Gardner syndrome is a rare inherited disorder now recognized as a variant of familial adenomatous polyposis (FAP). In this condition, dozens to thousands of small growths called adenomatous polyps develop along the inner lining of the colon and rectum. Over time, untreated polyps nearly always become cancerous, making routine monitoring and preventive surgery essential. In addition to intestinal polyps, people with Gardner syndrome develop non-cancerous tumors—such as bony growths in the skull (osteomas), small skin cysts (epidermoid cysts), and fibrous lumps under the skin—along with dental abnormalities like extra or impacted teeth NCBI.
The underlying cause of Gardner syndrome is a change (mutation) in the APC tumor suppressor gene on chromosome 5. The APC protein normally helps control cell growth; when it is defective, cells can divide uncontrollably, leading to the formation of polyps and tumors. Gardner syndrome follows an autosomal dominant pattern, meaning a person only needs one copy of the mutated gene—either inherited from a parent or arising anew—to develop the condition WikipediaCleveland Clinic.
Gardner syndrome is a rare inherited condition that causes growths in many parts of the body. It is a subtype of familial adenomatous polyposis (FAP), meaning people with Gardner syndrome develop hundreds to thousands of small growths (polyps) in their large intestine (colon) as teenagers or young adults. Over time, these polyps almost always turn into cancer if the colon is not removed. But in Gardner syndrome, changes go beyond the colon: benign (noncancerous) tumors such as osteomas (bone bumps), epidermoid cysts (skin lumps), and fibromas (soft-tissue nodules) often appear on the skull, jaw, and other bones, as well as under the skin. Dental abnormalities (extra or missing teeth, under-developed roots) and desmoid tumors (fibrous scars that can grow into organs) are also common. Because the underlying cause is a mutation in the APC gene passed down in families, Gardner syndrome tends to run in multiple generations. Early diagnosis through genetic testing and colonoscopy surveillance is critical: with timely management, people can live full lives with reduced risk of colorectal cancer and better control of outside-colon tumors.
Types of Gardner Syndrome
Classic Gardner syndrome
This form involves the development of hundreds to thousands of colon polyps, often beginning in the teenage years. Alongside polyps, affected individuals form osteomas (benign bone tumors), epidermoid cysts, fibromas, and other soft tissue growths. Without early colectomy (removal of the colon), nearly all patients develop colorectal cancer by age 40 Cleveland Clinic.
Attenuated Gardner syndrome
In attenuated FAP (AFAP), patients develop fewer polyps—typically 20 to 100—and at a later age (often after 40). Although the risk of colorectal cancer remains high, onset is delayed compared to classic Gardner syndrome. Extracolonic features (osteomas, cysts) still occur but may also appear later and with less severity Cleveland Clinic.
Sporadic (de novo) Gardner syndrome
Approximately 20% of cases arise from a new (de novo) mutation in the APC gene, with no family history of the condition. These individuals present the same spectrum of polyps and extracolonic tumors but have no inherited risk to pass on Medscape.
Causes of Gardner Syndrome
Gardner syndrome results from defects in the APC gene. The following are twenty distinct ways in which APC function can be lost or impaired, leading to Gardner syndrome:
Inherited germline APC mutation
Receiving one faulty APC gene copy from an affected parent is the most common cause of Gardner syndrome Cleveland Clinic.De novo APC mutation
A new change in the APC gene during egg or sperm formation can cause the syndrome in individuals with no family history Medscape.Nonsense point mutation
A single-letter change creates a premature “stop” signal, producing an incomplete APC protein Wikipedia.Frameshift insertion/deletion
Adding or removing letters shifts the gene’s “reading frame,” scrambling instructions for APC and truncating the protein Wikipedia.Missense mutation
One letter is swapped for another, altering a critical amino acid in the APC protein and reducing its function PMC.Large genomic deletion
A chunk of chromosome 5 that includes the APC gene is lost, removing the gene entirely or part of it Spandidos Publications.Insertion mutation
Extra DNA inserted into APC disrupts its sequence, leading to a faulty protein Spandidos Publications.Splice-site mutation
Changes at the boundary of coding and non-coding regions cause the cell to skip or misread parts of the APC message ScienceDirect.Somatic (post-zygotic) mosaicism
Mutation occurs after conception, so only some cells carry the faulty APC gene, leading to a milder or patchy presentation PMC.Promoter hypermethylation
Epigenetic “silencing” of the APC gene promoter prevents normal protein production without altering DNA sequence PMC.Repeat length variation
Changes in short repeated sequences within APC can destabilize the gene and impair its function (e.g., insertion of extra repeats) MDPI.Copy-number variation
Having extra or missing copies of the APC gene region on chromosome 5 alters gene dosage and disrupts normal control of cell growth Spandidos Publications.Chromosomal translocation
A piece of chromosome 5 bearing APC attaches to another chromosome, splitting the gene and inactivating it Spandidos Publications.Inverted segment
A flipped portion of DNA disrupts APC’s coding sequence, producing a non-functional protein Spandidos Publications.Untranslated region (UTR) mutation
Changes in APC’s “bookends” (5′ or 3′ UTR) can reduce gene stability or translation efficiency Wikipedia.MicroRNA binding alteration
Mutation creates or destroys a microRNA binding site in APC’s UTR, leading to inappropriate protein levels Wikipedia.DNA repair gene defects
Secondary mutations in genes like MUTYH, POLE, or POLD1 impair DNA repair and increase the chance of APC mutations, mimicking Gardner syndrome Nature.Oxidative DNA damage
Reactive oxygen species from inflammation or toxins can induce APC mutations over time, contributing to sporadic cases PLOS.Environmental mutagens
Exposure to chemicals (e.g., alkylating agents, nitrosamines) or radiation can damage DNA and trigger APC gene errors Wikipedia.Age-related replication errors
As cells divide with age, DNA copying mistakes accumulate, raising the risk of spontaneous APC mutations Wikipedia.
Symptoms of Gardner Syndrome
Abdominal pain
Persistent or crampy pain due to numerous intestinal polyps rubbing against the bowel wall Cleveland Clinic.Rectal bleeding
Tiny blood vessels in polyps can bleed into the stool, causing visible or hidden blood loss Cleveland Clinic.Diarrhea or constipation
Irregular bowel patterns emerge as polyps crowd the colon lining Cleveland Clinic.Colon obstruction
Large clusters of polyps may block stool passage, leading to distension and severe pain Cleveland Clinic.Colon cancer
Nearly inevitable by mid-adult life if the colon is not removed Cleveland Clinic.Osteomas
Hard, painless bony growths on the jaw or skull detected when a bump is felt or seen on X-ray Wikipedia.Epidermoid cysts
Small, painless lumps under the skin often on the face, scalp, or back Cleveland Clinic.Desmoid tumors
Fibrous, locally aggressive masses most often in the abdominal wall or trunk Wikipedia.Lipomas
Soft, movable fatty lumps under the skin that are usually harmless Cleveland Clinic.Fibromas
Firm nodules of connective tissue appearing on or under the skin Wikipedia.Dental abnormalities
Extra teeth, impacted teeth, or enamel defects visible on dental exam or X-ray Cleveland Clinic.Congenital hypertrophy of the retinal pigment epithelium (CHRPE)
Flat, non-cancerous pigmented spots seen on eye exam GARD Information Center.Anemia
Chronic blood loss from polyps can lower red cell count, causing fatigue and pallor Cleveland Clinic.Palpable abdominal mass
Large desmoid tumors or polyp masses may be felt on deep abdominal exam Cleveland Clinic.Weight loss
Due to malabsorption or cancer development in the colon Cleveland Clinic.
Diagnostic Tests for Gardner Syndrome
Physical Examination
Abdominal palpation for tenderness, masses, or distension.
Digital rectal exam to detect low-lying polyps or blood.
Skull/jaw palpation to feel osteomas under the skin.
Skin inspection for epidermoid cysts, fibromas, or lipomas Cleveland Clinic.
Manual Tests
Jaw and dental exam to count teeth, spot extra or impacted teeth.
Palpation of abdominal wall for firm desmoid nodules.
Lymph node exam to check for unusual lymph enlargement from soft-tissue tumors.
Skin cyst expression (squeezing) to inspect cyst contents when needed Cleveland Clinic.
Lab & Pathological Tests
Genetic testing for APC gene mutations in blood cells (gold standard, 95% detection).
Fecal occult blood test to detect hidden bleeding from polyps.
Colonic polyp biopsy during endoscopy to assess dysplasia or cancer.
Histopathology of osteoma or cyst to confirm benign nature.
Complete blood count (CBC) to screen for anemia from chronic bleeding.
Liver function tests (LFTs) when staging cancer or metastasis risk Cleveland Clinic.
Electrodiagnostic Tests
Electromyography (EMG) if desmoid tumors press on nerves, causing muscle weakness.
Nerve conduction studies (NCS) to evaluate nerve compression by abdominal or trunk tumors Cleveland Clinic.
Imaging Tests
Colonoscopy direct camera inspection of the colon to count and remove polyps.
CT scan of abdomen/pelvis to map desmoid tumor size and location.
MRI scan detailed soft tissue imaging for desmoids or liver metastases.
Skull X-ray to detect osteomas in jaw or skull bones Cleveland Clinic.
Non-Pharmacological Treatments
(Therapies and supportive measures that do not involve drugs)
Genetic Counseling
A specialized session with a genetics expert to explain the APC mutation, inheritance pattern, and testing options for family members. Its purpose is to help patients and relatives understand risk, make informed choices, and plan screening. Mechanistically, counseling provides education rather than altering the disease directly.Regular Colonoscopic Surveillance
Routine camera exams of the colon (every 1–2 years) detect new polyps early. The purpose is to remove or monitor polyps before they turn cancerous. The procedure mechanically visualizes and biopsies tissue for early intervention.Endoscopic Polypectomy
During colonoscopy, small instruments remove polyps. Purpose: to lower polyp burden and delay cancer. Mechanism: direct mechanical excision of growths prevents malignant transformation.Dental Monitoring and Orthodontic Care
Frequent dental X-rays and cleanings detect extra or impacted teeth and malformations. Purpose: to preserve oral health and plan interventions. Mechanism: identification of anomalies guides corrective braces or extractions.Dermatologic Surveillance
Regular skin checks by a dermatologist to watch skin cysts and fibromas. Purpose: early removal of bothersome or infected lesions. Mechanism: visual inspection and biopsy guide surgical removal when needed.Physical Therapy for Desmoid Tumors
Gentle stretching and strengthening exercises reduce pain and maintain mobility when desmoid tumors press on muscles. Purpose: improve function and quality of life. Mechanism: targeted movements promote circulation and reduce stiffness around fibrous growths.Pain Management Techniques
Heat packs, cold compresses, and TENS (transcutaneous electrical nerve stimulation) soothe aches from bone or soft-tissue tumors. Purpose: non-drug pain relief. Mechanism: thermal therapies and mild electric pulses interrupt pain signals.Nutritional Counseling
A dietitian advises on high-fiber, low-fat diets to support colon health and ease digestion. Purpose: slow polyp growth and improve gut comfort. Mechanism: fiber increases stool bulk, dilutes carcinogens, and speeds transit time.Psychological Support
Counseling or support groups help cope with diagnosis stress and family impact. Purpose: reduce anxiety, increase treatment adherence. Mechanism: talk therapy rewires stress responses and builds resilience.Occupational Therapy
Strategies to modify daily tasks and tools when bone lesions limit mobility or cause pain. Purpose: maintain independence at work and home. Mechanism: ergonomic adjustments reduce strain on affected areas.Laser Therapy for Cysts
Dermatologic lasers vaporize small skin cysts. Purpose: cosmetic improvement and prevention of infection. Mechanism: focused light energy breaks down cyst walls.Cryotherapy for Skin Lesions
Freezing skin fibromas with liquid nitrogen. Purpose: quick removal of small, bothersome nodules. Mechanism: extreme cold causes cellular destruction of lesion tissue.Photodynamic Therapy
For selected skin tumors, a light-activated drug is applied then activated by a specific wavelength to kill abnormal cells. Purpose: non-invasive lesion control. Mechanism: drug produces reactive oxygen species under light, destroying tumor cells.Regular Dermatologic Imaging
High-resolution ultrasound or MRI to monitor deep-seated fibromas. Purpose: plan timing of surgery or therapy. Mechanism: detailed imaging reveals growth rate and involvement of nearby organs.Sun Protection Measures
Wearing broad-spectrum sunscreen and protective clothing to reduce skin changes and cyst formation. Purpose: prevent sun-triggered cyst inflammation. Mechanism: UV blockers limit local skin damage and cyst enlargement.Intensive Dental Hygiene
Frequent brushing, flossing, and antimicrobial rinses to prevent infections around malformed teeth. Purpose: reduce dental complications and pain. Mechanism: lowers bacterial load in the mouth, limiting inflammation.Family Screening Programs
Organizing relatives for coordinated genetic testing and colonoscopy days. Purpose: early detection in at-risk family members. Mechanism: systematic scheduling encourages participation.Educational Workshops
Group sessions on Gardner syndrome basics, treatment options, and lifestyle tips. Purpose: empower patients with knowledge and peer support. Mechanism: structured teaching improves self-care behaviors.Yoga and Mind-Body Practices
Gentle yoga, meditation, and breathing exercises to reduce stress–a factor in desmoid tumor flare-ups. Purpose: lower cortisol and improve mood. Mechanism: relaxation response downregulates sympathetic overactivity.Hydrotherapy
Warm baths with Epsom salts to ease muscle tension and joint pain from osteomas. Purpose: soothe discomfort and improve sleep. Mechanism: magnesium in salts relaxes muscles and reduces inflammation.
Drug Treatments
(Evidence-based medications for key features of Gardner syndrome)
Sulindac (NSAID)
Class: Non-steroidal anti-inflammatory drug
Dosage: 150–200 mg twice daily
Timing: With meals to reduce stomach upset
Purpose: Shrink colon polyps and desmoid tumors
Mechanism: Inhibits COX-1/COX-2 enzymes, lowering prostaglandins that drive polyp growth
Side Effects: Stomach pain, ulcer risk, kidney effects
Celecoxib (COX-2 Inhibitor)
Class: Selective COX-2 inhibitor
Dosage: 200 mg twice daily
Timing: With food
Purpose: Reduce polyp number and size
Mechanism: Blocks COX-2 enzyme, reducing inflammation with less gastric risk
Side Effects: Cardiovascular risk, headache, diarrhea
Tamoxifen (Anti-Estrogen)
Class: Selective estrogen receptor modulator
Dosage: 20 mg once daily
Timing: Any time, consistent daily
Purpose: Slow desmoid tumor growth
Mechanism: Blocks estrogen receptors in tumor cells, inhibiting growth signals
Side Effects: Hot flashes, risk of blood clots
Imatinib (Tyrosine Kinase Inhibitor)
Class: TKI targeting PDGFR and c-KIT
Dosage: 400 mg once daily
Timing: With a light meal
Purpose: Treat aggressive desmoid tumors
Mechanism: Blocks signaling pathways that drive tumor cell division
Side Effects: Nausea, edema, muscle cramps
Sorafenib (Multi-Kinase Inhibitor)
Class: Multi-targeted TKI
Dosage: 400 mg twice daily
Timing: Morning and evening
Purpose: Manage advanced desmoid tumors
Mechanism: Inhibits RAF kinase and VEGFR, slowing tumor blood supply and growth
Side Effects: Hand-foot skin reaction, hypertension
Methotrexate (Low-Dose Chemotherapy)
Class: Antimetabolite
Dosage: 15 mg/week
Timing: Once weekly with folic acid supplements
Purpose: Slow desmoid and polyposis progression when other drugs fail
Mechanism: Disrupts DNA synthesis in rapidly dividing cells
Side Effects: Mouth sores, liver enzyme changes
Vinblastine (Chemotherapy)
Class: Vinca alkaloid
Dosage: 6 mg/m² IV every 3 weeks
Timing: In infusion center
Purpose: Treat aggressive desmoid masses
Mechanism: Prevents microtubule formation, stopping cell division
Side Effects: Hair loss, neuropathy
Doxorubicin (Anthracycline)
Class: Anthracycline antibiotic
Dosage: 60–75 mg/m² IV every 3 weeks
Timing: Infusion with cardiac monitoring
Purpose: Reduce large desmoid tumors resistant to other agents
Mechanism: Intercalates DNA, inhibiting topoisomerase II
Side Effects: Heart toxicity, nausea
Decitabine (Hypomethylating Agent)
Class: DNA methyltransferase inhibitor
Dosage: 20 mg/m² IV daily for 5 days (cycle)
Timing: 28-day cycles
Purpose: Experimental use to modify gene expression in polyps
Mechanism: Incorporates into DNA, reactivating tumor suppressor genes
Side Effects: Low blood counts, fatigue
Bevacizumab (Anti-VEGF Monoclonal Antibody)
Class: Angiogenesis inhibitor
Dosage: 5 mg/kg IV every 2 weeks
Timing: In infusion suite
Purpose: Starve aggressive desmoid tumors by blocking new blood vessel growth
Mechanism: Binds VEGF, preventing it from stimulating vessel formation
Side Effects: High blood pressure, risk of bleeding
Dietary Molecular Supplements
(Natural compounds that may help slow polyp growth or reduce inflammation)
Curcumin (Turmeric Extract)
Dosage: 500 mg twice daily
Function: Anti-inflammatory and antioxidant
Mechanism: Inhibits NF-κB and COX pathways, reducing pro-tumor signals
Green Tea Polyphenols (EGCG)
Dosage: 300 mg daily
Function: Antioxidant and anti-proliferative
Mechanism: Blocks Wnt/β-catenin signaling involved in polyp formation
Resveratrol
Dosage: 150 mg daily
Function: Antioxidant, anti-inflammatory
Mechanism: Activates SIRT1 pathways, promoting DNA repair and cell cycle arrest
Omega-3 Fatty Acids (Fish Oil)
Dosage: 1 g EPA/DHA daily
Function: Anti-inflammatory
Mechanism: Competes with arachidonic acid, lowering pro-inflammatory eicosanoids
Vitamin D₃
Dosage: 2,000 IU daily
Function: Regulates cell growth
Mechanism: Binds vitamin D receptor to modulate colonic cell proliferation
Calcium Citrate
Dosage: 1,200 mg daily
Function: Polyp-growth inhibitor
Mechanism: Binds free bile acids/toxins in gut, reducing mucosal irritation
Quercetin
Dosage: 500 mg daily
Function: Anti-oxidant, anti-proliferative
Mechanism: Inhibits PI3K/AKT signaling in tumor cells
Sulforaphane (Broccoli Sprouts)
Dosage: 30 mg daily
Function: Epigenetic modulator
Mechanism: Activates Nrf2 pathway, boosting detoxifying enzymes
Methylsulfonylmethane (MSM)
Dosage: 1,000 mg daily
Function: Anti-inflammatory and joint support
Mechanism: Donor of sulfur for connective tissue repair
Probiotic Blend (Lactobacillus & Bifidobacterium)
Dosage: 10 billion CFU daily
Function: Gut microbiome support
Mechanism: Restores healthy bacteria balance, reducing inflammation
Regenerative & Stem-Cell-Based Therapies
(Emerging approaches to repair tissue damage and modulate immune response)
Mesenchymal Stem Cell (MSC) Infusion
Dosage: 1–2 million cells/kg IV infusion monthly
Function: Immunomodulation and tissue repair
Mechanism: MSCs home to inflammation sites, release anti-inflammatory cytokines
Adipose-Derived Stem Cells
Dosage: 10 million cells injected near desmoid mass every 3 months
Function: Local anti-fibrotic effects
Mechanism: Secrete matrix-metalloproteinases that remodel scar tissue
Hematopoietic Stem Cell Transplant (HSCT)
Dosage: Single transplant after conditioning
Function: Reset immune system
Mechanism: New immune cells may better regulate fibrotic tumor activity
Induced Pluripotent Stem Cell (iPSC)-Derived Therapies
Dosage: Experimental infusions in clinical trials
Function: Replace damaged colon lining cells
Mechanism: iPSCs differentiate into healthy epithelial cells
Exosome-Based Treatment
Dosage: 50–100 µg exosome protein IV weekly
Function: Deliver regenerative signals
Mechanism: Exosomes carry microRNAs that reduce inflammation and fibrosis
CRISPR/Cas9 Gene Editing
Dosage: Single or repeat vector infusions (trial only)
Function: Correct APC gene defect at cellular level
Mechanism: Cas9 nuclease cuts mutated APC, template DNA repairs sequence
Key Surgeries
(Procedures to remove or prevent tumors and polyps)
Prophylactic Total Colectomy with Ileorectal Anastomosis
Procedure: Remove entire colon, connect small intestine to rectum
Why: Prevent colorectal cancer by eliminating polyp-bearing colon
Total Proctocolectomy with Ileal Pouch-Anal Anastomosis
Procedure: Remove colon and rectum, form internal pouch from small intestine to attach to anus
Why: For patients with rectal polyps or cancer risk in rectum
Polypectomy via Endoscopy
Procedure: Snare-or hot biopsy removal of individual polyps
Why: Delay or reduce need for colectomy by removing large or suspicious polyps
Desmoid Tumor Resection
Procedure: Surgical removal of fibrous masses
Why: Relieve pain or organ compression when tumors grow aggressively
Osteoma Excision
Procedure: Remove bone bumps on jaw or skull via small incisions
Why: Improve appearance, prevent nerve pressure or sinus blockage
Preventive Strategies
Early Genetic Testing for APC mutation in at-risk relatives
Timed Colonoscopic Surveillance beginning in adolescence
Prophylactic Colectomy when polyp burden becomes high
Regular NSAID Use (under doctor supervision) to lower polyp growth
High-Fiber Diet to reduce colonic irritants
Vitamin D and Calcium Supplementation to slow polyp progression
Avoidance of Tobacco and Alcohol which raise colon cancer risk
Sun Protection to guard against cyst inflammation
Stress Reduction Techniques to limit desmoid flares
Frequent Skin and Dental Checks for early removal of tumors
When to See the Doctor
New or Bleeding Polyps: Blood in stool or on toilet paper
Family History Update: Someone in the family tests positive for APC mutation
Rapid Tumor Growth: Pain or swelling from desmoids, osteomas, or cysts
Dental Changes: Loose, extra, or missing teeth causing discomfort
Digestive Symptoms: Persistent abdominal pain, diarrhea, or bowel obstruction
Skin Lesions: Cysts become red, painful, or infected
Unexpected Weight Loss or Fatigue: Signs of possible cancer progression
Joint or Bone Pain: Osteomas pressing on nerves or joints
Hormonal Changes: Risk factors that might alter treatment plan
Before Major Life Events: To plan surgery or intensive monitoring
Foods to Eat & Avoid
Eat: High-Fiber Foods (whole grains, beans) to promote healthy bowel movements
Eat: Colorful Fruits & Vegetables for antioxidants
Eat: Fatty Fish (salmon, mackerel) rich in omega-3
Eat: Low-Fat Dairy or Fortified Alternatives for calcium and vitamin D
Eat: Green Tea for polyphenols
Avoid: Processed & Red Meats linked to higher colon cancer risk
Avoid: High-Sugar Snacks that promote inflammation
Avoid: Excess Alcohol which irritates the gut lining
Avoid: Trans Fats & Fried Foods that may worsen polyp growth
Avoid: Tobacco Products which raise cancer risk
Frequently Asked Questions
What causes Gardner syndrome?
A change in the APC gene inherited from a parent causes uncontrolled cell growth in the colon and other tissues.Is Gardner syndrome the same as familial adenomatous polyposis (FAP)?
It is a variant of FAP with extra-intestinal tumors like osteomas, cysts, and desmoids.At what age do symptoms appear?
Colon polyps often appear in teenage years; other tumors may show up in the 20s–30s.How is Gardner syndrome diagnosed?
Genetic testing for APC gene mutations plus colonoscopy and imaging for tumors.Can polyps turn into cancer?
Yes—almost all colon polyps become cancer by age 40–50 if the colon is not removed.What surgeries are needed?
Colectomy (colon removal) is standard; other tumors are removed as needed.Are there medicines to slow polyp growth?
Yes—NSAIDs like sulindac and COX-2 inhibitors can shrink polyps and desmoids.Can diet help manage Gardner syndrome?
A high-fiber, low-fat diet with supplements (vitamin D, calcium) may slow polyp formation.What is the role of genetic counseling?
It helps family members understand their risk and decide on testing and screening.How often should I have a colonoscopy?
Usually every 1–2 years, but your doctor will tailor timing based on findings.Can dental problems be prevented?
Regular dental exams and X-rays help catch and treat tooth issues early.What are desmoid tumors?
Soft-tissue growths that can be painful and press on organs—treated with drugs, surgery, or radiation.Are stem cell or gene therapies available?
They are experimental but show promise in early trials to correct APC defects.What is my long-term outlook?
With early surgery and careful monitoring, many people live normal lifespans.How can I support mental health?
Joining support groups, seeking counseling, and practicing stress-reduction techniques help cope with the diagnosis.
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: August 04, 2025.
