Reduced tissue oxygenation and its reversibility by glycemic control in diabetic patients.
Relationship of transcutaneous oxygen pressure (TcP(O2)) to glycemic control and diabetic complications was investigated in patients with non-insulin dependent diabetes mellitus. TcP(O2) was measured in 103 patients with non-insulin dependent diabetes mellitus. Correlation of TcP(O2) to HbA1c, fasting blood sugar (FBS), age, duration of diabetes, serum lipids, hypertension, and diabetic complications were examined. We divided the patients into three groups according to their glycemic control: good control group (HbA1c < 7.0%), fair control group (HbA1c, 7.0-8.9%) and poor control group (HbA1c > or = 9.0). We compared TcP(O2) of these three groups with 19 non-diabetic controls. In 103 patients, TcP(O2) at baseline correlated with HbA1c, FBS and age (P < 0.001, P < 0.01 and P < 0.05, respectively), but did not correlate with duration of diabetes mellitus, neuropathy, nephropathy or retinopathy. TcP(O2) of good and fair control group was not reduced comparing to the non-diabetic control (63 +/- 11, 59 +/- 10 and 64 +/- 12 mmHg, respectively). The poor control group had significantly reduced TcP(O2) (55 +/- 10 mmHg) comparing to non-diabetic control (P < 0.005) and good control group (P < 0.005). Furthermore, in an independent study, TcP(O2), arterial oxygen pressure (Pa(O2)), oxygen pressure of dorsal pedal vein (PV(O2)) and erythrocyte 2,3-diphosphoglycerate (2,3-DPG) in eight patients with poor glycemic control were followed prospectively. Six patients with improvement of glycemic control showed a significant increase of TcP(O2) and Pa(O2) (P < 0.001 and P < 0.005, respectively). However, two patients without improvement of hyperglycemia had no change in TcP(O2) and Pa(O2). PV(O2) and 2,3-DPG levels of erythrocytes were not changed in six patients. These findings suggest that tissue oxygenation in diabetic patients was deteriorated in relation to hyperglycemia and was reversed with glycemic control. Improvement of Pa(O2) might contribute partly to the increase of TcP(O2).
Iino
K
K
Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka city, Japan.
Yoshinari
M
M
Doi
Y
Y
Shinohara
N
N
Iwase
M
M
Fujishima
M
M
D019794:2,3-Diphosphoglycerate; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001785:Blood Gas Monitoring, Transcutaneous; D001786:Blood Glucose / Q000378:metabolism*; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism*; D003925:Diabetic Angiopathies / Q000209:etiology / Q000378:metabolism*; D004163:Diphosphoglyceric Acids / Q000097:blood*; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism*; D011446:Prospective Studies; D012307:Risk Factors
D019794:2,3-Diphosphoglycerate; D001786:Blood Glucose; D004163:Diphosphoglyceric Acids; D006442:Glycated Hemoglobin; D008055:Lipids; D010100:Oxygen