Arterial hypertension and cognitive deficit

Cognitive impairment and dementia are more and more common in the elderly. The first begins, it advances silently and it leads to dementia in few years. Arterial hypertension represents the most important cerebrovascular risk factor after age. In numerous studies an inverse relationship between blood pressure values and cognitive performance emerges: it is possible that arterial hypertension plays a role in the pathogenesis of cognitive decline. Even in asymptomatic subjects the magnetic resonance signs of cerebral damage accompany cognitive impairment development. Antihypertensive therapy influence on cognitive function represents a subject of actual interest. The most studied drugs are calcium antagonists and ACE-inhibitors; they seem to have a protective effect on cognitive impairment, with regard to diuretics and beta-blockers. It would be important to study hypertensive patients, above all young asymptomatic hypertensives, even about cognitive functions, to prevent and consider cognitive decline and effective organ damage

Arterial hypertension: a cause of cognitive impairment and of vascular dementia

Arterial hypertension is a well-documented modifiable risk factor for cerebrovascular disease and for both cerebral infarction and intracerebral hemorrhage. Recent studies indicate a relationship between high blood pressure in midlife and dementia in late life and suggest that arterial hypertension may represent a cause of vascular dementia (VaD). This paper has reviewed the main evidence of a link between arterial hypertension and vascular cognitive impairment or VaD. Brain lesions induced by hypertension, diagnostic procedures for early diagnosis of vascular cognitive impairment in at risk subjects and the need to include cognitive assessment in patient's general visits in hypertension units are discussed

Bioequivalence study of nicardipine solution versus nicardipine tablets

The bioequivalence of a solution (investigational product) and a tablet (reference product) formulation of the dihydropyridine-type derivative Ca2+ antagonist nicardipine were investigated by measuring plasma levels of the compound after single randomized administration of 20 mg of the two formulations. Drugs were given orally in a single dose to 24 healthy volunteers (12 males and 12 females) at the beginning of the experiment and after a two weeks wash-out. Nicardipine is available in oral and intravenous formulations, the second being used for the short-term treatment of hypertensive crises. Oral formulations of nicardipine most diffused include immediate release (20 or 30 mg, three times a day administration), sustained release (30 mg, 45 mg or 60 mg, twice a day administration) and modified release (80 mg, once a day administration) tablets. A nicardipine solution is available only in Spain, but no published studies on the kinetics of this formulation are available. In the last 15 years, the main efforts were aimed to develop sustained or controlled release formulations of nicardipine to improve patient compliance by reducing the number of doses required each day. However, the use of twice a day or once a day administration of Ca2+ antagonists should be not overemphasized in particular situations like those of possible risk of cerebrovascular and/or coronary steal effect primarily in the elderly. The oral formulation of nicardipine investigated with a bioequivalence range > 70% compared to nicardipine immediate release tablets may represent an additional resource for treating elderly patients with concomitant cerebrovascular or coronary heart disease

A case of medullary thyroid carcinoma, parathyroid focal hyperplasia and pancreatic neuroendocrine tumor without RET and MEN1 mutations

Description of a case with unexplained multiple primary tumors (medullary thyroid carcinoma, parathyroid focal hyperplasia and pancreatic neuroendocrine tumor) without RET and MEN1 mutation