Why is acetaminophen (Tylenol) contraindicated in a patient with congenital disorder of glycosylation type Ib?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 21, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Acetaminophen Contraindication in CDG Type Ib

Acetaminophen (Tylenol) is NOT contraindicated in congenital disorder of glycosylation type Ib (CDG-Ib). There is no evidence in the medical literature or clinical guidelines establishing acetaminophen as contraindicated in this condition.

Understanding CDG Type Ib

CDG type Ib is caused by phosphomannose isomerase (PMI) deficiency, which affects the interconversion of fructose-6-phosphate and mannose-6-phosphate 1, 2. Unlike most CDG types, CDG-Ib presents primarily with:

  • Hepatic-intestinal disease without neurological involvement 1
  • Hypoglycemia, failure to thrive, and elevated transaminases 2
  • Protein-losing enteropathy with villous atrophy 2
  • Hypercoagulability and thrombotic complications 3, 2

Why This Misconception May Exist

The confusion likely stems from the hepatic involvement in CDG-Ib, which includes:

  • Elevated transaminases and hepatomegaly 2, 4
  • Coagulopathy affecting both pro- and anticoagulation proteins 3

However, the hepatopathy in CDG-Ib is fundamentally different from conditions where acetaminophen is truly contraindicated (such as acute liver failure or severe cirrhosis). The liver dysfunction in CDG-Ib results from abnormal glycosylation of hepatic proteins, not from hepatocellular damage that would impair acetaminophen metabolism 2.

Actual Treatment Considerations for CDG-Ib

The definitive treatment for CDG-Ib is oral mannose supplementation at 1 g/kg/day divided into 5 doses, which produces clinical and biochemical normalization 2, 4, 5. This therapy:

  • Normalizes transaminases and coagulation parameters 2
  • Resolves gastrointestinal symptoms 2
  • Corrects the abnormal transferrin glycosylation pattern 2

Clinical Pitfalls to Avoid

  • Do not withhold standard analgesics without specific contraindications 5
  • Monitor for hypercoagulability rather than focusing on medication restrictions, as thrombotic events are a significant risk in untreated CDG-Ib 3
  • Ensure mannose therapy is optimized before attributing symptoms to medication effects 2, 4

If your patient has been told to avoid acetaminophen, this recommendation should be re-evaluated with their metabolic specialist, as there is no published evidence supporting this restriction in CDG-Ib 1, 2, 5.

Related Questions

What part of the cell is affected by deficient glycosylation (glycosylation refers to the process of attaching carbohydrate molecules to target proteins or lipards)?
Should a child with congenital disorder of glycosylation (CDG) receive oral rehydration solution for dehydration caused by diarrhea?
What are the diagnostic and management approaches for a patient with a suspected protein glycosylation disorder?
Please draft a covering letter for a case report of Bohring‑Opitz syndrome in a [age]-year‑old [male/female] of [ethnicity] with characteristic facial dysmorphism, severe feeding difficulties, growth retardation, neurodevelopmental delay, seizures, a de novo pathogenic ASXL1 variant, and multidisciplinary management including levetiracetam (30 mg/kg/day) and a structured feeding program.
At 20 weeks gestation, an ultrasound shows an absent nasal bone; what is its significance and what are the recommended next steps?
At what age does testosterone level begin to decline in men?
Which therapeutic techniques are associated with increased positive neuroplastic change in adult patients undergoing neurological rehabilitation for stroke, traumatic brain injury, spinal cord injury, or other acquired neurological disorders?
In a patient with unresectable sinonasal squamous cell carcinoma who progressed after first‑line pembrolizumab combined with cisplatin and 5‑fluorouracil, what is the most appropriate next step in management?
What is the most likely cause of a patient with markedly elevated creatine phosphokinase (~4500 U/L), acute kidney injury (serum creatinine ~7.8 mg/dL) with anuria, severe thrombocytopenia (~50 ×10⁹/L), low complement levels, 1‑2 % schistocytes on peripheral smear, and altered mental status, while all blood cultures are negative?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.