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Requests for reprints should be addressed to Hajime Yasuda, Department of Hematology, Juntendo University School of Medicine, 2-1-1 Hongou, Bunkyo-ku, Tokyo, 113-8421 Japan.
Department of Hematology, Juntendo University School of Medicine, Tokyo, JapanDepartment of Cell Therapy and Transfusion Medicine, Juntendo University School of Medicine, Tokyo, Japan
A 76-year-old man with an 8-month history of suspected statis dermatitis was admitted to our institution because of weakness and painful dysesthesias in the hands and feet. A sensory-motor type polyneuropathy was evident in a stocking-and-glove distribution, and nerve conduction studies confirmed these clinical findings. Polyneuropathy was worse in the lower extremities, and he was unable to walk. Extensive testing including brain magnetic resonance imaging, spinal magnetic resonance imaging, and cerebral spinal fluid examinations were nondiagnostic. Subsequently, serum vitamin B6 (VB6) levels were found to be low at 3.5 ng/mL (normal values: 6.0-40.0 ng/mL for males). Oral supplementation with 60 mg/d of pyridoxal phosphate hydrate (PPH) was initiated, and 1 week later, VB6 levels rose to 39.3 ng/mL, and drastic improvements of polyneuropathy and dermatitis were observed. On a numerical rating scale, the painful dysesthesias in the lower extremities improved from 8 out of 10 to 3 out of 10 after 1 week of PPH administration, and to 0 out of 10 at 5 weeks after PPH administration. The patient was wheelchair-bound on admission but became able to walk unaided within 3 weeks after initiation of PPH. As for dermatitis, a clear regression of the brown-reddish pigmentations was observed (Figure).
FigureVitamin B6 deficiency dermatitis. (A) Photograph of lower limbs before vitamin B6 supplementation. (B) Photograph of lower limbs 5 weeks after vitamin B6 supplementation.
VB6 is essential as a cofactor in approximately 150 enzymatic reactions, and thus, deficiency can lead to diverse clinical manifestations, including dermatitis, polyneuropathy, anemia, seizures, stomatitis, and glossitis.
We demonstrate that the clinical picture of VB6 deficiency dermatitis can closely mimic statis dermatitis. Furthermore, statis dermatitis is basically a clinical diagnosis,
and we speculate that many cases of VB6 deficiency dermatitis are misdiagnosed as statis dermatitis. Meanwhile, VB6 deficiency polyneuropathy is as observed in the presented case typically sensory-motor, symmetrical, stocking-and-glove distribution, and more severe in the lower extremities. However, none of these features are specific to VB6 deficiency polyneuropathy. On top of this, approximately 40% of neuropathies of patients older than age 80 have been reported to be of unknown etiology,
and a significant number of VB6 deficiency polyneuropathy cases are most probably included.
VB6 deficiency is known to occur under situations such as malabsorption due to bowel disease and resection, alcoholism, eating disorders, hemodialysis, pregnancy, and administration of certain drugs (eg, isoniazid, cycloserine, and penicillamine).
The patient harbored none of these traits, and the cause of VB6 deficiency was unknown. However, the elderly, as the patient was, are known to be at higher risk of VB6 deficiency due to decreased food consumption, decreased absorption, increased catabolism, and impaired phosphorylation. In fact, a study of elderly nursing home patients demonstrated that approximately half of the participants had VB6 deficiency.
VB6 oral supplementation promptly improved both dermatitis and polyneuropathy in the presented case, and VB6 deficiency is an important but most probably underrecognized cause of dermatitis and polyneuropathy of the elderly. Testing for VB6 deficiency should be included in the routine workup when examining patients with unknown etiology dermatitis or polyneuropathy.
References
Calderon-Ospina CA
Nava-Mesa MO.
B vitamins in the nervous system: Current knowledge of the biochemical modes of action and synergies of thiamine, pyridoxine, and cobalamin.
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