To the Editor.—
Reading the CASE REPORT entitled "Pernicious Anemia, 18q Deletion Syndrome, and IgA Deficiency" (1982;248:1359), I arrive at conclusions different from those of the authors for the following reasons.
1. Antibodies that act against thyroid and parietal gastric cells are widely available commercially, and their mention would have lent support to the authors' conclusion of autoimmune processes accounting for both hypothyroidism and pernicious anemia. Such data, however, are
missing from the report, weakening their arguments.
2. The patient's chromosomal structure is more complex than the title indicates, since in the text two distinct karyotypes are described— 18q deletion (18q—) and 18r. This implies losses of chromosomal material from both sides of the centromere (ie, short [p—] and long [q] arm). Since short-arm deletions of both types— 18p deletion (18p—)1 and 18r—are known to be associated with thyroid dyshormonogenesis, an alternative interpretation of the observed hypothyroidism deserves consideration. The