Premature fusion of one or more epiphyses is an uncommon anomaly. It may occur as a complication of infection or trauma involving the epiphyseal cartilage plate (2). It has been reported following scurvy, probably as a result of a pathological fracture at the level of the epiphyseal line (4). The defect has been observed as a complication of hyper-vitaminosis A, in both children (3) and experimental animals (5). As a probable developmental error of cartilage formation, epiphyseal fusion may be seen in early life in the phalanges of the hands and feet, and sometimes in long bones of the extremities of patients with congenital chondrodystrophies (achondroplasia, Morquio's disease, Ellis-van Creveld disease, peripheral dysostosis, and others). Premature fusion of epiphyses is occasionally observed as an isolated lesion involving one or more phalanges and, rarely, long bones of the extremities in otherwise normal children (1). We have observed that premature fusion of epiphyses in long bones of the extremities occurs with relative frequency in patients with homozygous thalassemia. To our knowledge, this association has not been described previously. Our experience with this type of fusion, based on 11 cases, will be reported briefly. The cases were collected from a study of all available roentgenograms of patients with homozygous thalassemia previously seen or currently under treatment in this institution (The New York Hospital-Cornell Medical Center, New York). The number of cases surveyed, including the 11 affected patients, was 79. Of these, 63 were of thalassemia major, and 16, or 20 per cent, were of thalassemia intermedia. The age, at the time of the last roentgenograms of each bone examined, ranged from one to forty-nine years. Thirty-one patients were ten years of age or younger, 48 were older. Of the 16 with thalassemia intermedia, 4 were in the first decade, 12 were older (Table I). Of the 11 patients with premature epiphyseal fusion, 6 were males, 5, females. Seven had thalassemia major; 4, or 36 per cent, thalassemia intermedia. All were eleven years of age or older when the bony anomaly was first noted. In 4 instances previous films were available for this review and showed that the lesion was not present in the first decade of life (Table II). The incidence of the anomaly was 14 per cent when all 79 cases surveyed are included, but 23 per cent if only the 48 patients more than ten years of age are considered. Since the defect was not detected in any child in the first decade, the latter figure would seem to be a more accurate estimate of its frequency in patients with homozygous thalassemia. The lesion was diagnosed on the basis of demonstration of bony obliteration of the epiphyseal line plus deformity and shortening of the affected bone, except in older patients in whom all the epiphyseal lines were closed.