Helicobacter Pylori Infection

Helicobacter pylori is a gram negative, urease-producing spiral bacterium colonizing the gastric mucosa, acquired predominantly in childhood via fecal-oral or oral-oral routes, with prevalence closely tied to socioeconomic conditions and sanitation.

It is the dominant cause of chronic gastritis (see that entry), a major cause of peptic ulcer disease (see that entry), and is classified as a Group 1 (definite) carcinogen given its causal role in gastric adenocarcinoma and MALT lymphoma.

Non-invasive "test and treat" testing (for dyspepsia without alarm features, or before eradication confirmation): urea breath test or stool antigen test, both requiring PPI cessation for 2 weeks and antibiotic cessation for 4 weeks before testing to avoid false negatives
Serology detects past exposure but cannot distinguish active from cleared infection and is not useful for confirming eradication
Where endoscopy is already indicated (alarm features, age above threshold): rapid urease test (CLO test), histology, or culture (culture allows susceptibility testing, increasingly valuable given rising resistance)

First line triple therapy: PPI (e.g. omeprazole 20 mg bd) + amoxicillin 1 g bd + clarithromycin 500 mg bd, for 7 to 14 days (14 days increasingly preferred given modestly higher eradication rates than 7 days)
Given rising clarithromycin resistance in many regions, quadruple bismuth-based therapy is increasingly used first line where local resistance exceeds roughly 15%: PPI + bismuth subsalicylate/subcitrate + metronidazole 400 mg bd + tetracycline 500 mg qds, for 10 to 14 days
Penicillin allergy: substitute metronidazole 400 mg bd for amoxicillin in the triple regimen, or use bismuth quadruple therapy
Second line (after triple therapy failure): bismuth quadruple therapy if not already used, or a levofloxacin-based regimen (PPI + amoxicillin + levofloxacin) guided by local resistance data
Confirm eradication with urea breath test or stool antigen at least 4 weeks after completing antibiotics and 2 weeks off PPI, in all cases given the public health and malignancy-prevention importance of confirmed cure, not just symptom resolution
MALT lymphoma localized to the stomach frequently regresses with eradication therapy alone if early stage (see Gastric Cancer entry for further management if it does not)

Referral: gastroenterology for endoscopy where indicated, treatment failure after two eradication attempts, or confirmed MALT lymphoma/malignancy.

Cirrhosis

Also known as: Liver cirrhosis

End-stage result of chronic liver injury characterized by diffuse hepatic fibrosis and regenerative nodule formation, causing distortion of normal hepatic architecture and vasculature, leading to portal hypertension and progressive loss of synthetic/metabolic liver function. Represents the final common pathway of most chronic liver diseases.

Major etiologies:

Alcohol-related liver disease
Metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD/NASH) — increasingly common cause globally
Chronic viral hepatitis (HBV, HCV)
Autoimmune hepatitis
Cholestatic: primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC)
Metabolic/genetic: hemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency
Vascular: Budd-Chiari syndrome, chronic right heart failure (cardiac cirrhosis)
Drug-induced (methotrexate, amiodarone)

Classified by:

Compensated: asymptomatic or mild non-specific symptoms, no major complications
Decompensated: development of ascites, variceal hemorrhage, hepatic encephalopathy, or jaundice — marks major prognostic transition, median survival drops from ~12 years (compensated) to ~2 years (decompensated)
Severity/prognostic scoring: Child-Pugh (A/B/C) and MELD/MELD-Na scores — guide transplant listing and prognosis

Compensated (may be asymptomatic, found incidentally):

Fatigue, anorexia, weight loss, nausea
Signs of chronic liver disease: spider angiomata, palmar erythema, gynecomastia, testicular atrophy, Dupuytren's contracture, caput medusae, leukonychia, clubbing
Hepatomegaly (may become small/shrunken in advanced disease) ± splenomegaly (portal hypertension)

Decompensated:

Ascites: abdominal distension, shifting dullness, fluid thrill — most common decompensation event
Variceal hemorrhage: hematemesis, melena — from esophageal/gastric varices due to portal hypertension
Hepatic encephalopathy: confusion, asterixis (flapping tremor), altered sleep-wake cycle, progressing to stupor/coma (West Haven grading I–IV)
Jaundice: scleral icterus, generalized jaundice — reflects impaired bilirubin conjugation/excretion
Coagulopathy: easy bruising, bleeding (reduced synthesis of clotting factors)
Peripheral edema (hypoalbuminemia)
Muscle wasting/sarcopenia
Fetor hepaticus (sweet, musty breath odor)

Complications to actively screen for: hepatocellular carcinoma (HCC), spontaneous bacterial peritonitis (SBP), hepatorenal syndrome, hepatopulmonary syndrome, portal vein thrombosis.

Labs:
LFTs — may be normal in burnt-out cirrhosis; AST/ALT ratio >1 suggestive of alcohol-related disease
Synthetic function: low albumin, prolonged PT/INR
FBC: thrombocytopenia (earliest lab clue — portal hypertension/hypersplenism), anemia
U&E/creatinine: baseline renal function (hepatorenal syndrome risk)
Non-invasive fibrosis assessment (first-line, replacing biopsy in most cases):
Transient elastography (FibroScan): liver stiffness measurement in kPa — values vary by etiology, generally >12–15 kPa suggestive of cirrhosis
Serum fibrosis markers/scores: FIB-4 index, APRI score — screening tools, especially in MASLD
MR elastography: more accurate, less available
Liver biopsy: gold standard but reserved for diagnostic uncertainty or when etiology unclear despite non-invasive workup
Imaging: ultrasound — nodular liver contour, coarse echotexture, splenomegaly, ascites; also used for HCC surveillance
Etiology workup: viral hepatitis serology (HBsAg, anti-HCV), autoimmune markers (ANA, ASMA, anti-LKM, immunoglobulins), ferritin/transferrin saturation (hemochromatosis), ceruloplasmin (Wilson's, if young), alpha-1 antitrypsin level, lipid profile/HbA1c (MASLD risk factors)
Endoscopy (OGD): screening for esophageal/gastric varices at diagnosis of cirrhosis, repeated per surveillance interval based on findings
HCC surveillance: ultrasound ± AFP every 6 months in all cirrhotic patients

Differentials for decompensation presentations: other causes of ascites (malignancy, TB peritonitis, cardiac), other causes of encephalopathy (sepsis, uremia, drugs, intracranial pathology), other causes of UGIB (peptic ulcer).

General/etiology-specific:

Treat underlying cause: antiviral therapy (HBV — tenofovir/entecavir; HCV — direct-acting antivirals, near-100% cure rates), alcohol cessation (+ addiction support), weight loss/metabolic control for MASLD, immunosuppression for autoimmune hepatitis, venesection for hemochromatosis
Avoid hepatotoxic drugs, NSAIDs (renal risk in cirrhosis), sedatives (precipitate encephalopathy)
Vaccination: hepatitis A/B (if not immune), pneumococcal, influenza, COVID-19
Nutrition: adequate protein intake (1.2–1.5g/kg/day — do NOT protein-restrict, worsens sarcopenia), avoid prolonged fasting, late-evening snack recommended (reduces overnight catabolism)

Ascites management:

Sodium restriction (<2g/day)
Diuretics: spironolactone 100mg od (up titrate to max 400mg/day) ± furosemide 40mg od (up titrate to max 160mg/day), typical ratio 100:40 — monitor renal function/electrolytes closely
Large-volume paracentesis for tense/refractory ascites — albumin replacement 6–8g per liter removed if >5L drained (prevents post-paracentesis circulatory dysfunction)
Refractory ascites: consider TIPS (transjugular intrahepatic portosystemic shunt) or liver transplant referral

Variceal hemorrhage:

Primary prophylaxis (known varices, not yet bled): non-selective beta-blocker (propranolol, carvedilol) or endoscopic variceal band ligation
Acute bleed: resuscitation, restrictive transfusion strategy (target Hb ~7–8g/dL), IV terlipressin or octreotide (splanchnic vasoconstriction), prophylactic antibiotics (ceftriaxone 1g IV od — reduces mortality, prevents SBP/rebleeding), urgent endoscopy within 12 hours for band ligation/sclerotherapy
Secondary prophylaxis: combination beta-blocker + band ligation program

Hepatic encephalopathy:

Identify/correct precipitant (infection, GI bleed, constipation, electrolyte imbalance, sedatives, dehydration)
Lactulose 30mL PO tds-qds, titrate to 2–3 soft stools/day (traps ammonia as ammonium, laxative effect)
Rifaximin 550mg PO bd — add-on for recurrent episodes despite lactulose (reduces ammonia-producing gut flora)

Spontaneous bacterial peritonitis (SBP): diagnostic paracentesis if new/worsening ascites, fever, abdominal pain, or encephalopathy — ascitic fluid neutrophil count >250 cells/mm³ diagnostic; treat with IV cefotaxime/ceftriaxone + IV albumin (1.5g/kg day 1, 1g/kg day 3 — reduces hepatorenal syndrome risk); secondary prophylaxis with norfloxacin/ciprofloxacin after first episode

HCC: surveillance ultrasound ± AFP 6-monthly; management per BCLC staging (resection, ablation, TACE, systemic therapy, or transplant depending on stage)

Liver transplant referral: decompensated cirrhosis, MELD-Na ≥15, refractory complications (ascites, encephalopathy, recurrent variceal bleeding), HCC within transplant criteria (Milan criteria), or synthetic dysfunction (Child-Pugh C).

Helicobacter Pylori Infection

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management