B12 deficiency sans blood defects.

B.sub.12 deficiency sans blood defects

Scientists have developed two new tests for vitamin B.sub.12 deficiency, and in the process found that many people suffering from the deficiency do not have the characteristic blood disorders long thought to signal the problem. Instead, the researchers report, B.sub.12 deficiency "commonly" causes neurologic symptoms ranging from memory loss to an inability to walk. Such cases were believed to be rate in people deficient in B.sub.12..

Diagnosing the vitamin deficiency has long hinged on the presence of blood disorders--including anemia, a low white cell count and enlarged red cells--and on a test that measures B.sub.12 in the bloodstream. The new tests, now clinically available, aare more reliable and sensitive, say physicians John Lindenbaum of Columbia University in New York City and Robert H. Allen and Sally P. Stabler of the University of Colorado in Denver.

In a study of 323 patients with low vitamin B.sub.12 levels, 141 had neurologic symptoms and 40 of those did not have the characteristic blood disorders. The 40 suffered mild to marked neurologic and psychiatric symptoms, including dementia, depression, impotence and loss of balance. Aside from one patient who died during the first week of treatment from advanced complications of the deficiency, patients in this subgroup of 40 benefited from vitamin B.sub.12 injections, the standard treatment for the disorder. Most of these patients' symptoms disappeared completely, the physicians report in the June 30 NEW ENGLAND JOURNAL OF MEDICINE.

Earlier work had led Allen to question the reliability of the original B.sub.12 test. "So I tried to develop a new test to see how well the standard test was working," He says. "The gold-standard cases, the classic B.sub.12 deficiency cases, were no problem, but the rare cases -- without blood abnormalities -- were where the physicians needed extra help."

Originally known as "pernicious anemia," severe vitamin B.sub.12 deficiency was fatal until the 1920s, when experiments showed that patients recovered after eating liver. Physicians erroneously attributed this to the iron in liver, until the active dactor, cobalamin or vitamin B.sub.12., was identified in 1948. Why some patients with the deficiency have blood abnormalities and others have neurologic symptoms remains unknown.

In an editorial in the journal, William Beck of Massachusetts General Hospital in Boston issues a caveat, pointing out that in the past physicians have treated vague, diverse symptoms with B.sub.12 injections without adequate justification, and that further fonfirmation of these results is needed.