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Biomedical subjects

C Vitale

Publications and source records attributed to C Vitale.

At least 19 recordsLinked to original sources
PubMed2006

Low testosterone levels are associated with coronary artery disease in male patients with angina.

Historically, high androgen levels have been linked with an increased risk for coronary artery disease (CAD). However, more recent data suggest that low androgen levels are associated with adverse cardiovascular risk factors, including an atherogenic lipid profile, obesity and insulin resistance. The aim of the present study was to evaluate the relationship between plasma sex hormone levels and presence and degree of CAD in patients undergoing coronary angiography and in matched controls. We evaluated 129 consecutive male patients (mean age 58+/-4 years, range 43-72 years) referred for diagnostic coronary angiography because of symptoms suggestive of CAD, but without acute coronary syndromes or prior diagnosis of hypogonadism. Patients were matched with healthy volunteers. Out of 129 patients, 119 had proven CAD; in particular, 32 of them had one, 63 had two and 24 had three vessel disease, respectively. Patients had significantly lower levels of testosterone than controls (9.8+/-6.5 and 13.5+/-5.4 nmol/l, P<0.01) and higher levels of gonadotrophin (12.0+/-1.5 vs 6.6+/-1.9 IU/l and 7.9+/-2.1 vs 4.4+/-1.4, P<0.01 for follicle-stimulating hormone and luteinizing hormone, respectively). Also, both bioavailable testosterone and plasma oestradiol levels were lower in patients as compared to controls (0.84+/-0.45 vs 1.19+/-0.74 nmol/l, P<0.01 and 10.7+/-1.4 vs 13.3+/-3.5 pg/ml, P<0.05). Hormone levels were compared in cases with one, two or three vessel disease showing significant differences associated with increasing severity of coronary disease. An inverse relationship between the degree of CAD and plasma testosterone levels was found (r=-0.52, P<0.01). In conclusion, patients with CAD have lower testosterone and oestradiol levels than healthy controls. These changes are inversely correlated to the degree of CAD, suggesting that low plasma testosterone may be involved with the increased risk of CAD in men.

Adult↗
PubMed2006

Cervico-oculo-Acoustic syndrome in a male with consanguineous parents.

BACKGROUND: The cervico-oculo-acoustic syndrome comprises Klippel-Feil anomaly, sensorineural deafness and Duane's retraction syndrome. Polygenic, autosomal dominant, and X-linked inheritance have been hypothesized. The disorder has rarely been reported in males. CASE REPORT: A 42-year-old male, born of consanguineous parents, presented with Duane's syndrome, mixed hearing loss, C2-C3 fusion, neck stiffness, and right facial palsy. A variety of cardiac, neurological and urogenital anomalies occurred in his relatives. The electro-oculographic studies showed impaired abduction and adduction of the right eye and impaired abduction of the left eye. Vergence, vertical eye movements and peripheral vestibular responses were normal. Somatosensory evoked potentials showed absence of the N13 peak and brainstem auditory evoked potentials bilateral delay of the I-III interpeak latencies. CONCLUSIONS: Consanguinity of the patient's parents, not previously reported, suggests autosomal recessive inheritance, but autosomal dominant inheritance is indicated by the family history. The pattern of the oculomotor deficit is consistent with bilateral dysplasia of the abducens nuclei with preserved internuclear neurons in the right abducens nucleus. Neurophysiological investigations revealed lower brainstem and cervical cord involvement.

Abducens Nerve↗
PubMed2006

Managing cardiovascular risk in menopausal women.

Blood pressure control and prevention of glucose intolerance are primary factors in overcoming the increased cardiovascular risks in menopausal women. This heightened risk may partially be explained by the metabolic syndrome - a precursor of type 2 diabetes - in which the renin-angiotensin-aldosterone system may play a pivotal role. Once diabetes occurs, the cardiovascular risk is considerably greater in postmenopausal women than in men - especially if hypertension is also present. An additional risk factor, weight gain, is common in postmenopausal women not treated with hormone replacement therapy. Rigorous control of blood pressure has been shown to be particularly beneficial in women with metabolic syndrome; a reduction in blood pressure can reduce the mortality rate of ischemic stroke. The administration of hormone replacement therapy can also reduce the likelihood of coronary heart disease in postmenopausal women; therefore therapy should be started early in the menopausal transition to maximize cardiovascular protection. As such, an ideal hormone replacement therapy that can overcome hypertension, prevent body weight gain and control serum triglycerides offers an important advance in cardiovascular risk management during the menopause.

Age Factors↗
PubMed2006

Metabolic syndrome.

Metabolic and non metabolic cardiovascular risk factors tend to cluster in the same individual. The association of the cardiovascular risk factors is referred as metabolic syndrome (MS). This syndrome is associated with an increased risk of accelerated atherosclerosis and cardiovascular events. The cluster of cardiovascular risk factors of the MS includes: insulin resistance with or without glucose intolerance or diabetes, abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, a proinflammatory and prothrombotic state. MS is one of the major issues in the management of cardiovascular disease because of its epidemic proportion and its impact on increasing risk of developing both cardiovascular disease and type 2 diabetes. The main therapeutic goal in the management of patients with the MS is to reduce risk for clinical cardiovascular events and to prevent type 2 diabetes. In particular, for individuals with established diabetes, risk factors management must be intensified to reduce their higher cardiovascular risk. Lifestyle changes have a critical role in the clinical management of the risk factors predisposing to MS, such as overweight/obesity, physical inactivity. A large body of evidence suggests the use of Metformin and Acarbose for the treatment of the syndrome as these drugs have consistently shown to reduce cardiovascular events and mortality. Most anti-hypertensive drugs have unfavorable metabolic profile while b-blockers, centrally acting agents and drugs targeting the renin angiotensin system should always be considered for the treatment of hypertension in patients with MS.

Atherosclerosis↗
PubMed2005

Metformin improves endothelial function in patients with metabolic syndrome.

BACKGROUND: Metabolic Syndrome (MS) is associated with impaired endothelial function and increased cardiovascular risk. Insulin resistance is a key feature of MS and plays an important role in the pathogenesis of endothelial dysfunction. Aim of the present study was to evaluate the effect of metformin on endothelial function and insulin resistance, assessed by the homeostasis model (HOMA-IR, homeostasis model assessment-insulin resistance), in patients with MS. METHODS: Sixty-five subjects (37 men and 28 women, mean age 54 +/- 6 years) with MS were allocated to receive metformin 500 mg twice daily (n = 32) or placebo (n = 33) for 3 months. Before and after treatment we assessed endothelial function, using flow-mediated dilatation of the brachial artery, and HOMA-IR. RESULTS: Patients who received metformin demonstrated statistically significant improvement in endothelium-dependent vasodilation compared with those treated with placebo (from 7.4 +/- 2.1% to 12.4 +/- 1.9% vs. 7.3 +/- 2.5% to 6.9 +/- 2.7%, P = 0.0016, metformin vs. placebo respectively), without significant effect on endothelium-independent response to sublingual glyceryl trinitrate (P =0.32). Metformin improved insulin resistance compared with placebo group (HOMA-IR from 3.39 to 2.5 vs. 3.42 to 3.37; 26% reduction in HOMA-IR, P = 0.01). An association between the improvement in insulin resistance and the improvement in endothelial function (r = -0.58, P = 0.0016) was found. CONCLUSION: Metformin improves both endothelial function and insulin resistance in patients with MS. These findings support the central role of insulin resistance in the development of endothelial dysfunction and the role of metformin for the treatment of patients with MS.

Brachial Artery↗
PubMed2004

Coeliac disease associated with Sjögren's syndrome, renal tubular acidosis, primary biliary cirrhosis and autoimmune hyperthyroidism.

Although coeliac disease may occur in patients affected by another immune-mediated disorder, its coexistence with multiple autoimmune diseases is not frequently described. We report here the case of a 45-year-old woman referred to our centre because of diarrhoea and weight loss, who had already received a diagnosis of primary biliary cirrhosis, Sjögren's syndrome and renal tubular acidosis. Following the development of diarrhoea we established the diagnosis of coeliac disease, based on the presence of anti-endomysium antibodies and a compatible duodenal biopsy. Despite gluten withdrawal she went on to develop an autoimmune hyperthyroidism. The patient tested positive for HLA DRB1*03 and DQB1*02. The association is unlikely to be casual and may be explained by autoimmune mechanisms, genetic susceptibility and favouring environmental factors commonly shared by the diseases of our patient.

Acidosis, Renal Tubular↗
PubMed2004

Comparative vascular effects of hormone replacement therapy and raloxifene in women at increased cardiovascular risk.

Hormone replacement therapy (HRT) improves endothelial function in postmenopausal women while the effects of raloxifene, a selective estrogen receptor modulator, are still under debate. The aim of this study was to evaluate endothelium-dependent flow-mediated vasodilatation in the brachial artery and plasma levels of nitrite, nitrate and endothelin-1 in 20 postmenopausal women with increased cardiovascular risk treated with either HRT or raloxifene for 4 weeks in a randomized double-blind single cross-over study. Patients had an endothelium-dependent flow-mediated dilatation of 4% prior to initiation of the study. Treatment with HRT resulted in a 67% increase in dilatation compared with baseline (from a 7.4% increase to a 12.4% increase, p < 0.01). Raloxifene treatment resulted in no change in vasodilatation from baseline. Endothelium-dependent dilatation was significantly improved by HRT compared with raloxifene treatment (12.4+/-0.6% vs. 6.1+/-2.0%; p < 0.01). Compared with baseline values, nitrate plus nitrite levels increased significantly (p < 0.05) with HRT but not with raloxifene. Similarly, endothelin-1 decreased from baseline with both treatments, but only the HRT-induced decrease was statistically significant (p < 0.05). In conclusion, HRT improved endothelial function and reduced plasma levels of endothelin-1 in postmenopausal women at risk of coronary artery disease. These beneficial effects were not shared by raloxifene.

Aged↗
PubMed2001

Effect of estradiol valerate alone or in association with cyproterone acetate upon vascular function of postmenopausal women at increased risk for cardiovascular disease.

OBJECTIVES: a large body of evidence has been accumulated suggesting that impairment of vascular endothelial function is an initial step in the development of atherosclerosis. Recent studies have shown that estrogen replacement therapy in postmenopausal women (PMW) improves endothelium-dependent, flow-mediated dilatation (FMD) while the cyclical adjunct of a progestin may reverse this effect. METHODS: the purpose of this study was to evaluate endothelium-dependent, FMD in the brachial artery and the plasma levels of Endothelin-1 in menopausal females treated with estradiol valerate with and without cyclical cyproterone acetate in 20 PMW (mean age 64+/-6 years) with more than one risk factor for coronary artery disease. After a baseline evaluation, PMW entered a double-blinded, placebo controlled single cross-over study and were randomized to receive either estradiol valerate (2 mg) for 21 days or estradiol valerate (2 mg) for 11 days and estradiol valerate (2 mg) and cyproterone acetate (1 mg) for 10 days. Patients were crossed-over the complementary treatment 7 days after completing the first treatment phase. The study of forearm blood flow was repeated at the end of each treatment period. RESULTS: estradiol valerate significantly increased FMD as compared with baseline (12+/-3 vs. 7+/-4%, P<0.01) the adjunct of cyproterone acetate did not affect the effect of estradiol valerate upon FMD (12+/-3 vs. 11+/-4%, P=NS). Similarly reactive hyperemic flow increased after estradiol valerate alone (24%) or in association with cyproterone acetate (24%) compared with baseline. Plasma levels of Endothelin-1 were significantly reduced by estradiol valerate alone or in association with cyproterone acetate. CONCLUSIONS: in conclusion hormone replacement therapy with estradiol valerate and cyproterone acetate improves endothelial function and reduces plasma levels of Endothelin-1 in PMW at risk of coronary artery disease. These effects may be relevant for cardioprotection.

Brachial Artery↗
PubMed2001

Surface expression and function of p75/AIRM-1 or CD33 in acute myeloid leukemias: engagement of CD33 induces apoptosis of leukemic cells.

p75/AIRM-1 is a recently identified inhibitory receptor expressed by natural killer and myeloid cells displaying high homology with CD33. Crosslinking of p75/AIRM-1 or CD33 has been shown to sharply inhibit the in vitro proliferation of both normal myeloid cells and chronic myeloid leukemias. In this study, we analyzed acute myeloid leukemic cells for the expression of p75/AIRM-1. p75/AIRM-1 marked the M5 (11/12) and M4 (2/2) but not the M1, M2, and M3 subtypes according to the French-American-British classification. Cell samples from 12 acute myeloid leukemias were cultured in the presence of granulocyte/macrophage colony-stimulating factor. Addition to these cultures of anti-CD33 antibody resulted in approximately 70% inhibition of cell proliferation as assessed by [(3)H]thymidine uptake or by the recovery of viable cells. Anti-p75/AIRM-1 antibody exerted a strong inhibitory effect only in two cases characterized by a high in vitro proliferation rate. After crosslinking of CD33 (but not of p75/AIRM-1), leukemic cells bound Annexin V and displayed changes in their light-scattering properties and nucleosomal DNA fragmentation, thus providing evidence for the occurrence of apoptotic cell death. Remarkably, when anti-CD33 antibody was used in combination with concentrations of etoposide insufficient to induce apoptosis when used alone, a synergistic effect could be detected in the induction of leukemic cell death. These studies provide the rationale for new therapeutic approaches in myeloid leukemias by using both chemotherapy and apoptosis-inducing mAbs.

Acute Disease↗
PubMed2001

No evidence of association between CAG expansions and essential tremor in a large cohort of Italian patients.

Essential tremor (ET) is one of the most common movement disorders. However the pathogenesis is as yet unknown, although a genetic cause has long been recognised. Clinical and molecular evidences suggested that the ET gene might contain a CAG expanded region. In a cohort of Italian ET patients Repeat Expansion Detection (RED) approach did not demonstrate large CAG expansions. We extended the study towards specific targets: the channel proteins hSKCa3 and CACNL1A4. Direct assessment of CAG stretches within these two genes did not demonstrate any CAG expansion in affected subjects. Also a case-control analysis failed to reveal any evidence of association, thus excluding these genes as a cause of ET.

Aged↗
PubMed2001

Unawareness of dyskinesias in Parkinson's and Huntington's diseases.

We performed a clinical study to evaluate the unawareness of dyskinesias in patients affected by Parkinson's disease (PD) and Huntington's disease (HD). Thirteen PD patients with levodopa-induced dyskinesias and 9 HD patients were enrolled. Patients were asked to evaluate the presence of dyskinesias while performing specific motor tasks. The Abnormal Involuntary Movement Scale (AIMS) and Goetz dyskinesia rating scale were administered to determine the severity of dyskinesias. The Unified Parkinson's disease rating scale (UPDRS) and Unified Huntington's Disease Rating Scale (UHDRS) were used in PD and HD patients, respectively. In PD we found a significant negative relationship between unawareness score at standing and AIMS score and between unawareness score at hand pronation-supination and AIMS score for upper limbs. In HD we found a significant positive relationship between total unawareness score and UHDRS score and between total unawareness score and disease duration. In PD the unawareness seems to be inversely related with severity of dyskinesias, while in HD it is directly related to disease duration and severity.

Aged↗
PubMed2001

p75/AIRM1 and CD33, two sialoadhesin receptors that regulate the proliferation or the survival of normal and leukemic myeloid cells.

Inhibitory receptors originally identified in natural killer (NK) cells have also been detected in other leukocyte types, thus suggesting that they may play a more general role in the control of leukocyte function. Here we report data on p75/adhesion receptor molecule 1 (AIRM1), a surface inhibitory receptor of the sialoadhesin family originally identified in NK cells that is also expressed by normal and leukemic myeloid cells. Given the homology between p75/AIRM1 and CD33, we also reanalyzed CD33, a major myeloid marker of still unknown function. We discuss recent data indicating that engagement of p75/AIRM1 or CD33 sharply inhibits the in vitro proliferation/differentiation of CD34+ myeloid precursors induced by stem cell factor and granulocyte-macrophage colony-stimulating factor. Importantly, a similar in vitro inhibitory effect occurs in monocyte/macrophages as well as in chronic or acute myeloid leukemias. While CD33 appears to act via the induction of apoptosis, p75/AIRM1 blocks cell proliferation but does not appear to induce apoptosis. A synergistic effect in the induction of apoptosis has also been documented between antibodies specific for CD33 and the chemotherapic agent etoposide. Taken together, the use of appropriate ligands against CD33 or p75/AIRM1 may represent a new therapeutic tool for treatment of myeloid leukemias or diseases characterized by overwhelming macrophage activation.

Antigens, CD↗
PubMed2001

How progestins influence the cardiovascular effect of hormone replacement therapy.

Hormone replacement therapy aims to protect against osteoporosis and alleviate fastidious menopausal symptoms such as hot flushes, depression, sleep disturbances and vaginal dryness. In view of the acknowledgement of estrogen deficiency as a major trigger for the acceleration of cardiovascular risk after menopause, hormone replacement therapy may also be proposed as a substantial beneficial cardioprotective agent. The effects of progestins on lipoprotein profile and vasomotor tone are dependent on the chemical structure and the scheme of administration of progestins, with androgenic progestins and cyclical therapy having a potential detrimental effect. Prospective primary and secondary prevention studies, however, suggest that the adjunct of non-androgenic progestins to estrogen therapy is at least as effective as estrogen replacement therapy in reducing cardiovascular mortality and morbidity. Data from recent randomized secondary prevention studies have to be viewed with caution.

Animals↗
PubMed2001

Spinal-cord compression due to extradural amyloidosis of the cervico-occipital hinge, in a hemodialysed patient. A case report.

Long-term dialysed patients can develop an arthropathy, called dialysis arthropathy, due to the deposition and transformation of the beta2 microglobulin into amyloid. The involvement of the spine, called destructive spondyloarthropathy (DSA), occurs between 10 and 25 percent; of these patients, and sometimes causes neurological damage. The disc space narrowing, vertebral body erosion and pseudocystis, in presence of polyarthropathy, chronic renal failure, and carpal tunnel syndrome, allows to make a diagnosis of DSA, which is proved by histological finding of beta2 microglobulin-amyloid. We report a rare case of spinal cord compression due to beta2 microglobulin-amyloid deposit in extradural space of cervico-occipital hinge.

Adult↗