Kensou Ohsawa

Elevated serum levels of soluble vascular cell adhesion molecule-1 in NIDDM patients with proliferative diabetic retinopathy

We studied 68 Japanese NIDDM patients (38 men and 30 women), aged 56.9+/-1.2 years (range 33-75 years), with a BMI of 23.1+/-0.5 kg/m2 without hypertension, dyslipidemia, and diabetic macroangiopathy for evaluating the relationship between serum soluble vascular cell adhesion molecule-1 (sVCAM-1) levels and the severity of diabetic retinopathy. Fundus examination was performed by an ophthalmologist using an ophthalmoscope, and the findings were graded as: (1) no signs of diabetic retinopathy (NDR), (2) background diabetic retinopathy (BDR), or (3) proliferative diabetic retinopathy (PDR). Serum sVCAM-1 levels were measured in duplicate by enzyme-linked immunosorbent assay using the soluble VCAM-1 KIT (R&D Systems Ltd., Ablingdon, Oxfordshire, UK). There was no difference in serum sVCAM-1 levels between patients with BDR (n = 17) and patients with NDR (n = 40) (1035.3+/-104.4 and 978.8+/-48.9 ng/ml, respectively, P = 0.8), but patients with PDR (n = 11) showed a significant increase of serum sVCAM-1 levels compared with patients with NDR (1281.8+/-166.3 and 978.8+/-48.9 ng/ml, respectively, P = 0.02). Although serum sVCAM-1 levels were correlated, not only with age but also with the known diabetic duration (r = 0.39, P = 0.001, and r = 0.40, P = 0.0007, respectively), age-adjusted sVCAM-1 levels were still significantly higher in the PDR group than in the NDR group. In contrast. serum sVCAM-1 levels were not related to the presence of diabetic nephropathy or HbA1c levels. Our results suggest that sVCAM-1 might be implicated in the development of the diabetic retinopathy, and measurement of serum sVCAM-1 levels in NIDDM patients maybe clinically useful for assessing the severity and possibly the activity of diabetic retinopathy.

The First Case of Insulin-Dependent Diabetes mellitus with Prominent Spurious Hyperglucagonemia due to Interference of Immunoglobulin G in Glucagon Radioimmunoassay (OAL-123) System

A 51-year-old male was admitted to our hospital because of diabetic ketoacidosis. His symptoms were promptly improved with intensive insulin therapy, but his plasma glucagon immunoreactivity measured by the OAL-123 radioimmunoassay (RIA) system showed persistently high values (3,090-3,210 pg/ml). A computed tomographic scan, abdominal angiography and endoscopic examination of his gastrointestinal tract showed no evidence of glucagonoma. After removing the immunoglobulin fraction from the plasma, his immunoreactive plasma glucagon level returned to normal. Moreover, the immunoglobulin G fraction purified from the patients plasma inhibited the binding of [125I]glucagon to rabbit antiglucagon antiserum, OAL-123. Dot-blot analysis demonstrated that the immunoglobulin G of this patient cross-reacted against OAL-123. Therefore, it was considered that the prominent hyperglucagonemia in this patient was due to the presence of IgG, which interfered with the measurement of plasma-immunoreactive glucagon.