[Efficacious changes in blood volume: interactions between circulation components and water-electrolyte metabolism].
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Blood Circulation↗
Biomedical subjects
S Vinci
Publications and source records attributed to S Vinci.
[The pathogenesis of arterial hypertension in diabetes mellitus and its role in nephropathy].
This paper synthesizes the pathogenic steps of arterial hypertension in diabetes mellitus: hyperosmolarity due to the hyperglycemia and increased sodic tubular reabsorption accounting for the expansion of the extracellular volume with hypervolemia; abnormalities of the ionic membrane pumps leading to abnormal intracellular calcium distribution, thereby inducing an increased vascular tone; atypical vasomotor reactivity to cathecolamines; modifications of the renin-angiotension-aldosterone system. The pathophysiological derangements by which hypertension could induce nephropathy are examined: the vasodilatation which can be detected from the onset of diabetes, may be a determinant in the transmission of systemic hypertension to the glomerular microcirculation with resulting enhancement of the hydrostatic transglomerular pressure gradient (i.c. the major factor producing glomerular injury), glomerular plasmatic flow and filtration rate. The nephron hyperfiltration increases the movement of plasmatic proteins across the glomerular capillary wall with subsequent mesangial hyperactivity and sclerosis. Antihypertensive treatment in diabetes follows general guidelines and it should be instituted even in the case of microhypertension being facilitated in this setting the appearance of microalbuminuria i.e. the starting point of nephropathy. Even if experimental studies are to favor ACE inhibitors as the first-line drugs for abating glomerular hypertension by mitigation of the direct effect of angiotensin II on the efferent arteriolar tone, clinical observations suggest that, regardless of type of treatment, the normalization of systemic arterial pressure, by reversing glomerular hypertension may be effective in preventing diabetic nephropathy.
Diabetes Complications↗
[Current approach in the prevention and treatment of diabetic nephropathy].
Diabetic renal microangiopathy accounts for enormous morbidity and mortality, particularly in patients who develop diabetes in childhood or early youth; in the last few years its pathogenesis has been therefore extensively studied, aiming to prevent renal complications or at least of slowing down its progression toward uremia. Though not always in accordance with theoretical expectations, the results of clinical trials have nevertheless widened our therapeutic possibilities; in fact, besides the attainment of an optimal metabolic control, other possible interventions include a careful correction of albeit minimal elevations in arterial pressure; the interference with intrarenal hemodynamic parameters; the correction of insulin-independent metabolic pathways, abnormally activated in the diabetic, such as non enzymatic glycation and polyol pathway; the treatment of endothelial and platelet alterations; the improvement of the rheologic properties of blood.
Blood Coagulation Disorders↗
[The physiopathologic bases of the neurotoxicity of phosphorus chelating agents containing soluble aluminum salts in patients with renal insufficiency].
To what extent can damage to the central and peripheral nervous systems be ascribed to chronic aluminum (Al) intoxication taken as a chelating agent for phosphorus, to limit hyperphosphatemia in uremic patients? Since Al is normally eliminated by the renal route, its accumulation in uremia has to be ascribed to a reduced or abolished renal clearance of the metal, which results in preferential toxicity for certain tissues, especially nervous tissue, which shows difficulty in eliminating Al, even after intake has been stopped. This review discusses, on the basis of toxicologic, experimental and clinical data, the possible pathogenic steps of Al neurotoxicity in uremia, considering: the damage to axonal transport in which Al intoxication tends to affect the components of the cytoskeleton, the polymerization phase of the alpha and beta tubulin constituents of neurotubules, and the normal translocation of neurofilaments from the perikaryon to more distal positions of the axon; the abnormalities in the brain pool of adrenergic, cholinergic and GABA neurotransmitters; the increase in permeability and changes in perm-selectivity of the blood-brain-barrier, with further loss of neurotransmitters and with acquisition, from the systemic circulation, of neurotransmitter-like substances such as hormones, monoamines and peptides, which may adversely modulate synaptic and membrane functions; the cerebral energy metabolism and particularly the hexokinase reaction, by Al replacement of the Mg-ion in the Mg-ATP complex, so that phosphorylation of glucose to G6P is blocked; the interaction of Al with calmodulin by displacement of the Ca-ion and subsequent formation of a stable Al-calmodulin complex with a cytotoxic effect due to the increase in the intracellular calcium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
Aluminum↗
Gallbladder duplication: MR cholangiography demonstration.
Gallbladder duplication is a rare anatomic malformation. We present a case of gallbladder duplication in a patient who underwent laparoscopic cholecystectomy in which breath-hold magnetic resonance cholangiography showed the biliary anomaly, allowing a correct preoperative differentiation of the specific type of duplication.
Aged↗
MR white lung sign: incidence and significance in pulmonary consolidations.
PURPOSE: The presence of a pulmonary consolidation with a signal intensity comparable with that of the static fluid on heavily T2-weighted MR images has been named the "MR white lung sign." This sign has been described in mucinous bronchioloalveolar carcinoma (BAC). Our purpose was to establish the frequency and significance of this sign in pulmonary consolidations of varied causes. METHOD: In this prospective study, 83 patients with pulmonary consolidation underwent MR examination between January and December 1999. Segmental or lobar consolidations were due to pneumonia without central obstruction (n = 22), pneumonitis with central obstruction (n = 21), cicatricial atelectasis (n = 8), passive atelectasis (n = 10), radiation pneumonitis (n = 8), mucinous BAC (n = 5), infarction (n = 3), bronchiolitis obliterans organizing pneumonia (n = 3), nonmucinous BAC (n = 2), and lymphoma (n = 1). The MR white lung sign was considered present when the signal intensity of a pulmonary consolidation was comparable with that of the static fluid on heavily T2-weighted images obtained with MR hydrography sequences. Interobserver agreement, sensitivity, and specificity of the white lung sign in diagnosing mucinous BAC were calculated. RESULTS: The MR white lung sign was present in 7 (8%) of 83 consolidations, including 5 (100%) of 5 cases of mucinous BAC and 2 (10%) of 21 cases of obstructive pneumonitis. The frequency of the white lung sign was 100% in mucinous BAC and 2.6% in consolidations due to other causes. The difference was statistically significant (p < 0.05). CONCLUSION: The white lung sign is an uncommon finding in pulmonary consolidations evaluated with heavily T2-weighted sequences. However, the sign is characteristic of mucinous BAC and adds specificity to the radiologic diagnosis.
Adenocarcinoma, Bronchiolo-Alveolar↗
Perineural spread in a case of sinonasal sarcoidosis: case report.
We report a case of sinonasal sarcoidosis with perineural spread along the trigeminal and vidian nerves in which primarily MR imaging but also CT allowed excellent visualization of this infiltration.
Biopsy↗
Treatment of biguanide-induced lactic acidosis: reproposal of the "physiological" approach and review of the literature.
We report a case of severe biguanide-induced lactic acidosis which did not respond to symptomatic alkali treatment via either intravenous bicarbonate infusion or bicarbonate-dialysis. We thus initiated a therapeutic strategy based on insulin and thiamine only in order to reactivate the pyruvate oxidative pathway, in which both drugs play important roles as cofactors. This original "physiological" approach proved effective, and further alkali administration was unnecessary. Our results prompted a review of the literature on the treatment of biguanide-induced lactic acidosis, a situation in which the absence of precise therapeutic rules can undoubtedly affect both the evolution and the prognosis of the syndrome.
Acidosis, Lactic↗