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Biomedical subjects

R Boeri

Publications and source records attributed to R Boeri.

16 recordsLinked to original sources
PubMed1989

[Well's syndrome with eosinophilic vasculitis, coronary aneurysms and myocardial infarction].

This report describes a 40-year-old man suffering from Well's syndrome (recurrent granulomatous dermatitis with eosinophilia) who presented an anterior myocardial infarction complicated by shock and 3rd degree A-V block. The patient died within 12 hours of admission to the hospital. At autopsy, both main coronary arteries showed proximal aneurysms occluded by thrombi. On light microscopy, the aneurysmatic coronary walls were infiltrated by numerous eosinophils, lymphocytes and plasma cells. Similar cellulitis, mainly perivascular, was found in kidneys and anterior mediastinum. Because the patient had been treated with large doses of diclofenac and piroxicam owing to painful arthralgias, the Authors discuss the possible allergic pathogenesis of the vasculitis.

Adult↗
PubMed1988

Immunohistochemical evaluation of a panel of monoclonal antibodies for the diagnosis of small cell lung cancer.

Monoclonal antibodies (mAbs) with a high sensitivity and specificity for small cell lung cancer (SCLC) may be of potential diagnostic and therapeutic use. We selected five different mAbs generated against SCLC cell lines and tested them on paraffin-embedded SCLC and non SCLC (NSCLC) clinical samples in a retrospective study using immunohistochemical techniques. The results showed that the contemporary use of mAbs that react with different antigens allowed all the examined SCLC to be detected indicating that this panel of mAbs was extremely sensitive. Analysis of the reactivity of these mAbs with NSCLC showed that 4 of the 5 antibodies reacted also with a few NSCLC. Using higher dilutions of these mAbs their specificity improved substantially. The 5 different mAbs presented marked heterogeneity of antigenic expression within and between SCLC. This panel of antibodies may be very useful in the diagnosis of SCLC whereas their application, in vivo, in therapeutic trials, is limited by the heterogeneity of antigenic expression.

Antibodies, Monoclonal↗
PubMed1987

Amiodarone induced phospholipidosis. Biochemical, morphological and functional changes in the lungs of rats chronically treated with amiodarone.

Amiodarone, an antiarrhythmic drug, causes pulmonary fibrosis in some patients during chronic treatment but the mechanism is unknown. We studied the effects of amiodarone on pulmonary biochemistry, morphology and function at doses of 25 and 50 mg/kg/12 hr given to rats by gavage for four weeks. Plasma and pulmonary phospholipids were significantly augmented, 13% and 88% respectively, in the group given amiodarone 50 mg/kg/12 hr compared to pair-fed controls. Typical phospholipidosis-like light and electron microscopic alterations were seen in the lung, their severity related to the extent of biochemical changes induced by amiodarone. Pulmonary function tests revealed mild but not significant changes in O2 and CO2 alveolar exchange efficiency and lung compliance (P-V curve) of treated animals in comparison to pair fed controls. Plasma average concentrations of amiodarone and its main metabolite, desethylamiodarone, after four weeks were 2.46 +/- 0.18 and 0.73 +/- 0.13 micrograms/ml, respectively, in the 50 mg/kg/12 hr group. In the same group amiodarone and desethylamiodarone concentrations in lung were 163 +/- 26 and 569 +/- 153 times higher than those in plasma. A highly significant correlation was found between amiodarone concentrations in plasma and lung and phospholipid content in the lung. A subgroup of animals received amiodarone 50 mg/kg/12 hr for 8 weeks. The pulmonary phospholipidosis-like lesions were similar to those observed after one month of treatment, no fibrosis was evident on light microscopic examination.

Amiodarone↗
PubMed1985

[An unusual cause of arterial and venous pulmonary hypertension].

A 49 year old woman with syphilis of recent onset was repeatedly admitted to the hospital on account of recurrent dyspnoea and hemoptysis. The symptoms and radiological signs indicated the presence of a "cardiac lung". The ECG disclosed right ventricular overload which was confirmed by echocardiography. The left heart was normal, not only on echocardiography but also on cardiac catheterization, which documented severe pulmonary hypertension, partly precapillary, partly postcapillary. The presence of chronic lung congestion in the absence of pathological findings pertaining to the left heart lead to the diagnosis of pulmonary venous occlusive disease. However, pulmonary angiography showed notable and widespread arterial amputations which are not present in this syndrome. Autopsy provided the correct diagnosis: sclerosing mediastinitis localized at the hilum with prevalent involvement of both arterial and venous pulmonary vessels.

Female↗