Hepatic Jaundice

Hepatic jaundice is a condition where the liver struggles to remove bilirubin, a yellow pigment produced during the normal breakdown of red blood cells. This results in a yellowish discoloration of the skin, eyes, and mucous membranes.

Types of Hepatic Jaundice:

1. Hepatocellular Jaundice: Caused by liver diseases such as hepatitis or cirrhosis.
2. Obstructive Jaundice: Due to obstruction of bile flow, often caused by gallstones or tumors.
3. Hemolytic Jaundice: Resulting from excessive breakdown of red blood cells, seen in conditions like sickle cell anemia or malaria.

Causes of Hepatic Jaundice:

1. Liver infections like hepatitis A, B, or C.
2. Liver cirrhosis caused by chronic alcoholism or other factors.
3. Gallstones blocking the bile ducts.
4. Liver cancer or tumors.
5. Genetic disorders affecting bilirubin metabolism like Gilbert’s syndrome.
6. Medications that can harm the liver.
7. Hemolytic anemia.
8. Pancreatic cancer.
9. Bile duct disorders.
10. Infections such as malaria or leptospirosis.
11. Autoimmune diseases affecting the liver.
12. Liver injury due to trauma.
13. Wilson’s disease, a genetic disorder causing copper accumulation in the liver.
14. Alpha-1 antitrypsin deficiency.
15. Congestive heart failure.
16. Pancreatitis.
17. Sepsis.
18. Liver ischemia.
19. Alcoholic liver disease.
20. Liver abscess.

Symptoms of Hepatic Jaundice:

1. Yellowing of the skin and eyes (jaundice).
2. Dark urine.
3. Pale stools.
4. Itchy skin.
5. Fatigue.
6. Abdominal pain.
7. Nausea and vomiting.
8. Loss of appetite.
9. Swelling in the abdomen.
10. Weight loss.
11. Fever.
12. Confusion.
13. Bleeding easily.
14. Enlarged liver or spleen.
15. Swollen legs or ankles.
16. Jaundice-related itching.
17. Jaundice-related changes in urine color.
18. Jaundice-related changes in stool color.
19. Weakness.
20. Jaundice-related changes in mental state.

Diagnostic Tests for Hepatic Jaundice:

1. Liver Function Tests: Measures levels of liver enzymes and bilirubin.
2. Blood Tests: To check for infections, hepatitis, or other liver diseases.
3. Ultrasound: Imaging test to visualize liver and bile ducts.
4. CT Scan: Detailed imaging of the liver and surrounding organs.
5. MRI: Provides detailed images of liver and bile ducts.
6. Liver Biopsy: Sample of liver tissue to check for damage or disease.
7. Endoscopic Retrograde Cholangiopancreatography (ERCP): Examines bile ducts using a scope.
8. Magnetic Resonance Cholangiopancreatography (MRCP): Special MRI to assess bile ducts.
9. Abdominal X-ray: To check for any blockages or abnormalities.
10. Endoscopic Ultrasound: Combines endoscopy and ultrasound to examine bile ducts.
11. Liver Scans: Nuclear imaging to assess liver function and blood flow.
12. Cholecystogram: X-ray to visualize the gallbladder and bile ducts after contrast dye injection.
13. Biopsy of Liver Lesions: To determine if any liver tumors are cancerous.
14. Genetic Testing: To diagnose genetic liver disorders.
15. Laparoscopy: Surgical procedure to directly view the liver and surrounding organs.
16. Transient Elastography (FibroScan): Measures liver stiffness to assess fibrosis.
17. Blood Clotting Tests: To check for liver function in clotting blood.
18. Liver Doppler Ultrasound: Checks blood flow in the liver.
19. Liver Autoantibodies Testing: To diagnose autoimmune liver diseases.
20. Liver Angiography: X-ray imaging to assess blood flow in the liver.

Treatments for Hepatic Jaundice:

1. Dietary Changes: Low-fat, low-sodium diet to ease the workload on the liver.
2. Hydration: Drinking plenty of fluids to help flush toxins from the body.
3. Avoiding Alcohol: Alcohol can worsen liver damage.
4. Medication Management: Avoiding medications that can harm the liver.
5. Treating Underlying Conditions: Addressing infections, liver diseases, or other contributing factors.
6. Liver Transplant: In severe cases of liver failure, a transplant may be necessary.
7. Phototherapy: Light therapy to help break down excess bilirubin.
8. Bile Duct Surgery: To remove obstructions.
9. Chemotherapy: For liver cancer treatment.
10. Embolization Therapy: Blocking blood supply to liver tumors.
11. Radiofrequency Ablation: Using heat to destroy liver tumors.
12. Percutaneous Ethanol Injection: Injecting alcohol into tumors to destroy them.
13. Cholecystectomy: Surgical removal of the gallbladder for gallstone-related issues.
14. Stent Placement: To keep bile ducts open.
15. Liver Resection: Surgical removal of part of the liver.
16. Palliative Care: To manage symptoms and improve quality of life in advanced cases.
17. Liver Drainage Procedures: To relieve bile duct blockages.
18. Antibiotic Therapy: To treat infections affecting the liver.
19. Fluid Drainage: Removing excess fluid buildup in the abdomen (ascites).
20. Nutritional Support: Providing essential nutrients for liver health.

Drugs Used in Hepatic Jaundice:

1. Ursodeoxycholic acid (ursodiol): Helps dissolve gallstones.
2. N-acetylcysteine: Antidote for acetaminophen overdose.
3. Rifampicin: Antibiotic used in certain liver infections.
4. Corticosteroids: For autoimmune liver diseases.
5. Interferon: Antiviral medication for hepatitis.
6. Ribavirin: Antiviral medication for hepatitis.
7. Lamivudine: Antiviral medication for hepatitis B.
8. Entecavir: Antiviral medication for hepatitis B.
9. Tenofovir: Antiviral medication for hepatitis B and C.
10. Sofosbuvir: Antiviral medication for hepatitis C.

Drug treatments

Doses are typical adult ranges and must be individualized by your clinician, especially with impaired liver function.

1) Ursodeoxycholic acid (UDCA)
Class: Bile acid (hydrophilic).
Dose/Time: 10–15 mg/kg/day in 2–3 divided doses, long-term if indicated.
Purpose: Improve cholestasis in diseases like primary biliary cholangitis and some intrahepatic cholestasis states.
Mechanism: Replaces toxic bile acids, stabilizes hepatocyte membranes, improves bile flow.
Side effects: Mild GI upset, weight gain, rare hair thinning.

2) Cholestyramine (for cholestatic pruritus)
Class: Bile acid sequestrant.
Dose/Time: 4 g 1–4 times daily; take ≥4–6 h apart from other meds.
Purpose: Reduce itching from bile acids.
Mechanism: Binds bile acids in gut, lowers enterohepatic circulation.
Side effects: Constipation, bloating, poor absorption of fat-soluble vitamins.

3) Rifampin (second-line anti-pruritic; specialist use)
Class: Enzyme inducer antibiotic.
Dose/Time: 150–300 mg twice daily if benefits outweigh risks.
Purpose: Refractory cholestatic itch.
Mechanism: Induces microsomal enzymes and pregnane X receptor pathways that modify pruritogens.
Side effects: Hepatotoxicity, drug interactions, orange body fluids.

4) Naltrexone (anti-pruritic; off-label)
Class: Opioid receptor antagonist.
Dose/Time: Start 12.5–25 mg daily, increase to 50 mg daily as tolerated.
Purpose: Break itch-scratch cycle mediated by endogenous opioids.
Mechanism: Blocks μ-opioid receptors; shifts itch signaling.
Side effects: Nausea, insomnia, withdrawal-like symptoms if on opioids.

5) Sertraline (itch adjunct in some patients)
Class: SSRI antidepressant.
Dose/Time: 50–100 mg daily.
Purpose: Reduce itch perception, improve mood/sleep; sometimes helps in cholestatic itch.
Mechanism: Central modulation of serotonin pathways.
Side effects: GI upset, sexual dysfunction, hyponatremia in elderly.

6) Vitamin K (phytonadione) for coagulopathy
Class: Fat-soluble vitamin.
Dose/Time: 5–10 mg PO/IV daily for 1–3 days if deficiency suspected (e.g., prolonged INR from cholestasis/malabsorption).
Purpose: Correct vitamin K deficiency–related bleeding risk.
Mechanism: Restores γ-carboxylation of clotting factors II, VII, IX, X.
Side effects: Rare anaphylactoid reaction with IV (use slow infusion).

7) Prednisolone/Prednisone ± Azathioprine (autoimmune hepatitis)
Class: Corticosteroid ± antimetabolite.
Dose/Time: Prednisolone 30–40 mg/day taper; add azathioprine 1–2 mg/kg/day for steroid-sparing; months to years under specialist care.
Purpose: Suppress immune attack on hepatocytes and resolve jaundice.
Mechanism: Broad anti-inflammatory and T-cell suppression.
Side effects: Infection risk, weight gain, diabetes, bone loss; azathioprine can cause cytopenias and cholestasis.

8) N-Acetylcysteine (NAC) in acetaminophen toxicity and sometimes acute liver failure
Class: Antidote/antioxidant.
Dose/Time: IV or PO protocols per hospital (e.g., IV 150 mg/kg load then infusions).
Purpose: Stop ongoing injury and improve survival in acute toxic injury.
Mechanism: Replenishes glutathione; detoxifies NAPQI; antioxidant effects.
Side effects: Nausea, rare anaphylactoid reaction (treatable).

9) Direct-acting antivirals for hepatitis C (e.g., sofosbuvir/velpatasvir)
Class: Antiviral combination.
Dose/Time: Fixed-dose tablet once daily for 12 weeks (typical).
Purpose: Cure HCV, reduce inflammation, resolve jaundice over time.
Mechanism: Inhibits viral polymerase/NS5A replication complex.
Side effects: Headache, fatigue; major drug-drug interaction checks required.

10) Antivirals for hepatitis B (e.g., tenofovir disoproxil fumarate or entecavir)
Class: Nucleos(t)ide analogs.
Dose/Time: Tenofovir DF 300 mg daily or entecavir 0.5–1 mg daily, long-term.
Purpose: Suppress HBV, limit inflammation/fibrosis, prevent flares.
Mechanism: Inhibits HBV polymerase.
Side effects: Tenofovir: renal/bone monitoring; Entecavir: generally well tolerated.

Other common supportive meds your clinician may use (not counted in the 10 above): lactulose/rifaximin for encephalopathy, diuretics for ascites, fat-soluble vitamin A/D/E/K replacement, antibiotics for infections, and PPIs/H2 blockers if steroid therapy or variceal risks are present.

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Dietary molecular supplements

Supplements can interact with medications and some are harmful in liver disease. Discuss every supplement with your clinician. Avoid multi-herb “detox” products with unknown ingredients.

1) Coffee (brew, not energy drinks)
Dose: 2–4 cups/day if tolerated.
Function: Associated with lower liver fibrosis and HCC risk in studies.
Mechanism: Antioxidants, diterpenes, and adenosine modulation reduce inflammation and fibrosis.

2) Omega-3 fatty acids (EPA/DHA)
Dose: 1–2 g/day combined EPA+DHA.
Function: Improves triglycerides and may help fatty liver.
Mechanism: Anti-inflammatory lipid mediators; lowers hepatic fat synthesis.

3) Vitamin E (for non-diabetic NASH, specialist-guided)
Dose: 800 IU/day (alpha-tocopherol) if appropriate.
Function: Antioxidant that may improve steatohepatitis.
Mechanism: Scavenges reactive oxygen species in hepatocytes.
Caution: Possible bleeding risk/long-term safety debates; avoid if cirrhosis/diabetes unless advised.

4) Zinc
Dose: 25–50 mg elemental zinc/day for limited periods; add copper monitoring if long-term.
Function: Supports ammonia handling and immune function.
Mechanism: Cofactor for urea cycle enzymes and antioxidant defense.

5) Selenium
Dose: 100–200 mcg/day.
Function: Antioxidant support.
Mechanism: Integral to glutathione peroxidases, reduces oxidative stress.

6) S-adenosyl-L-methionine (SAMe)
Dose: 800–1600 mg/day in divided doses.
Function: May improve cholestasis and mood symptoms in some patients.
Mechanism: Donates methyl groups; supports glutathione synthesis.

7) TUDCA (tauroursodeoxycholic acid) supplement
Dose: Common over-the-counter doses range 250–500 mg/day; medical-grade dosing varies—ask your doctor.
Function: Bile flow support and cellular stress reduction.
Mechanism: Hydrophilic bile acid that reduces ER stress and stabilizes membranes.

8) Curcumin (turmeric extract standardized)
Dose: 500–1000 mg/day with piperine-free or carefully monitored formulas (piperine can raise drug levels).
Function: Anti-inflammatory and antioxidant effects.
Mechanism: NF-κB pathway modulation; free radical scavenging.
Caution: Rare hepatotoxicity reported—stop if enzymes rise.

9) Betaine (trimethylglycine)
Dose: 2–6 g/day divided.
Function: Methyl donor; may help fatty liver in some small studies.
Mechanism: Supports homocysteine methylation and hepatic fat export.

10) Phosphatidylcholine (PC)
Dose: 1.2–2.7 g/day.
Function: Cell-membrane support and bile composition aid.
Mechanism: Supplies membrane phospholipids; may improve VLDL export.

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Regenerative / stem-cell-related” therapies

These are not self-treatments. Several remain investigational and are used only in trials or specialist centers. I’ll note typical research dosing when established; otherwise, dosing varies and is determined by protocols.

1) Pegylated Interferon-α (for HBV/HDV in selected patients)
Dose: PegIFN-α2a 180 mcg once weekly (duration and eligibility vary).
Function/Mechanism: Immune modulation to clear or suppress hepatitis viruses; can improve hepatic inflammation and jaundice over time.
Cautions: Flu-like symptoms, depression, cytopenias; not for decompensated cirrhosis.

2) Thymosin alpha-1 (used in some countries for chronic hepatitis)
Dose: 1.6 mg subcutaneously twice weekly (regimens vary).
Function/Mechanism: Enhances T-cell function and antiviral responses.
Cautions: Variable evidence; use only under specialist guidance.

3) Granulocyte colony-stimulating factor (G-CSF) in acute-on-chronic liver failure (ACLF) — investigational
Dose in trials: ~5 µg/kg/day SC for 5 days; protocols vary.
Function/Mechanism: Mobilizes bone-marrow stem cells; may aid liver regeneration in some studies.
Cautions: Mixed evidence; infection/leukocytosis risks.

4) Mesenchymal stem cell (MSC) infusions — clinical trials
Dose: Protocol-defined; no over-the-counter use.
Function/Mechanism: Paracrine anti-inflammatory and anti-fibrotic effects; potential hepatocyte support.
Cautions: Experimental; seek ethics-approved trials only.

5) Albumin dialysis systems (MARS, Prometheus) — bridge therapy
Dose: Per hospital protocol (sessions hours–days).
Function/Mechanism: Removes protein-bound toxins (bile acids, bilirubin) to stabilize patients with severe cholestasis or liver failure while underlying cause is treated.
Cautions: ICU-level care; not a cure.

6) Hepatocyte or auxiliary liver transplantation — highly specialized
Dose: Surgical/procedural; selection criteria strict.
Function/Mechanism: Replaces failing hepatocyte function; definitive for end-stage disease or acute liver failure not recovering.
Cautions: Lifelong immunosuppression, infection risk, rejection, cost.

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Surgeries/procedures

Many cases of hepatic jaundice are not surgical. Procedures are used for diagnosis, complications, mixed pathology, or end-stage disease.

1) Liver biopsy (percutaneous or transjugular)
Procedure: Needle samples liver tissue; transjugular route used when clotting risk is high.
Why done: Confirm cause (autoimmune, NASH, drug-induced, cholestatic diseases) and stage fibrosis, which guides therapy.

2) ERCP with limited intrahepatic intervention (selected cholestatic disorders)
Procedure: Endoscopic scope into bile duct to treat strictures or stones; stents can be placed.
Why done: If imaging shows intrahepatic duct strictures or stone migration causing a mixed cholestatic picture.

3) Percutaneous transhepatic biliary drainage (PTBD)
Procedure: Radiologist places a catheter through the liver into bile ducts to drain bile.
Why done: Severe cholestasis with segmental obstruction not accessible by ERCP in secondary sclerosing cholangitis or complex strictures.

4) Transjugular intrahepatic portosystemic shunt (TIPS)
Procedure: Creates a channel between portal and hepatic veins.
Why done: Not for jaundice directly, but for complications (refractory ascites/variceal bleeding) that worsen overall liver function and can indirectly affect bilirubin handling.

5) Liver transplantation
Procedure: Replace diseased liver with a donor liver.
Why done: End-stage liver disease or acute liver failure with poor recovery chances—definitive solution for persistent hepatic jaundice when the liver cannot recover.

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Preventions

1. Get vaccinated against hepatitis A and B if not immune.

2. Do not drink alcohol if you have any liver disease; never binge drink.

3. Use medicines carefully: follow doses; avoid double-dosing combination cold/pain pills that contain acetaminophen.

4. Avoid risky injections or needle sharing; use sterile equipment for tattoos/piercings.

5. Practice safer sex; use condoms to reduce viral hepatitis spread.

6. Keep a healthy weight; aim for a waistline and BMI in a healthy range.

7. Control diabetes, blood pressure, and lipids with food, activity, and prescribed meds.

8. Avoid raw/undercooked shellfish and unsafe water, especially when traveling.

9. Check herbs and supplements with your clinician; avoid unknown “liver cleanses.”

10. Routine checkups if you take long-term potentially hepatotoxic drugs (e.g., TB therapy, methotrexate); do scheduled labs.

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When to see a doctor urgently

• Rapidly deepening yellow color of skin/eyes over days.

• Very dark urine and clay-colored stools lasting more than 24–48 hours.

• Severe itching preventing sleep.

• Confusion, drowsiness, personality change, or tremor (possible hepatic encephalopathy).

• Easy bruising or bleeding, nosebleeds, or black stools.

• Severe right-upper abdominal pain, fever, or vomiting.

• New swelling of the belly or legs, or sudden weight gain from fluid.

• Inability to keep food/fluids down, fainting, or signs of dehydration.

• If pregnant and jaundiced—seek care immediately.

• Any jaundice in a newborn or child should be assessed promptly.

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What to eat and what to avoid

What to eat

1. Lean proteins: fish, skinless poultry, beans, tofu, low-fat dairy—support healing.

2. High-fiber carbs: oats, brown rice, barley, whole-grain bread—support gut microbiome and bile acid metabolism.

3. Colorful vegetables and fruits: antioxidants that fight liver inflammation (e.g., leafy greens, berries, citrus).

4. Healthy fats: olive oil, avocado, nuts, and seeds—improve lipid profile and satiety.

5. Plenty of water—supports circulation and kidney function; limit sugary drinks.

What to avoid

1. Alcohol—even “social” amounts can harm a diseased liver.
2. Very high-sugar and refined carb foods—sodas, pastries, candy; these drive fat accumulation in the liver.
3. Large amounts of deep-fried foods and trans fats—increase oxidative stress.
4. Raw/undercooked shellfish—infection risk.
5. Unregulated herbal mixtures or bodybuilding supplements—common source of drug-induced liver injury.

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Frequently asked questions

1) Can hepatic jaundice go away?
Yes—if the cause is treated. Viral hepatitis cured or suppressed, alcohol stopped, toxic drugs removed, and fatty liver improved can reverse jaundice over days to weeks. Long-standing scarring (cirrhosis) may take longer or need transplant if advanced.

2) How long until the yellow color fades?
It varies. Mild hepatitis may clear in 1–3 weeks after the cause is fixed. Severe cholestasis or chronic disease can take months to normalize.

3) Is acetaminophen safe for pain?
Use only if your clinician says it’s okay, at the lowest effective dose and never above 2 g/day in chronic liver disease (many patients are advised to avoid or limit strictly). Avoid combining multiple products that contain it.

4) Are NSAIDs (ibuprofen, naproxen) safe?
Often not preferred in advanced liver disease or if you have fluid retention/varices because they can cause bleeding and kidney injury. Ask your doctor.

5) Why is my urine dark and stools pale?
Bilirubin spills into urine (making it tea-colored) and less reaches the intestine, so stools can turn pale. As liver function improves, these colors normalize.

6) What helps cholestatic itching at home?
Cool showers, moisturizers, loose clothes, and avoiding heat help. If severe, medicines like cholestyramine are more effective—speak with your clinician.

7) Can I take vitamins?
Yes, but do not self-dose high amounts. In cholestasis, doctors often replace A, D, E, K carefully and monitor levels. Too much vitamin A or niacin can harm the liver.

8) Is coffee really good for my liver?
Observational studies link 2–4 cups/day with lower fibrosis and liver cancer risk. If you tolerate it and your doctor agrees, it’s reasonable.

9) Do I need a liver biopsy?
Sometimes. If the cause is unclear or staging will change treatment, a biopsy provides definitive tissue diagnosis.

10) Can exercise worsen jaundice?
Gentle to moderate activity is helpful. Avoid extreme workouts during acute illness; build up slowly as you recover.

11) Will jaundice hurt my eyes permanently?
The yellow color is from bilirubin in tissues and does not damage vision. If you have eye pain or visual changes, get checked—another issue may be present.

12) Can I still eat protein if I had encephalopathy before?
Most patients should eat adequate protein; do not restrict without clinician guidance. The quality and timing of protein can be adjusted individually.

13) When is transplant considered?
In end-stage disease (decompensated cirrhosis) or acute liver failure with poor chances of recovery, after evaluation at a transplant center.

14) Are herbal “liver cleanses” safe?
Many are not. Some cause serious liver injury. Always review products with your clinician and prefer evidence-based care.

15) Can stress cause jaundice?
Stress alone does not raise bilirubin, but it can worsen habits (alcohol, poor sleep, poor diet). Managing stress supports recovery.

 

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. Thank you for giving your valuable time to read the article.

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