Depending on the specific dietary habits, they may have a deficiency of one or more of the following: thiamine (vitamin B1), pyridoxine (vitamin B6), pantothenic acid and biotin, vitamin B12, folic acid, niacin (vitamin B3), and vitamin A.

Acetaldehyde
It is also thought there is perhaps a genetic predisposition for some alcoholics that results in increased frequency of alcoholic polyneuropathy in certain ethnic groups. During the bodys processing of alcohol, ethanol is oxidized to acetaldehyde mainly by alcohol dehydrogenase; acetaldehyde is then oxidized to acetate mainly by aldehyde dehydrogenase (ALDH). ALDH2 is an isozyme of ALDH and ALDH2 has a polymorphism (ALDH2*2, Glu487Lys) that makes ADLH2 inactive; this allele is more prevalent among Southeast and East Asians and results in a failure to quickly metabolize acetaldehyde. The neurotoxicity resulting from the accumulation of acetaldehyde may play a role in the pathogenesis of alcoholic polyneuropathy. History
The first description of symptoms associated with alcoholic polyneuropathy were recorded by John C. Lettsome in 1787 when he noted hyperesthesia and paralysis in legs more than arms of patients. Jackson has also been credited with describing polyneuropathy in chronic alcoholics in 1822. The clinical title of alcoholic polyneuropathy was widely recognized by the late nineteenth century. It was thought that the polyneuropathy was a direct result of the toxic effect alcohol had on peripheral nerves when used excessively. In 1928, George C. Shattuck argued that the polyneuropathy resulted from a vitamin B deficiency commonly found in alcoholics and he claimed that alcoholic polyneuropathy should be related to beriberi.
Keratoderma blennorrhagicum etymologically meaning keratinized (kerato-) skin (derma-) mucousy (blenno-) discharge (-rrhagia) (also called keratoderma blennorrhagica) are skin lesions commonly found on the palms and soles but which may spread to the scrotum, scalp and trunk. The lesions may resemble psoriasis. : 195 Keratoderma blennorrhagicum is commonly seen as an additional feature of reactive arthritis in almost 15% of male patients. The appearance is usually of a vesico-pustular waxy lesion with a yellow brown colour. These lesions may join to form larger crusty plaques with desquamating edges. See also
Keratoderma
Keratosis
Blennorrhea
List of cutaneous conditions

References


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