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INTRODUCTION

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Patients can develop neuropathies due to inadequate nutrition and subsequent vitamin deficiency (Table 18-1). Nutritional deficiency-related polyneuropathies are currently uncommon, especially in developed countries. However, these neuropathies do occur and are important because they are potentially treatable. Malnutrition may occur in chronic alcoholics and in patients with chronic illness, unusual diets, and obesity surgery. Some vitamin deficiencies (e.g., vitamins B12 and E) often occur because of impaired gastrointestinal absorption rather than poor dietary intake. In other cases, neuropathy may develop secondary to the effects of medications (e.g., isoniazid causing vitamin B6 deficiency). The clinical and laboratory features of most nutritional polyneuropathies are similar to those of the more common polyneuropathies. Timely and accurate diagnosis is important because patients can improve with replacement therapy.

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TABLE 18-1.NUTRITIONAL DEFICIENCY ASSOCIATED WITH PERIPHERAL NEUROPATHY
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THIAMINE (VITAMIN B1) DEFICIENCY

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CLINICAL FEATURES

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Thiamine deficiency or beriberi is uncommon nowadays and primarily occurs as a consequence of chronic alcohol abuse, recurrent vomiting, total parenteral nutrition, inappropriately restrictive diets, and perhaps bariatric surgery.1 The symptoms arising from insufficient dietary intake of thiamine are known as beriberi and may present in two forms: dry beriberi and wet beriberi. The difference between these two types of beriberi is simply the presence (wet beriberi) or absence (dry beriberi) of congestive heart failure and lower limb edema. Affected individuals usually present with numbness, tingling, and burning in the distal lower extremities, which subsequently spread to involve the proximal legs and upper extremities.2 On examination, a mild-to-moderate reduction in all sensory modalities is noted in a stocking distribution along with diminished muscle stretch reflexes. Mild, predominantly distal weakness may be appreciated. Congestive heart failure with edema of the lower legs is seen in the so-called wet beriberi.

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LABORATORY FEATURES

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Measuring thiamine concentration in serum and urine is not very reliable.3 Assay of erythrocyte transketolase activity and the increase in activity after adding thiamine pyrophosphate (TPP) appears to be more accurate and reliable.47 Sensory nerve conduction studies (NCS) reveal reduced or absent sensory nerve action potentials (SNAPs) amplitudes with relative preservation of distal sensory latencies and conduction velocities.2 The motor NCS may be normal or demonstrate slightly reduced amplitudes.

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HISTOPATHOLOGY

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Sural nerve biopsies reveal loss of primarily large myelinated axons.1,8 Necropsy studies have demonstrated chromatolysis of the anterior horn cells and dorsal root ganglia cells along with axonal degeneration and secondary demyelination of the posterior columns.

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PATHOGENESIS

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Most meats and vegetables contain adequate amounts of thiamine, in particular unrefined ...

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