Multiple organ damage in severe acute respiratory syndrome (SARS) patients is 
common; however, the pathogenesis remains controversial. This study was to 
determine whether the damage was correlated with expression of the SARS 
coronavirus receptor, angiotensin converting enzyme 2 (ACE2), in different 
organs, especially in the endocrine tissues of the pancreas, and to elucidate 
the pathogenesis of glucose intolerance in SARS patients. The effect of clinical 
variables on survival was estimated in 135 SARS patients who died, 385 
hospitalized SARS patients who survived, and 19 patients with non-SARS 
pneumonia. A total of 39 SARS patients who had no previous diabetes and received 
no steroid treatment were compared to 39 matched healthy siblings during a 
3-year follow-up period. The pattern of SARS coronavirus receptor-ACE2 proteins 
in different human organs was also studied. Significant elevations in oxygen 
saturation, serum creatinine, lactate dehydrogenase, creatine kinase MB 
isoenzyme, and fasting plasma glucose (FPG), but not in alanine transaminase 
were predictors for death. Abundant ACE2 immunostaining was found in lung, 
kidney, heart, and islets of pancreas, but not in hepatocytes. Twenty of the 39 
followed-up patients were diabetic during hospitalization. After 3 years, only 
two of these patients had diabetes. Compared with their non-SARS siblings, these 
patients exhibited no significant differences in FPG, postprandial glucose 
(PPG), and insulin levels. The organ involvements of SARS correlated with organ 
expression of ACE2. The localization of ACE2 expression in the endocrine part of 
the pancreas suggests that SARS coronavirus enters islets using ACE2 as its 
receptor and damages islets causing acute diabetes.