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TDP<br />

85753<br />

of sera from patients with HP (4%).(2)<br />

Reference Values:<br />

0-12 years: < or =6.6 mg/L<br />

13-18 years: < or =11.0 mg/L<br />

>18 years: < or =23.9 mg/L<br />

Clinical References: 1. Fink JN, Zacharisen MC: Hypersensitivity pneumonitis. In Allergy<br />

Principles and Practice. Vol. 1. 5th edition. Edited by E Middleton Jr, CE Reed, EF Ellis, et al. St. Louis,<br />

MO, Mosby Year Book Inc., 1998, Chapter 19 2. Anderson E, Jacob GL, Roberts GD, Homburger HA:<br />

Comparative evaluation of enzyme immunoassay and immunodiffusion for detection of IgG antibodies to<br />

hypersensitivity pneumonitis antigens. Poster Presentation AAAAI Annual Meeting, San Diego, CA,<br />

March 3-8, 2000. J Allergy Clin Immunol 2000;105:S304<br />

Thiamin (Vitamin B1), Whole Blood<br />

Clinical Information: Thiamin (vitamin B1) is an essential vitamin required for carbohydrate<br />

metabolism, brain function, and peripheral nerve myelination. Thiamin is obtained from the diet. Body<br />

stores are limited and deficiencies can develop quickly. The total thiamin pool in the average adult is<br />

about 30 mg. An intake of 0.5 mg per 1,000 kcal per day is needed to maintain this pool. Due to its<br />

relatively short storage time, marginal deficiency can occur within 10 days and more severe deficiency<br />

within 21 days if intake is restricted. Approximately 80% of all chronic alcoholics are thiamin deficient<br />

due to poor nutrition. However, deficiency also can occur in individuals who are elderly, have chronic<br />

gastrointestinal problems, have marked anorexia, are on cancer treatment, or are receiving diuretic<br />

therapy. The signs and symptoms of mild-to-moderate thiamin deficiency are nonspecific and may<br />

include poor sleep, malaise, weight loss, irritability, and confusion. Newborns breast fed from deficient<br />

mothers may develop dyspnea and cyanosis; diarrhea, vomiting, and aphonia may follow. Moderate<br />

deficiency can affect intellectual performance and well-being, despite a lack of apparent clinical<br />

symptoms. Severe deficiency causes congestive heart failure (wet beriberi), peripheral neuropathy (dry<br />

beriberi), Wernicke encephalopathy (a medical emergency that can progress to coma and death), and<br />

Korsakoff syndrome (an often irreversible memory loss and dementia that can follow). Rapid treatment of<br />

Wernicke encephalopathy with thiamin can prevent Korsakoff syndrome. Symptoms of dry beriberi<br />

include poor appetite, fatigue, and peripheral neuritis. Symptoms of wet beriberi include cardiac failure<br />

and edema. Patients with Wernicke encephalopathy present with behavior change (confusion, delirium,<br />

apathy), diplopia (often sixth nerve palsies), and ataxia. A late stage, in which the patients may develop an<br />

irreversible amnestic confabulatory state, is referred to as the Wernicke-Korsakoff syndrome. The<br />

response to thiamin therapy in deficient patients is usually rapid. Thiamin deficiency is a treatable, yet<br />

under diagnosed, disorder in the United States. A heightened level of awareness of the possibility of<br />

thiamin deficiency is necessary to identify, intervene, and prevent thiamin deficiency's dire consequences.<br />

It appears that no conditions are directly attributable to thiamin excess and that thiamin administration is<br />

safe except in extremely rare cases of anaphylaxis from intravenous thiamin. Whole blood thiamin testing<br />

is superior to currently available alternative tests for assessing thiamin status. Serum or plasma thiamin<br />

testing suffers from poor sensitivity and specificity, and

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