Trend of hospital utilization for encephalitis.

Encephalitis generally results in a serious illness requiring hospitalization. The aim of this study was to describe the epidemiology of hospitalization for encephalitis in Italy, taking into account the geographical distribution, aetiology, seasonality and evolution of hospitalization rates over recent years. The mean hospitalization rate was 5·88/100 000. For most of these hospitalizations (n=13 119, 55·6%), no specific cause of encephalitis was reported. The most common aetiological category was 'viral', which accounted for 40·1% (n=4205) of such hospitalizations (rate 1·05/100 000). Within this category, herpes virus was the leading causative agent (n=1579, 0·39/100 000). This report highlights a significant increase of 'viral encephalitis not otherwise specified' (ICD-9 code 049·9) vs. a reduction of all other causes. A seasonal pattern was noted in people aged ≥65 years in this group. Specific surveillance of encephalitis without known origin should be reinforced in order to identify the potential role of emerging pathogens and to design preventive interventions.

Perioperative antibiotic prophylaxis: improved compliance and impact on infection rates.

The aims of this study were to determine adherence to the perioperative antibiotic prophylaxis (PAP) protocol used at a large Italian teaching hospital during a 6-year period, to assess the variables associated with inappropriate administration, and to measure the impact on surgical site infection (SSI) rates. There were 28 621 patients surveyed of which 74·6% received PAP. An improvement in adherence to the PAP protocol was registered for 58·8% of patients. Significant risk factors were an American Society of Anesthesiologists (ASA) score ≥ 2 [odds ratios (OR) from 1·28 (95% confidence interval (CI) 1·19-1·37) to 1·87 (95% CI 1·43-2·44)], prolonged duration of surgery (OR 1·68, 95% CI 1·56-1·82) and urgent surgery (OR 2·16, 95% CI 1·96-2·37). During the study period, a significant reduction in SSIs rates was detected. We concluded that the global reduction of inadequate PAP administration signifies the efficacy of a multidisciplinary quality improvement initiative on antimicrobial utilization, and this is supported by the observed reduction of the SSI rate.

Fluconazole susceptibility of Candida spp. isolates collected over nine years in a teaching hospital of Ancona, Italy.

The in vitro activity of fluconazole was investigated against 476 yeast isolates collected during a 9-year period (1997-2005) from patients hospitalised in a teaching hospital of Ancona. They included 373 isolates of Candida albicans, 53 of Candida glabrata and 50 of Candida parapsilosis. Minimum inhibitory concentrations (MICs) determined in accordance with the Clinical Laboratory Standards Institute methodology showed that 96% of the isolates were susceptible (MIC < or =8.0 microg/ml). The uncommon, resistant isolates (MIC > or =64 microg/ml) were randomly distributed over time. Our data show that resistance to fluconazole in this geographical area is a rare event and suggest that this triazole can still represent first-line therapy in our institution.

In-vitro activity of the synthetic protegrin IB-367 alone and in combination with antifungal agents against clinical isolates of Candida spp.

The in vitro activity of the peptide IB-367, alone or combined with either fluconazole (FLU) or amphotericin B (AMB), was investigated against 25 Candida isolates belonging to five species. IB-367 minimum inhibitory concentrations (MICs) ranged from 2.0 to 32 microg/ml and it was active against both FLU-susceptible and - resistant isolates. A rapid fungicidal activity was observed. Synergism was documented in 41.6% and 44% of IB-367/FLU and IB-367/AMB interactions, respectively. Antagonism was never observed. The broad antifungal activity and the positive interactions with AMB and FLU suggest that IB-367 represents a promising candidate against infections due to Candida spp.

Antihypertensive effect of insulin reduction in diabetic-hypertensive patients.

Body weight, urinary volume, sodium and potassium excretion, and blood pressure were evaluated for six days in twelve type II diabetic women, taking insulin doses over their need, after insulin daily dosage reduction. Six of them were suffering from essential hypertension. A significant decrease in body weight with an increase in urinary volume and in urinary sodium excretion was found in all patients. However, no significant variation in plasma renin activity and urinary aldosterone output was observed. Urinary potassium excretion remained unchanged. In normotensive subjects no variation of blood pressure levels occurred. On the contrary, hypertensive patients exhibited, after insulin reduction, a fall in systolic and diastolic blood pressure, which correlated directly with body weight decrease and inversely with urinary volume and urinary sodium excretion increases. Hypotheses relating insulin action to hypertension are discussed.

Insulinemia and blood pressure. Relationships in patients with primary and secondary hypertension, and with or without glucose metabolism impairment.

In order to investigate the relationships between insulinemia and hypertension, fasting insulinemia has been assessed in 117 subjects: 69 normotensive subjects, 36 with essential hypertension, and 12 with renovascular hypertension, all untreated and newly diagnosed, classified in subgroups (euglycemic nonobese, euglycemic obese, with impaired glucose tolerance and with non-insulin-dependent diabetes mellitus). In the patients with essential hypertension fasting insulinemia was significantly higher than in normotensive subjects (P less than .0005). The patients with secondary hypertension and the normotensive subjects had similar fasting insulinemia values. In each subgroup fasting insulinemia was higher in hypertensive patients than among normotensive subjects (P less than .05). A significant correlation between fasting insulinemia and mean blood pressure has been found in patients with essential hypertension (r = 0.408, P less than .05), but not in patients with renovascular hypertension. Our data suggest a possible direct relationship between fasting insulinemia and blood pressure, especially in obese patients or patients with impaired glucose metabolism, and that increased blood pressure per se is not an insulin resistant state.

[Paroxysmal nocturnal hemoglobinuria with multiple venous thrombosis and acute renal insufficiency. Description of a case]. / Emoglobinuria parossistica notturna con trombosi venose multiple ed insufficienza renale acuta. Descrizione di un caso.

Oral anticoagulants were administered to a young woman suffering from P.N.H. after the development of portal vein thrombosis. She interrupted the treatment and developed multiple splanchnic thromboses followed by acute renal failure, from which she recovered four weeks later. Although the pathogenetic mechanism could include renal vascular microthrombosis, the possibility of renal ischemic damage due to massive blood pooling within the splanchnic district is discussed.

[Disseminated intravascular coagulation and acute hepatic necrosis at the end of pregnancy. A case report]. / Coagulazione intravascolare disseminata e necrosi epatica acuta a termine di gravidanza. Descrizione di un caso.

A 30-year-old woman in the 36th week of her second pregnancy, suddenly developed jaundice with remarkable liver necrosis, accompanied by generalized bleeding due to disseminated intravascular coagulation (DIC). She underwent a caesarean and a dead foetus was extracted from the uterus. Heparin and frozen plasma infusion resulted in a prompt recovery from the haemostatic disorder. The course of the disease involved the successive appearance of haemorrhagic shock, intestinal ileus and pulmonary embolism all of which she recovered from. The liver biopsy showed severe cholestasis without derangement of the lobular structure. Hypotheses of acute veno-occlusive disease caused by the DIC, and acute fatty liver of pregnancy are discussed.

[Increase of circulating levels of insulin and C-peptide: common factors in essential hypertension and overweight]. / Aumento dei livelli circolanti di insulina e C-peptide: fattore commune nell'ipertensione essenziale e nel sovrappeso.

The aim of our study was to investigate the hypothesis that insulin resistance is involved in the pathogenesis of essential hypertension, and to explain whether hyperinsulinemia in this condition is the result of either pancreas overproduction or defective hepatic insulin clearance. In 14 lean normotensive, 17 overweight normotensive, 17 lean essential hypertensive, and 20 overweight essential hypertensive subjects, we measured, after overnight fasting, blood glucose, serum insulin, and serum C-peptide, and calculated the glucose/insulin and the insulin/C-peptide ratios, which can be commonly taken as indexes of peripheral sensitivity to insulin and hepatic insulin clearance, respectively. When compared to lean normotensives, overweight and/or hypertensive patients exhibited higher serum insulin and C-peptide concentrations, and a lower glucose/insulin ratio. No difference was found in the insulin/C-peptide ratio between normotensive and hypertensive subjects. Diastolic blood pressure was directly correlated with serum insulin (p less than 0.01) and C-peptide (p less than 0.01), and inversely correlated with the glucose/insulin ratio (p less than 0.02). We conclude that insulin resistance is present in both essential hypertensive and overweight subjects. Considering the normality of the insulin/C-peptide ratio when taken as the hepatic insulin clearance index, we believe that hyperinsulinemia is caused by a beta-cell hypersecretory response to the defective peripheral action of the hormone.

Insulin resistance and beta-cell hypersecretion in essential hypertension.

To determine whether a decreased sensitivity to insulin is involved in the pathogenesis of essential hypertension, fasting blood glucose, serum insulin, serum C peptide, the glucose:insulin ratio and the insulin:C-peptide ratio were measured in 14 lean normotensives, 17 overweight normotensives, 17 lean hypertensives and 20 overweight hypertensives. Compared with the lean normotensives, the patients who were overweight, those with hypertension and those who were both overweight and hypertensive showed increased fasting serum insulin and C-peptide levels, and a lower glucose:insulin ratio. No significant difference between the normotensive and the hypertensive subjects was found in the insulin:C-peptide ratio. Diastolic blood pressure was directly correlated with serum insulin (P less than 0.01) and with C-peptide levels (P less than 0.01), and inversely correlated with the glucose:insulin ratio (P less than 0.02). We conclude that insulin resistance is present in both essential hypertensive and overweight subjects. Since the present study showed that hepatic insulin clearance was normal in hypertensives, the hyperinsulinaemia in essential hypertension appears to be due to beta-cell hypersecretion in response to a defective peripheral action of the hormone.

In vivo comparative efficacy of three surgical hand preparation agents in reducing bacterial count.

BACKGROUND: Besides objective efficacy, the choice between an antiseptic-based liquid soap, or an alcohol-based hand rub for surgical hand preparation technique is based on personal preference. Glycerol is often added to the formulations in order to enhance tolerability; however, it has been recently reported as a factor reducing the sustained effect of surgical hand rubs. AIM: To compare the efficacies of three commercial products for hand decontamination. METHODS: The in vivo efficacy of an alcohol-based hand rub (isopropyl alcohol 40%; N-propyl alcohol 25%; glycerin 1.74%; triethanolamine salt of carbomer <1%) was compared with other widely used products in surgical hand antisepsis (chlorhexidine and povidone-iodine). All products were used according to the manufacturers' instructions. FINDINGS: The best results were achieved with the alcohol-based hand rub and these were sustained for a period of 3h. Some volunteers experienced skin peeling off the hands when using alcohol-based hand rub; in this group of participants, the bacterial count was reduced only by 0.91 ± 1.67 log10 compared with 2.86 ± 1.22 log10 in the group who did not show this phenomenon. CONCLUSION: Besides confirming the importance of alcohol-based hand rubs for surgical hand decontamination, the results suggest the value of assessing the characteristics, and response of healthcare workers' skin, that may contribute to the development of skin peeling, and the subsequent possibility of a paradoxical overcolonization of hands after surgical preparation with alcohol-based hand rub.

Evaluation of insulin-induced changes in the renal response to furosemide in normal subjects.

Over the last years, a large mass of information has accumulated indicating that changes in the serum insulin concentration can affect renal electrolyte excretion. We analyzed the response of the kidney to furosemide in 5 healthy men, in the presence of both normal physiological serum insulin levels and levels at the upper limit of the physiological range, obtained by the hyperinsulinemic-euglycemic clamp technique. After furosemide administration, glomerular filtration rate, urine flow, urine sodium excretion, free water clearance, urine pH, plasma renin activity and plasma aldosterone exhibited the same behavior in the presence of both serum insulin concentrations. The rise in urinary potassium excretion following furosemide administration was significantly lower in the presence of high insulin concentrations. Although we observed a slight decrease in plasma potassium levels during the equilibration phase of the clamp required before the administration of furosemide, a significantly lower increase in potassium fractional excretion indicated a direct tubular effect of insulin. Thus, in conditions in which natriuresis is mildly stimulated, as in the case of the administration of low doses of furosemide, insulin does not affect the rate of renal sodium reabsorption. Conversely, the hormone has an appreciable influence on the modulation of tubular potassium exchanges.

[Insulinemia and intraerythrocytic sodium in normotensive normal-weight subjects with and without a family history for essential arterial hypertension]. / Insulinemia e sodio intraeritrocitario in soggetti normotesi normopeso con e senza familiarità per ipertensione arteriosa essenziale.

To investigate whether the hyperinsulinemia observed in essential hypertensive subjects anticipates the onset of hypertension, and if it may play a role in predisposing to hypertension, we examined the relationships between fasting insulinemia (F.IRI), C-peptide (C-pep), and some known predictive factors of essential hypertension (EH), such as prehypertensive blood pressure, erythrocyte sodium concentration (ESC) and family history of hypertension. Sixty-two normotensive, lean, euglycemic subjects with no family history of diabetes were subdivided in 2 groups: 32 subjects without (F-) and 30 with (F+) family history of EH (at least one parent). The groups were matched for age, sex and body mass index. Systolic (SBP) and diastolic (DBP) blood pressures (p < 0.01 and p < 0.025, respectively), F.IRI (p < 0.0005), C-pep (p < 0.005), and ESC (p < 0.025) were significantly higher, and glucose/insulin ratio (p < 0.0005) lower in F+ than in F-. SBP (r = 0.43, p < 0.001) and DBP (r = 0.415, p < 0.001) were directly correlated to F.IRI and C-pep (respectively r = 0.418, p < 0.001 and r = 0.368, p < 0.01). A direct correlation was also found between mean blood pressure and ESC (r = 0.297, p < 0.05) and between ESC and F.IRI (r = 0.320, p < 0.05). In a separate analysis on the 2 subgroups F+ and F-, the above mentioned parameters were still correlated in the group with but not in the group without family history of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum insulin, insulin sensitivity, and erythrocyte sodium metabolism in normotensive and essential hypertensive subjects with and without overweight.

Increased insulin circulating levels and perturbations of intracellular sodium metabolism have been reported in essential hypertensive patients, leading to postulate their involvement in the pathophysiology of the disease. In-vitro studies have shown that insulin modulates the activity of some transmembrane sodium transporters. The aim of this investigation was to assess in subjects with essential hypertension and/or overweight, the levels of fasting serum insulin, the activity of sodium transporters and their possible relationships. In 18 lean normotensive, 12 overweight normotensive, 18 untreated lean essential hypertensive, and 16 untreated overweight essential hypertensive subjects, we measured the fasting levels of blood glucose and serum insulin, and calculated the glucose/insulin ratio as an index of sensitivity to insulin. In addition, in the red blood cells of these subjects, we evaluated the maximal rate of ouabain-sensitive Na/K pump, furosemide-sensitive outward Na/K cotransport, Nai/Lio countertransport, and the constant rate of passive permeability to Na. When compared to lean normotensive, overweight normotensive, lean hypertensive, and overweight hypertensive subjects exhibited significantly higher fasting insulin levels, with lower glucose/insulin ratio. No significant difference was found in the activity of Na/K pump, Na/K cotransport, and passive permeability to Na. The Nai/Lio exchange was significantly increased in both hypertensive groups. Mean blood pressure correlated positively and independently with body mass index and fasting insulinemia, and inversely with the glucose/insulin ratio. No relationships were found between blood pressure, fasting insulin levels or glucose/insulin ratio and the activity of sodium transport systems. We conclude that hyperinsulinemia and insulin resistance are associated with essential hypertension independently of overweight. These data lend support to the hypothesis that insulin is involved, concurrently with other factors, in the pathogenesis of essential hypertension in both lean and obese subjects.

In vitro action of insulin on erythrocyte sodium transport mechanisms: its possible role in the pathogenesis of arterial hypertension.

The effects of insulin on sodium and potassium metabolism have been well known for many years; clinical observation and laboratory experience showed different results about the insulin effect on the sodium-potassium pump. Moreover, studies about the insulin effect on the sodium-potassium cotransport are not available. Therefore, the effects of insulin on Na+,K+ pump and Na+,K+ cotransport were evaluated. Results show that insulin inhibits Na+,K+ pump, while Na+,K+ cotransport is markedly activated. The possible link between pathogenesis of arterial hypertension in hyperinsulinemic subjects and present data is examined.

Evidence for a direct and non-receptor-mediated action of 5HT2 antagonists on transmembrane cation transport systems.

Changes in transmembrane sodium fluxes have been reported in normotensive and in hypertensive subjects after ketanserin administration. In this study, the effects of the serotonergic system on transmembrane sodium transport mechanisms have been investigated in vitro. In erythrocytes drawn from ten healthy subjects, we studied the effects of serotonin (5HT) on the Na/K pump, Na/K cotransport, Na/Li countertransport, and passive permeability of Na. No significant changes were found. A direct, non-receptor-mediated action of ketanserin was then suspected, and the effects of two concentrations of ketanserin (5 x 10(-8) and 5 x 10(-7) M) were evaluated in erythrocytes from 12 normal volunteers. Both concentrations of ketanserin significantly decreased the activity of the Na/K pump and increased the activity of Na/Li countertransport. Na/K cotransport and passive permeability were not affected. Indirect evidence of the action of ketanserin on sodium transmembrane fluxes came from other experiments. In the red blood cells taken from five normal subjects and incubated for 2 hours in a plasma pool, we evaluated the changes in intracellular sodium concentration induced by the presence of 5HT or ketanserin. A significant decrease in intracellular sodium concentration occurred only with ketanserin. This study indicates that ketanserin has a direct influence on transmembrane sodium fluxes. If this action were also present in other cells, it might contribute to the actions of the drug at vascular, nervous, and renal tubular levels.

Effects of ketanserin on transmembrane sodium transport in erythrocytes.

Ketanserin, an antagonist of 5-HT2-serotonergic and alpha 1-adrenergic receptors, has come into use for the therapy of mild to moderate arterial hypertension. Quite recent observations have shown changes in transmembrane sodium (Na) transport after the acute administration of high doses of this drug to normal subjects. It is well known that some of these transport systems have an altered activity in essential hypertension. We evaluated the effects of long-term (3 months) administration of ketanserin (40-80 mg/day) on Na and potassium (K) intracellular concentrations and transmembrane fluxes in red blood cells (RBCs) from 12 essential hypertensive patients. In addition the present study describes the in vitro effects of two different concentrations of the drug (5 x 10(-8) and 5 x 10(-7) M) on erythrocytes in normal subjects. In the first study, both systolic and diastolic blood pressure were significantly lowered by the treatment with ketanserin (from 165/103 to 143/89; p less than 0.001). Na and K intraerythrocyte concentrations fell markedly during ketanserin administration (both p less than 0.001). A marked decrease in Na,K-pump activity (p less than 0.001) and an increase in Na,lithium(Li)-countertransport function (p less than 0.001) were observed. Na outward cotransport, Na leak, and K leak were not modified by the therapy. Direct correlation was found between the fall in mean blood pressure and in Na and K intraerythrocyte concentration (respectively, p less than 0.01 and p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)