Blood Sugar Level Following Intravenous Glucose in Rheumatoid Arthritis

Since the majority of patients with rheumatoid arthritis show a slower fall in the blood sugar level after the intravenous injection of glucose than do the normal controls, the alteration cannot be explained on the basis of gastrointestinal dysfunction. Differences in the renal threshold of glucose do not explain the altered glucose tolerance, since approximately the same amount of glucose is lost in the urine in both groups. Blood samples taken at 3 and 5 minutes following the injection of the glucose showed the height of the blood sugar level to be approximately the same in the patients with rheumatoid arthritis and in normals. The slower fall in the blood sugar level of the former is therefore not a simple function of a greater rise following the intravenous administration of the glucose. Although the patients with severe poliomyelitis had as much or more atrophy than the rheumatoid arthritic patients, there was no delay in rate of fall of the blood sugar level after the intravenous administration of glucose. In view of the fact that the hepatic homeostatic control regulates the blood sugar level, faulty utilization of glucose by extrahepatic tissues cannot be considered the primary factor responsible for the alteration of the glucose tolerance. The altered glucose tolerance in rheumatoid arthritis is explainable on the basis of an altered threshold of the hepatic homeostatic control of the blood sugar. Additional studies must be done to determine whether this derangement emanates directly from extrahepatic influences.