The sensitivity of clinical diagnostic methods in the diagnosis of diabetic neuropathy.

This study assessed the sensitivity of various methods for the clinical diagnosis of diabetic peripheral neuropathy. A total of 147 randomly selected patients with diabetes mellitus and 65 age- and sex-matched healthy controls were evaluated by various clinical (the neuropathy symptom score [NSS], the neuropathy disability score [NDS], vibration perception thresholds [VPTs], Tinel's sign and Phalen's sign), laboratory (fasting plasma glucose and glycosylated haemoglobin levels) and electro-physiological (nerve conduction studies, H-reflex and F-wave measurements) methods. In the patient group, 8.2% had an abnormal NSS, 28.5% had a positive Phalen's sign, 32.6% had a positive Tinel's sign, 42.8% had an abnormal VPT and 57.1% had an abnormal NDS. Significant correlations were found between electro-physiologically confirmed neuropathy and the two provocation tests and abnormal VPTs. In conclusion, assessment with a complete neurological examination and standard electrophysiological tests is very important for the diagnosis of diabetic peripheral neuropathy and the prevention of morbidity in patients with or without symptoms.

The relationship between left ventricular mass index and insulin sensitivity, postprandial glycaemia, and fasting serum triglyceride and adiponection levels in patients with type 2 diabetes.

The relationship between left ventricular mass index (LVMI) and insulin sensitivity, postprandial glycaemia, fasting serum triglyceride and adiponectin was investigated in 70 patients with type 2 diabetes. Serum fasting insulin, C-peptide, high-sensitivity C-reactive protein (hs-CRP), glycated haemoglobin (HbA1c), postprandial glycaemia, lipids and fasting serum adiponectin levels were measured. Ventricular hypertrophy was assessed at rest by electrocardiography and echocardiography. Insulin sensitivity was assessed using the homeostasis model assessment index (HOMA-IR). LVMI was assessed using the Devereux formula. Study patients had lower than normal HOMA-IR, and higher than normal serum fasting insulin levels and LVMI, and tended to have reduced insulin sensitivity. Pearson's correlation coefficient showed a statistically significant correlation between fasting serum adiponectin and LVMI, fasting serum insulin, HOMA-IR, HbA1c, serum postprandial glucose and hs-CRP. There were no statistically significant correlations between LVMI and serum hs-CRP or HOMA-IR. The results indicate the importance of fasting serum adiponectin in the development of cardiovascular complications, such as increased LVMI.

Biochemical composition of benign thyroid cyst fluid.

Although the availability of thyroid cyst fluid is easy by fine-needle aspiration, less is known about the biochemical composition of thyroid cyst fluid. The authors have, therefore, determined the biochemical composition of 18 benign thyroid cyst fluid specimens. They found that the activities of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and the concentrations of total protein, total bilirubin, and uric acid were highly increased in thyroid cyst fluid specimens when compared with normal human serum specimens. The concentrations of glucose, cholesterol, and triglycerides in cyst fluid were within normal serum limits. Selenium (Se) concentrations in most cyst fluids were low. Moreover, there was no correlation between Se and other biochemical parameters. Protein electrophoresis of cyst fluid specimens yielded high concentrations of alpha 1 and especially alpha 2 globulin fractions indicating an inflammation. The concentrations or activities of biochemical analytes were not significantly different in pure and mixed cysts. Those parameters were also not significantly different between cyst fluids of different colors. The gross appearance of the fluid and the presence of certain biochemical analytes were consistent with a hemorrhagic origin of most of the cyst fluid specimens. However, some biochemical markers indicate that autolysis or necrosis of thyroid tissue may also contribute the composition of thyroid cyst fluid. The reason for lower Se concentration in the thyroid cyst fluid may be the lower Se concentration in the Turkish population. These results also suggest that the fluid color or nature of cyst, e.g., pure or mixed cyst, is not a main determinant of biochemical composition of benign thyroid cyst fluid.

The effects of valsartan on insulin sensitivity in patients with primary hypertension.

Insulin resistance is an important risk factor of cardiovascular disease. This study was performed to determine the effects of valsartan on insulin sensitivity in patients with primary hypertension. In this study, non-obese subjects with primary hypertension and a reference group of healthy subjects matched by age, sex and body mass index were evaluated; patients with any other causes of peripheral insulin resistance and hyperlipidaemia were excluded. The effect of valsartan on insulin resistance, assessed by homeostasis model assessment (HOMA-IR), fasting serum insulin levels, determined by radioimmunoassay, and fasting blood glucose concentrations, measured by the glucose oxidase method, were evaluated. All obtained data were evaluated by Pearson correlation analysis. Before valsartan treatment, the fasting serum insulin levels were significantly elevated in the 20 hypertensive patients with primary hypertension compared with the 20 subjects in the reference group (19.6 +/- 7.1 versus 8.7 +/- 1.9 microIU/ml). The fasting serum insulin levels correlated with HOMA-IR. Correlation analysis also showed a significant relationship between HOMA-IR and both systolic and diastolic blood pressures (r = 0.71 and r = 0.77, respectively). In our study, we showed that patients with primary hypertension have a decreased insulin sensitivity that was reflected in high serum fasting insulin levels. Anti-hypertensive treatment with valsartan increases insulin sensitivity.

Effects of fluvastatin treatment on insulin sensitivity in patients with hyperlipidaemia.

This study aimed to determine the effects of fluvastatin treatment on insulin sensitivity in patients with hyperlipidaemia. Non-obese, normoglycaemic, normotensive patients with hyperlipidaemia (n = 20) and a reference group of healthy subjects of similar age, sex, and body mass index (n = 20) were evaluated. Patients with other causes of peripheral insulin resistance were excluded. All participants underwent a diagnostic protocol, which included measurements of insulin sensitivity index and other metabolic parameters. Insulin sensitivity was assessed by Homeostasis Model Assessment (HOMA). Serum insulin levels were tested by radioimmunoassay. Patients were treated with fluvastatin 40 mg once daily for 3 months. Before fluvastatin treatment, fasting serum insulin levels were significantly raised in patients with hyperlipidaemia compared with subjects from the reference group (19.1 +/- 13.4 versus 8.1 +/- 3.4 microIU/ml). The fasting serum insulin levels and HOMA-estimated insulin sensitivity were correlated in the whole group. Correlation analysis showed a significant relationship between HOMA-estimated insulin resistance and plasma cholesterol and triglyceride concentrations. Patients with hyperlipidaemia had reduced insulin sensitivity that was reflected by high serum fasting insulin levels. Anti-hyperlipidaemic treatment with fluvastatin increases insulin sensitivity.