Biomedical subjects
Publications and source records attributed to P Carfagna.
We report a case of miliary tuberculosis (MTB) occurring after extracorporeal shock-wave lithotripsy in a 51-year-old man. The MTB was complicated by pancytopenia and CD4(+) T-lymphocytopenia, which was responsible for Pneumocystis carinii pneumonia. Hematological parameters returned to normal in response to antituberculous treatment.
Anticonvulsant hypersensitivity syndrome is an uncommon side effect of phenytoin. It is characterized by fever, skin reactions, lymphadenopathy, and severe multiorgan involvement. Atypical clinical features have rarely been described. We observed a unique case of anticonvulsant hypersensitivity syndrome in a 77-year-old woman in whom fever and monoarthritis were the main clinical features. Symptoms dramatically subsided after phenytoin withdrawal.
Several studies have indicated that the serine protease urokinase-plasminogen-activator (uPA) is an important factor in host defense against pulmonary pathogens. To gain a better insight into the role of uPA in Pneumocystis carinii (P. carinii) pneumonia (PCP), we evaluated PA production in alveolar macrophages (AMs) obtained from rats with steroid-induced PCP. Treatment with cortisone acetate favored PCP in 91% of rats. In the bronchoalveolar lavage (BAL) samples of immunosuppressed rats both with and without PCP, we observed a decrease in uPA activity as well as a decrease in cell number. Urokinase-PA production by AMs was reduced in rats treated with cortisone alone. However, an increase in cell-associated uPA was observed in rats with PCP. This increase appears to be produced in response to P carinii infection. In fact, when AMs obtained from untreated healthy or immunosuppressed uninfected rats were challenged with P carinii, a significant increase in PA activity in cell lysates was observed, though a lower response was obtained in cortisone-treated animals. Our results suggest that healthy AMs respond to the presence of P carinii with an increase in uPA production and that this response in immunodepressed rat-AMs is partially impaired.
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We recently observed (February 1999) a 68-year old patient with endocarditis on a prosthetic biologic valve caused by a vancomycin-resistant Enterococcus faecalis. Broth dilution tests showed susceptibility to ampicillin (MIC=0.5 microg/ml), no high resistance to aminoglycosides (MIC for gentamicin <500 microg/ml) and resistance to vancomycin (MIC >256 microg/ml) and teicoplanin (MIC >16 microg/ml). A PCR assay detected vanA gene in this strain. A transthoracic echocardiogram did not show valvular vegetations. A possible endocarditis was diagnosed and the patient received ampicillin for 8 weeks and gentamicin for 6 weeks. The patient remained afebrile after a 4-month follow-up when he underwent surgical replacement of the dysfunctional bioprosthetic valve. Mitral valve was sterile on culture, but histology confirmed the diagnosis of previous endocarditis. This is the third case of endocarditis caused by vancomycin-resistant E. faecalis reported to date.
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Heart failure, still nowadays an important cause of morbidity and mortality in many countries, is a complex of symptoms related to inadequate peripheric perfusion and often to the retention of fluid, that results from an impaired left ventricular pump function. Treatment of heart failure has seen considerable changes in the last years. Short term goals of therapy are directed towards the relieve of symptoms that can be commonly managed by the use of vasodilators, diuretics, digoxin, in order to obtain an improvement in myocardial functional capacity and quality of life of patients. Nevertheless, it is important to recognize that improvement of symptoms is not necessarily correlated with correction of left ventricular dysfunction and, most important, with improvement of survival. In late 1980s both experimental and clinical observations carried out in an attempt to explain the progression of the disease and its poor long-term survival, led the physicians to think about heart failure as a neurohormonal disorder. This new conceptual model has first led to the widespread introduction of angiotensin converting inhibitors in clinical practice; then, the evidence that sympathetic activation might play an important role in the progression of heart failure, led the investigators to propose that beta-blocking agents might be useful in the management of heart failure. Accumulating clinical evidence indicates that beta blocker therapy, particularly with third generation beta-blocking agents, not only improves left ventricular function but also may reduce and reverse pathological remodeling in the heart. Ongoing large scale clinical trials may confirm the mounting evidence, from numerous clinical studies, that these agents may prolong survival in patients with heart failure.
Changes in antibiotic susceptibility was evaluated in 77 consecutive nosocomial clinical isolates of Staphylococcus aureus collected from 1986 to 1994 at the Umberto I Polyclinic of the University of Rome (63 isolates) and from 7 other Roman hospitals (14 isolates). Oxacillin resistance in these isolates increased from 39% during the 1980s to 69% during the 1990s. Significant increases in resistance to ciprofloxacin, clindamycin and rifampicin were observed among oxacillin-resistant strains. No resistance to glycopeptides was observed although both teicoplanin and vancomycin had slightly reduced antistaphylococcal activity.
Fourteen patients (11 men and 3 women) with Streptococcus bovis infective endocarditis have been observed by the Infectious Disease Section of our Department of Clinical Medicine between the years 1988-1998. The mean age was 63.2 years (range 35-85 years); 5 patients previously suffered valvular disease or had a valvular prosthesis, the infection involved the mitral valve in 6 patients, the aortic in 8, the prosthetic valve in 1. No patient developed cardiac failure or died during hospitalization; only 1 episode of major embolism (spleen) was observed. No patient required cardiac surgery. All patients became afebrile after starting antibiotic treatment; no cases of Streptococcus bovis relapse have been observed, during a six-month follow-up after antibiotics discontinuation, in 13 patients fully evaluated. The remaining patient was lost to follow-up. An underlying asymptomatic colonic neoplasm was diagnosed at colonoscopy in 7 of 11 evaluated patients. This study confirms that Streptococcus bovis infective endocarditis is relatively benign, but it stresses the frequency and potential severity of the associated colonic lesions, requiring colonoscopy and making the treatment of high risk lesion mandatory.
Systemic infections induced by Salmonella arizonae have been described in patients with underlying cell-mediated immunodeficiencies, usually resident in southern countries of U.S. and in Mexico. This peculiar geographic distribution is probably due to the ingestion of meat or drugs from rattlesnakes, that Salmonella arizonae colonize in the intestinal tract and that live in the above areas. In this article we describe two cases of systemic Salmonella arizonae infections, that represent, to our knowledge, the first report in European literature.
Our aim was to investigate the effect of GnRH-agonist (GnRH-a) induced suppression of plasma sex steroids on serum GH, insulin like growth factor-I (IGF-I) and insulin levels after an oral glucose load (OGTT) in women with polycystic ovary syndrome (PCOS). Serum insulin, GH and IGF-I levels during a 75-g 4-h OGTT were measured in 3 nonobese and 7 obese hyperandrogenic women with PCOS and normal glucose tolerance before and after 10 weeks of treatment with the GnRH-a triptorelin (3,75 mg im every 28 days). Basal estrogen and androgen levels were also measured at time 0 of the first and the second OGTT. After the therapy serum estrogens and androgens were significantly suppressed. Body weight remained unchanged. Basal GH significantly increased after the treatment while fasting IGF-I and insulin levels decreased from (mean +/- SE) 349.3 +/- 31.8 to 278.7 +/- 33.2 ng/mL and from 22.4 +/- 4.1 to 18.8 +/- 4.4 microU/mL, respectively. The insulin response to OGTT (area under curve) was also reduced (from 16,017 +/- 2598 to 11,736 +/- 2317 microU/mL/240 min). Our results suggest that the GnRH-a induced suppression of ovary secretion may modify the serum GH and IGF-I levels and the insulin response to an OGTT in women with PCOS.
OBJECTIVE: To evaluate the sensitivity of GH secretion to the suppressive effect of oral glucose administration in women with polycystic ovary syndrome (PCOS). DESIGN: Comparison of the GH response to an oral glucose load in women with PCOS and in weight-matched normally menstruating women (controls). SETTING: Reproductive endocrinology unit. PATIENT(S): Eighteen obese and 11 nonobese patients and 10 obese and 10 nonobese controls. INTERVENTION(S): After an overnight fast, each woman underwent a 75-g, 3-hour oral glucose tolerance test (OGTT). MEAN OUTCOME MEASURE(S): Growth hormone, glucose, and insulin responses to OGTT. RESULT(S): No significant differences in the glycemic and insulinemic responses were found between the patients and the weight-matched controls. No decrease in plasma GH was observed in both obese and nonobese patients and in obese controls during the OGTT, whereas a significant GH decrease occurred in nonobese controls 60 and 120 minutes after glucose intake. CONCLUSION(S): Oral glucose administration was unable to suppress GH levels in nonobese as well as in obese women with PCOS and in obese control women. These data suggest that both PCOS and obesity are associated with a reduced sensitivity of GH secretion to glucose suppression.
The purpose of this work was to investigate the relationship of gonadotropin levels to body weight and insulin levels in woman with polycystic ovary syndrome (PCOS). Specifically, we wished to test the hypothesis that circulating luteinizing hormone (LH) and insulin levels are different in obese and normal weight patients with PCOS. The basal plasma levels of gonadotropins, estrogens, androgens and sex hormone-binding globulin, the gonadotropin responses to gonadotropin releasing hormone (GnRH) and the insulin and C-peptide responses to a 3-hour oral glucose tolerance test (OGTT) were measured in 19 obese and 19 normal weight patients with PCOS and 7 obese and 8 normal weight ovulatory controls. Data of the patients were evaluated according to body weight (obese vs normal weight) and basal LH (high vs normal). There was no significant difference in basal LH and androgen levels and in the insulin response to oral glucose between obese and normal weight patients with PCOS. Compared to the weight matched controls, both obese and non obese patients showed significantly higher LH responses to GnRH and C-peptide responses to OGTT. When the high LH patients (no = 18) were compared those with normal LH (no = 20), the high LH subjects exhibited significantly higher androstenedione levels. Both obese (no = 10) and normal weight (no = 8) patients with high LH showed significantly greater C-peptide responses to OGTT than obese (no = 9) and non obese (no = 11) patients with normal LH. However, as compared with the weight matched controls, both the high LH and normal LH patients had significantly greater C-peptide responses to OGTT. We conclude that obese and non obese patients with PCOS do not seem to differ in the prevalence of elevated LH levels or in the LH secretory pattern. Insulin resistance, expressed by an enhanced pancreatic sensitivity to oral glucose, is present in both the high LH and the normal LH subjects, even though the PCOS patients with elevated LH tend to be more insulin resistant and hyperandrogenic than the normal LH patients.
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