Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening blood disorder. Tiny clots form inside many of the body’s smallest blood vessels. These clots use up platelets (the cells that stop bleeding), so the platelet count falls. As red blood cells squeeze past the clots, they break, causing anemia. The clots also block blood flow and can damage the brain, heart, kidneys, and other organs. Without fast treatment, TTP can be fatal; with modern care, most people survive. NCBINational Organization for Rare Disorders
Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy—a disease where tiny blood clots form in small vessels. TTP happens when the blood-clotting helper protein VWF becomes too sticky because the ADAMTS13 enzyme is very low or blocked. The ultra-sticky VWF catches platelets and forms micro-clots, which use up platelets (causing low platelet count and easy bruising/bleeding) and slice red blood cells (causing hemolytic anemia). People can develop headache, confusion, stroke-like symptoms, chest pain, shortness of breath, fever, abdominal pain, dark urine, and kidney problems. Doctors diagnose TTP with blood tests (very low platelets, anemia with schistocytes on smear, high LDH, low haptoglobin), an ADAMTS13 activity test (<10% strongly supports TTP), and risk tools like the PLASMIC score while waiting for the enzyme test. Treatment must start right away and usually includes daily plasma exchange, steroids, caplacizumab, and often rituximab. Congenital TTP is treated with enzyme replacement (recombinant ADAMTS13) or plasma infusion. ADZYNMAepicurism.infoUnderstanding TTPU.S. Food and Drug Administration
A protein-cutting enzyme called ADAMTS13 normally trims very large strands of von Willebrand factor (VWF) so platelets do not clump too much. In TTP, ADAMTS13 activity is severely low. Ultra-large VWF strings remain in the blood, platelets stick to them, and widespread micro-clots form. This causes microangiopathic hemolytic anemia (broken red cells) and thrombocytopenia (low platelets). A blood test showing ADAMTS13 activity <10% strongly supports the diagnosis. PMCAsh Publications
Types of TTP
Immune-mediated (acquired) TTP (iTTP). The immune system makes antibodies that block or clear ADAMTS13. This is the most common form in adults and often presents suddenly. It may relapse. Ash Publications
Congenital (inherited) TTP (cTTP, Upshaw–Schulman syndrome). A person is born with two faulty copies of the ADAMTS13 gene, so enzyme levels are very low from birth. Attacks may begin in infancy, childhood, or later, and can be triggered by stressors like infections or pregnancy. GARD Information Center
Clinicians also describe clinical courses such as acute, relapsing, and refractory disease (not responding to initial treatment), but the underlying type is immune-mediated vs congenital. NCBI
Causes
TTP itself is caused by severe ADAMTS13 deficiency. Below are common underlying causes or triggers that can start an attack or uncover a tendency to TTP:
Autoantibodies against ADAMTS13 (iTTP). The immune system inappropriately targets ADAMTS13 so it cannot work. Ash Publications
ADAMTS13 gene mutations (cTTP). Inherited changes produce too little working enzyme. GARD Information Center
Bacterial or viral infections. Infections can inflame blood vessels and provoke iTTP episodes. NCBI
Pregnancy or the postpartum period. Pregnancy increases VWF and can reveal or trigger both iTTP and cTTP. Ash PublicationsFrontiers
Autoimmune diseases (for example, lupus). Immune activation can generate anti-ADAMTS13 antibodies. NCBI
HIV infection. Immune dysregulation and endothelial injury can precipitate TTP-like illness, including iTTP. NCBI
Quinine. Immune-mediated drug reaction linked to TMA and TTP. PubMed
Ticlopidine. Early thienopyridine antiplatelet agent historically associated with TTP. New England Journal of Medicine
Clopidogrel. Rare early complication after starting therapy; typically within 2 weeks. New England Journal of Medicine
Calcineurin inhibitors (cyclosporine, tacrolimus). Dose-related endothelial toxicity may lead to TMA/TTP. PubMed
Chemotherapy agents (e.g., mitomycin C, gemcitabine). Can damage endothelium and provoke TMA; some cases behave like TTP. Ash Publications
Interferon-based therapies. Reported in drug-induced TMA/TTP reviews. ResearchGate
VEGF-pathway or anti-angiogenic drugs. Endothelial effects can trigger TMA; careful evaluation is required. Ash Publications
Immune checkpoint inhibitors (rare). Immune activation has been linked to TMA; workup must exclude iTTP. Ash Publications
Solid organ or stem-cell transplantation (rare). Immunosuppressants and endothelial injury can cause TMA; ADAMTS13 testing helps separate iTTP from other TMA. ScienceDirect
Pancreatitis. Systemic inflammation may precipitate TMA episodes. NCBI
Major surgery. Physiologic stress can trigger relapse in susceptible individuals. NCBI
Malignancy. Cancer-related TMAs occur; ADAMTS13 testing clarifies if iTTP is present. acrjournals.onlinelibrary.wiley.com
Severe hypertension (as a confounder/trigger). Can cause TMA; distinction from iTTP requires labs and ADAMTS13 testing. acrjournals.onlinelibrary.wiley.com
COVID-19 or other systemic viral illnesses (rare). Case reports and series describe TMA with low ADAMTS13 in some patients; careful diagnostic workup is needed. NCBI
Note: Many entries above are triggers or look-alikes within the thrombotic microangiopathy (TMA) spectrum. Confirming true TTP relies on severely reduced ADAMTS13 activity together with the clinical picture. PMC
Common symptoms and signs
Easy bruising and purple spots (purpura/petechiae). Low platelets make the skin bruise or spot easily. National Organization for Rare Disorders
Bleeding from the nose, gums, or heavier menstrual bleeding. Platelet shortage reduces normal clotting. National Organization for Rare Disorders
Fatigue and weakness. Red cell destruction causes anemia and low oxygen delivery. NCBI
Pale skin. A visible sign of anemia. GARD Information Center
Jaundice (yellowing of skin/eyes). Broken red cells release bilirubin. NCBI
Dark urine. From hemolysis and kidney involvement. NCBI
Fever. Inflammatory response to widespread clotting and hemolysis. NCBI
Headache. Brain is sensitive to reduced blood flow. National Organization for Rare Disorders
Confusion, slowed thinking, or trouble speaking. Micro-clots can briefly reduce blood flow in the brain. National Organization for Rare Disorders
Fainting or dizziness. From anemia or brain involvement. National Organization for Rare Disorders
Seizures. Severe brain involvement can provoke seizures. National Organization for Rare Disorders
Stroke-like weakness or numbness. Small clots may cause focal neurologic symptoms. National Organization for Rare Disorders
Shortness of breath or chest pain. Anemia and micro-clots can stress the heart and lungs. NCBI
Abdominal pain, nausea, vomiting. From intestinal or pancreatic involvement or general illness. NCBI
Swelling or decreased urine (kidney strain). Micro-clots can injure kidneys. NCBI
How doctors make the diagnosis
TTP is a clinical emergency. Doctors often start treatment immediately when suspicion is high, while tests are pending. A widely used bedside tool, the PLASMIC score, estimates the chance that ADAMTS13 is severely low and helps guide urgent decisions. Definitive diagnosis rests on ADAMTS13 testing. NCBI
A) Physical examination
Vital signs and general appearance. Fever, fast heart rate, low blood pressure, and signs of severe illness raise concern for TTP in the right context. NCBI
Skin and mucosa check. Petechiae, purpura, and mucosal bleeding reflect thrombocytopenia. National Organization for Rare Disorders
Neurologic exam. Brief confusion, weakness, speech problems, or seizures suggest brain involvement. National Organization for Rare Disorders
Cardio-renal exam. Chest pain, shortness of breath, edema, or decreased urine may indicate heart/kidney stress. NCBI
B) Manual/bedside assessments
These are quick tests or structured scores performed at the bedside to document severity; they do not by themselves prove TTP.
- Orthostatic blood pressure/heart rate. Looks for volume depletion or autonomic effects in a sick patient. NCBI
- Capillary refill time and peripheral perfusion check. Screens for poor microcirculation. NCBI
7) Glasgow Coma Scale (GCS) / brief cognitive screen. Tracks level of consciousness and confusion during neuro involvement. NCBI - NIH Stroke Scale (focused bedside neuro scoring). Quantifies focal deficits if present. (Used to track severity; not specific for TTP.) NCBI
C) Laboratory and pathological tests — the heart of diagnosis
Complete blood count (CBC). Low platelets and anemia are typical. NCBI
Peripheral blood smear. Shows schistocytes (fragmented red cells); this is a key clue for microangiopathic hemolysis. NCBI
Lactate dehydrogenase (LDH). Usually high due to cell breakdown; correlates with hemolysis and tissue ischemia. NCBI
Haptoglobin (low) and indirect bilirubin (high). Support hemolysis. NCBI
Reticulocyte count (high). Bone marrow response to anemia. NCBI
Coagulation tests (PT/INR, aPTT). Often normal in TTP; this helps distinguish TTP from DIC, where they are prolonged. NCBI
Creatinine and urinalysis. Evaluate kidney involvement (protein, blood, casts). NCBI
ADAMTS13 activity with inhibitor/antibody testing. Activity <10% (sometimes <10 IU/dL, depending on the assay) is strongly diagnostic in the right clinical picture; detection of anti-ADAMTS13 antibodies supports iTTP. PMCen.iacld.com
Practical point: Because ADAMTS13 results may take time, clinicians often start treatment right away if the PLASMIC score is high and the smear shows schistocytes. NCBI
D) Electrodiagnostic tests — to assess complications
Electrocardiogram (ECG). Heart strain, ischemia, or rhythm problems can occur in TTP; ECG helps detect them early. NCBI
Electroencephalogram (EEG). If seizures or unexplained confusion occur, EEG helps document abnormal brain activity. (This tracks complications; it does not prove TTP.) NCBI
E) Imaging tests — to look for organ damage
Brain CT or MRI. Used when there are neurologic symptoms to rule out bleeding or stroke and to measure injury from micro-clots. NCBI
Echocardiogram or cardiac enzymes with imaging as needed. Some patients develop heart injury; echo and troponin help detect and follow this. NCBI
Non-pharmacological treatments (therapies & supportive care)
These are “non-drug” actions or procedures. In TTP, the most important one is a procedure: therapeutic plasma exchange (TPE).
Therapeutic plasma exchange (TPE) – the cornerstone: removes inhibitory antibodies and ultralarge VWF; replaces ADAMTS13 with donor plasma. Usually daily 1–1.5 plasma volumes until platelets and hemolysis normalize for a few days. NCBI
Plasma infusion (esp. cTTP) when TPE isn’t available, or as short-term bridge; it provides ADAMTS13 but doesn’t remove antibodies. NCBI
ICU-level monitoring for neuro, cardiac, and kidney complications; rapid response saves organs. ADZYNMA
Avoid routine platelet transfusions—they can worsen clotting; only for life-threatening bleeding or urgent procedures, under specialist guidance. PMC
Red blood cell transfusion for symptomatic anemia to improve oxygen delivery. ADZYNMA
Central venous catheter placement to perform plasma exchange safely and repeatedly. ScienceDirect
Twice-daily TPE (temporarily) in refractory disease or organ deterioration. The Blood Project
Renal support (IV fluids, careful diuretics; dialysis if acute kidney injury is severe). ADZYNMA
Cardiac care for chest pain or elevated troponin; ECG monitoring, oxygen, and cardiology support. PMC
Seizure control protocols and neurocritical care when needed (EEG, airway protection). PMC
Infection control (cultures, source control) because infection can trigger or mimic TTP. ADZYNMA
Stop likely culprit drugs (e.g., quinine, certain antiplatelets, calcineurin inhibitors) after hematology review. PMC
Pregnancy-specific planning (maternal–fetal medicine + hematology) for acute episodes or for cTTP prophylaxis. U.S. Food and Drug Administration
Early steroid-sparing strategy planning (because long steroid courses have side effects)—ties into drug therapy below. NCBI
VTE prevention individualized—mechanical methods early; pharmacologic prophylaxis considered when platelets recover, guided by your team. NCBI
Nutrition support for healing (iron, folate, protein) once acute phase is controlled. ADZYNMA
Rehabilitation/physiotherapy after neurologic events to regain function. ADZYNMA
Psycho-social support (counseling, peer groups); TTP is frightening and often recurs—support helps adherence and recovery. ADZYNMA
Education and a medical alert plan (wallet card, emergency letter) for future episodes. ADZYNMA
Close follow-up with ADAMTS13 monitoring during remission; preemptive rituximab may be offered if ADAMTS13 falls, to prevent relapse. PMC
Drug treatments
Doses below are typical/commonly cited; exact regimens are individualized. Always defer to your treating hematologist.
Caplacizumab (Cablivi) • anti-VWF nanobody
Dose: 11 mg IV before first TPE, then 11 mg SC after each TPE; continue daily for 30 days after the last TPE; may extend ~28 days if ADAMTS13 remains low.
When/Purpose: Start at diagnosis of iTTP, with TPE + immunosuppression; rapidly stops new micro-clots, speeds platelet recovery, and reduces relapse.
Mechanism: Blocks the VWF–platelet GPIbα interaction.
Key side effects: Bleeding, especially mucosal; caution around procedures. FEP BlueHealth NetPrednisone / Methylprednisolone • corticosteroid
Dose: Prednisone ~1 mg/kg/day; some centers use IV methylprednisolone 10 mg/kg/day for 3 days in severe cases, then taper.
Purpose: Calm antibody production and inflammation quickly.
Mechanism: Broad immunosuppression.
Side effects: High blood sugar, mood/sleep changes, infection risk, fluid retention. NCBIRituximab • anti-CD20 monoclonal antibody
Dose: 375 mg/m² IV weekly × 4 (timed around TPE so it isn’t removed).
When/Purpose: Often added up-front in iTTP; definitely used for refractory/relapsing disease and preemptively in remission with low ADAMTS13.
Mechanism: Depletes B cells that make anti-ADAMTS13 antibodies.
Side effects: Infusion reactions, infection risk (HBV reactivation—screen first). PMC+1Recombinant ADAMTS13 (ADZYNMA) • enzyme replacement
Dose: For cTTP, IV prophylaxis every other week; on-demand daily during acute events (label-guided dosing).
Purpose: Replaces the missing enzyme in congenital disease, preventing and treating episodes (including in pregnancy).
Mechanism: Restores VWF-cleaving activity.
Side effects: Infusion reactions; hypersensitivity (rare). U.S. Food and Drug AdministrationMolina HealthcareCyclophosphamide (CTX) • cytotoxic immunosuppressant (off-label)
Dose: Regimens vary in refractory iTTP (e.g., ~500 mg/m² IV once or pulses; other dosing exists).
Purpose: For refractory cases to silence antibody production.
Mechanism: Alkylates proliferating lymphocytes.
Side effects: Low blood counts, infection, hemorrhagic cystitis, infertility risk. PMCCyclosporine (CsA) • calcineurin inhibitor (off-label)
Dose: Often ~2–4 mg/kg/day in divided doses with level monitoring in refractory disease.
Purpose: Maintenance or refractory control of autoimmunity.
Mechanism: Blocks T-cell activation.
Side effects: Kidney toxicity, hypertension, tremor, drug interactions. PMCBortezomib • proteasome inhibitor (off-label)
Dose: Commonly 1.3 mg/m² SC/IV on days 1, 4, 8, 11 of a 21–28-day cycle in refractory iTTP.
Purpose: Depletes antibody-secreting plasma cells in rituximab-refractory iTTP.
Mechanism: Proteasome blockade → plasma cell apoptosis.
Side effects: Neuropathy, cytopenias, shingles risk (often give antiviral prophylaxis). Wiley Online LibraryVincristine • anti-mitotic (off-label)
Dose: Single ~1–2 mg IV dose has been used adjunctively in refractory cases (dosing varies; neurotoxicity limits use).
Purpose: Rescue immunosuppression when others fail.
Mechanism: Stops rapidly dividing immune cells.
Side effects: Neuropathy, constipation, hair loss. PMCMycophenolate mofetil (MMF) • antimetabolite (off-label)
Dose: Often 500 mg twice daily, titrated to 1 g twice daily if tolerated (maintenance or steroid-sparing).
Purpose: Prevent relapses / maintain remission.
Mechanism: Inhibits lymphocyte purine synthesis.
Side effects: GI upset, infection risk, teratogenicity (pregnancy avoidance needed). Council of Health InsuranceN-acetylcysteine (NAC) • mucolytic/antioxidant (adjunct, off-label)
Dose: High-dose IV regimens (e.g., ~150 mg/kg/day in case series) used with standard therapy in refractory iTTP.
Purpose: Experimental adjunct to reduce VWF ultra-large multimers.
Mechanism: Breaks disulfide bonds within VWF; may reduce its stickiness.
Side effects: Nausea, rare anaphylactoid reaction; evidence is limited—specialist only. PMC+1
Dietary “molecular” supplements
No vitamin or supplement treats TTP or replaces plasma exchange/caplacizumab/immunosuppression. Discuss every product with your hematology team to avoid interactions (for example, some supplements can increase bleeding).
Folic acid (e.g., 1 mg/day) – supports red-cell production after hemolysis.
Vitamin B12 (per labs; oral or IM) – supports healthy red blood cells.
Iron (only if iron deficiency is proven) – helps rebuild hemoglobin.
Vitamin D (per labs) – supports immune balance and bone health; steroid use raises the need.
Vitamin C (100–500 mg/day) – supports iron absorption and antioxidant defense.
Protein/essential amino acids – aids healing; prioritize food sources.
Omega-3 fatty acids (ask first; may affect bleeding) – anti-inflammatory support.
Probiotics (if appropriate) – gut support during/after antibiotics; evidence in TTP is indirect.
Zinc (short term if deficient) – immune function; avoid excess.
Multivitamin (standard doses) – general nutritional back-stop.
Important cautions: avoid quinine-containing products (including some “tonic water” brands), high-dose garlic/ginkgo/ginseng, and other herbal “blood thinners” unless your doctor okays them. PMC
Advanced / immune-directed” therapies
There are no approved stem-cell or regenerative drugs for TTP. When cases are refractory or relapsing, specialists may use advanced immune-directed approaches:
Recombinant ADAMTS13 (ADZYNMA) – cTTP enzyme replacement (prevents and treats episodes; pregnancy-friendly planning). U.S. Food and Drug Administration
Rituximab – B-cell depletion to stop anti-ADAMTS13 production. PMC
Bortezomib – plasma-cell depletion when rituximab fails. Wiley Online Library
Cyclophosphamide – cytotoxic pulses in severe refractory iTTP. PMC
Cyclosporine – maintenance immunosuppression strategy in selected patients. PMC
Daratumumab (anti-CD38) – case reports/series show benefit in refractory iTTP; considered only by experts. Wiley Online Library
Procedures/surgeries
Central venous catheter placement – needed to perform plasma exchange reliably. ScienceDirect
Therapeutic plasma exchange procedure – technically a procedure rather than a drug; repeated daily until remission. NCBI
Dialysis (temporary) – if acute kidney failure develops. ADZYNMA
Splenectomy – rarely used now; historical rescue in relapse before modern biologics. PMC
Airway/feeding procedures (intubation, tracheostomy, feeding tube) – only if severe neurologic complications occur.
Prevention & relapse-reduction steps
Specialist follow-up at a TTP-experienced center.
Regular ADAMTS13 monitoring in remission; a falling level often predicts relapse. PMC
Preemptive rituximab if ADAMTS13 drops (your team will discuss pros/cons). PMC
Avoid known triggers, especially quinine, and review all new medications with your hematologist. PMC
Pregnancy planning (hematology + maternal-fetal medicine) with a plan for cTTP prophylaxis or iTTP monitoring. U.S. Food and Drug Administration
Vaccinations (non-live when on rituximab; time doses before B-cell depletion if possible).
Medical alert ID noting “history of TTP—avoid platelets unless life-threatening bleeding.” PMC
Rapid care pathway for any future symptoms (you and your family know what to do).
Healthy lifestyle—sleep, stress control, balanced diet, no smoking; these don’t cure TTP but support recovery.
Infection prevention (hand hygiene; prompt evaluation), as infections can trigger episodes. ADZYNMA
When to see a doctor—immediately if you notice:
Sudden bruising/petechiae, bleeding gums/nose plus fatigue or dark urine.
Any neurologic symptoms (confusion, weakness, slurred speech, seizures).
Chest pain or shortness of breath.
During pregnancy: any of the above or unexplained severe fatigue and bruising.
TTP care is urgent. Go to the emergency department and say, “I’m worried about TTP.” Early plasma exchange + steroids + caplacizumab saves lives. Understanding TTP
What to eat” and “what to avoi
Eat more of:
Iron- and folate-rich foods (beans, lentils, leafy greens, lean meats) to support blood rebuilding.
Protein (fish, eggs, dairy/soy, legumes) to heal tissues.
Vitamin-C–rich fruits/vegetables (citrus, berries, peppers) to help iron absorption.
Whole grains for steady energy.
Hydration (water) to support kidney function and plasma exchange.
Avoid / limit:
Quinine-containing products (including some tonic waters / leg-cramp tablets). PMC
Alcohol (raises bleeding risk and interacts with meds).
Herbal/botanical “blood thinners” (high-dose garlic, ginkgo, ginseng, etc.).
Grapefruit if you’re on cyclosporine (drug interaction). PMC
Raw or undercooked foods if you’re significantly immunosuppressed.
High-sugar/high-salt diets (steroids can raise sugars and cause fluid retention).
NSAIDs (like ibuprofen) unless your doctor okays them—bleeding risk.
Unapproved supplements—always clear with your team first.
Energy drinks and excess caffeine (can raise BP/HR).
Smoking/vaping (vascular harm).
Frequently asked questions (FAQ)
1) Is TTP the same as HUS (hemolytic uremic syndrome)?
No. Both are thrombotic microangiopathies, but TTP is defined by severely low ADAMTS13; HUS is usually due to shiga-toxin or complement problems. Treatments differ. ADZYNMA
2) What is the “classic pentad”?
Old textbooks listed fever, neurologic symptoms, kidney dysfunction, thrombocytopenia, and hemolytic anemia. In real life, most patients don’t have all five—low platelets + hemolysis + clinical suspicion are enough to start therapy. ADZYNMA
3) What is the PLASMIC score and why does it matter?
It’s a 7-item bedside score that estimates the chance of severe ADAMTS13 deficiency so doctors can start treatment immediately while the ADAMTS13 test is pending. epicurism.info
4) How long does plasma exchange continue?
Usually daily until platelets are stable and signs of hemolysis have resolved for a couple of days, then stopped. NCBI
5) Do all adults with iTTP get caplacizumab?
Current practice often includes caplacizumab with TPE and steroids because it speeds platelet recovery and lowers early recurrence; individual factors and bleeding risk are considered. Understanding TTP
6) Why avoid platelet transfusions?
Adding platelets can “fuel the fire” by providing more platelets for VWF to grab; they’re reserved for life-threatening bleeding or urgent surgery. PMC
7) Can TTP relapse?
Yes. ADAMTS13 monitoring helps predict relapse risk; preemptive rituximab can prevent attacks in some people when levels drop. PMC
8) How is congenital TTP (cTTP) managed long-term?
With scheduled recombinant ADAMTS13 prophylaxis and on-demand dosing during stressors or pregnancy; some centers used plasma infusions before rADAMTS13 became available. U.S. Food and Drug Administration
9) What if my TTP doesn’t respond to first-line therapy?
Teams escalate with twice-daily TPE, add/continue rituximab, and consider bortezomib, cyclophosphamide, cyclosporine, or other expert-level options. The Blood Project
10) Are aspirin or anticoagulants used?
Antithrombotic drugs are not first-line in acute iTTP and are used cautiously because of bleeding—decisions are individualized after platelets recover. Medscape
11) Can I get pregnant after TTP?
Many people do, but pregnancy needs close planning (especially in cTTP, where prophylactic rADAMTS13 may be used) and monitoring in iTTP. U.S. Food and Drug Administration
12) What about vaccines and infections?
Vaccines protect you from infections that may trigger relapses, but timing around rituximab matters (non-live vaccines before B-cell depletion when possible). PMC
13) Are there foods I must avoid forever?
Beyond quinine-containing drinks/products and high-risk herbs, there’s no special TTP diet—aim for balanced nutrition and follow your team’s advice. PMC
14) Is stem-cell therapy used for TTP?
No—there is no established role for stem-cell transplant or “regenerative drugs” in TTP. Care focuses on TPE + targeted immunotherapy and, in cTTP, enzyme replacement. U.S. Food and Drug Administration
15) How likely am I to recover?
With today’s rapid, combined therapy, most people achieve remission; early recognition and adherence to follow-up are critical. Understanding TTP
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 17, 2025.
