Vitamin B-12 (cobalamin) deficiency: a heretofore undescribed control mechanism for plasma corticosteroid-binding globulin concentration in man.

Six of eight patients with Addisonian pernicious anemia were found to have diminished corticosteroid-binding globulin (CBG) concentrations, which returned within 2 weeks to normal after the im administration of cobalamin. T4-binding globulin was found to be completely normal before and after cobalamin replacement. Other estrogen-responsive proteins, i.e. ceruloplasmin, alpha 1-trypsin inhibitor, haptoglobin, transferrin, and alpha 2-macroglobulin, also did not follow CBG concentration in a parallel fashion. The immunoglobulins similarly did not follow a course parallel to that of CBG. The CBG concentration in two untreated patients had a normal increase in response to estrogen administration, similar to that described in CBG deficiency from other causes. No clue was found regarding the mechanism by which B12 influences the putative hepatic control of CBG concentration. It is speculated that at least two control points may be necessary for a normal CBG concentration. Patients with a genetic deficiency of CBG may also have to have cobalamin deficiency in order for them to reach a concentration approaching zero.