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Page 2 of Niacin deficiency
Secondary deficiency may be due to diarrhea, cirrhosis, or
alcoholism. Pellagra also may occur in carcinoid syndrome
(tryptophan is diverted to form 5-hydroxytryptophan and serotonin)
and in Hartnup disease (absorption of tryptophan by the intestine
and kidneys is defective).
Symptoms and Signs
Pellagra is characterized by skin, mucous membrane, CNS, and GI
symptoms. Pellagra can cause a symmetric photosensitive rash,
stomatitis, glossitis, diarrhea, and dementia. Symptoms may appear
alone or in combination.
Skin symptoms include several types of lesions, which are usually
bilaterally symmetric. The distribution of lesions—at pressure
points or sun-exposed skin—is more pathognomonic than the form of
the lesions. Lesions can develop in a glovelike distribution on the
hands (pellagrous glove) or in a boot-shaped distribution on the
feet and legs (pellagrous boot). Sunlight causes Casal's necklace
and butterfly-shaped lesions on the face.
Mucous membrane symptoms affect primarily the mouth but may also affect
the vagina and urethra. Glossitis and stomatitis characterize acute
deficiency. As the deficiency progresses, the tongue and oral mucous
membranes become reddened, followed by pain in the mouth, increased
salivation, and edema of the tongue. Ulcerations may appear, especially
under the tongue, on the mucosa of the lower lip, and opposite the molar
GI symptoms early in the deficiency include burning in the pharynx and
esophagus and abdominal discomfort and distention. Constipation is
common. Later, nausea, vomiting, and diarrhea may occur. Diarrhea is
often bloody because of bowel hyperemia and ulceration.
CNS symptoms include psychosis, encephalopathy (characterized by
impaired consciousness), and cognitive decline (dementia). Psychosis is
characterized by memory impairment, disorientation, confusion, and
confabulation; the predominant symptom may be excitement, depression,
mania, delirium, or paranoia.
Diagnosis and Treatment
Diagnosis is clinical and may be straightforward when skin and mouth
lesions, diarrhea, delirium, and dementia occur simultaneously. More
often, the presentation is not so specific. Differentiating the CNS
changes from those in thiamin deficiency is difficult. A history of a
diet lacking niacin and tryptophan may help establish the diagnosis. A
favorable response to treatment with niacin can usually confirm it. If
available, laboratory testing can help confirm the diagnosis,
particularly when the diagnosis is otherwise unclear. Urinary excretion
of N1-methylnicotinamide (NMN) is decreased; < 0.8 mg/day (< 5.8
µmol/day) suggests a niacin deficiency.
Because multiple deficiencies are common,
a balanced diet, including other B vitamins (particularly riboflavin and
pyridoxine), is needed. Nicotinamide is usually used to treat
deficiency, because nicotinamide, unlike nicotinic acid (the most common
form of niacin), does not cause flushing, itching, burning, or tingling
sensations. Nicotinamide is given in doses ranging from 40 to 250 mg/day
po in divided doses 3 to 4 times a day.
Niacin (nicotinic acid) in large amounts is sometimes used to lower LDL
cholesterol and triglyceride levels and to increase HDL cholesterol
levels. Symptoms may include flushing and, rarely, hepatotoxicity.
Immediate- and sustained-release preparations of niacin.
(but not nicotinamide) may improve lipid levels. Flushing, which is
prostaglandin-mediated, is more common with immediate-release
preparations. It may be more intense after alcohol ingestion, aerobic
activity, sun exposure, and consumption of spicy foods. Flushing is
minimized if niacin is taken after meals or if aspirin (325 mg) is taken
30 to 45 min before niacin. The chance of severe flushing can be reduced
by starting immediate-release niacin.
at a low dose (eg, 50 mg tid) and increasing it very slowly. At
intermediate doses (1000 mg/day), triglyceride levels decrease 15 to
20%, and HDL cholesterol levels increase 15 to 30%. Reductions in LDL
cholesterol are modest (< 10%). Higher doses of niacin
(3000 mg/day) reduce LDL cholesterol 15 to 20% but may cause jaundice,
abdominal discomfort, blurred vision, worsening of hyperglycemia, and
precipitation of preexisting gout. People with a liver disorder probably
should not take high-dose niacin.
Hepatotoxicity may be more common with some sustained-release
preparations. Some authorities recommend checking levels of uric acid,
blood glucose, and plasma transaminases q 6 to 8 wk until the dose of
niacin has been stabilized
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