Intra-arterial iloprost for limb ischaemia.
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Adult↗
Biomedical subjects
E Motz
Publications and source records attributed to E Motz.
Hyperglycemia-induced thrombin formation in diabetes. The possible role of oxidative stress.
Diabetes is characterized by the existence of a thrombosis-prone condition, possibly related to hyperglycemia. However, the mechanism linking hyperglycemia to the activation of the coagulation cascade is still unclear. It has been recently suggested that diabetes is accompanied by increased oxidative stress. In this work, the possibility that oxidative stress may be involved in the hyperglycemia-induced coagulation activation has been evaluated. Prothrombin fragment 1 + 2 (F1 + 2), which represents a reliable marker of the amount of thrombin released in the circulation, has been chosen for studying thrombin formation in vivo. In nine type II diabetic patients and in seven healthy control subjects, matched for age and body mass index, three different experiments were performed: oral glucose tolerance test (OGTT), intravenous antioxidant glutathione (GSH) administration for 2 h, and OGTT plus intravenous GSH administration. Samples were drawn at -15 min and every 30 min from 0 to 180 min. During the OGTT, F1 + 2 significantly increased in both diabetic and healthy subjects. GSH administration during OGTT normalized this phenomenon. GSH administration alone significantly decreased F1 + 2 in diabetic patients, while no effect was observed in the normal subjects. These data suggest that hyperglycemia may induce thrombin activation, possibly inducing an oxidative stress, and that antioxidant GSH may counterbalance this effect.
Aged↗
Fibrinogen plasma levels as a marker of thrombin activation in diabetes.
This study attempted to verify the existence of a correlation between fibrinogen, a major cardiovascular risk factor in diabetes, and indexes of thrombin generation and action, prothrombin fragment 1 + 2 (F1 + 2), and D-dimer (D-D), in a group of diabetic subjects compared with a matched control group. Forty insulin-dependent diabetes mellitus patients and 30 matched healthy control subjects participated in this study. The subjects were tested for the following parameters: fibrinogen, prothrombin F1 + 2, D-D, fasting glycemia, and HbA1c. In addition, 5 diabetic subjects who maintained stable fibrinogen plasma levels > 300 mg/dl for at least 6 months before the study were treated with 12,500 U/day subcutaneous heparin for 7 days. Diabetic subjects showed increased levels of fibrinogen, prothrombin F1 + 2, and D-D plasma levels. Simple linear regression analysis detected a positive correlation between fibrinogen and prothrombin F1 + 2, D-D, and glycosylated HbA1c. In the five diabetic subjects treated with heparin fibrinogen, prothrombin F1 + 2 and D-D levels decreased at the end of the treatment. All these parameters returned to baseline after 7 days of washout. These data indicate that fibrinogen plasma levels are correlated to parameters of thrombin activation in plasma in diabetic patients and suggest that high fibrinogen plasma levels might be a risk marker for cardiovascular disease in diabetes because it is an expression of an existing thrombophilia.
Adult↗
Fibrinogen plasma levels as a marker of thrombin activation: new insights on the role of fibrinogen as a cardiovascular risk factor.
Fibrinogen has recently emerged as a major risk factor for atherothrombosis. However, the pathophysiologic mechanism linking high fibrinogen concentration to cardiovascular disease is unclear. In this study 136 subjects (75 males, 61 females, age 51.7 +/- 14.4 years, mean +/- standard deviation, range 17-82) were tested for total and HDL-cholesterol, total triglycerides, apolipoprotein AI, apolipoprotein B, fibrinogen, prothrombin fragment and D-dimer. Moreover, 5 subjects who had hyperfibrinogenemia (range 450 to 950 mg/dl) for at least 6 months by repeated measurements, were treated with a short 7-day course of heparin 12,500 U/day subcutaneously. The effect of heparin on all the above mentioned parameters was observed at the end of treatment and after 7 days of wash-out. Simple regression analysis detected a positive correlation between fibrinogen and age, prothrombin fragment and D-dimer, and a negative correlation between fibrinogen and HDL-cholesterol and apolipoprotein AI. A direct correlation between age and both prothrombin fragment and D-dimer was also demonstrated. Multivariate analysis showed a persistent correlation between fibrinogen and prothrombin fragment, D-dimer and age, that was not influenced by sex, smoking habit and body mass index. In the 5 hyperfibrinogenemic subjects, heparin administration significantly reduced fibrinogen (625.4 +/- 211.1 vs 455.2 +/- 112.3 mg/dl, p < 0.03), prothrombin fragment (0.97 +/- 0.1 vs 0.63 +/- 0.2 nM, p < 0.002) and D-dimer (336 +/- 101.8 vs 275.2 +/- 78.5 ng/ml, p < 0.03). All these parameters returned to baseline after 7 days of wash-out (fibrinogen 632.5 +/- 198.2 mg/dl, prothrombin fragment 0.96 +/- 0.2 nM, D-dimer 325.8 +/- 98.65 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Serum tissue polypeptide antigen (TPA) in thyroid cancer.
Serum tissue polypeptide antigen, (TPA), carcinoembryonic antigen (CEA), calcitonin (CT) and thyroglobulin (Tg) have been measured by specific radioimmunoassays in 174 patients with various types of thyroid cancer previously submitted to thyroidectomy. Elevated serum TPA concentrations were found in 12 of 13 patients with local invasion or distant metastases from undifferentiated thyroid cancer or thyroid lymphosarcoma, while serum Tg and CEA values were normal or undetectable. In 123 patients with well differentiated thyroid cancer serum TPA was usually normal regardless of the presence or absence of functioning metastases. On the contrary, 14 of 15 patients with "dedifferentiated" metastases from previously differentiated thyroid cancer had elevated serum TPA values, while serum CEA was normal and serum Tg variable. Serum CT was confirmed as the most sensitive marker of metastatic medullary thyroid carcinoma, but elevated serum TPA values were also found in most of these cases. The present data indicate that serum TPA provides a new humoral marker in the follow-up of undifferentiated and "dedifferentiated" thyroid carcinoma and may also be usefully employed as an additional marker for medullary thyroid carcinoma.
Adolescent↗
Serum myoglobin in primary hypothyroidism and effect of L-thyroxine therapy.
Serum myoglobin (Mb) concentrations have been measured by radioimmunoassay in normal subjects, in hypothyroid patients examined 20 days after withdrawal of thyroid hormone therapy ("short-term" hypothyroidism), and in untreated hypothyroids ("long-term" hypothyroidism). In "short-term" hypothyroids, serum Mb levels were significantly higher (p less than 0.01) than those observed in normal controls, although only a minority or patients showed elevated Mb levels. In "long-term" hypothyroids, serum Mb concentrations were significantly higher than that found in normal controls (p less than 0.0001) and in "short-term" hypothyroids (p less than 0.001). In "long-term" hypothyroidism a significant inverse correlation was found between serum thyroid hormones and Mb, whereas no similar correlation was observed in "short-term" hypothyroidism. The administration of progressively increasing doses of L-T4 untreated hypothyroids was followed by normalization of serum Mb, but serum TSH levels still remained elevated. These data indicate that the duration and the severity of hypothyroidism are important factors in the rise of serum Mb, and that the normalization of serum Mb is faster than that of serum TSH and requires less L-T4 than that needed for normal TSH secretion.
Adolescent↗
Hyperglycemia counterbalances the antihypertensive effect of glutathione in diabetic patients: evidence linking hypertension and glycemia through the oxidative stress in diabetes mellitus.
Diabetes mellitus is associated with hypertension. An antihypertensive effect of the antioxidant glutathione has been recently demonstrated. It has been suggested that hyperglycemia may contribute to the pathophysiology of hypertension in diabetes by generating an oxidative stress. In this study, three different tests were performed in ten hypertensive and ten nonhypertensive diabetic subjects: (1) an oral glucose tolerance test, (2) glutathione i.v. administration (1 g/m2 bolus + 1 g/m2 in 2 h), and (3) oral glucose tolerance test + glutathione administration. At -15', 0', 30', 60', 90', 120', and 180' systolic and diastolic blood pressure, plasma glucose, and insulin were measured. Variations in plasma glucose and insulin levels were not different during each test in the two groups of patients and in test (1) compared to (3). Glutathione administration reduced systolic and diastolic blood pressure in both hypertensive and nonhypertensive diabetic subjects from 30' to 120'. This phenomenon was abolished as glycemia increased after oral glucose loading. In hypertensive, but not in nonhypertensive diabetic subjects, a significant increase of systolic and diastolic blood pressure was observed at 90' and 120' of the oral glucose tolerance test (p < 0.01). These data show that hyperglycemia can counteract the hypotensive effects of the antioxidant glutathione, suggesting that glucose may impair arterial relaxation by producing free radicals. Also, it appears that hypertension in diabetic patients is aggravated by high glucose plasma levels.
Antihypertensive Agents↗