[Confusional states of epileptic nature with onset at menopause. Clinical studies of a case].
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Biomedical subjects
F Franchi
Publications and source records attributed to F Franchi.
Ocular toxicity of systemic chemotherapy with megadoses of carmustine and mitomycin.
The use of chemotherapeutic agents in high doses in the treatment of advanced-stage cancer enhances drug toxicity, and ocular complications are not uncommon. In this article, we discuss the ocular toxicity in six patients with advanced nonpretreated colorectal cancer who received megadoses of carmustine and mitomycin with the support of autologous bone marrow transplantation. The results obtained did not reveal any subjective or objective pathologic conditions of the ocular apparatus with particular attention to orthoptic examinations, the anterior segment, and the fundus. No patient had changes in visual acuity. Tonometry did not demonstrate significant variations. There were, however, qualitative and quantitative changes in the tear films of all patients, leading to damage to the corneal and conjunctival epithelium.
Antineoplastic Combined Chemotherapy Protocols↗
[Brain natriuretic peptide].
Brain natriuretic peptide (BNP) is a cardiac hormone with a spectrum of activities quite similar to those of atrial natriuretic peptide (ANP), including diuretic, natriuretic, hypotensive and smooth muscle relaxant activities. These effects are due to the stimulation of guanylate cyclase-linked natriuretic peptide receptors, leading to an increase in cyclic GMP concentration in target cells. BNP has a lower affinity than ANP for C (clearance) receptors, and is less susceptible to degradation by neutral endopeptidase-24.11, resulting in a longer half-life. In the kidney, BNP increases the glomerular filtration rate and inhibits sodium reabsorption in the distal tubule. It also inhibits the release of renin and aldosterone. Unlike ANP, produced by the atria, BNP is mainly synthesized and released into circulation by the left ventricle and is therefore influenced by stimuli involving this cardiac chamber, such as an increase in arterial pressure, left ventricular hypertrophy and dilation. Plasma BNP levels are very low in healthy subjects, and respond modestly, although significantly to physiological stimuli such as changes in posture or sodium intake. In contrast, plasma BNP concentrations increase in disease states such as cirrhosis with ascites, hypertension, chronic renal failure, acute myocardial infarction and congestive heart failure. In the latter condition, plasma BNP concentration is a reliable prognostic index. Evidence obtained by administering BNP to healthy subjects and hypertensive patients suggests that BNP, at physiological and pathophysiological plasma concentrations, markedly influences cardiovascular homeostasis, mainly due to its effects on sodium excretion and the renin-aldosterone axis.
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