Frontal Behavioural Inventory in the differential diagnosis of dementia.

OBJECTIVE: To evaluate diagnostic properties of the Frontal Behavioural Inventory (FBI) in patients suffering from different forms of dementia. METHODS: The FBI was administered with other psychometric tests investigating cognitive performances and behavioral scales to the caregivers of 35 patients with the frontal variant of frontotemporal dementia (fv-FTD), 22 patients with Alzheimer's disease (AD) and 15 with vascular dementia (VaD). All patients were comparable for degree of dementia severity and level of executive impairment. RESULTS: The FBI showed high concurrent validity, internal consistency and good inter-rater and test-retest reliability. The discriminant validity was also very high. A new FBI cut-off score of 23 gave 97% sensitivity and 95% specificity in distinguishing fv-FTD from non-FTD patients. Conversely, the Neuropsychiatic Inventory (NPI) score was unable to differentiate fv-FTD from AD. CONCLUSIONS: The FBI is a neurobehavioral tool suitable to distinguish fv-FTD from other forms of dementia also when data from cognitive testing or other behavioral scales fail to support the differential diagnosis.

The management of psychogeriatric patient.

The exponential growth in the prevalence of cognitive impairment of old patients leads the physicians to deal with a larger incidence of behavioral disorders (such as excitement,aggressiveness), and psychotic symptoms (such as delirium and visual hallucinations). The presence of psychotic troubles in dementia causes a remarkable distress to caregivers and involves higher difficulties in the patient management. The estimates of such troubles range between 15 and 75 %. Geriatric assessment and the management of behavioral troubles require a prompt evaluation of all their possible causes. As a matter of fact, their appearance often reveals a physical disturbance (pain, fever, etc.), or adverse environmental conditions, or it could also be a consequence of a multiple drug therapy. For this reason,the use of antipsychotics should always be preceded by an accurate clinical diagnosis.Anxiolytic, anti-depressive, anti-convulsive and anti-psychotic drugs are among the therapeutic strategies for the management of the psychogeriatric patient. Atypical antipsychotics seem to be able to decrease the psychotic symptoms, with low levels of therapeutic failure. They also reduce extrapyramidal effects and the growth of prolactine hormone, which is quite useful when dealing with very old patients. Risperidone and olanzapine are two atypical anti-psychotics, which already proved to be adequate and well tolerated during the treatment of schizophrenia and of acute maniacal disorders. Our experience, with a population of patients followed by our Alzheimer Evaluation Unit (AEU), confirms that a low dose of olanzapine (5mg/day) and risperidone (0.5-1.0 mg/day) are effective in lowering behavioral disturbances, and psychotic symptoms due to dementia. Even in the long run,low doses of these drugs are still well tolerated. Higher levels of risperidone (> 1 mg/die)often caused extra-pyramidal symptoms such as rigidity and dyskinesia, whereas higher levels of olanzapine (> 5 mg/day) lead to an exceeding sedation. The management of behavioral disturbances is one of the most important goals in the global treatment of patients affected by dementia, to the extent of improving the quality of life. Atypical antipsychotics are preferable compared to old-generation drugs, therefore, they are the key therapeutic strategy we cannot renounce.

[Association of visceral Leishmaniosis and pulmonary tuberculosis: description of a patient] / Associazione di Leishmaniosi viscerale e tubercolosi polmonare: descrizione di un caso clinico.

Leishmaniosis, whether localised or disseminated, is mainly correlated to cell-mediated immunodeficiency. Immunodeficient patients are also particularly prone to diseases due to Mycobacterium tuberculosis, in whom either the disseminated form or a localisation of the lungs prevails. We report a rather uncommon association of both pathologies successufully treated with N-methylglucamine antimonium followed by an association of rifampycin, isoniazid and ethambutol. The ethiopathogenetic mechanisms, are described.

Abnormalities of sodium handling and of cardiovascular adaptations during high salt diet in patients with mild heart failure.

BACKGROUND: Sodium retention and hormonal activation are fundamental hallmarks in congestive heart failure. The present study was designed to assess the ability of patients with asymptomatic to mildly symptomatic heart failure and no signs or symptoms of congestion to excrete ingested sodium and to identify possible early abnormalities of hormonal and hemodynamic mechanisms related to sodium handling. METHODS AND RESULTS: The effects of a high salt diet (250 mEq/day for 6 days) on hemodynamics, salt-regulating hormones, and renal excretory response were investigated in a balanced study in 12 untreated patients with idiopathic or ischemic dilated cardiomyopathy and mild heart failure (NYHA class I-II, ejection fraction < 50%) (HF) and in 12 normal subjects, who had been previously maintained a 100 mEq/day NaCl diet. In normal subjects, high salt diet was associated with significant increases of echocardiographically measured left ventricular end-diastolic volume, ejection fraction, and stroke volume (all P < .001) and with a reduction of total peripheral resistance (P < .001). In addition, plasma atrial natriuretic factor (ANF) levels increased (P < .05), and plasma renin activity and aldosterone concentrations fell (both P < .001) in normals in response to salt excess. In HF patients, both left ventricular end-diastolic and end-systolic volumes increased in response to high salt diet, whereas ejection fraction and stroke volume failed to increase, and total peripheral resistance did not change during high salt diet. In addition, plasma ANF levels did not rise in HF in response to salt loading, whereas plasma renin activity and aldosterone concentrations were as much suppressed as in normals. Although urinary sodium excretions were not significantly different in the two groups, there was a small but systematic reduction of daily sodium excretion in HF, which resulted in a significantly higher cumulative sodium balance in HF than in normals during the high salt diet period (P < .001). CONCLUSIONS: These results show a reduced ability to excrete a sodium load and early abnormalities of cardiac and hemodynamic adaptations to salt excess in patients with mild heart failure and no signs or symptoms of congestion.

[Dose-response study of bunazosin in the treatment of light-to-moderate arterial hypertension]. / Studio dose-risposta sulla bunazosina nel trattamento dell'ipertensione arteriosa lieve-moderata.

INTRODUCTION: The antagonists of alpha-adrenergic receptors were introduced in the therapy of arterial hypertension in 1950, but have had limited use due to the poor efficacy and safety of some drugs belonging to this pharmacological class. A recent molecule from this class, bunazosin, is a highly selective alpha 1-antagonist, whose long half-life allows a single daily administration. The aim of this study was to identify the minimum effective dose of bunazosin in the treatment of mild-moderate arterial hypertension. MATERIALS AND METHODS: Patients of both sexes, aged over eighteen years, suffering from mild/moderate essential arterial hypertension were admitted to the study. The experimental design was controlled between patients; and the study was carried out in accordance with the principles of Helsinki anf Tokyo. Dosage was of 3 and 6 mg/day per os; after 2 weeks' treatment, if DBP in clinostatism > or = 95 mmHg, the dose was doubled. Treatment lasted four weeks. RESULTS: At the end of treatment, in the group of patients initially treated with 3 mg/day, SBP, in clinostatism fell by 10.0% and DBP by 8.4% (p < 0.01 between times); in the group of patients initially treated with 6 mg/day, the reductions were of 9.2% and 6.5% respectively (p < 0.01 between times). Heart rate, electrocardiograph traces and laboratory parameters showed no clinically significant modifications. The safety profile of the treatment was excellent in 80% of the patients treated overall. DISCUSSION: This study allowed the minimum effective dose of bunazosin, equal to 3-6 mg/day, to be identified, as well as confirming the antihypertensive efficacy of the drug and its ample safety margin. In fact, this range of daily dosage led to a fall in pressure values, without causing clinically significant alterations of heart rate, electrocardiograph traces and laboratory parameters. CONCLUSIONS: In conclusions, in mild/moderate arterial hypertension, bunazosin in monotherapy at the dosage of 3-6 mg/day, is an effective and safe treatment.

Insulin reduces reflex forearm sympathetic vasoconstriction in healthy humans.

Previous in vitro studies indicate that insulin modifies vascular reactivity to different agents. We have previously demonstrated that in normotensive humans physiological hyperinsulinemia is associated with an increase of forearm norepinephrine release but does not modify vascular resistance. To explore whether insulin modulates peripheral vasoconstriction induced by reflex sympathetic activation, we studied its effects on forearm hemodynamics (strain-gauge plethysmography) during graded levels of lower body negative pressure (-5, -10, -15, and -20 mm Hg, each for 5 minutes) in normotensive subjects. For this purpose, eight subjects received an intrabrachial artery infusion of regular insulin at a systemically ineffective rate (0.05 milliunits/kg per minute) so that deep-venous insulin levels increased in the experimental forearm from 16.5 +/- 2.9 to 379.6 +/- 30 pmol/L (p < 0.01), whereas arterial insulin levels remained unchanged (from 40.9 +/- 8.6 to 43.1 +/- 7.9 pmol/L, NS). In the control arm, forearm vascular resistance (units) increased from 52.3 +/- 3 to a peak of 78.4 +/- 5 (p < 0.001) during lower body negative pressure. In the insulin-exposed forearm, vascular resistance (46.4 +/- 2 at baseline) remained unchanged during insulin infusion (45.8 +/- 3, NS) and rose to a peak of 54.8 +/- 6 (p < 0.05) during lower body negative pressure. The response of forearm vascular resistance to lower body negative pressure was different in the two forearms (F = 4.506, p < 0.01, repeated-measures analysis of variance with grouping factor). Our results demonstrate that in normotensive subjects local physiological hyperinsulinemia reduces the forearm vasoconstrictive response to reflex sympathetic activation.

Effects of the single and repeated administration of benazepril on systemic and forearm circulation and cardiac function in hypertensive patients.

The hemodynamic and cardiac effects of the new angiotensin-converting enzyme inhibitor, benazepril, were studied in 28 hypertensives in a double blind, placebo-controlled, between-patient study. Hemodynamic studies were performed noninvasively by means of M-mode echo (central hemodynamics and left ventricular systolic function), 2-D echo-Doppler (left ventricular diastolic function), and pulsed Doppler flowmetry (forearm circulation). Examinations were done at the end of a placebo run-in period and 3 hours after benazepril administration, both on the first day and after 6 weeks of treatment (10 or 20 mg once daily, according to patient response). In comparison with placebo, benazepril reduced systolic (p = 0.04) and diastolic (p = 0.003) blood pressure, because of a significant reduction in systemic vascular resistance (p = 0.03), while cardiac output was unchanged. Forearm vascular resistance was reduced and brachial artery compliance increased, although not to a statistically significant level (both p = 0.07). Both systolic and diastolic left ventricular function were positively influenced by the afterload reduction: End-systolic stress was reduced by 12% (p = 0.07), as was the late diastolic peak flow velocity (p = 0.02). All hemodynamic changes were evident after acute benazepril administration, and no differences was observed between acute and repeated treatment. We conclude that, similar to other ACE-inhibitors, benazepril reduces blood pressure through a reduction in vascular resistance, while cardiac output and heart rate are unaffected. These hemodynamic effects occur as early as after the first administration and exert a favorable influence on left ventricular dynamics.

Reversal of cardiac and large artery structural abnormalities induced by long-term antihypertensive treatment with trandolapril.

In 15 patients with untreated mild to moderate essential hypertension and left ventricular hypertrophy, we assessed blood pressure, echocardiographic left ventricular mass index, brachial artery compliance (pulsed doppler flowmetry), and calculated forearm vascular resistance (strain gauge plethysmography) before, during (6 and 12 months) and after (1 month washout period) 1 year of satisfactory (blood pressure < or = 140/90 mm Hg) antihypertensive therapy with the angiotensin-converting enzyme inhibitor trandolapril (2.0 mg orally once daily). During the antihypertensive effective treatment, we observed a significant reduction of systolic and diastolic blood pressures, left ventricular mass index, and forearm vascular resistance at both 6 and 12 months. In addition, brachial artery compliance was significantly increased. After washout, systolic (156 +/- 3 mm Hg) and diastolic (102 +/- 1 mm Hg) blood pressures returned to levels comparable to baseline. However, left ventricular mass index (132 +/- 4; p < 0.01) and brachial artery compliance (1.53 +/- 0.01; p < 0.01) were still different from baseline. These results demonstrate that chronic antihypertensive treatment with trandolapril is associated with a stable regression of cardiac and vascular abnormalities, which is partially unrelated to the blood pressure lowering effect.

Prevalence of peripheral arterial disease and related risk factors in elderly institutionalized subjects.

Blood pressure was measured at the posterior tibial artery by Doppler ultrasonography in 124 elderly subjects (37 men and 87 women) living in two retirement homes in Naples (Italy). Ankle-to-arm systolic pressure ratios below 0.97 and 0.90 was considered as a probable and definite pathological sign of peripheral arterial disease, respectively. Half of the subjects (48% of men and 51% of women) gave a value below 0.97, while a third (35% of men and 33% of women) had a value below 0.90. By multiple regression analysis, mean blood pressure, plasma cholesterol levels and cigarette smoking were all negatively correlated with ankle systolic pressure values with a progressively lower significance. Most of the patients with pathological Doppler examination were asymptomatic at a questionnaire for intermittent claudication.

Abnormal hormonal and renal responses to saline load in hypertensive patients with parental history of cardiovascular accidents.

BACKGROUND: Acute cardiac and cerebrovascular accidents are more frequent in hypertensive subjects with a family history of acute vascular accidents. The mechanisms underlying the susceptibility to vascular disease in these subjects are unknown. We investigated whether a parental history of premature heart attack or stroke in hypertensive subjects is associated with abnormalities of sodium handling. METHODS AND RESULTS: Patients with mild, uncomplicated essential hypertension were divided into two subgroups according to family history: a subgroup with a parental history of premature heart attack or stroke (FV+, n = 18) and a subgroup with a family history completely negative for vascular accidents (FV-, n = 14). The two subgroups were comparable with respect to age, weight, sex distribution, blood pressure, duration of hypertension, cardiovascular risk factors, renal function, and organ damage. Baseline plasma renin activity (PRA), concentrations of aldosterone (PA), atrial natriuretic factor (ANF), and norepinephrine, and urinary electrolyte excretion were also comparable in the two subgroups. Despite these similarities, the responses to an acute saline load, measured under controlled metabolic and experimental conditions, were different in the two subgroups. In the FV+ subgroup at 60 minutes of saline load, PRA fell by 1.0 +/- 0.2 ng/ml/hr and PA concentration by 89.4 +/- 26 pg/ml and ANF concentration increased by 38 +/- 9 pg/ml, whereas in the FV- subgroup the corresponding responses were -2.3 +/- 0.3 ng/ml/hr (p less than 0.005), -190 +/- 43 pg/ml (p less than 0.05), and 80 +/- 13 pg/ml (p less than 0.005), respectively. Urinary sodium excretion was delayed in the FV+ subgroup (270 +/- 67 mu eq/min at 60 minutes) compared with the FV- subgroup (555 +/- 157 mu eq/min at 60 minutes, p less than 0.05). At 120 minutes of saline load, significant (p less than 0.005) differences in PRA and ANF concentration were still observed. In a control group of eight normal subjects the responses to a saline load were comparable to those in the FV- subgroup but greater than those in the FV+ subgroup at 60 minutes. CONCLUSIONS: These results provide evidence that the hormonal and renal adjustments to an acute salt load are impaired in hypertensive patients with a parental history of vascular accidents. We speculate that abnormalities of sodium handling may represent markers of a more rapid development of vascular injury in human hypertension.

Converting enzyme inhibition prevents the effects of atrial natriuretic factor on baroreflex responses in humans.

The aim of this study was to assess the influence of atrial natriuretic factor (ANF) on arterial baroreflex chronotropic responses and to investigate whether this effect of ANF is affected by angiotensin converting enzyme inhibition (CEI). For this purpose, in 13 normal volunteers, the reflex chronotropic responses to arterial baroreceptor stimulation (phenylephrine, 25-100 micrograms i.v.) or deactivation (nitroglycerin, 25-100 micrograms i.v.) were evaluated in control conditions and during the steady-state phase of a sustained infusion of ANF (50 ng/kg/min) or placebo, before and during prolonged treatment with the converting enzyme inhibitor enalapril (20 mg p.o. for 5 days). ANF infusion, which raised plasma ANF levels from 48 +/- 19 to 1,765 +/- 203 pg/ml, was associated with a slight decrease in systemic blood pressure and no change in heart rate. In addition, it caused a significant increase of the regression slope obtained with phenylephrine (from 11.3 +/- 2 to 18.5 +/- 2 msec/mm Hg) and a significant reduction of slope of the nitroglycerin-produced regression line (from 9.3 +/- 1 to 5.6 +/- 0.6 msec/mm Hg). After sustained CEI, which raised plasma renin activity from 1.4 +/- 0.4 to 19.9 +/- 5 ng/ml/hr, ANF infusion induced an increase in plasma ANF levels and a reduction in blood pressure comparable to those observed in control conditions. During CEI, however, ANF infusion had no significant effect on the chronotropic baroreflex responses produced by phenylephrine or nitroglycerin. Chronotropic and pressor responses to cold exposure were unchanged after CEI and during ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood and plasma viscosity after acipimox treatment in hypertriglyceridemic patients.

Acipimox, a nicotinic acid analog, is known to reduce the plasma lipid concentration in hyperlipidemic patients. In a study to check whether the drug improved hemo-rheological parameters, 21 patients (17 M, 4 F) with asymptomatic hypertriglyceridemia were treated with acipimox (250 b.i.d.) for 30 days. Plasma lipid concentrations were measured before and after therapy, together with blood and plasma viscosity. Mean plasma cholesterol and triglyceride levels decreased from 234 +/- 51 (SD) mg/dl to 202 +/- 53 mg/dl (p less than 0.01) and from 515 +/- 231 mg/dl to 298 +/- 130 mg/dl (p less than 0.01) respectively. Blood viscosity decreased (p less than 0.05 and less than 0.01) (range of reduction 6-20%) at all shear rates examined (from 2.25 s-1 to 450 s-1); plasma viscosity was significantly reduced only at lower shear rates (2.25 and 4.50 s-1). Changes in blood and plasma viscosity after acipimox treatment were not related to changes in plasma triglycerides. Acipimox seems to act beneficially on hemo-rheological parameters, independently of its hypolipidemic effect and could be usefully prescribed to patients with clinical signs of arteriosclerosis.

Effect of oral mesoglycan on plasma lipoprotein concentration and on lipoprotein lipase activity in primary hyperlipoproteinemia.

Mesoglycan extracted from calf aorta was orally administered (96 mg/day) to 15 patients with primary hyperlipoproteinemia: 4 type IIA, 4 type IIB, 6 type IV and one type V. In the seven hypertriglyceridemic patients the drug after two months of treatment reduced total and VLDL-triglyceride from 701 mg/dl to 423 mg/dl (p less than 0.025) and from 562 mg/dl to 377 mg/dl (p less than 0.025) respectively and increased lipoprotein lipase activity from 19.7 mumol/l/min to 27.8 mumol/l/min (p less than 0.05). No change was observed in the group with type IIA-IIB hyperlipoproteinemia.

[Hemorrheological anomalies: an element of additional risk in arterial diseases]. / Le anomalie emoreologiche: elemento di rischio aggiuntivo nelle arteriopatie.

Arterial blood flow to different tissues and organs is influenced by blood viscosity. The main determinants of blood viscosity are hematocrit and plasma protein concentration. Venesection and consequent reduction of hematocrit are very useful in various pathological conditions. Plasma-exchange removes proteins in excess (such as LDL in familial hypercholesterolemia) from plasma and thereby improves plasma viscosity, erythrocyte deformability and blood flow to the body tissues.