Mannosyltransferase 8 deficiency—the condition more precisely known as ALG12-congenital disorder of glycosylation (ALG12-CDG, formerly CDG-Ig). Inside our cells is a factory called the endoplasmic reticulum (ER). Proteins entering this factory receive a special sugar tree (an N-glycan). The ALG12 enzyme adds the eighth mannose to this tree. When ALG12 is faulty, the sugar tree is incomplete. Incomplete sugars lead to proteins that don’t fold or travel properly. This can cause low muscle tone, developmental delay, unusual facial features, small head size, recurrent infections from low antibodies (low IgG), and in some boys undescended testes or a small penis. Symptoms start in infancy and vary from mild to severe. Diagnosis typically starts with a transferrin isoelectric focusing (or mass-spec) screen and is confirmed by genetic testing. Treatment today is supportive (treating symptoms and protecting organs); there is no proven cure yet. PMC+3MedlinePlus+3NCBI+3
Mannosyltransferase 8 deficiency is a rare, inherited metabolic disease. It happens when a gene called ALG12 does not work properly. This gene makes an enzyme (a tiny machine) that adds a special sugar molecule (a mannose) to a growing sugar chain inside the endoplasmic reticulum of our cells. These sugar chains are later attached to many proteins so those proteins can fold, travel, and work in the body. If ALG12 is not working, the sugar chain is left unfinished. As a result, many proteins are poorly glycosylated (“undertagged” with sugars), and they do not function correctly. Because glycosylation is needed in almost every organ, the illness can affect the brain, muscles, immune system, liver, gut, heart, hearing, eyes, growth, and development. It is autosomal recessive, which means a child must inherit one faulty copy of the ALG12 gene from each parent to have the disease. PubMed+2MedlinePlus+2
Other names
Doctors and researchers may use several names for the same condition. Common synonyms include:
ALG12-CDG
Congenital disorder of glycosylation type Ig (CDG-Ig)
CDG1G / CDG-Ig / congenital disorder of glycosylation type 1G
Carbohydrate-deficient glycoprotein syndrome type Ig
All of these refer to mannosyltransferase 8 deficiency due to variants in ALG12. MedlinePlus
Inside the endoplasmic reticulum (ER), cells build a 14-sugar “starter tag” on a lipid carrier (dolichol). ALG12’s job is to add the eighth mannose in an alpha-1,6 linkage to that growing tag. Later, this entire tag is moved onto new proteins (N-glycosylation). Without ALG12, the tag stalls one step too early, so many proteins get attached to the wrong sugar pattern or get too few sugars. Those proteins then misfold or are unstable, which leads to the multi-system problems seen in this disease. UCSC Genome Browser+1
Types
There is only one genetic disease here—ALG12-CDG—but people can look different. Clinicians often talk about three clinical patterns to help with care:
Severe early-infancy form. Symptoms start in the first months of life with poor growth, weak muscle tone, feeding problems, frequent infections, and developmental delay. Some babies also have small head size (microcephaly), distinctive facial features, and low immunoglobulin levels (hypogammaglobulinemia). MedlinePlus+1
Attenuated (milder) childhood form. Children still have low muscle tone and delayed milestones, but may have longer survival and fewer organ crises. Learning difficulties and recurrent infections can still occur. ScienceDirect
Antenatal or mixed form. Some babies show signs even before birth (for example, growth concerns), and then follow one of the above pathways after delivery. The mix and severity depend on which ALG12 variants are present. PubMed
Causes
Important note: The primary cause is always pathogenic variants (mutations) in the ALG12 gene that reduce or abolish mannosyltransferase 8 function. The items below explain how this can happen and what can modify the course. Think of them as genetic causes plus real-world factors that can make the disease worse or more noticeable.
Biallelic loss-of-function variants in ALG12. When both gene copies are non-working (nonsense or frameshift variants), the enzyme level is very low and disease is usually severe. PubMed
Harmful missense variants in ALG12. A single amino-acid change in the catalytic region can slow the sugar-adding step and cause disease, sometimes with a milder or variable picture. PubMed
Splice-site variants. Changes at the borders of exons and introns can lead to skipped exons or unstable RNA, lowering the enzyme. Wiley Online Library
Promoter or regulatory variants. Rare changes that reduce ALG12 gene expression can lower enzyme amount. (Documented for ALG12 and similar CDG genes generally.) Frontiers
Compound heterozygosity. Two different harmful variants (one from each parent) together cause deficiency. PubMed
Homozygous founder variants in certain families. In some communities, a shared ancestral variant can appear in homozygous form and cause disease in multiple related families. Wiley Online Library
Consanguinity increases risk in autosomal recessive diseases. When parents are related, the chance of inheriting the same rare variant from both sides is higher. (CDG general principle.) Frontiers
ER quality-control stress. Because many proteins are mis-glycosylated, the ER becomes stressed, which worsens cell function—this amplifies disease features. (CDG mechanism, broadly described.) PMC
Limited dolichol-linked sugar supplies under illness or fasting. During fever or catabolic stress, the glycosylation pathway strains, and symptoms can flare. (General CDG observation.) Frontiers
Coexisting variants in other glycosylation genes. Very rarely, an additional change elsewhere can modify severity. (CDG literature recognizes complexity.) Frontiers
Low immunoglobulins (immune weakness) as a disease consequence. This is not a separate cause of ALG12-CDG, but it causes frequent infections that worsen nutrition and growth. Frontiers in Glycosylation
Protein-losing enteropathy. Again, not a genetic cause, but it causes low protein levels (like albumin), leading to swelling and poor healing, making the disease appear worse. (Seen in CDG cohorts.) PMC
Liver involvement. If the liver is inflamed or not working well, many glycoproteins in blood become abnormal, which causes more bleeding and swelling problems. PMC
Poor feeding and malnutrition. Feeding difficulty causes weight loss and delays, compounding the underlying disorder. MedlinePlus
Intercurrent infections. Common colds or other infections cause metabolic stress and may reveal previously subtle symptoms. MedlinePlus
Certain medications that stress the liver or gut can cause temporary worsening. Care teams usually review drugs carefully in CDG. (General safety guidance in CDG practice.) Frontiers
Surgery or anesthesia stress. Fluid shifts and infections after procedures can cause decompensation; teams plan extra monitoring in CDG. PMC
Dehydration with diarrhea. Losing fluids and minerals causes weakness and can worsen low blood proteins. PMC
Unrecognized coagulopathy. Low clotting factors cause bleeding risks and may trigger complications until treated. (CDG cohorts show frequent coagulopathy.) PMC
Delayed diagnosis. Without supportive care, preventable problems (nutrition, infections) cause extra harm; earlier recognition improves management. (CDG practice frameworks.) PMC
Common symptoms and signs
Low muscle tone (hypotonia). Babies feel “floppy,” have delayed head control, and get tired quickly because mis-glycosylated muscle and nerve proteins work poorly. MedlinePlus
Developmental delay. Milestones like sitting, walking, and talking come late because brain development and muscle control are affected. MedlinePlus
Feeding problems and poor weight gain. Sucking, swallowing, and digestion can be hard, leading to failure to thrive. MedlinePlus
Recurrent infections. Low immunoglobulin levels are common, so children catch colds and chest infections more often. Frontiers in Glycosylation
Small head size (microcephaly) in some children. This reflects effects on brain growth. MedlinePlus
Facial differences (dysmorphism). Doctors may note features like prominent forehead, large ears, or thin upper lip—helpful clues for diagnosis but not harmful themselves. Orpha.net
Hearing loss (often sensorineural). Mis-glycosylation affects inner ear structures and nerves, so hearing checks are important. Frontiers in Glycosylation
Eye problems. Strabismus, nystagmus, or other visual issues may appear and need ophthalmology care. Frontiers in Glycosylation
Heart findings in some patients. A minority may have structural heart issues; all children should get a screening exam. Frontiers in Glycosylation
Liver problems. Raised enzymes, big liver (hepatomegaly), trouble making proteins and clotting factors; this can lead to swelling and easy bruising. PMC
Protein-losing enteropathy and diarrhea. The gut leaks proteins into the stool; children can have swelling and low albumin. PMC
Swelling (edema) and ascites. Low blood proteins from gut loss and liver issues can cause puffiness of legs and belly fluid. PMC
Learning difficulties or intellectual disability (range varies). Supports at school are often needed. Frontiers in Glycosylation
Male genital hypoplasia or undescended testes in some boys. This is a recognized feature in ALG12-CDG. Frontiers in Glycosylation
Bone or skeletal changes in some patients. Skeletal dysplasia or limb features have been reported in case series. Frontiers in Glycosylation
Diagnostic tests
A) Physical exam (bedside observation)
Growth and nutrition check (weight, length/height, head size). Tracks failure to thrive and microcephaly. A simple growth chart helps guide feeding support. MedlinePlus
Neurologic tone and reflex exam. Doctors look for hypotonia, weak reflexes, and delayed motor skills to support the suspicion of a glycosylation disorder. PMC
Skin and edema check. Looking for swelling of legs or belly and skin changes related to low albumin from protein-losing enteropathy. PMC
Liver and spleen palpation. Feeling for enlarged organs points to hepatic involvement and guides further tests. PMC
Ear, nose, and throat review. Clues to recurrent infections and possible hearing issues, prompting formal audiology. Frontiers in Glycosylation
B) Manual tests (simple clinical maneuvers without machines)
Feeding assessment and swallow observation. Clinician watches a feed to spot poor latch, fatigue, or choking, guiding feeding therapy. MedlinePlus
Developmental screening (age-appropriate tasks). Simple play-based tests check motor and language skills to document delay and plan therapies. Frontiers
Abdominal girth and pitting-edema check. Tape-measure and fingertip pressure monitor ascites and fluid retention over time. PMC
Bedside hearing/vision screens. Whisper tests and tracking of objects can suggest the need for formal audiology or ophthalmology testing. Frontiers in Glycosylation
Orthostatic and hydration checks. Pulse and capillary refill help assess dehydration when diarrhea is active. PMC
C) Laboratory and pathological tests
Transferrin isoform analysis (isoelectric focusing or mass spectrometry). This is the classic screening test for N-glycosylation disorders. In ALG12-CDG, a Type I pattern is typical (reduced tetrasialo-transferrin, more disialo/asialo forms). PMC+2Frontiers+2
Total plasma N-glycan profiling. Mass spectrometry of serum glycans can show the accumulation of high-mannose structures that fit ALG12’s block and supports the diagnosis. PMC
Genetic testing of ALG12 (NGS panel or exome/genome). Confirms the exact variants and helps with family counseling. MedlinePlus
Lipid-linked oligosaccharide (LLO) analysis in fibroblasts (specialized). Shows build-up of Man7 structures, which is the biochemical signature of ALG12 deficiency. CDG Hub
Liver function tests and proteins. ALT/AST, bilirubin, albumin, and clotting studies (PT/INR, specific factors) track liver involvement and coagulopathy. PMC
Immunology panel. Immunoglobulin levels (IgG, IgA, IgM) check for hypogammaglobulinemia that explains recurrent infections. Frontiers in Glycosylation
Stool alpha-1 antitrypsin and fecal protein tests. Detect protein-losing enteropathy when edema or low albumin is present. PMC
Metabolic screen to exclude look-alikes. Basic amino acids, acylcarnitines, and endocrine checks help rule out other inborn errors while ALG12-CDG is being confirmed. (CDG diagnostic algorithms recommend broad screening.) PMC
D) Electrodiagnostic tests
EEG (electroencephalogram) when seizures or spells occur. Looks for abnormal brain activity to guide anti-seizure care. (Neurologic involvement is well described across CDG.) PMC
Nerve conduction studies/EMG in selected cases. If weakness or reduced reflexes are unexplained, these tests check for neuropathy or myopathy. (Used across CDG when indicated.) PMC
E) Imaging tests
Abdominal ultrasound. Non-invasive way to look for hepatomegaly, fatty change, or ascites and to monitor over time. BioMed Central
Echocardiogram (heart ultrasound). Screens for structural heart differences reported in some ALG12-CDG patients. Frontiers in Glycosylation
Brain MRI (when clinically indicated). Assesses brain structure, myelination, and potential causes of developmental delay or seizures. (Common in CDG evaluations.) PMC
Hearing tests (otoacoustic emissions or ABR). Objective tests confirm sensorineural hearing loss and direct early interventions. Frontiers in Glycosylation
Skeletal survey when dysplasia is suspected. X-rays can document bone changes that sometimes accompany ALG12-CDG. Frontiers in Glycosylation
Non-pharmacological treatments (therapies & other supports)
(Each includes description, purpose, and simple mechanism.)
Physiotherapy for low tone and motor delay
Gentle, regular exercises improve posture, joint stability, and gross motor skills. Purpose is better movement and fewer contractures. It works by repeating movement patterns to strengthen muscles and train the brain–muscle connection. BioMed CentralOccupational therapy (OT)
Helps with hand skills, dressing, feeding, and daily tasks. Purpose is independence at home and school. Mechanism is task-specific practice with adaptive tools (grips, splints). BioMed CentralSpeech and feeding therapy
Targets speech clarity and safe swallowing. Purpose is better communication and nutrition. Mechanism is oromotor exercises and pacing during feeds. BioMed CentralHigh-calorie, high-protein nutrition plan
Small, frequent meals plus calorie boosters prevent failure to thrive. Mechanism is energy repletion to match higher needs. MedlinePlusMCT-enriched diet when protein-losing enteropathy (PLE) is present
Medium-chain triglycerides absorb directly to the blood (not via lymph), reducing protein loss. Purpose is to raise albumin and reduce edema. PMC+1Edema care (compression, limb elevation, skin care)
Reduces swelling and protects skin. Mechanism is improving venous/lymph return and reducing fluid leakage. UVA School of MedicineVision support and low-vision aids
Glasses, lighting, and classroom positioning help children with cataract/retinal issues. Mechanism is optimizing remaining vision. Frontiers in GlycosylationIndividualized education plan (IEP)
Extra learning support for attention, autism-spectrum, or intellectual disability features. Mechanism is structured, paced teaching. PMCInfection-prevention habits
Hand hygiene, early fever response, and up-to-date vaccinations reduce infections in low-IgG states. Mechanism is lower exposure and boosted adaptive immunity. MedlinePlusSafe-seizure plan and caregiver training
Positioning, timing, and rescue steps improve safety during seizures. Mechanism is risk reduction while medical therapy works. BioMed CentralPhysiologic reflux measures
Upright feeds, slower flow, and thicker feeds (if advised) ease reflux. Mechanism: gravity and pacing reduce regurgitation. BioMed CentralConstipation program
Fiber, fluids, toileting routine to avoid discomfort and feeding setbacks. Mechanism: stool softening & motility. BioMed CentralSleep hygiene
Regular bedtime, dark room, and minimal screens improve development and behavior. Mechanism: stable circadian rhythm. BioMed CentralPhysical bracing/orthotics
Ankle–foot orthoses support gait and prevent contractures. Mechanism: alignment + load distribution. BioMed CentralRespiratory physiotherapy (if recurrent infections)
Airway clearance, positioning. Mechanism: mucus mobilization lowers pneumonia risk. MedlinePlusSocial work & care-coordination
Connects families to services and reduces caregiver burnout. Mechanism: resource navigation. BioMed CentralGenetic counseling
Explains inheritance (autosomal recessive) and future family planning. Mechanism: risk clarification. CDG HubPhysical activity within tolerance
Low-impact play maintains strength and mood. Mechanism: graded conditioning without exhaustion. BioMed CentralDental prevention
Fluoride care and cleanings reduce infection risk in low-IgG states. Mechanism: lower oral bacterial load. MedlinePlusPalliative/supportive care for severe disease
Focuses on comfort, symptom control, and family goals. Mechanism: holistic support alongside active care. BioMed Central
Drug treatments (what they’re for & how they work)
Important: Medicines and dosing are highly individual in ALG12-CDG because of liver, coagulation, and nutrition issues. Use specialist care; examples here explain purposes and mechanisms, not personal prescriptions. Most CDG types (including ALG12) do not respond to “sugar replacement” like mannose (that helps MPI-CDG, a different disease). PMC
Levetiracetam for seizures — reduces neuronal excitability by modulating synaptic vesicle protein SV2A. Often well-tolerated in metabolic disorders. BioMed Central
Topiramate for seizures — enhances GABA and inhibits glutamate receptors to stabilize neurons. BioMed Central
Clobazam as adjunct — benzodiazepine that enhances GABA signaling for seizure control. BioMed Central
Vitamin K if coagulopathy/bleeding tendency — supports gamma-carboxylation of clotting factors. BioMed Central
Fresh frozen plasma (FFP) or factor concentrates during procedures/bleeds — temporarily replaces missing/low glycosylated factors. BioMed Central
Antithrombin concentrate in documented deficiency with thrombosis risk — restores natural anticoagulant balance. BioMed Central
Ursodeoxycholic acid for cholestasis — improves bile flow and protects hepatocytes. BioMed Central
Albumin infusion for severe hypoalbuminemia/PLE — raises oncotic pressure; often paired with diuretics. PMC
Loop diuretic (e.g., furosemide) post-albumin to mobilize edema — increases salt/water excretion. UVA School of Medicine
Octreotide in refractory PLE — reduces intestinal lymph flow and protein loss. PMC
Proton pump inhibitor for reflux/esophagitis — lowers gastric acid to protect lining. BioMed Central
Antimicrobials for infections (culture-guided) — treat promptly due to low IgG. MedlinePlus
IVIG (intravenous immunoglobulin) in significant hypogammaglobulinemia with recurrent infections — supplies pooled IgG to improve defense. PMC
Iron supplementation for iron-deficiency anemia — restores hemoglobin and oxygen delivery. ScienceDirect
Vitamin D + calcium for bone health (limited mobility/nutrition) — supports mineralization. ScienceDirect
Zinc if deficiency — supports growth and immune function. ScienceDirect
Prokinetics or laxatives (as clinically indicated) — improve GI motility/constipation for feeding success. BioMed Central
Antiemetics for severe vomiting — reduce nausea for hydration/nutrition. BioMed Central
Antihistamines/inhaled therapies if co-existing atopy/asthma — symptom relief to reduce infection stressors. BioMed Central
Vaccines (routine + clinician-advised extras) — not a “drug” but essential medicines that prime immunity in low-IgG contexts; household contacts should also be up-to-date. MedlinePlus
Dietary molecular supplements
(Always discuss with your team—needs differ in CDG.)
MCT oil (if PLE) — quick energy, bypasses lymph; may lessen protein loss burden. PMC
Omega-3 fatty acids — anti-inflammatory support for general health. ScienceDirect
Vitamin A — fat-soluble vitamin for vision/epithelium (monitor levels). ScienceDirect
Vitamin D — bone and immune support. ScienceDirect
Vitamin E — antioxidant; monitor to avoid excess. ScienceDirect
Vitamin K — supports clotting; diet source complements medical dosing. BioMed Central
Iron — treats iron-deficiency anemia if present. ScienceDirect
Zinc — growth/immune function. ScienceDirect
Selenium — antioxidant enzymes; consider if low intake. ScienceDirect
Probiotics — may support gut barrier and stool regularity; evidence variable. ScienceDirect
Immunity-booster / regenerative / stem-cell” drug ideas
There are no approved regenerative, stem-cell, or gene therapies for ALG12-CDG today. Research in CDG broadly explores gene therapy, mRNA therapy, pharmacological chaperones, proteostasis regulators, and substrate-pathway tweaking, but these remain experimental. Enroll only via recognized studies/registries. PMC+1
AAV/viral gene therapy concepts (experimental): deliver a working ALG12 gene copy.
mRNA therapy concepts: provide a temporary message to make the enzyme.
Pharmacological chaperones: stabilize misfolded enzyme variants.
Proteostasis modulators: improve folding/ER quality control.
Substrate supplementation: helps some CDGs (e.g., oral mannose for MPI-CDG) but not proven for ALG12-CDG.
Genome editing (CRISPR) concepts: long-term goal; not clinic-ready. PMC+1
Surgeries or procedures (what & why)
Gastrostomy tube (G-tube) — for poor oral intake; ensures safe calories, meds, and fluids.
Cataract extraction — to improve vision if significant lens opacity develops. Frontiers in Glycosylation
Orchiopexy — for undescended testes in boys; protects fertility and reduces malignancy risk. MedlinePlus
Hernia repair — if symptomatic or incarcerated hernia occurs (increased with connective-tissue weakness).
Central line placement — when repeated albumin/IV therapies are necessary (with infection-prevention safeguards). PMC
Prevention tips
Keep vaccinations current (child and household). MedlinePlus
Use hand hygiene and quick evaluation for fever/cough. MedlinePlus
Build a nutrition plan early; monitor growth curves. MedlinePlus
For edema/PLE, follow MCT diet guidance and clinic follow-up. PMC
Avoid hepatotoxic drugs/herbals unless cleared by the team. BioMed Central
Plan for procedures with hematology (bleeding/clotting risks). BioMed Central
Keep a seizure action plan and rescue steps at home/school. BioMed Central
Maintain dental care to reduce infection sources. MedlinePlus
Ensure regular vision and hearing checks to support development. Frontiers in Glycosylation
Engage genetic counseling for family planning and carrier testing. CDG Hub
When to see a doctor urgently
Fever, breathing trouble, lethargy, seizure cluster, or feeding refusal.
New/worse swelling, rapid weight gain, abdominal distension, or diarrhea (possible PLE). UVA School of Medicine
Bleeding/bruising, prolonged nosebleeds, or before any surgery/dental procedure. BioMed Central
Yellow eyes/skin (worsening cholestasis), poor urine, or severe dehydration. BioMed Central
What to eat & what to avoid
Do aim for small, frequent, high-calorie meals with protein at each feed. MedlinePlus
Do consider MCT-enriched fats if PLE is present (clinic-guided). PMC
Do include fruits/vegetables, whole grains, and adequate fluids for gut health. ScienceDirect
Do take prescribed vitamins/minerals (A, D, E, K, iron, zinc) as advised. ScienceDirect
Do keep food safety high (avoid unpasteurized foods) due to low IgG. MedlinePlus
Avoid very fatty long-chain meals during active PLE; prefer MCT sources. PMC
Avoid alcohol/hepatotoxic herbals in adolescents/adults with liver issues. BioMed Central
Avoid prolonged fasting; use bedtime snacks if weight gain is hard. MedlinePlus
Avoid excessive added sugars replacing nutrient-dense calories. ScienceDirect
Avoid new supplements without team review (interactions, liver effects). BioMed Central
FAQs
Is ALG12-CDG the same as “mannosyltransferase 8 deficiency”?
Yes. ALG12 adds the eighth mannose during N-glycan assembly; that’s why some texts call it mannosyltransferase 8 deficiency. NCBIHow is it inherited?
Autosomal recessive—a child inherits one non-working copy from each parent. CDG HubHow common is it?
Very rare—only a small number of patients reported worldwide. CDG HubWhat are the main symptoms?
Low tone, developmental delay, distinctive facial features, low IgG with infections, and in some boys genital differences. MedlinePlusHow is it diagnosed?
Screen with transferrin isoelectric focusing (or MS-based glycan tests), confirm with genetic testing. FrontiersIs there a cure?
Not yet; care is supportive and tailored to the child’s needs. PMCCan oral mannose help?
Not for ALG12-CDG. Mannose therapy helps some other CDGs (like MPI-CDG), not this one. PMCWhy are infections frequent?
Many patients have hypogammaglobulinemia (low IgG), weakening antibody defenses. MedlinePlusWhat is protein-losing enteropathy (PLE) and why does swelling occur?
Protein leaks through the gut, lowering albumin and causing edema; MCT diet, albumin/diuretics, and sometimes octreotide can help. UVA School of Medicine+1Are eyes affected?
Some patients develop cataracts/retinal changes; regular eye checks matter. Frontiers in GlycosylationIs surgery ever needed?
Yes, for feeding access (G-tube), cataracts, hernias, or orchiopexy in boys—case by case. Frontiers in GlycosylationCan adults be diagnosed?
Yes; milder cases may be recognized later as testing expands. BioMed CentralAre clinical trials available?
CDG research networks and registries sometimes run studies—ask your team about enrollment. rarediseasesnetwork.orgWhich specialists are involved?
Clinical genetics, neurology, gastro/hepatology, immunology, ophthalmology, nutrition, PT/OT/SLP, and social work. BioMed CentralWhat does good follow-up look like?
Regular growth checks, labs (albumin, coagulation, immunoglobulins), seizure tracking, vision/hearing exams, and vaccination reviews. BioMed Central
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: September 12, 2025.
