A case of type 2 diabetes manifested by hypokalemic periodic paralysis.
- Author:
Dong Han YEOM
1
;
Ha Young KIM
;
Byoung Hyun PARK
;
Chung Gu CHO
Author Information
1. Department of Internal Medicine, Wonkwang University School of Medicine, Iksan, Korea. stemcell@hanafos.com
- Publication Type:Case Report
- Keywords:
Hyperinsulinemia;
Hypokalemic periodic paralysis;
Type 2 diabetes
- MeSH:
Adenosine Triphosphatases;
Adenosine Triphosphate;
Adrenocorticotropic Hormone;
Aldosterone;
Diabetes Mellitus;
Diabetes Mellitus, Type 2;
Diuretics;
Eating;
Glucose;
Glucose Tolerance Test;
Humans;
Hydrocortisone;
Hyperinsulinism;
Hypokalemia;
Hypokalemic Periodic Paralysis;
Insulin;
Male;
Middle Aged;
Muscle Weakness;
Plasma;
Potassium;
Renin;
Thyroid Gland
- From:Korean Journal of Medicine
2009;76(4):499-501
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Hypokalemic periodic paralysis may be precipitated by stress, rest after exercise, or events that lower serum potassium levels, such as carbohydrate ingestion or the use of insulin or diuretics. In healthy subjects, insulin activates Na+/K+ ATPase, which elicits potassium influx and transient hypokalemia; however, hypokalemia is compensated by K+ ATP channel activation. Recently, we encountered a 49-year-old male patient with type 2 diabetes mellitus and hyperinsulinemic hypokalemic periodic paralysis. The patient had no family history of muscle weakness or diabetes mellitus. At the time of the attack, plasma glucose was 142.4 mg/dL, plasma insulin was 116.86 micronIU/mL, serum potassium was 2.08 mEq/L, and thyroid hormone, renin, aldosterone, ACTH, and cortisol levels were normal. Symptoms improved rapidly upon potassium replacement. Oral glucose tolerance testing revealed high glucose and insulin levels at 2 h, and serum potassium and phosphate levels decreased from 5.1 to 4 mEq/L and 3.6 to 2.0 mg/dL, respectively.
