PubMed Health⌕ Search

Biomedical subjects

C De Martinis

Publications and source records attributed to C De Martinis.

At least 19 recordsLinked to original sources

Cardiac troponin I in acute coronary ischemic syndromes. Epidemiological and clinical correlates.

UNLABELLED: The present study was aimed to investigate the variability of cardiac troponin I (cTnI) in the first week of acute myocardial infarction (AMI) course with regard to some epidemiological and clinical parameters and in patients with non-AMI acute coronary ischemic disease. Serum cTnI was assayed in 82 patients, 42 affected with AMI and 40 with non-AMI acute coronary ischemic disease, on admission in coronary care unit, within 6 h after the onset of symptoms, and, in AMI group, on 24 and 48 h and 7th day of illness course. cTnI is increased within the first 6 h, remaining above normal until 7th day. However, some distinctive features in the subgroups scheduled for this study are present. (1) The mean values of cTnI in AMI patients who died, >60 years old and with anterolateral necrosis are constantly higher than in survivors, <60 years old and with inferoposterior necrosis, respectively. (2) The cTnI concentration is already returned in normal range at 7th day of illness course in survivors and in patients with inferoposterior AMI. (3) The 24-h peak level of cTnI is significantly higher in fibrinolysed than in patients who didn't undergo fibrinolysis. (4) A direct correlation between the cTnI value and the Killip class is present either in the whole group or in any subset of patients and the progressive decrease of the cTnI concentration along the AMI course doesn't occur in Killip>2 group. (5) cTnI is higher in unstable than in stable anginous patients and normal subjects but not in stable angina with respect to healthy controls. CONCLUSIONS: (1, 2) The less increase and the early return in normal range of cTnI serum levels which occur in AMI subgroups with a better prognosis could be regarded as favourable prognostic signs. (3) The persistent higher values of cTnI in fibrinolysed subjects being associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent relase of cTnI from myocardium represents a reliable biochemical marker following the wash-out associated to a successful reperfusion. (4) The persistent increase of cTnI in AMI patients with advanced Killip class suggests that the high cTnI values are not only a strong index of myocardial necrosis but also of ongoing myocyte injury and hemodynamic impairment predictive of poor outcome. (5) The hypothesis can be reasonably advanced that the higher values of cTnI in unstable angina are due to focal areas of myocardial necrosis undetectable by the conventional serum markers or to a clinically silent AMI occurred in the week or so before in-hospital admission.

Adult↗

Polyclonal expansion of CD3(+)/CD4(+)/CD56(+) large granular lymphocytes and autoimmunity associated with dysregulation of Fas/FasL apoptotic pathway.

Evidence is accumulating regarding CD95/CD95 ligand (Fas/FasL) pathway dysregulation in clonal diseases of the lymphohaemopoietic lineages. According to these observations, it has been proposed that this defect may represent one of the mechanisms of tumour progression. In large granular lymphocyte (LGL) leukaemia, dysregulated apoptosis may represent a key event in the development of malignancy and autoimmunity. This case report describes dysregulation of the Fas/FasL pathway in a chronic polyclonal expansion of CD3(+) LGLs associated with numerous serological immune abnormalities.

Antibodies, Monoclonal↗

[Troponin I in acute ischemic cardiopathy].

BACKGROUND: The present study was aimed at investigating cardiac troponin I values in the first week of acute myocardial infarction and in non-infarct acute coronary ischemic syndromes. METHODS: Eighty-two patients, 42 with acute myocardial infarction, 10 with stable angina and 30 with primary unstable angina, were enrolled in the study. Blood was collected within 6 hours of symptom onset and, in the group with acute myocardial infarction, after 24 and 48 hours, and on day 7. RESULTS: Serum troponin I increased within the first 6 hours of myocardial infarction, reached the peak after 24 hours, at 48 hours it decreased, and remained above the normal range until day 7. However, troponin I values 1) were constantly higher in patients who died, in those > 60 years old and in those with antero-lateral necrosis than in survivors, in those < 60 years old and in those with infero-posterior necrosis, respectively; 2) returned to normal range on day 7 in survivors and in patients with infero-posterior acute myocardial infarction; 3) were significantly higher in fibrinolysed patients than in those who did not undergo thrombolysis; 4) were higher in patients classified as Killip class > 2. Serum troponin I values were in the normal range in non-infarct acute coronary ischemic syndromes, but were higher in unstable than in stable angina. CONCLUSIONS: The lesser increase and the early return to the normal range of cardiac troponin I levels in the subgroups of patients with myocardial infarction having a better clinical course could be regarded as a favorable prognostic sign. Since the persistent higher values of cardiac troponin I in fibrinolysed subjects are associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent post-thrombolysis release of cardiac troponin I from the myocardium represents a biochemical marker of a successful reperfusion. The persistent high cardiac troponin I values in patients with advanced Killip class suggest that the neuropeptide is an index of ongoing myocyte injury and hemodynamic impairment as well. The higher values of cardiac troponin I in unstable angina are probably due to focal areas of myocardial necrosis undetectable by conventional enzymatic serum markers.

Acute Disease↗

[Vasoactive intestinal peptide in heart failure].

BACKGROUND: The aim of our study was to investigate the pathophysiological role of the vasoactive intestinal peptide (VIP), a vasodilating neuropeptide with positive inotropic and chronotropic properties, in heart failure. METHODS: The study was carried out in 35 patients with heart failure due to dilated cardiomyopathy, who underwent a peripheral venous blood sample for radioimmunoassay of VIP within the first in-hospital day. RESULTS: The plasma concentration of VIP: 1) is not higher than normal in the whole group of patients with heart failure; 2) is higher in younger than in elderly healthy subjects but does not significantly change in relation to age in heart disease patients; 3) is higher in elderly (> 60 years) but not in younger (< 60 years) patients compared to healthy subjects of the same age; 4) is higher in NYHA functional class 2 than in NYHA functional class > 2 groups and in normal subjects; 5) is not correlated with echocardiographic parameters; 6) does not significantly change with respect to the etiology of dilated cardiomyopathy. CONCLUSIONS: The plasma concentration of VIP in heart failure is conditioned by some epidemiological and clinical variables. Unlike the healthy group, differences are not detectable with respect to the age of patients; thus, in elderly heart disease subjects the neuropeptide productive potentiality is preserved. Taking into account the physiological properties of VIP, its plasma increase in the initial phase of heart failure can be reasonably regarded as a further mechanism to restore the compromised hemodynamic balance. Its decrease, related to worse clinical conditions, could be due to a progressive depletion from the pre-synaptic nerve endings and to a deficiency in the neurogenic productive capacity of the molecule.

Adult↗

Effect of age and relation to mortality on serial changes of vasoactive intestinal peptide in acute myocardial infarction.

Plasma levels of vasoactive intestinal peptide increase early after acute myocardial infarction (AMI) and are significantly higher during the first 2 weeks of AMI in survivors and younger patients (<60 years) than in those who died and in older (>60 years) patients. Data suggest that vasoactive intestinal peptide is involved in neuroendocrine activation occurring in AMI and could be regarded as a marker of the course of AMI.

Adult↗

[Neuroendocrine activation in acute myocardial infarction: state of the art and preliminary results on intestinal vasoactive peptide].

Acute myocardial infarction (AMI) is known to be associated with a complex neuroendocrine activation, especially concerning sympathetic and renin-angiotensin systems, cortisol, atrial natriuretic peptide and endothelin. Results of our study show that the vasoactive intestinal peptide (VIP), also, is early involved in the neuroendocrine activation occurring in AMI. Plasma concentration of VIP, significantly increased in AMI patients within 6 hours after the onset of chest pain, soon decreased and remained below than normal along the first week. At the 14th day of the AMI, plasma levels of VIP returned into the normal range. A significant increase of VIP plasma concentration is detectable in the first hours of AMI in survived as compared with died patients. The phenomenon seems to be a suitable process to provide an endogenous support to the ischemic heart and to counteract the negative effects of other neuroendocrine activated factors.

Adult↗

[The physiopathological role and prognostic value of the vasoactive intestinal peptide in acute myocardial infarct].

Aim of our study was to investigate the pathophysiological role of vasoactive intestinal peptide (VIP) in the neuroendocrine activation occurring in acute myocardial infarction (AMI). Plasma VIP concentration has been assayed in 30 patients with AMI, 22 males and 8 females, aged 41-82 years, without other important diseases. VIP plasma values, assayed on admission to the Coronary Care Unit, within 4-6 hours after the onset of chest pain, everyday for the first week and on day 14, were significantly higher in survivors and in patients aged < 60 years. VIP plasma concentration was not statistically correlated with CPK and CPK-MB. VIP seems to play a pathophysiological role in the neuroendocrine activation occurring in AMI. Low VIP plasma levels are associated with an unfavorable short-term prognosis. Moreover, it appears that VIP secretion is negatively influenced by aging.

Adult↗

[Efficacy of L-thyroxine (L-T4) therapy on the volume of the thyroid gland and nodules in patients with euthyroid nodular goiter (ENG)].

The efficacy of treatment with TSH suppressive doses of L-thyroxine was evaluated by echography in 35 patients with euthyroid nodular goiter. Patients have been subdivided in two groups comparable for sex age and size of the goiter. Sixteen patients were treated for nine months with suppressive doses of thyroxine and nineteen were followed without therapy as control. Patients in treatment were then followed up for additional 9 months without therapy. The mean decrease of thyroid volume at nine months was 25% (27 +/- 10 ml vs 20 +/- 8 ml; p < 0.01). After discontinuation of treatment thyroid volume increased and had returned to base line values after nine months of follow up. In the control group mean thyroid volume had increased by 17.7% at nine months (28 +/- 17 vs 33 +/- 19 ml; p < 0.001). Thyroid nodules in response to thyroid hormone treatment showed a variable behaviour: 30.7% (4/13) of the nodules responded to the therapy with a reduction > to 25% at the ninth month; the remaining nodules were insensitive to the therapy. In conclusion suppressive thyroxine treatment is effective in reducing the goiter, nodules instead are only in part sensitive to the treatment. Thyroxine therapy of euthyroid nodular goiter must be followed for long term since upon thyroxine discontinuation there is a prompt reappearance of the goiter.

Adult↗

Tissue-specific antibodies against the fibroblast insulin receptor in a patient with lupus nephritis and hypoglycemia.

We recently reported that the serum from a patient with lupus nephritis, insulin resistance, and hypoglycemia contains multiple populations of antibodies directed at the human insulin receptor. In the present study, we found a subpopulation of antibodies (eluted from a protein A-Sepharose affinity column at pH 4.3) directed at the human fibroblast insulin receptor. When tested against human placental membranes, IM-9 lymphocytes, circulating monocytes and erythrocytes, and isolated adipocytes, the antibody subpopulation did not compete with 125I-insulin for binding to its receptor. In contrast, the antibody subpopulation competed with 125I-insulin for binding to the human fibroblast insulin receptor. This antibody subpopulation stimulated [3H]alpha-aminoisobutyric acid [( 3H]AIB) uptake to these cells. Unlike the effect of insulin, however, this regulation of transport was not antagonized by a mouse monoclonal antibody to the human insulin receptor that inhibits 125I-insulin binding. These studies indicate, therefore, that a tissue-specific antibody subpopulation can occur spontaneously in patients with antibodies to the human insulin receptor. Furthermore, they indicate the presence of anti-insulin receptor autoantibodies specifically directed against a tissue that is not primarily involved in glucose metabolism.

Animals↗

Decreased insulin receptors but normal glucose metabolism in Duchenne muscular dystrophy.

Compared to matched controls, 17 patients with Duchenne muscular dystrophy showed decreased insulin binding to monocytes due to decreased receptor concentration. These patients showed no signs of altered glucose metabolism and retrospective analysis of the clinical records of a further 56 such patients revealed no modification in carbohydrate metabolism. These data suggest that reduced insulin receptor number does not produce overt modifications of glucose metabolism in Duchenne muscular dystrophy.

Adolescent↗

Insulin receptors on monocytes and erythrocytes from obese patients.

Insulin receptors were studied in monocytes and erythrocytes [red blood cells (RBC)] isolated from 15 normal and 15 nondiabetic obese outpatients on an unrestricted diet. Insulin binding on both monocytes (P < 0.001) and RBC (P < 0.01) was higher in normal than in obese subjects due to different receptor concentrations. In some obese patients, binding to monocytes was decreased, while binding to RBC was normal. These data demonstrate that obese out-patients on an unrestricted diet have a reduced number of insulin receptors. It is suggested that interpretation of insulin binding based upon RBC should be used with caution, since a discrepancy exists in some subjects in the results obtained with these cells and monocytes.

Adult↗

[Role of 17-beta-estradiol in the synthesis and secretion of prolactin].

In 5 post-menopausal women TSH and prolactin secretions, induced by TRH, were studied before and after treatment with mg 20 of polyestradiol valerate. After this drug, plasma prolactin concentration increased, but no difference was observed in TSH secretion. The data suggest that 17-beta-estradiol doesn't increase the number of TRH receptors on pituitary cell surface, but stimulates prolactin synthesis.

Age Factors↗

[Influence of cimetidine on hypoglycemia-induced GH secretion].

Dopaminergic drugs inhibit prolactin and stimulate GH secretion. On the contrary antidopaminergic drugs stimulate prolactin and decrease hypoglycemia-induced GH secretion. According to the hypothesis that Cimetidine, an H2-receptor antagonist, decreases hypothalamic dopamine secretion, it was evaluated GH response to hypoglycemia after this drug. It was demonstrated that Cimetidine decreases hypoglycemia-induced GH secretion.

Adult↗

[Prolactin after repeated intravenous injections of cimetidine].

To 4 normal women a bolus of mg 400 of cimetidine was injected intravenously once an hour for three hours in succession and plasma prolactin behaviour studied. No depletion in prolactin pituitary storage was observed in all subjects. The possible usefulness of cimetidine for clinical diagnostic purposes is discussed.

Adult↗