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V Foresti

Publications and source records attributed to V Foresti.

At least 37 records · Page 2Linked to original sources
PubMed1990

Malignant pleural effusions: meaning of pleural-fluid pH determination.

In 36 patients with malignant pleural effusions, we determined the pH and the glucose concentration of the pleural fluid. Twenty-one of 36 patients (58.3%) had a low pH (less than 7.30) and 15 had a normal pH (greater than or equal to 7.30; 7.13 +/- 0.12 vs. 7.37 +/- 0.05; p less than 0.0005). The patients with low pH had significantly lower glucose concentrations than those with normal pH (2.7 +/- 1.4 vs. 6.3 +/- 2.9 mmol/l; p less than 0.0005). Twenty-one of 34 patients (61.7%) had a glucose concentration lower than a cut-off value of 4.4 mmol/l; of these, 17 (81%) had a low pH. The mean survival in the low-pH group was 4.8 +/- 4.4 months, whereas the mean survival in the normal-pH group was 5 +/- 8 months (p greater than 0.4). Twelve of 36 patients (33.3%) were treated with intrapleural Corynebacterium parvum (CBP) injections. Fourteen of 21 low-pH patients (66.6%) survived more than 2 months, and 4 of them are still alive. Six of 15 normal-pH patients (40%) survived more than 2 months, and 1 of them is still alive. Three of the 5 living patients were treated with CBP (2 in the low-pH group and 1 in the normal-pH groups). Our results confirm that pH and glucose concentrations in the pleural fluid of patients with malignant effusions are frequently low. However, the survival and the response to CBP pleurodesis in patients with low-pH malignant effusions are the same as those in patients with normal-pH malignant effusions.

Adolescent↗
PubMed1990

[EDTA-induced pseudothrombocytopenia].

EDTA-induced pseudothrombocytopenia is a laboratory artifact caused in vitro by platelet aggregation, due to IgG or IgM class antibodies reacting with antigenic binding site of the GP IIb glycoprotein. Pseudothrombocytopenia is rarely found (about 1% of platelets counts), but must be considered in the differential diagnosis of thrombocytopenia, since it could lead to useless investigations and therapies. We report three patients with pseudothrombocytopenia, one of whom underwent bone marrow biopsy and danazol treatment, before establishing the correct diagnosis. The absence of hemorrhagic manifestations with persisting low platelets counts led to a re-examination of peripheral blood smear and to the diagnosis of pseudothrombocytopenia. Therefore a morphological platelets evaluation and their count on citrate-anticoagulated blood must be performed in every patient under assessment for thrombocytopenia.

Aged↗
PubMed1989

Antithyroid antibodies during amiodarone treatment.

In 44 euthyroid and goitre-free patients, 23 treated with amiodarone (group A) and 21 treated with other antiarrhythmic drugs (group B), antimicrosomal antibodies and antithyroglobulin antibodies were determined before the beginning of treatment and after 7, 15, 30, 60, and 180 days. In group A, none of the patients had antithyroid antibodies before treatment. 1 of 15 patients (6.7%) had antimicrosomal antibodies (titre 1:100) on day 7 only, and 1 of 18 (5.5%) had antithyroglobulin antibodies (titre 1:80) on day 180. In group B. 1 of 21 patients (4.8%) had antimicrosomal antibodies (IgG class) at titre 1:400 before the beginning of treatment, which was negative on day 180, and 2 of 17 (11.8%) had antimicrosomal antibodies (titre 1:100) on day 60 only. None of these patients showed clinical and/or laboratory signs of hyper- or hypothyroidism. These data indicated that antithyroid antibodies rarely appear in amiodarone-treated patients and do not differ significantly from patients treated with other antiarrhythmic drugs. The role of autoimmunity and the meaning of antithyroid antibodies in the pathogenesis of amiodarone-induced thyroid dysfunction (mainly of hypothyroidism) in patients without pre-existent thyroid diseases is still unclear.

Aged↗
PubMed1989

[Transitory efficacy of potassium perchlorate in hypothyroidism caused by amiodarone].

We report a case of a patient with hypothyroidism due to amiodarone. The short-term administration (1 g/die for 10 days) of potassium perchlorate (KClO4) led to normalization of serum thyroid hormone concentrations and marked reduction of thyrotropic hormone. The reduction of KClO4 (400 mg/die) and its following withdrawal led to reappearance of hypothyroidism signs. No side-effects or toxic reactions occurred during KClO4 therapy. This anion competitively inhibits thyroid iodide transport, reducing intrathyroidal iodide content and removing thyroid hormone synthesis inhibition. We suggest KClO4 therapy when amiodarone-associated hypothyroidism impairs a pre-existent cardiac disease and when a quick restoration of euthyroidism is necessary. Nevertheless, we emphasize that its effect can be transitory in cases of short-term treatment or low doses.

Aged↗
PubMed1989

Angiotensin-converting enzyme as a possible marker for lung toxicity in amiodarone-treated patients.

Since it has been observed that in vitro amiodarone induces morphological alterations in endothelial cells similar to those observed in patients with lung toxicity and that the angiotensin-converting enzyme (ACE) seems to be a marker for perturbation of the alveolar-capillary membrane, serum ACE concentrations have been determined in 44 patients, 23 treated with amiodarone (group A) and 21 treated with other anti-arrhythmic drugs (group B), before the beginning of treatment and after 7, 15, 30, 60 and 180 days. Serum ACE concentrations in group A were lower than the basal values (15.8 +/- 5.9 mU/ml) on day 7 (12.7 +/- 4.5 mU/ml) and were higher on day 60 (17.9 +/- 3.8 mU/ml), then returned to basal values by day 180 (15.9 +/- 5.5 mU/ml), but none of the differences were statistically significant. In group B, serum ACE concentrations were significantly higher than basal values (15.2 +/- 4.0 versus 14.2 +/- 3.5 mU/ml, p less than 0.05) only on day 15. In group A serum ACE concentrations were significantly higher than in group B only on day 60 (17.9 +/- 3.8 versus 14.7 +/- 4.5 mU/ml, p less than 0.025). During the period of the study none of the patients showed any clinical or radiological signs of lung toxicity or reduction of lung diffusion capacity for carbon monoxide (DLCO). Serum ACE levels were normal even in three patients who developed pulmonary fibrosis and in four whose DLCO was reduced by more than 20% from the basal values after the study was completed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Hospital pseudo-infections caused by Mycobacterium gordonae].

Sputum specimens from 15 patients with respiratory disease were reported to have positive cultures for Mycobacterium gordonae, an organism generally considered to be non-pathogenic for man. None showed typical radiological changes for mycobacteriosis. Mycobacterium gordonae was also isolated from some components of the aerosol therapy instrument. Because aerosol therapy was used for 4 patients only, we were not able to establish whether the Mycobacterium gordonae was only a colonizer. We suggest that its isolation in culture must be evaluated in an adequate clinical context before concluding that it is pathogenic.

Aged↗
PubMed1989

[Anatomical study of the fibrosing action of Corynebacterium parvum in malignant pleural effusion].

Intrapleural injection of Corynebacterium parvum (CBP) has recently been used for the treatment of recurrent neoplastic pleural effusions and its mechanism of action has been suggested to be either a local fibrosis-stimulating effect or immunostimulation. The case is reported of a patient with pleuritis secondary to metastases of mammary carcinoma, treated with CBP plus methylprednisolone, who died five days after the treatment because of an acute myocardial infarction. The pathologic examination showed fibrinous pleuritis with an interconnecting network between the visceral and parietal pleura.

Breast Neoplasms↗
PubMed1989

[Is malignant mesothelioma of the pleura only an occupational disease?].

Ten cases of pleural malignant mesothelioma identified histologically at the Department of General Medicine in May 1983-June 1987, are examined in this paper. Occupational risk factors and clinical features are discussed. Only one patient (10%) was subjected to occupational risk of asbestos exposure (as a smith) while the other nine patients showed a negative anamnesis for direct or indirect asbestos exposure. However, one of these patients was a tram-driver. The patients' mean age was 69 years old. 7 patients were males. 7 patients were born in an industrialized urban environment, 3 were born in an agricultural environment: all had been living in Milan for many years. Pleural fluid cytology was only useful in the diagnosis of 2 cases. This study suggests that pleural malignant mesothelioma is a neoplasm which also affects people not exposed to asbestos at work and that its frequency is increasing. The most probable cause is environmental contamination by asbestos of urban industrialized areas. Thus, it is necessary to eliminate this mineral from all manufacturing processes in which asbestos is not indispensable.

Aged↗
PubMed1988

Primary hypothyroidism due to leukemic infiltration of the thyroid gland.

We describe a patient with acute B-lymphocyte lymphoblastic leukemia who developed laboratory changes (not detectable free thyroxine, TSH 66 microIU/ml) suggesting severe primary hypothyroidism. Histological examination at autopsy showed massive leukemic infiltration of the thyroid gland: the progressive reduction of thyroid hormone levels with concomitant increase in TSH levels observed over a three-month period from the onset of the hemopathy suggests a cause-effect relationship between leukemic infiltration of the thyroid gland and hypothyroidism.

Acute Disease↗
PubMed1988

[Hypertrophic cardiomyopathy mimicking clinical picture of Budd-Chiari syndrome].

A case of a patient with clinical picture of hepatosplenomegaly, portal hypertension, dilatation of hepatic veins and inferior vena cava, without venous thrombosis or other causes of obstruction of right-sided heart, is described. This picture is compatible with the Budd-Chiari syndrome. Echocardiography has shown a hypertrophic cardiomyopathy causing relevant dilatation of both atria and it has allowed us to exclude the presence of a constrictive pericarditis. The hypertrophic cardiomyopathy is first considered as a cardiac cause of cirrhosis mimicking the Budd-Chiari syndrome.

Aged↗
PubMed1988

[Budd-Chiari syndrome secondary to thrombosis of the inferior vena cava in myeloproliferative disease].

A case with abdominal pain, hepatosplenomegaly and ascites is reported. Ultrasonography and computed tomography showed a thrombus localized in the inferior vena cava at the confluence of the hepatic veins. The diagnosis of Budd-Chiari syndrome was made two years after clinical and laboratory findings appeared. The patient was affected by a Philadelphia-positive myeloproliferative disease that was the predisposing condition to the inferior vena cava thrombosis. We suggest that the diagnosis of Budd-Chiari syndrome must be considered in patients presenting conditions associated with thrombotic diathesis: so a suitable therapy can be started before an irreversible hepatic damage.

Aged↗