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Hypokalemic Periodic Paralysis due to the Sjögren Syndrome in Chinese Patients

Kin-Kee Pun, MD; Cheuk-Kit Wong, MD; Elaine Yee-Ling Tsui, MD; Sidney Chi-Fai Tam, MD; Annie Wai-Chee Kung, MD; and Christina Chun-Lun Wang, MD
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Requests for Reprints: K. K. Pun, MD, Department of Medicine, University of Hong Kong, Pokfulam Road, Hong Kong.

Current Author Addresses: Drs. Pun, Wong, Tsui, Tam, Kung, and Wang: Department of Medicine, University of Hong Kong, Pokfulam Road, Hong Kong.

Ann Intern Med. 1989;110(5):405-406. doi:10.7326/0003-4819-110-5-405
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This excerpt has been provided in the absence of an abstract.

The Sjögren syndrome is complicated by distal renal tubular acidosis in about 40% of the patients (1). Three patients presented with hypokalemic paralysis as a result of renal tubular acidosis that occurred 2 to 7 years before xerostomia or xerophthalmia. Hypokalemic paralysis occurs more frequently in Orientals as a result of thyrotoxicosis (2, 3), hyperaldosteronism (4), barium poisoning (5), and as a side effect of glossypol, a fertility regulating agent used in China (6).

Cases: A 34-year-old southern Chinese woman was hospitalized because of sudden onset of quadriparesis caused by exertion followed by a heavy meal. On admission, there was


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