Clinical biochemistry of neuron specific enolase.

The soluble brain protein 14-3-2 first described by Moore and McGregor in 1965 is now known to be a cell specific isoenzyme of the glycolytic enzyme enolase (EC 4.2.1.11), designated neuron specific enolase (NSE). It is not only a marker for all types of neurons, but also for all neuroendocrine or paraneuronal cells. The appearance of NSE is a late event in neural differentiation, thus making NSE a useful index of neural maturation. The demonstration that tumors of the nervous system and of neuroendocrine origin contain NSE has promoted the study of NSE as a possible tumor marker. Immunocytochemistry has been used to identify NSE in cytologic preparations from several types of tumors, offering useful indications for differential diagnosis. NSE levels in serum from tumor patients are not useful in the diagnosis of early stage disease. However, serum NSE levels have been shown to be helpful in the identification of advanced small cell lung cancer, neuroblastoma and several other neoplasms. The main use of serum NSE is the monitoring of chemotherapy and the detection of a relapse in these cases.

No effect of insulin treatment or glycemic improvement on plasma carnitine levels in type 2 diabetic patients.

Carnitine is an essential factor for the transport of long-chain fatty acids and is important for the heart muscle. A longitudinal study in type 2 diabetic patients was carried out. Carnitine levels were observed before and during metabolic intervention with dietary measures and either sulfonylurea or insulin treatment. In both treatment groups a significant glycemic improvement was observed after 3 months (insulin treatment group: hemoglobin A1c 11.3 +/- 2.8 versus 7.0 +/- 1.0; sulfonylurea treatment group; hemoglobin A1c 11.3 +/- 1.4 versus 7.3 +/- 0.9). Carnitine levels did not differ from a control group and did not change significantly during the observed period.

[Decreased plasma carnitine in Type I diabetes mellitus]. / Vermindertes Plasmacarnitin bei Typ-I Diabetes mellitus.

Realizing the importance of carnitine for the lipid and carbohydrate metabolism and the possible role for glucose utilization and myocardial function carnitine concentrations in type I and type II diabetic patients in plasma, erythrocytes and 24 h urine were determined. The plasma levels of carnitine were significantly diminished in type I diabetic patients compared to controls, while carnitine concentrations in erythrocytes and 24 h urine did not differ from controls. Plasma carnitine levels did not change significantly during the diurnial profile. No correlation between HbA1c and carnitine levels was observed in the diabetic patients.

Hypomagnesaemia in type 2 (non-insulin-dependent) diabetes mellitus is not corrected by improvement of long-term metabolic control.

Low levels of magnesium have frequently been reported in diabetes mellitus especially in poorly controlled Type 1 (insulin-dependent) diabetic patients. Furthermore hypomagnesaemia might contribute to insulin resistance in Type 2 (non-insulin-dependent) diabetes. As the influence of improved metabolic control on plasma magnesium levels is unknown in Type 2 diabetic patients we studied magnesium plasma levels in 50 patients 1) before, 2) one and 3) three months after the initiation of insulin therapy or intensified treatment with oral hypoglycaemic agents. Magnesium plasma levels were measured by a colorimetric method and were significantly reduced in diabetic patients compared to healthy control subjects (0.79 +/- 0.01 mmol/l vs 0.88 +/- 0.01 mmol/l; p less than 0.0001). Metabolic control was significantly improved as documented by reduced HbA1C levels in both insulin-treated patients or the patients on oral hypoglycaemic agents (p less than 0.003). However, plasma magnesium levels remained unchanged during the follow-up in the insulin-treated group (1: 0.79 +/- 0.02 mmol/l; 2: 0.81 +/- 0.02 mmol/l; 3: 0.79 +/- 0.01 mmol/l) as well as in the patients on oral hypoglycaemic agents (1: 0.79 +/- 0.03 mmol/l; 2: 0.78 +/- 0.02 mmol/l; 3: 0.84 +/- 0.04 mmol/l). This study shows that even marked improvement of glycaemic control does not correct hypomagnesaemia in Type 2 diabetes. We conclude that hypomagnesaemia might be related to the insulin-resistant state and that possible beneficial effect of chronic magnesium administration should be evaluated in these patients.