Copper deficiency associated with alkali therapy in a patient with renal tubular acidosis.

slight excess obse r ve d m a y be expl icab le to s o m e ex ten t by cases o f sickle cell-B" tha l a s semia or sickle cellhe red i t a ry pers i s tence o f fetal h e m o g l o b i n , which it m a y not be poss ib le to d i f fe ren t ia te f rom SS d isease du r ing the first yea r o f life in the absence o f fami ly studies. Unless d i sc repanc ies in gene f r equenc i e s are r e p o r t e d by o the r centers , there is no reason at p r e sen t to ques t ion our u n d e r s t a n d i n g o f the way in which sickle h e m o g l o b i n is inher i ted . R E F E R E N C E S