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G Vezzoli

Publications and source records attributed to G Vezzoli.

40 records · Page 3Linked to original sources
PubMedDate not supplied

[Diagnostic imaging of Budd-Chiari syndrome in adults and children].

Budd-Chiari syndrome is caused by the obstruction of the hepatic veins or of the inferior vena cava. It is characterized by the classic symptomatological triad: ascites, hepatomegaly, and abdominal pain. In 2/3 cases its etiology remains unknown. Budd-Chiari syndrome may be associated with polycythemia vera, neoplasms, chronic leukemia, congenital abnormalities, hypercoagulation conditions, pregnancy, oral contraceptives, and constrictive pericarditis. Even though its clinical diagnosis is difficult, radiology plays a decisive role with US, CT, MR imaging and, above all, angiography; the latter, together with liver biopsy, generally provides with an unquestionable diagnosis. Through the definition of stage of the disease, of level (intrahepatic, venous, caval, cardiac), of type (intrinsic or extrinsic), and degree of both obstruction and consequent development of collateral channels, radiology determines which patients should undergo a medical or a surgical treatment. In some case, percutaneous angioplasty can be performed. Four cases of Budd-Chiari syndrome, including two children, were investigated with US, CT, angiography, and liver biopsy; MR imaging was also employed in one case. The underlying cause was identified in 3 patients: constrictive pericarditis of probable congenital origin and web occlusion of the inferior vena cava near the right atrium in the 2 children; hepatic vein thrombosis due to essential thrombocythemia in the third case. In the fourth patient, thrombosis of the inferior vena cava and hepatic veins was unexplained. The diagnosis was established by means of liver biopsy and phlebography of the hepatic veins. Good diagnostic information was also supplied by non-invasive techniques, such as US, CT, and MR imaging.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Malignant lymphomas with thoracic localization. Problems of semeiology and radiological staging].

A series of 234 malignant lymphomas (121 Hodgkin lymphomas and 113 non-Hodgkin lymphomas) observed at the Brescia City Hospital between 1981 and 1987 has been reviewed. This paper is aimed at assessing: 1) in which sectors of the staging radiology is indicated; 2) which radiological techniques are needed for the staging of chest lymphomas; 3) which impact they have on the therapeutic program. All patients underwent chest X-ray, which was integrated by conventional tomography in 80% of cases. Only 76 patients underwent CT: 35 times for staging, and 69 times for restaging (overall figure: 104). The two techniques were compared: in untreated patients CT gave supplementary information in 19 out of 35 cases (54.3%). In 7 patients (20%) the findings were such as to determine a change in the previous staging; only in a case (2.8%) was the management affected; in treated patients CT proved to be superior to conventional radiology in 28 out of 69 cases (40.56%) and allowed the possibility of a recurrence (which was suggested by clinical and radiological findings) to be ruled out in 23 patients (33.3%). In our opinion, CT should not be used as a routine investigation in the staging of malignant thoracic lymphomas; on the contrary, it should be limited to selected cases, when a radical radiotherapy is to be performed, or when clinics and plain radiographs proved unable to assess the nature of a pathologic thoracic condition.

Adolescent↗
PubMedDate not supplied

Genotype-phenotype correlations in normotensive patients with primary renal tubular hypokalemic metabolic alkalosis.

Among the different forms of hereditary renal tubulopathies associated with hypokalemia, metabolic alkalosis and normotension, two main types of disorders have been identified: Gitelman disease, which appears to be a homogeneous post-Henle's loop disorder, and Bartter syndrome, a heterogeneous Henle loop disorder. A specific gene has been found responsible for Gitelman disease, encoding the thiazide-sensitive Na-Cl cotransporter (TSC) of the distal convoluted tubule. From a phenotypic point of view the characteristic findings of this disease are hypocalciuria, hypomagnesemia and tetanic crises appearing during childhood or later. Many subjects are asymptomatic. At least three different genes have been shown to be responsible for Bartter syndrome, characterized by mutations in the proteins encoding respectively the bumetanide-sensitive Na-K-2Cl cotransporter, the inwardly-rectifying renal potassium channel and a renal chloride channel, all protein transports located in the ascending limb of Henle's loop. Mutations in the first two transport proteins have been demonstrated in patients with the hypercalciuric forms of Bartter syndrome associated with nephrocalcinosis (respectively Bartter syndrome type I and II), who were often born after pregnancies complicated by polyhydramnios and premature delivery. Mutations in the gene encoding a renal chloride channel were recently recognized in patients with a Henle tubular defect not associated with nephrocalcinosis (Bartter syndrome type III). Most of the latter group of patients were normo-hypercalciuric and presented dehydration and life-threatening hypotension in the first year of life. However, these three genes do not explain all the patients with Bartter syndrome which unlike Gitelman disease, appears to be a very heterogeneous disorder. Clearance studies, especially if done during furosemide and/or hydrochlorothiazide administration, have been helpful in identifying the site of tubular involvement. Considering both phenotypic and genotypic data, we propose a clinical-pathophysiological and molecular approach to diagnose the different tubulopathies associated with hypokalemic metabolic alkalosis.

Alkalosis↗