Congenital Bile Acid Synthesis Defect Caused by Mutation in HSD3B7

Congenital bile acid synthesis defect caused by mutation in HSD3B7 is a rare inherited liver and metabolism disease. It is also called congenital bile acid synthesis defect type 1. In this condition, the body cannot make normal primary bile acids well because the HSD3B7 gene does not work properly. This gene normally helps liver cells make an enzyme called 3β-hydroxy-Δ5-C27-steroid oxidoreductase. When that enzyme is weak or missing, the liver makes too little normal bile acid and too many unusual bile acid by-products. These abnormal chemicals can injure the liver, reduce bile flow, and make it hard to digest fat and absorb vitamins A, D, E, and K. Many babies become jaundiced or develop cholestasis early in life, but some children or adults are diagnosed later. Without treatment, the disease can progress to cirrhosis or liver failure, but it is one of the rare liver disorders that can improve greatly when found early.

Congenital bile acid synthesis defect type 1, usually caused by harmful changes in the HSD3B7 gene, is a rare inherited liver disease. The body cannot make normal primary bile acids well. Because of this, bile flow becomes weak, digestion of fat becomes poor, and unusual bile acid by-products can build up and injure the liver. It often starts in infancy or childhood with jaundice, cholestasis, poor growth, vitamin deficiency, enlarged liver, bleeding tendency, or later cirrhosis and portal hypertension. Early diagnosis matters because this disease is often treatable when recognized in time.

The basic problem is simple: the HSD3B7 enzyme normally helps convert cholesterol into normal bile acids. When both copies of the gene are not working well, the liver makes abnormal intermediates instead of healthy bile acids. Normal bile acids are needed to move bile, digest fat, and absorb vitamins A, D, E, and K. Without them, the child may have pale stools, poor weight gain, rickets, easy bruising, itching, or liver damage. Doctors usually confirm the disease with urine bile acid testing by mass spectrometry and genetic testing.

A very important evidence point is that oral cholic acid is the main disease-specific treatment. The FDA label for CHOLBAM says it is indicated for bile acid synthesis disorders due to single enzyme defects, and current liver guidelines recommend an oral primary bile acid for patients with HSD3B7 deficiency. Long-term studies also show that cholic acid can improve liver tests, reduce toxic bile acid production, and help many children keep their own liver.

Other names

Other names used for this disease include congenital bile acid synthesis defect type 1, bile acid synthesis defect, congenital, 1, CBAS1, BAS defect type 1, 3β-hydroxy-Δ5-C27-steroid oxidoreductase deficiency, 3β-HSD deficiency, and HSD3B7 deficiency. These names all point to the same core problem: a defect of bile acid production caused by disease-causing changes in the HSD3B7 gene.

Types

There is not one universally accepted official subtype list for HSD3B7 deficiency itself, but doctors often describe the illness in practical patterns based on how it appears. One pattern is early infantile cholestatic disease, where a baby develops jaundice, poor growth, or liver trouble in the first weeks or months of life. Another pattern is later-onset liver disease, where diagnosis happens in older children or adults. A third pattern is atypical or mild presentation, where the disease first shows up as vitamin deficiency, rickets, abnormal liver tests, or unexplained liver scarring rather than obvious newborn jaundice.

Causes

The true direct cause of this disorder is usually the same in all affected people: a person inherits two disease-causing HSD3B7 variants, one from each parent, in an autosomal recessive pattern. The 20 items below are simple cause-related genetic situations that can lead to this disease.

1. A homozygous missense mutation can cause the disease. This means the child receives the same harmful spelling change in both copies of the HSD3B7 gene, and the enzyme is made incorrectly.

2. A compound heterozygous missense mutation can also cause it. This means there are two different harmful changes, one on each copy of the gene.

3. A nonsense mutation can be the cause. This type of change creates an early stop signal, so the enzyme becomes too short to work well.

4. A frameshift mutation can cause the disease by changing the reading pattern of the gene, which often produces a severely damaged protein.

5. A small deletion in the gene can be causal. MedlinePlus notes that many disease-causing changes remove one or two DNA building blocks.

6. A small insertion can also damage the gene and stop the enzyme from doing its normal job in bile acid synthesis.

7. A splice-site mutation can cause disease because the gene message is cut and joined incorrectly before the protein is made.

8. A mutation that changes an important amino acid in the enzyme active area can reduce or destroy enzyme activity.

9. A mutation that makes the enzyme unstable can be causal because the protein breaks down too quickly inside liver cells.

10. A mutation that prevents correct folding of the enzyme can also cause disease, because badly folded proteins usually cannot work normally.

11. A mutation that changes how the enzyme sits in the endoplasmic reticulum membrane may lead to disease, since this is where the enzyme normally functions in liver cells.

12. A mutation that causes very low enzyme activity can lead to severe early disease because normal primary bile acids are not produced in enough amount.

13. A mutation that causes partial enzyme activity may still produce the disease, but sometimes with later or milder presentation.

14. Two carrier parents are a common cause-related family situation. The child develops the disease only when both parents pass down a harmful gene copy.

15. Consanguinity, meaning the parents are biologically related, can increase the chance that a child receives the same harmful HSD3B7 variant from both sides of the family.

16. A family-specific private variant can cause disease. Some families carry their own rare mutation not seen often in others.

17. A novel mutation can also be causal. Studies have reported many newly discovered HSD3B7 variants in affected patients.

18. A founder mutation can be the cause in some populations, where the same inherited harmful variant appears again in unrelated families from the same background.

19. The disease is caused not only by lack of normal bile acids but also by buildup of atypical toxic bile acid intermediates, which injure liver cells and reduce bile flow.

20. In simple words, the final cause is a failure of a key step in bile acid synthesis. The HSD3B7 enzyme normally helps convert early sterol substances into normal bile acid pathway products. When that step fails, cholestasis and malabsorption follow.

Symptoms

1. Jaundice is one of the most common symptoms. The skin and eyes look yellow because bile pigments build up in the body during cholestasis.

2. Dark urine can happen because conjugated bilirubin passes into the urine when the liver cannot move bile properly.

3. Pale or clay-colored stools may appear because too little bile reaches the intestine.

4. Enlarged liver or hepatomegaly is common. The liver becomes swollen because it is under stress from toxic bile acid intermediates and ongoing injury.

5. Enlarged spleen can occur in some patients, especially when liver disease becomes more advanced.

6. Poor weight gain or failure to thrive is common in babies because fat digestion and calorie absorption are poor.

7. Fat malabsorption is a major symptom. The body cannot handle fats well because normal bile acids are needed for fat absorption.

8. Mild steatorrhea can happen. This means fatty, greasy, or bulky stools because undigested fat stays in the bowel.

9. Easy bruising or bleeding may develop because vitamin K absorption falls, and vitamin K is needed for normal blood clotting.

10. Rickets or soft weak bones can appear, especially from poor vitamin D absorption over time.

11. Bone pain or delayed bone growth may happen as part of vitamin D deficiency and rickets.

12. Tiredness and weakness can occur in children with chronic liver disease, poor nutrition, and vitamin deficiency.

13. Poor appetite may be present in infants or children with liver dysfunction and malabsorption.

14. Signs of cirrhosis can develop if the disease is not treated early. This may include abdominal swelling, bigger spleen, and worsening liver function.

15. Late unexplained liver disease can itself be the symptom pattern in some older children or adults. Instead of obvious newborn illness, they may first show liver enzyme problems, fibrosis, or vitamin deficiency.

Diagnostic tests

1. General physical examination is the first step. The doctor checks skin color, eye color, hydration, alertness, and overall sickness level. This helps detect jaundice and chronic liver disease signs.

2. Growth measurement is important. Weight, length, and head size are measured because poor growth can be a clue to chronic cholestasis and fat malabsorption.

3. Abdominal inspection is used to look for a swollen belly, visible distension, or signs of chronic liver disease.

4. Liver palpation is a manual bedside test. The doctor gently feels the abdomen to see whether the liver edge is enlarged.

5. Spleen palpation is another manual test. It checks for splenomegaly, which may suggest more advanced liver involvement.

6. Stool and urine color review is a simple but very useful bedside assessment. Pale stool and dark urine strongly support cholestasis in an infant.

7. Serum total and direct bilirubin testing is a basic blood test. It helps confirm cholestatic jaundice.

8. ALT and AST are liver enzyme tests. They show liver cell injury, although they do not by themselves name the exact disease.

9. Gamma-glutamyl transferase (GGT) is very important. In HSD3B7 deficiency, GGT is often normal or low, which is a useful clue because many other cholestatic diseases have high GGT.

10. Routine serum total bile acids may be measured. In this disease they can be normal or low, which can look surprising in a child with cholestasis.

11. Coagulation tests, such as PT and INR, are done to look for vitamin K deficiency and liver synthetic failure. They can become abnormal in affected infants.

12. Fat-soluble vitamin levels are checked, especially vitamins A, D, E, and K. These help show malabsorption from lack of normal bile acids.

13. Serum cholesterol may be measured because low cholesterol has been described in this disorder.

14. Urine bile acid mass spectrometry is one of the key diagnostic tests. It looks for the typical abnormal 3β-hydroxy-Δ5 bile acids that strongly suggest HSD3B7 deficiency.

15. Plasma bile acid profiling by LC-MS/MS can also help by showing unusual bile acid intermediates in blood.

16. Molecular genetic testing of HSD3B7 confirms the diagnosis by finding disease-causing variants in both gene copies.

17. Broader cholestasis gene panel testing may be used when the diagnosis is not clear at the start, because many genetic liver diseases can look alike.

18. Liver ultrasound is an imaging test used to look at liver size, spleen size, bile ducts, and to help rule out structural causes such as biliary obstruction.

19. Hepatobiliary scintigraphy may be used in the work-up of infant cholestasis when doctors need more information about bile flow and to separate medical from surgical causes.

20. Liver biopsy is a pathological test. It may show cholestatic liver injury, giant cell hepatitis, fibrosis, or cirrhosis, but it is usually combined with bile acid profiling and genetics because biopsy alone cannot prove HSD3B7 deficiency.

Non-pharmacological treatments, therapies, and supportive care

1. Early specialist follow-up. Regular follow-up with a pediatric hepatologist or metabolic liver specialist helps detect worsening cholestasis, vitamin deficiency, fibrosis, and growth failure early. The purpose is to prevent silent liver damage. The mechanism is simple: frequent review leads to faster adjustment of therapy, lab tests, imaging, and nutrition.

2. Genetic counseling. This disease is usually autosomal recessive, so parents may both be carriers. The purpose is family planning and early testing of siblings. The mechanism is identification of inheritance risk, carrier testing, and informed reproductive decisions.

3. Urine bile acid profiling. This is a key diagnostic and monitoring test. The purpose is to identify abnormal bile acid metabolites and to follow treatment response. The mechanism is laboratory detection of atypical bile acids, which fall when primary bile acid replacement works.

4. Molecular genetic testing. DNA testing confirms the HSD3B7 mutation. The purpose is an exact diagnosis. The mechanism is direct identification of the disease-causing gene change, which can stop years of misdiagnosis.

5. Liver function monitoring. Repeated checks of bilirubin, AST, ALT, GGT, INR, and albumin help measure liver injury. The purpose is early warning. The mechanism is trend tracking over time, not one single test.

6. Growth monitoring. Measuring weight, height, and head growth is essential, especially in infants. The purpose is to detect malabsorption and undernutrition. The mechanism is that poor bile acid production reduces fat and vitamin absorption, slowing growth.

7. Fat-soluble vitamin monitoring. Vitamin A, D, E, and K levels should be checked regularly. The purpose is to prevent eye, bone, nerve, and bleeding problems. The mechanism is simple replacement guided by lab results.

8. Nutrition counseling. A trained dietitian can help choose calorie-dense, easy-to-digest meals. The purpose is better growth and less deficiency. The mechanism is improved meal planning, vitamin support, and better intake during cholestasis.

9. Bone health surveillance. Chronic vitamin D malabsorption can lead to rickets or weak bones. The purpose is bone protection. The mechanism is monitoring vitamin D status, calcium, growth, and sometimes bone imaging.

10. Liver ultrasound. Ultrasound checks liver size, texture, spleen size, and possible portal hypertension. The purpose is to look for structural damage. The mechanism is noninvasive imaging that shows chronic liver disease signs.

11. Elastography or fibrosis assessment. This may help estimate liver stiffness. The purpose is to detect fibrosis early. The mechanism is noninvasive measurement of tissue stiffness that can suggest worsening liver scarring.

12. Itch skin care. Gentle bathing, moisturizers, trimmed nails, and cool rooms may reduce damage from scratching. The purpose is skin protection and better sleep. The mechanism is lowering skin irritation even when cholestatic itch is still present.

13. Hydration support. Good fluid intake helps children with diarrhea, poor intake, or fever. The purpose is to avoid dehydration. The mechanism is maintaining circulation and kidney function during illness or poor feeding.

14. Developmental assessment. Chronic illness and malnutrition can affect development. The purpose is early support for speech, movement, and learning. The mechanism is early therapy referral when milestones are delayed.

15. Infection prevention routines. Hand hygiene, vaccination review, and quick care for fever are important in chronic liver disease. The purpose is to reduce stress on the liver. The mechanism is lowering infection-triggered decompensation.

16. Physical activity as tolerated. Gentle age-appropriate activity supports appetite, muscle, and bone health. The purpose is general health. The mechanism is improved strength and physical development, while avoiding exhaustion in advanced disease.

17. Psychosocial support. Rare diseases cause fear, stress, and family burden. The purpose is better quality of life. The mechanism is counseling, support groups, and education that improve treatment adherence and coping.

18. Endoscopy surveillance when portal hypertension is present. If cirrhosis develops, doctors may check for varices. The purpose is bleeding prevention. The mechanism is finding enlarged veins before they rupture.

19. Liver transplant evaluation in advanced disease. This is not first-line care, but it is important when liver failure progresses. The purpose is survival. The mechanism is replacement of the damaged liver when medical therapy is no longer enough.

20. Family screening of siblings. Brothers and sisters may have the same disorder or may be carriers. The purpose is early diagnosis. The mechanism is testing before severe liver injury appears.

Drug treatment: what is directly proven, and what is supportive

1. Cholic acid (CHOLBAM). This is the most important drug for HSD3B7 deficiency. Drug class: primary bile acid replacement. FDA dosage is 10 to 15 mg/kg/day, in 1 or 2 doses, adjusted by response; some patients with poor control may need higher specialist-guided doses. Time: taken daily, long term. Purpose: replace the missing primary bile acid, improve bile flow, suppress harmful abnormal bile acid synthesis, and improve fat and vitamin absorption. Mechanism: feedback inhibition of bile acid production plus physiologic bile acid replacement. Side effects can include diarrhea, reflux, abdominal pain, liver test worsening in some patients, and the need for close monitoring.

2. Ursodiol (ursodeoxycholic acid). Drug class: hydrophilic bile acid. It is not the main FDA-labeled drug for HSD3B7 deficiency, but some doctors use it as supportive treatment in cholestatic liver disease. Dose is individualized by age and weight. Purpose: improve bile flow and reduce cholestatic stress. Mechanism: changes bile composition and may protect liver cells. Side effects may include diarrhea and abdominal discomfort. Important caution: guidelines for HSD3B7 favor primary bile acid replacement such as cholic acid, not ursodiol alone as definitive therapy.

3. Phytonadione (vitamin K1). Drug class: fat-soluble vitamin replacement. Oral or injectable dosing is individualized by age, INR, bleeding risk, and deficiency severity. Purpose: prevent easy bruising and dangerous bleeding caused by fat-soluble vitamin malabsorption. Mechanism: restores hepatic production of clotting factors that depend on vitamin K. Side effects are usually mild with oral use; injectable use can rarely cause serious hypersensitivity reactions. This is supportive care, not a cure for the bile acid defect.

4. Calcitriol or vitamin D therapy. Drug class: active vitamin D analog or vitamin D replacement. Dose depends on age, calcium level, and bone status. Purpose: correct vitamin D deficiency and protect bones from rickets or weakness. Mechanism: increases calcium absorption and supports bone mineralization. Side effects can include high calcium, constipation, weakness, or kidney stone risk if overdosed. In HSD3B7 deficiency, it treats a consequence of malabsorption, not the gene defect itself.

5. Multivitamin support including vitamins A, D, E, and K. Drug class: vitamin supplementation. Dose is individualized and should be specialist-guided because cholestatic children may need careful monitoring. Purpose: correct combined deficiency from poor fat absorption. Mechanism: restores body stores needed for vision, immunity, bone, nerves, and clotting. Side effects depend on the vitamin and dose; too much can also be harmful. This is supportive but essential.

6. Hydroxyzine. Drug class: antihistamine/anxiolytic. Dose varies by age and weight. Purpose: sometimes used for itch and sleep disturbance, even though cholestatic itch is not purely histamine-driven. Mechanism: sedating antihistamine effect may reduce scratching at night. Side effects include sleepiness, dry mouth, and dizziness. It treats symptoms only and does not correct abnormal bile acid synthesis.

7. Cholestyramine. Drug class: bile acid sequestrant. Dose depends on age and tolerance. Purpose: sometimes used for cholestatic pruritus. Mechanism: binds bile acids in the intestine, but it can also worsen absorption of fat-soluble vitamins, so it must be used carefully in this disease. Side effects include constipation, bloating, and vitamin loss. This is symptom management only.

8. Furosemide. Drug class: loop diuretic. Label-supported use includes edema associated with cirrhosis of the liver. Dose is individualized. Purpose: reduce fluid overload, swelling, or ascites in advanced liver disease. Mechanism: increases urinary sodium and water loss. Side effects include dehydration, low potassium, low sodium, kidney stress, and hearing issues at high doses. It is for complications, not for the metabolic defect itself.

9. Spironolactone. Drug class: aldosterone antagonist potassium-sparing diuretic. Dose is individualized. Purpose: often used in ascites and edema related to liver disease. Mechanism: blocks aldosterone-driven sodium retention. Side effects include high potassium, low blood pressure, breast tenderness, and dehydration. In liver patients it is commonly paired with monitoring of weight, electrolytes, and kidney function.

10. Lactulose. Drug class: nonabsorbable disaccharide. Dose is adjusted to bowel response. Purpose: used when advanced liver disease leads to hepatic encephalopathy. Mechanism: lowers ammonia production and absorption in the gut. Side effects include bloating, cramps, and diarrhea. This is only for severe liver complications and not for routine early HSD3B7 care.

11. Rifaximin. Drug class: gut-selective antibiotic. FDA label dose for hepatic encephalopathy recurrence reduction in adults is 550 mg twice daily. Purpose: lower recurrence of hepatic encephalopathy, usually with lactulose. Mechanism: changes intestinal bacteria and reduces ammonia-related toxin production. Side effects may include nausea, edema, dizziness, and C. difficile risk. This is complication treatment, not disease-specific therapy.

12. Propranolol or 13. Nadolol. Drug class: nonselective beta-blockers. Doses are individualized. Purpose: used when portal hypertension and varices are present to reduce bleeding risk. Mechanism: lowers portal venous pressure. Side effects include slow pulse, low blood pressure, fatigue, and bronchospasm risk. These are not used in every patient, only selected patients with specialist guidance.

14. Omeprazole. Drug class: proton pump inhibitor. Dose depends on age and indication. Purpose: treat reflux, gastritis, or ulcer risk in selected patients. Mechanism: suppresses gastric acid. Side effects may include headache, diarrhea, and, with prolonged use, nutrient absorption concerns. It is supportive only.

15. Ceftriaxone and other antibiotics. Drug class: cephalosporin antibiotic. Dose depends on infection type and age. Purpose: treat proven bacterial infections in decompensated liver disease. Mechanism: kills susceptible bacteria. Side effects include diarrhea, allergy, biliary sludge, and microbiome disturbance. Use only when infection is suspected or confirmed.

For the remaining “drug” items often discussed in care plans—vitamin A, vitamin E, calcium, zinc, albumin infusion, and specialized enteral formulas—the need is real, but the exact product and dose are individualized and often not backed by disease-specific FDA approval for HSD3B7 deficiency. They should be chosen by a liver specialist based on labs, age, bleeding risk, bone status, growth, and complications.

Dietary and molecular supplements

The most useful “molecular supplements” in this disorder are usually fat-soluble vitamin replacement and high-calorie nutrition support, not immune-boosting products. In simple terms, the body cannot absorb fat normally when bile acids are missing, so vitamins A, D, E, and K often need planned replacement. Some children also need calcium, extra calories, or tube-feeding support if growth is poor. Exact dosage must be individualized. The function is to repair deficiency. The mechanism is replacement of nutrients that are not being absorbed well because bile flow is weak.

Immunity booster, regenerative, and stem-cell drugs

At present, there are no established immunity-booster drugs, no approved regenerative drugs, and no approved stem-cell drugs specifically for HSD3B7 deficiency. Standard care is still early diagnosis, bile acid replacement, vitamin correction, and management of complications. Research in liver regeneration and cell therapy exists in hepatology in general, but it is not standard evidence-based treatment for this specific condition. Any clinic selling “immune boosting” or “stem-cell cure” for HSD3B7 deficiency should be viewed with caution.

Surgeries or procedures and why they are done

Liver transplantation is the main major surgery when liver failure, severe cirrhosis, or progressive decompensation continues despite treatment. It is done to replace the diseased liver and save life.

Upper GI endoscopy with variceal banding may be needed if portal hypertension causes esophageal varices. It is done to prevent or control life-threatening bleeding.

Liver biopsy may be used when diagnosis is unclear or when doctors need histology, although modern biochemical and genetic tests reduce the need in some cases. It is done to assess fibrosis, hepatitis pattern, or cirrhosis.

Feeding tube placement may be needed in children with severe poor intake or failure to thrive. It is done to improve calorie delivery and growth when oral feeding is not enough.

Paracentesis may be needed in advanced liver disease with tense ascites. It is done to remove fluid, relieve discomfort, and sometimes test for infection.

Prevention, when to see a doctor, and what to eat or avoid

10 prevention tips: get early testing in jaundiced infants; do not delay specialist referral; follow cholic acid exactly as prescribed; monitor vitamins A, D, E, K; check growth often; keep vaccination and hygiene up to date; avoid unproven supplements; avoid alcohol later in life; use medicines only with doctor approval because the liver is vulnerable; screen siblings when advised. These steps do not prevent the gene mutation, but they can prevent severe liver injury, bleeding, bone disease, and delayed diagnosis.

When to see a doctor urgently: jaundice, dark urine, pale stools, poor weight gain, vomiting, belly swelling, bleeding, bruising, severe itching, sleepiness, confusion, fever, black stool, or vomiting blood. These can signal cholestasis, vitamin deficiency, portal hypertension, infection, or liver failure.

What to eat: regular balanced meals, enough calories, protein as advised, fruits, vegetables, tolerated grains, and prescribed vitamin supplements. What to avoid: alcohol, unregulated herbal products, random “liver detox” products, unnecessary fat-blocking drugs, and any supplement that interferes with vitamin absorption without medical supervision. The best diet is individualized by a metabolic dietitian.

FAQs

1. Is HSD3B7 deficiency curable? It is a genetic disease, so the gene change is not reversed, but early treatment can control the disease very well in many patients.

2. What is the main treatment? Oral cholic acid is the key evidence-based treatment.

3. Can it be fatal? Yes, if untreated it can progress to liver failure, but early therapy improves outcomes.

4. Is it inherited? Yes, usually autosomal recessive inheritance.

5. Can adults have it too? Yes. Some are diagnosed late, even after years of unexplained liver disease.

6. Why are vitamins low? Because bile acids are needed to absorb fat and fat-soluble vitamins.

7. Does every patient need surgery? No. Many improve on medical therapy and never need transplant.

8. Can ursodiol replace cholic acid? It may help cholestasis in some settings, but it is not the main proven disease-specific therapy for HSD3B7 deficiency.

9. What tests confirm the diagnosis? Urine bile acid analysis and genetic testing are most important.

10. Can siblings also have it? Yes, so family testing may be recommended.

11. Is there a proven stem-cell cure? No proven standard stem-cell drug or stem-cell cure exists for this disease today.

12. Does itching always happen? Not always, but cholestatic itch can occur, especially in more advanced disease.

13. Why is early diagnosis so important? Because treatment can stop ongoing toxic bile acid injury before severe cirrhosis develops.

14. Can liver tests become normal? In many treated patients, liver chemistry improves a lot, especially when treatment starts early.

15. What is the long-term outlook? Outlook is often good with early recognition, cholic acid therapy, vitamin support, and close follow-up, but delayed cases may still develop portal hypertension or need transplant.

For this rare condition, the most evidence-based summary is very clear: diagnose early, start cholic acid, replace vitamins, monitor growth and liver health, and treat complications fast. That is the approach most strongly supported by the FDA label, genetic references, and current cholestatic liver disease guidelines.

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. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. 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. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: March 10, 2025.