Vitamin B

5.5.2.1. Vitamin B6 Deficiency. Although V-B6 deficiency was identified following the development of seizures and anemia in infants given purified diets (196), experimental depletion in adults was achieved using an anti-metabolite, desoxypyridoxine. Vilter et al. (197) described seborrheic dermatitis of the nasolabial folds, eyebrows, angles of the mouth, retroauricular spaces, and scalp as the primary lesion, evolving after 19-21 days of desoxypyridoxine treatment. Dermatitis was followed by glossitis, glossodynia, and red, hypertro-phied filiform papillae on the lateral aspects of the tongue. Sensory neuritis began as tingling, numbness in the hands and feet, and ascended quickly as extremities became hyperesthetic to pinprick.

Microcytic anemia accompanies V-B6 deficiency resulting from the role of plasma pyridoxal phosphate (PLP) in synthesizing aminole-vulinate synthase, an essential enzyme in the first step for heme synthesis (198). Without heme to sequester iron, differential smears may reveal sideroblasts, immature erythroid cells with mitochondrial granules of non-heme iron (199).

Functional deficits of deficiency include depression, confusion (200), and hypoactive deep tendon reflexes (197). Neurological sequelae are not well understood, but may result from altered PLP function in metabolism of synaptic transmitter amines, noradrenalin, adrenaline, tyramine, dopamine, and serotonin (201). Accumulation of abnormal tryptophan metabolites within the brain is thought to exacerbate neuropsychiatry symptoms (202), as V-B6 is required in tryptophan conversion to nicotinic acid (198). PLP is also necessary to form the singular inhibitory neurotransmitter, gamma-aminobutyric acid, whose absence may predispose to seizure activity, recalcitrant to anti-seizure medications, in severe V-B6 deficiency (203,204).

Drug therapies can contribute to V-B6 deficit. Loop diuretics deplete V-B6 in early kidney failure as they decrease tubular resorption of water. V-B6, vitamin C, and oxalate losses have been shown to

Drug/Nutrient Interactions: Antituberculars

Isoniazid (INH) (262) Antihypertensives Hydralazine (Forms hydrazone complex with pyridoxal making it unavailable for enzyme reactions (206).

Loop Diuretics Furosemide (205)

V-Bg supplementation recommendations were 25 mg per day during INH therapy (262), later researchers showed g mg day was required in high dose INH therapy (263).

Zinc and Riboflavin are required to phosphorylate pyridoxal-5'-phosphate (264 ).

Biochemical Evaluation: Plasma 5' Pyridoxal Phosphate (PLP) at least 20 nmol/L

PLP is a good indicator of V-B6 tissue stores and has been chosen by the National Academy of Sciences as the primary criterion to assess the Recommended Dietary Allowance (RDA).

Function/Absorption/Elimination: Function: Coenzyme in metabolism of amino acids, glycogen, and sphingoid bases. Absorbed: Throughout small intestine by nonsaturable passive diffusion, which has implications for risk of toxicity.

Biological Half Life:

Approximately 25 days

Medical Diagnoses//Comorbidities: Alcohol Misuse Dialysis Patients Congestive Heart Failure

CAPD/CCPD Losses/day (nmol):

8 ± 2 Pyridoxal Phosphate 545 ± 61 total V-B6 (f) HD Losses (ml/min): Cuprophan 86 ± 61.7

Cellulose Triacetate 73 ± 90.2 (375 ml/min blood flow rate (212)

Isonicotinyl Hydrazone Pyridoxal

Food Sources: (> 0.8 mg/svg) Highly fortified ready to eat (RTE) cereals, beef liver, soy-based meat substitutes; fortified instant oatmeal.

US Diet Sources: RTE Cereals, mixed foods (sandwiches containing meats), white potatoes, non-citrus fruits, beef, pasta, rice, cooked cereals.

1.5 mg Female

Upper Limit: 100 mg with adverse effect peripheral neuropathy Total Body Store : Males - 110

Physical Findings/Functional Deficits: DEFICIENCY:

Oral: Filiform papillary hypertrophy progressing to atrophy, Glossodynia (197).

Dermatologic: Seborrheic-like dermatitis in nasolabial folds, eyebrows (197). Hematologic: Microcytic, Sideroblastic Anemia (265), Lymphocytopenia (197, 266). Neurologic: Depression, Confusion (197), Epileptiform convulsions from accumulation of abnormal tryptophan metabolites (267), Hyperesthesias (197), Hypoactive deep tendon reflexes (DTR's) (197). TOXICITY Muscular: Gait imbalance, Ataxia (214), Fasciculations (215,216), Diminished DTR's (214), Preserved muscle strength (214). Neurologic: Numbness (215), Perioral numbness (214), tingling in toes, limbs, hands, fingers, face (215), Lhermitte's Sign (214,215, 216), (+) Romberg (215), Thermal, vibratory insensitivity (268), Reduced proprioception (269). Also Important: Bilateral, stocking-glove distribution of symptoms (216 ), Dose-Response to severity of symptoms (268), Duration exposed of significance (268), "Coasting" may follow cessation (268).

Fig. 7. Comprehensive vitamin B6 (V-B6) assessment in renal failure. If not annotated otherwise, data cited from refs (198,150-195).

correlate with water diuresis (205). The antihypertensive medication, hydralazine, forms hydrazone with PLP, compromising V-B6 decarboxylase activity (206). Isoniazid (INH), used as an anti-tubercular, combines with pyridoxine to form isonicotinyl hydrazine, which can result in PLP-mediated INH neurotoxicity in low V-B6 intake, that is, in alcoholic, malnourished, (207), or CKD populations (208-211).

V-B6 losses through the dialyzer are significant, which double with high efficiency, high flux cellulose triacetate membranes, compared to cuprophan membranes (212). Losses through the peritoneal membrane

Hypertrophied Papillae Tongue

A. Filiform papillary hypertrophy with fused papilla Plasma Pyridoxal Phosphate (PLP) 1.3 ng/mL (R 3.6-18) ©Steve Castillo

Steve Castillo

C. Erosion of papilla with longstanding V-B6 deficit PLP 3.1 ng/mL (R 3.6-18) ©Steve Castillo

B. Filiform papillary hypertrophy Lateral view PLP 1.3 ng/mL (R 3.6-18) ©Steve Castillo

  1. Tearing of eyes V-B6 depletion PLP 6.4 ng/mL (R 3.6-18) ©Steve Castillo
  2. Seborrheic-like dermatitis Nasolabial fold, nares PLP 1.3 ng/mL (R 3.6-18) ©Steve Castillo Fig. 8. Nutrient-based lesions associated with laboratory validated vitamin B6 (V-B6) deficit.

Photographs may not be reproduced, copied, projected, televised, digitized, or used in any manner without photographers' express written permission.

are lower than HD membranes, but dietary intake alone has not been able to sustain PLP concentrations (213).

A comprehensive V-B6 assessment is shown in Fig. 7. The primary lesion photographed by Castillo in deficient HD patients was filiform papillary hypertrophy (Fig. 8). Mild seborrheic-like dermatitis and increased tearing were also identified in patients with PLP concentrations between 1.3 and 6.4ng/mL (laboratory range 3.6-18.0). PLP is believed to reflect tissue stores of the nutrient, which was used by the NAS to estimate the RDA for V-B6.

5.5.2.2. Vitamin B6 Toxicity. High doses of V-B6 present in foods do not cause toxicity, but V-B6 accumulates with supplementation due to its non-saturable passive absorption process. Toxicity is generally relegated to the dorsal root ganglia with its increased blood vessel permeability, unlike the blood-brain barrier that insulates the brain (214). Clinical symptoms of V-B6 toxicity include numbness, paresthesias, ataxia, Lhermitte's sign, and pain. Symptoms documented are sensory deficit, sensory ataxia, (+) Romberg's sign, and loss of Achilles reflexes (215). Neuropathy associated with V-B6 toxicity presents in a bilateral, stocking-glove distribution barring injury, beginning at the distal digits (216). Limited clearance of V-B6 in dialysis patients has been associated with elevated PLP concentrations with supplementation as low as 50 mg daily (217). With its potential for both deficiency and toxicity, it is good nutrition practice to document PLP concentrations when renal vitamin intake is uncertain or when supplemental V-B6 is prescribed with anti-tubercular or cardiovascular treatments.

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