Lp (a) has been considered an independent risk factor for coronary atherosclerosis. Recent papers in the literature have demonstrated elevations of Lp (a) in diabetic subjects. The clinical significance of hyper-Lp (a)-emia as a risk factor for diabetic vascular complications, however, is still unclear. We investigated the significance of Lp (a) as a risk factor for diabetic nephropathy cross-sectionally. Lp (a) was determined in 235 NIDDM patients and 105 non diabetic controls. Diabetic subjects were classified into those with normoalbuniinuria (group N), microalbuminuria (group M) and overt nephropathy (group P).
1) Lp (a) was significantly higher in the diabetics than in the controls, and Lp (a) in the diabetic females was significantly higher than in the males.
2) In the male diabetics, Lp (a) was significanty higher in both group P and group M than in group N. In female diabetics, Lp (a) was significantly higher in group P than in group N.
3) Discriminant analysis suggested the importance of hypertension, the duration of diabetes, and Lp (a) as independent risk factors for overt nephropathy.

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Abnormalities of endoneurial microvessels have been implicated in the pathogenesis of diabetic neuropathy. To investigate endoneurial microvascular abnormalities in relation to changes in nerve fibers, the tibial nerves of rats with chronic streptozotocin induced diabetes were exmined by light and electron microscopy with morphometric analysis.
Reduced mean myelinated fiber size and increased myelinated fiber density consistent with the data reported previously, were demonstrated in the diabetic rats. The vascular area, luminal area and basement membrane area of the endoneurial vessels were increased in some diabetic rats, although their mean values were not significantly different from the normal controls. In contrast, pericyte area was significantly reduced in diabetic rats. There was no evidence of occluded vascular lumens or endothelial proliferation in the diabetic rats. Although changes in the endoneurial microvessels were relatively modest in diabetic rats, compared with those found in human diabetic paients, the changes suggest that alterations in the microcirculation of peripheral nerves may play a role in the progression of diabetic neuropathy.

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Of the 134 patients with non-insulin-dependent diabetes mellitus (NIDDM) who participated in this study, the serum IgA concentration exceeded the upper normal limit in 62 patients (45.6%). However this parameter showed no significant correlation with patient's age, disease duration, fasting blood glucose, HbA_1c or fructosamine. The mean IgA levels were significantly higher (P<0.005) in the preproliferative (N=23) and proliferative diabetic retinopathy groups (N=15) than in the non retinopathic group (N=75) and the group with simple retinopathy (N=21).T hey were also significantly elevated (P=0.0001) in the groups with microalbuminuria (N=36) and overt proteinuria (N=31) compared with the normoalbuminuric group (N=67). In sum, the serum IgA concentration was elevated with high frequency in NIDDM and tended to increase as microangiopathy was aggravated. The serum IgA concentration, therefore, is considered not to be useful for differentiating IgA nephropathy from diabetic nephropathy in proteinuric NIDDM.

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We measured transcutaneous oxygen tension (TcPO₂) in 40 lower limbs of non-diabetic subjects without peripheral vascular disease (PVD, API≥1.0) and 122 limbs of diabetic subjects. Measurements were made on the subclavicular region and metatarsal area of each foot in the supine position, and leg elevation (40cm) was employed to assess limb vascular reserve. Regional perfusion index (RPI) was calculated as foot TcPO₂/subclavicular TcPO₂ in each position.
RPI values in diabetic subjects without PVD (API≥1.0) were similar in the supine position, but were significantly lower after leg elevation compared with those in non-diabetic subjects. Diabetic subjects with PVD (API≥0.8) demonstrated lower RPI in the supine position, and the decreases in RPI caused by leg elevation were more pronounced. RPI values were significantly correlated to API in the supine position (r=0.56, p<0.001), and the relation was more significant after leg elevation (r=0.72, p<0.001). Legs with the history of gangrene or ulcer showed lower API as well as marked decreases in both TcPO₂ and RN after the leg elevation.
These results indicate that TcPO₂ measurement with the leg elevation is a sensitive method for the evaluaton of limb ischemia in diabetic subjects.

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A 56-year-old man presenting with general lassitude, thirstiness and disorientation was admitted to his local hospital. His blood glucose level was 1228 mg/dl, and arterial blood gas analysis revealed pH 7.253 and HCO₃^- 16.4 mEq/l. A diagnosis of diabetic ketoacidosis was made, and the patient was transferred to our hospital. Laboratory examination on admission revealed thrombocytopenia, decreased anithrombin III activity, and increased blood urea nitrogen and creatinine levels. We made a diagnosis of diabetic ketoacidosis with disseminated intravascular coagulation (DIC) and acute renal failure. We successfully treated his hyperglycemia, ketoacidosis, DIC and acute renal failure, but the chest x-ray on the third hospital day showed interstitial infiltration. The patient became progressively more dyspneic and died on the seventh hospital day. At autopy there were numerous nodules filled with Aspergillus species. The pancreatic islets were markedly diminished. Histochemical staining showed normal glucagon-and somatostatin containing cells but no insulin-staining cells. Many lymphocytes, especially T-lymphocytes, had infiltrated around the vessels and islets of the pancreas. The patient was therefore believed to have IDDM with insulitis.
Patients with diabetic ketoacidosis are usually in a state of reduced immunocompetence. Therefore, we must treat them with care with regard to infectious complications, especially fungal infections, which have recently been increasing.

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We experienced a 73-year-old female patient with diabetes mellitus of 9 years or more duration who had high fasting plasma glucose levels because of a possible rebound phenomenon after delayed gastric emptying.
We measured her plasma glucose levels overnight by continuous monitoring and found hypoglycemia followed by fasting hyperglycemia.Domperidone, 10 mg, was then administered to the patient at 9: 00 pm, and this was followed by marked improvement of the patient's high fasting plasma glucose levels. Before treatment with domperidone, the patient's growth hormone level at 3: 00 am and glucagon, adrenocorticotropic hormone and cortisol levels at 6: 00 am had been high. All of them decreased to within the normal range after the high fasting plasma glucose levels had been improved by treatment with domperidone.These counter-regulatory hormones appeared to have augmented the fasting plasma glucose levels.The above results suggest that it is important to try domperidone in patients suffering from rebound high fasting plasma glucose as a result of gastroparesis.

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We report a case of insulin-dependent diabetes mellitus (IDDM) which developed in acute painless pancreatitis. After the general symptoms of a common cold, a 60 year old man was admitted to the hospital because of acute pancreatitis diagnosed on the basis of elevated serum amylase activity (1259 Somogyi units/100ml) and a moderately swollen pancreas and confirmed by abdominal ultrasonography and computed tomography. Several days after the onset of acute pancreatitis, a marked increase in blood glucose concentration (734mg/100ml) was found, and insulin administration was required, although serum amylase levels returned to normal and the size of the swollen pancreas became normal within 2 weeks.Based on the following observations, this patient was diagnosed as having IDDM:(1) the abrupt onset of the diabetes mellitus:(2) undetectable low urinary excretion of C-peptide (CPR), which was 46.7μg/day on admission; and (3) no response of plasma CPR to glucagon injection or arginine infusion, suggesting complete destruction of pancreatic B-cells.The cytomegalovirus (CMV) antibody titer determined by complement fixation was×32 on admission.It increased to×512 after 127 days, and remained elevated throughout the period of observation.It is conceivable that CMV infection caused not only the patient's acute painless pancreatitis but his IDDM.

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We encountered a case of severe hyperglycemia after a-interferon (IF) administration for type C hepatitis. The subject was a 41 year old woman. The diagnosis of type C viral hepatitis due to blood transfusion for aplastic anemia was made in 1990.The patient was found to have diabetes mellitus in 1989.Her plasma glucose had been well controlled by diet and oral hypoglycemic agent therapy (glibenclamide 1.25 mg/day) until IF was started.After IF was started on March, 1991, high fever, general malaise, thirstiness, and polyuria with severe hyperglycemia developed abruptly. Urinary C peptide (CPR) was reduced, but no ketosis was observed. Insulin was then started. After IF was discontinued in May, 1991, both glycemic control and urinary CPR secretion gradually improved.The precise mechanism of the acute deterioration of glycemic control after IF administration is not clear, but it appears that reduced insulin secretion due to pancreatic beta-cell damage and/or increased insulin resistance may have been one of the mechanisms of the IF-induced hyperglycemia. When IF is started in a patient with diabetes, plasma glucose should be monitored carefully.

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The case of a patient who had acute emphysematous pyelonephritis with diabetes mellitus followed by disseminated intravascular coagulation is presented. A 63 year old woman was admitted to our hospital because of high fever and left abdominal pain.Physical examination revealed acute pyelonephritis with diabetes mellitus. She was immediately treated with intensive intravenous antibiotics and injected insulin. On the second day after admission, she developed disseminated intravascular coagulation.Anticoagulant therapy was then administered.Acute emphysematous pyelonephritis was subsequently diagnosed based upon the findings of gas on abdominal roentogenograms and swelling of a low density area around the left kidney on CT scan.Despite increasing the amount of antibiotics, the gas on the roentogenograms and the inflammation did not disappear. The patient then underwent left nephrectomy. Macroscopic observation revealed an abscess in part of the left kidney.Microscopic analysis revealed a xantogranulomatous lesion and infiltration composed of lymphocytes and plasma cells.The clinical course of the patient after nephrectomy was good.Early diagnosis, intensive chemotherapy and treatment of the underlying disease and its complications are important, because acute emphysematous pyelonephritis usually has a severe clinical course. If conservative therapy is not effective or if there is an obstructive lesion of the urethral tract, we recommend adequate chemotherapy and timely surgical treatment to ensure a good course.

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Enzyme immunoassay for insulin using a monoclonal antibody has been developed. The IRI value obtained by this new technique (dIRI) was reported to be similar to that obtained by the conventional method.In this study, we compared the dIRI values to those assayed using a polyclonal antibody (eIRI) in insulinoma patients. The dIRI values were about half of the eIRI values. The difference between IRI values in the two methods was significantly correlated to the proinsulin concentration in plasma. Considering the specificity of the antibodies, higher values of eIRI are likely due to the abundant proinsulin in insulinoma patients. Insulinoma indices such as the Fajan index (IRI/PG) and evaluation of IRI hyperresponse after glucagon administration are directly affected by IRI values. In diagnosing insulinoma, dIRI values should be judged carefully since hypersecretion of proinsulin is ignored in the dIRI assay.

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