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JAMES D. C. GOWANS, MD; ITALO EVANGELISTA, MD; MARY ANN O'SULLIVAN, MD

Arch Intern Med. 1964;113(5):744-747.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Despite an extensive accumulation of peripheral knowledge, the etiology of rheumatoid arthritis remains enigmatic. Extensive research, including recent studies of the immunologic aspects of the disease, has, thus far, failed to provide any real understanding of its cause. The role of environment, thought to be important, also remains obscure. A high familial incidence has been clearly established and stands out as one of the basic clues which might eventually clarify some of the underlying and predisposing conditions. Whether the reasons for family aggregations are genetic, environmental, or a combination of both is not yet known.

Before 1950, although a high familial incidence was strongly suspected, the accuracy of observations was questionable because of a common failure to distinguish rheumatoid from other forms of arthritis. Since then a number of more reliable studies, such as those by Lewis-Fanning ¹ and Barter,² have been published. In 1952, Short and co-workers³ . . . [Full Text PDF of this Article]

Author Affiliations
BOSTON

Footnotes
Received for publication Feb 28, 1963; accepted Dec 5.

Assistant Professor of Medicine (Dr. Gowans); Arthritis and Rheumatism Foundation Clinical Fellow in Medicine (Dr. Evangelista); Research Associate, Department of Preventive Medicine, Tufts University Medical School (Dr. O'Sullivan). From the departments of medicine, New England Center Hospital and Tufts University Medical School.

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