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T Wiesendanger

Publications and source records attributed to T Wiesendanger.

At least 37 records · Page 2Linked to original sources
PubMed1985

[Chronic idiopathic eosinophilic pneumopathies. A study of 16 cases].

We report 16 cases of chronic idiopathic interstitial pneumonia (P.C.I.E.). P.C.I.E. has well defined clinical, radiological and biological characteristics which enable the eosinophilic pulmonary infiltrates to be recognised and the diagnosis to be confirmed without histological proof. The data from broncho-alveolar lavage (L.B.A.) show that besides the radiological infiltrates, there is a diffuse alveolar eosinophilia; sometimes confirming the pulmonary function results, which show a similar pattern to diffuse interstitial pneumonia (P.I.D.). The frequent association of asthma (50%) and extra-pulmonary signs (30%) may suggest a vasculitis or more particularly the Churg-Strauss syndrome, all the more so without a lung biopsy; however the evolution of the disease and the response to low dose steroid therapy is against the latter two being considered in the differential diagnosis. The prognosis for P.C.I.E. is good in the short and medium term; nevertheless during the period under observation (mean 6.3 years) steroid therapy could only be stopped in 3 out of 16 patients. The other patients were stable with a low dose of Cortisone. No patient with P.C.I.E. associated with asthma or hypergammaglobulinaemia or extra-pulmonary signs could be weaned from steroids. The authors advocate that the dose of steroids should be adjusted as low as possible to maintain an eosinophilia below 500/mm3.

Adult↗
PubMed1985

[Pneumopathy caused by hypersensitivity to isocyanates. Value and dangers of a realistic provocation test].

Organic isocyanates are responsible for bronchial pathology and in rare cases of hypersensitivity pneumonia. We present a new observation supported by a complete lung function assessment, histology of a transbronchial biopsy and a positive bronchial challenge test. The progress of the disorder was followed by repeated lung function measurements and bronchoalveolar lavage. The alveolar response at first showed an alveolar leukocytosis, then a mixed picture, finally becoming a pure lymphocytosis. The activity of the alveolar cells was assessed for T lymphocytes by cytofluorimetry, the presence of DRa like and LMR antigens and lastly for macrophages with Gallium scans. The inflammatory response was followed by analysing the proteins in the lavage liquid. The value of studying alveolar cell-activity and equally alveolar protein content is underlined in this study and reminds one of the character, sometimes unpredicted and dangerous, of challenge tests using isocyanates.

Bronchi↗
PubMed1984

[Amiodarone: a new etiology of diffuse interstitial pneumopathy? Apropos of 2 personal cases and 10 cases from the literature].

Diffuse Interstitial Pneumonia (PID) is probably, although rarely, a complication of Amiodarone therapy. We describe two new cases and review 19 from the recent literature. The first patient was a man treated solely with Amiodarone for three years (total dose 185 g). He presented clinically with a picture of PID with slight dyspnoea, weight loss of 4 kilos and a dry cough. There were pulmonary crackles on auscultation, diffuse reticulo-nodular shadows radiographically and compatible pulmonary function tests. Broncho-alveolar lavage (LBA) was lymphocytic (30%). Stopping Amiodarone without resorting to steroids led to the disappearance of the clinical signs within 15 days and the return to normal of the LBA and pulmonary radiograph within six months though the pulmonary function was unchanged. The second case was a 78 year old man treatment with Amiodarone for six months (total dose 20 g). He presents acutely with grade IV dyspnoea and low grade fever. There were pulmonary crackles on auscultation and a bilateral pulmonary infiltrate on the chest radiograph. The pulmonary function tests were compatible with PID showing a restrictive ventilatory defect, a reduced Carbon Monoxide transfer (single breath) and hypoxia. The diagnosis was confirmed by a transbronchial biopsy showing a parieto-alveolar infiltration with increased cellularity and collagen formation. The LBA was predominantly polymorphonuclear. Stopping the Amiodarone associated with steroid treatment produced a normal chest radiograph within six weeks, whilst moderate dyspnoea and less severe restrictive ventilatory defects persisted. The clinical, radiological, functional and histological features of our patients were comparable to those 19 cases reported in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

[Diffuse pulmonary carcinomatous lymphangitis. Study of respiratory function in 18 cases].

Respiratory function studies were carried out in 18 patients with diffuse and isolated pulmonary lymphangitis (LCP) diagnosed on radiological and cyto-histological grounds. Restrictive ventilatory defects were found in 17 out 18 cases CPT: 75,3% (DS = 5), CV: 56.7% (DS = 14,5). The Tiffeneau coefficient was less than 65% in 50% of cases but the DEM/CV was reduced in 77% of cases, evidence of the great frequency of airflow obstruction. The measure of the (formula; see text) was normal in 5 out of 17 cases, implying the absence of an alveolar neoplastic lesion or obliteration by arteritis or capillaritis in LCP. The alveolar-arterial oxygen gradient on hyperoxia was normal (less than 27 kPa) 14 times out of 18 and slightly increased in 4. Important hypoxaemia at rest was present 17 times out of 18; PaO2: 8 kPa (DS = 1). There was no patient with alveolar hyperventilation: PaCO2: 4.3 kPa (DS = 0.5). On exercise, hypoxaemia remained stable 4 times, improved 5 times and worsened 9 times. A pathophysiological interpretation was given for each disturbance of respiratory function. In conclusion, a characteristic respiratory function profile of LCP is proposed, with a restrictive ventilatory disturbance or moderate mixed picture, a DLCO/VA ratio generally normal, almost constant hypoxaemia at rest and improvement or worsening on exercise. CPT = Mean total lung capacity. CV = Mean vital capacity. DS = Standard deviation.

Aged↗
PubMed1982

[Perfusion and ventilation pulmonary scintigraphy in the diagnosis of the operability of primary bronchial cancers].

Ventilation scintigraphy using Munsch's technique with Xenon 133 combined with perfusion scintigraphy using 99m Tc albumin particles in microspheres are of considerable interest in the preoperative evaluation of bronchogenic carcinoma. Basing themselves on 95 cases, the authors discuss the manner in which the tumor affects ventilation and perfusion. In the 70 cases of matching ventilatory and perfusion scans, scintigraphy alone is not sufficient to demonstrate the exact perfusion obstruction mechanism. On the other hand, if there is a V/Q mismatch (21 cases) and if the perfusion defect is more extensive than the ventilation defect or the radiological opaque area, this normally implies a mediastinal extension of the tumor, and tends to make any carcinologically valid ablation highly risky. Comparison of the perfusion and ventilation scans with the radiological data and spirometric values showed that 9 patients presented with abnormal pulmonary radiographs outside the tumor areas. Six of these cases involved tuberculous sequelae. Forty-four of the ninety five patients (46.3%) showed normal ventilation and perfusion scans outside the tumor areas. Of the 91 patients undergoing spirometry, 39 suffered from ventilatory obstruction and pathological ventilation and perfusion scans and 18 presented with scintigraphic anomalies outside the tumor are a but did not suffer from ventilatory obstruction.

Adult↗