There is effective treatment for methemoglobinemia, and acquired cases are usually reversible, but there is not a one‑time “permanent cure” for all congenital (inherited) forms. Instead, management focuses on quickly reversing episodes when they occur and, for chronic inherited disease, using ongoing therapies to keep methemoglobin levels low.
Acquired methemoglobinemia
- The mainstay treatment is stopping the offending drug/chemical and giving high‑flow oxygen plus intravenous methylene blue, which rapidly converts methemoglobin back to normal hemoglobin.
- If methylene blue is unavailable, contraindicated (for example in G6PD deficiency), or ineffective, options include high‑dose vitamin C (ascorbic acid), exchange transfusion, and sometimes hyperbaric oxygen.
Congenital methemoglobinemia
- In hereditary forms caused by enzyme deficiency (cytochrome b5 reductase), patients often have lifelong mild cyanosis but can be managed with chronic low‑dose oral methylene blue or, in some cases, vitamin C to reduce methemoglobin levels.
- These therapies control symptoms rather than permanently correcting the genetic defect; definitive cure would require correcting the underlying mutation, which is not standard clinical practice at present.
Prognosis
- With prompt recognition and appropriate treatment, outcomes for both acquired and many congenital cases are generally good, and patients can live normal lives between episodes.
- Severe untreated cases, especially with methemoglobin levels above about 50–70%, can be life‑threatening, so rapid emergency care is critical if symptoms like sudden cyanosis, shortness of breath, confusion, or loss of consciousness occur.
