Question:hard
A 30-year-old woman presents with easy fatigability, exertional dyspnea and weight loss. She also reports frequent falls. On examination there is a bilateral decrease in vibration sense. Her hemoglobin is 8.2 g%. She was treated with folate; her anemia improved but her neurological symptoms worsened. What is the most probable reason for her condition?
A 30-year-old woman presents with easy fatigability, exertional dyspnea and weight loss. She also reports frequent falls. On examination there is a bilateral decrease in vibration sense. Her hemoglobin is 8.2 g%. She was treated with folate; her anemia improved but her neurological symptoms worsened. What is the most probable reason for her condition?
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Anemia improves but the cord signs worsen, what happens to B12 stores when you push folate alone?
Updated On: Jun 23, 2026
- Folate was not absorbed
- Unmasked pyridoxine deficiency
- Deficiency of folate reductase in the CNS
- Folate therapy caused rapid use of vitamin B12 stores, aggravating symptoms
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The Correct Option is D
Solution and Explanation
Read the trap: hematologic response but neurologic decline after folate is the signature of an underlying vitamin B12 deficiency, so option 4 is correct.
Her vibration loss and frequent falls reflect subacute combined degeneration of the dorsal columns, a B12 lesion. B12 normally recycles methyltetrahydrofolate back to tetrahydrofolate for DNA synthesis. When you flood the system with folate, you bypass that block, so red cell production resumes and the anemia improves. The catch is that the renewed DNA synthesis rapidly draws down the already low B12 reserves, and folate offers no protection to the nervous system, so the myelopathy progresses.
The other options do not fit: folate clearly was absorbed (the anemia corrected), pyridoxine deficiency causes a different picture, and a CNS folate-reductase defect is not the mechanism here. Always check B12 before treating megaloblastic anemia with folate.
Ref: Standard hematology texts.
Her vibration loss and frequent falls reflect subacute combined degeneration of the dorsal columns, a B12 lesion. B12 normally recycles methyltetrahydrofolate back to tetrahydrofolate for DNA synthesis. When you flood the system with folate, you bypass that block, so red cell production resumes and the anemia improves. The catch is that the renewed DNA synthesis rapidly draws down the already low B12 reserves, and folate offers no protection to the nervous system, so the myelopathy progresses.
The other options do not fit: folate clearly was absorbed (the anemia corrected), pyridoxine deficiency causes a different picture, and a CNS folate-reductase defect is not the mechanism here. Always check B12 before treating megaloblastic anemia with folate.
Ref: Standard hematology texts.
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