Pyridoxine deficiency overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Overview
The classic clinical syndrome for Pyridoxine deficiency (or B6 deficiency) is a seborrheic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy.[1] Vitamin B6 is a co-factor for glutamic acid decarboxylase, an enzyme that converts Glutamate to GABA. Therefore, the concurrent increase in the excitatory neurotransmitter, Glutamate, and decrease in inhibitory neurotransmitter, GABA, resultant from B6 deficiency, may manifest itself in the form of seizures.
Historical Perspective
Historical Perspective
Classification
Classification
Pathophysiology
Pathophysiology
Causes
Causes
Differentiating Pyridoxine deficiency from Other Diseases
Differentiating Pyridoxine deficiency from Other Diseases
Epidemiology and Demographics
Epidemiology and Demographics
Risk Factors
Risk Factors
Screening
Screening
Natural History, Complications, and Prognosis
Natural History, Complications, and Prognosis
Diagnosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Imaging Findings
Other Diagnostic Studies
Treatment
Treatment
Medical Therapy
Surgery
Prevention
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