiviral dose especially Peg-IFN, delayed or canceled invasive procedures for diagnosis and therapy related to surgery. Thrombocytopenia therapy in patients with chronic hepatitis C can be divided into two: pharmacological treatments, including steroid administration, platelet transfusion, targeted thrombopoiesis therapy, thrombopoietin recepto r activation therapy, and non-pharmacological therapy, including splenectomy and partial splenic embolization. Steroid administration for thrombocytopenia treatment in chronic hepatitis C infection is not used because it can worsen liver damage. Some pharmacological therapies still require further research and are still in the experimental stage in regard to their effectiveness and safety in thrombocytopenia treatment in chronic hepatitis C infection.

Irritable bowel syndrome (IBS) is a large bowel functional disorder characterized by abdominal pain or discomfort and is associated with bowel habit changes without organic disorder. IBS is affected by many factors and is suspected of involving central and peripheral mechanisms, such as gastrointestinal dysmotility, bowel visceral/mucosal hypersensitivity, increased bowel permeability and interaction among the luminal factors including food and bowel microbiota changes, bowel epithelial barrier, mucosa immunity, genetic factor and biopsychosocial and brain gut axis which are suspected to affect IBS pathophysiology. Understanding the various factors and mechanisms underlying IBS helps in the consideration of management and repair of patients’ prognosis

Achlorhydria is defined as a decrease in secretion quantity or decrease in the acidity of gastric acid. Gastric acid has several functions including activating other digestive enzymes, deciphering the food particles in the digestive process, essential vitamins and minerals absorption, and eliminating most of the microorganisms that enter with the food. There is no specific management for achlorhydria. Patients with achlorhydria in addition to experiencing disorders of HCl formation generally also suffer from pepsin deficiency. Therefore, pepsin is usually given to support the provision of betaine HCl. Patients with achlorhydria should be periodically monitored for early diagnosis of anemia due to iron deficiency and/or cobalamin. Calcium and vitamin D deficiency can be monitored through serum 25 hydroxyvitamin D level as well as bone density examination

A 21-year-old male patient was admitted to the Emergency room of Dr. Soetomo General Hospital with a chief complaint of decrease in consciousness. Jaundice and mental status changes were found. Laboratory testing showed hyperbilirubinemia, progressive rise in serum alanine and aspirate aminotransferase levels, rise in prothrombin time and International Normalized Ratio (INR), positive IgM anti HAV. Diagnosis of this patient was acute liver failure due to acute hepatitis A. The patient was treated treatment with O2 nasal 3-4 lpm, a low-protein diet, fluid therapy including NaCl 0.9%, dextrose 10% and Branch Chain Amino Acids (BCAA), inj. ranitidine 2x1 amp, vitamin K 3x1 amp, FFP transfusion 10 cc/kg (first hour) followed by 1 cc/hour, lactulose syrup 4x30 cc, L-ornithine-L-aspartate 4 ampoule/PZ 100 cc for 4 hours. The patient was discharged in good condition. Three weeks later, the patient was monitored at the outpatient clinic, and jaundice was not found.

Constipation is a symptom characterized by defecation frequency less than three times a week or fecal impaction. Chronic constipation is characterized by a sense of rectal dissatisfaction, bowel movement difficulty, or both. This literature review will explain the latest pathophysiology of constipation, diagnosis based on international clinical criteria (ROME III), and national consensus of the Indonesian Society of Gastroenterology, as well as the selection of evidence-based therapy. Factors causing chronic constipation include mechanical, metabolic, neuropathic, myopathic and idiopathic. Diagnosis needs to be systematically evaluated from anamnesis, identification of alarm symptoms, physical examination and investigation. Management of chronic constipation depends on the type of constipation. It is performed comprehensively to restore normal physiological defecation function and evaluate constipation causes. Constipation treatment may be pharmacological and non-pharmacological. Cons tipation complications include pelvic organ prolapse, hemorrhoids, hemorrhoid bleeding, fissure ani, fecal impaction causing colonic or stercoraceous ulcer obstruction, resulting in bleeding/perforation and recurrent urinary tract infections due to ureter compression due to stool mass

Over the past decade, significant advances have been made in the noninvasive assessment of liver fibrosis in patients with chronic liver disease. Transient elastography appears to be excellent in assessing liver fibrosis. For the interpretation of liver stiffness measurements, the doctor should know the disease clinically, biologically and morphologically and its parameters. In chronic liver disease, especially in chronic hepatitis C, the value of liver stiffness is strongly correlated with fibrosis stage according to the histology score. Patients with similar fibrosis but high alanine aminotransferase levels tend to have higher liver stiffness values, especially in chronic hepatitis B, and diagnostic performance for low-stage fibrosis can be affected when ALT is elevated. Transient elastography is an excellent tool for early detection of cirrhosis. Although TE cannot completely fulfill the need for liver biopsy, it can be used as an important noninvasive tool that allows the setting up of more efficient and custom management strategies for patients with chronic liver disease

Ulcerative colitis is one part of inflammatory bowel disease and a chronic illness characterized by diffuse inflammation in the colonic mucosa. Ulcerative colitis is also influenced by lifestyle such as smoking, a diet high in sugar and fat, drug use, and stress. Genetic factors also have a role in ulcerative colitis. This study aimed to review the diagnosis and management of ulcerative colitis. The pathogenesis of inflammatory bowel disease is a result of continuous antigen stimulation by commensal enteric bacteria, fungi and viruses causing chronic inflammation in hosts with a genetic disorder and defects in mucosal barrier function as well as immunoregulation. The main clinical symptoms of ulcerative colitis are diarrhea with blood and mucus and abdominal pain. The diagnosis of ulcerative colitis is established based on typical clinical symptoms, stool examination, colonoscopy, and biopsy checks. These steps are performed to confirm the presence of colitis and to exclude infection. A typical endoscopic and histological outcome with negative outcomes from evaluation for infectious diseases will support the diagnosis of ulcerative colitis. Treatment of ulcerative colitis should be adjusted to the severity of the disease, divided into therapeutics for maintenance and therapy for remission. The goal of therapy is to induce and maintain remission conditions to improve patients’ quality of life, reduce long-term steroid requirements and minimize cancer risk. Patients' prognosis is generally quite good despite the often-deteriorating quality of life.

Paralytic ileus is a disease with transport disturbance of intestinal contents due to decreased smooth muscle activity in the small intestine or colon. Complications will occur when paralytic ileus is not treated adequately. Intestinal passage interference occurs in paralytic ileus; therefore, the food cannot be digested. Paralytic ileus causes include postoperative ileus, inflammation, electrolyte disorders, metabolic disorders, drugs, intestinal obstruction and trauma. Paralytic ileus treatment can be divided into two: supportive therapy and etiology therapy. The prognosis of paralytic ileus patients is generally good

Short bowel syndrome (SBS) is malabsorption due to intestinal surface area insufficiency. In Europe, the incidence of home Total Parenteral Nutrition (TPN) is approximately three cases per million people per year, and the prevalence is four cases per million per year, whereas most people who get home TPN are patients with SBS at 35%. There are three types of SBS bowel resection types, namely ileocolonic, jejunocolonic, and jejunostomy. The main causes of SBS in adults are bowel resection associated with vascular disorders and Crohn's disease. Clinical manifestations of SBS are malabsorption of macronutrients, fluids, and electrolytes, vitamin and mineral deficiencies, diarrhea, gastric hypersecretion, wound healing and infection. SBS management includes nutrition management, pharmacological management, and surgical management. SBS complications include gallstones, oxalate kidney stones, liver diseases, d-lactate acidosis, peptic ulcers, and metabolic bone disease. This study is a lite rature review aiming to discuss treatment options for short bowel syndrome

Barrett's esophagus (BE) is a displacement of the squamocolumnar border (SCJ) site to proximal to the gastroesophageal junction (GEJ) accompanied by the presence of intestinal metaplasia. BE develops when reflux-induced stomach acid destroys the squamous epithelial layer of the esophagus and this lesion heals via a metaplasia process in which the damaged squamous epithelial layer is replaced by columnar colon-type epithelium. BE prevalence in the general population is about 1.6-1.7%. Patients with gastroesophageal reflux disease (GERD) may progress to BE. This report concerns two cases of patients with Barrett's esophagus. In both these patients BE was found without dysplasia. A diagnosis was made on the basis of anamnesis, physical examination, laboratory, radiological, endoscopy and anatomical pathology. The management of BE is aimed at three main objectives: reduction of symptoms due to GERD, avoiding progression to strictures and ulcers, and preventing progression to adenocarcinom a. Both patients were given a PPI, a prokinetic and chemoprevention NSAID which achieved clinical improvement. Neither patient had ablation, photodynamic or mucosal resection. BE survival is much better than in groups without BE (5 years survival 61% vs. 28%, P = 0.001)

Portal hypertension is a clinical syndrome characterized by pathological elevation of portal venous pressure and all its consequences. In portal hypertension, there is an increase in pressure in the veins that carry blood from the splanchnic organs to the liver. The main factors of portal hypertension include increased intrahepatic resistance to portal blood flow due to degenerative nodules and increased splanchnic blood flow secondary to vasodilation in the splanchnic vascular bed. Clinical symptoms indicated in portal hypertension are varicella hemorrhage with hematemesis or vomiting of blood (vomitus may be red blood mixed with clumps or coffee grounds), and/or melena, i.e. red or black defecation-like petis (shrimp paste). The goal of treatment of patients with portal hypertension is to reduce portal pressure. Drugs for portal hypertension should be able to lower blood vessel portal pressure without lowering arterial pressure, which may aggravate hyperdynamic circulation and incre ase the risk of renal failure. Most of the drugs often used in clinical practice are splanchnic vascular vasoconstrictors vasopressin derivatives (terlipressin), somatostatin, somatostatin analogs (octreotide and vapreotide), Nonselective β-Blocker and Carvedilol.