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Patients with end-stage renal disease treated by hemodialysis with bioincompatible membranes are exposed during the dialysis period to acute effects on lung microcirculation, which may result in pulmonary fibrosis and diffusion defects in long-standing dialysis. To investigate the occurrence of these possible chronic pulmonary alterations, we determined lung function in patients with chronic renal failure not undergoing hemodialysis and in patients who had been receiving regular hemodialysis both for short and long periods of time. Forty-three patients divided into three groups were studied: 17 patients before dialysis with a mean (SD) creatinine clearance of 14.1 (6.8) ml/min 11.73 m2, 10 patients receiving regular hemodialysis for a period of less than 12 months (mean 6.4 +/- 3.5 months), and 16 patients receiving regular hemodialysis for more than 5 years (mean 8.3 +/- 3.6 years). First-use bioincompatible cellulosic dialysis membranes were used in all the cases. The following parameters were recorded: forced vital capacity (FVC), forced expiratory volume in 1s (FEV1), total lung capacity (TLC), residual volume (RV), carbon monoxide transfer factor (TLCO), accessible lung volume (VA), carbon monoxide transfer factor/accessible lung volume (KCO- that is, TLCO/VA), and arterial blood gases. Patients receiving regular hemodialysis for more than 5 years showed significantly lower values of TLCO and KCO than patients before dialysis and patients receiving regular hemodialysis for less than 12 months. Seventy-five percent of patients on long-term hemodialysis had markedly reduced TLCO or KCO values (below 80% of the reference value) as compared with 17% of patients before dialysis and 10% of patients dialyzed for less than 12 months (P < 0.001). Differences among groups for the remaining parameters were not observed. In conclusion, patients undergoing long-term regular hemodialysis with a bioincompatible membrane showed a selective reduction in pulmonary diffusing capacity possibly due to chronic pulmonary fibrosis.

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Bronchomalacia in adults develops secondary to bronchial disease processes (chronic bronchitis, tuberculosis, neoplasm) or to lesions resulting from prolonged intubation, surgery, trauma, or lung transplantation. We report the case of an 84-year-old woman with no history of any of the aforementioned associations in whom we detected severe idiopathic bronchomalacia of the main left bronchus. The identified lesion caused recurrent pneumonias leading to death. We show images obtained by bronchoscopy, revealing the severity of the lesion and its functional repercussions.

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Lymphangioleiomyomatosis (LAM) is a rare lung disease that mainly affects women of childbearing age. Pulmonary disease that is indistinguishable from LAM appears in 1% of patients with tuberous sclerosis (TS). At present we can not say whether we are looking at an association of two rare diseases or at a single disease with different clinical profiles. To date, open lung biopsy has been required for definitive diagnosis. We report the case of a women with TS and LAM in whom a diagnosis of pulmonary involvement was based on clinical signs and high resolution computerized tomography of the chest.

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Pulmonary sequestration is a congenital malformation in which the pulmonary parenchyma is isolated from the rest of the lung and receives irrigation. Traditionally this malformation has been diagnosed by arteriography, but in recent years the usefulness of magnetic resonance, a technique that can probably substitute for arteriography on many occasions, has been emphasized. We report 3 cases of intralobar pulmonary sequestration diagnosed by magnetic resonance, a procedure that provided adequate presurgical assessment. The magnetic resonance images were later shown to be consistent with anatomical findings.

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UNLABELLED: Portable devices might be an alternative method to diagnose patients suspected for obstructive sleep apnea syndrome (OSAS). We have analized one hundred patients consecutively referred to our especialized out-patient clinic for sleep breathing disorders. We have used a previously validated portable device-Polygraphics CNS-which records thoracoabdominal movement, nasobuccal airflow, ECG, oxymetry, body position, and continuous positive airway pressure (CPAP). Sixty patients showed an apnea/hypopnea index (AHI) > 15. Seven patients showed an AHI > 10f plus symptoms suggestive of OSAS. Two patients had an AHI between 5-10 and very high suspicion for OSAS; a subsequent CPAP treatment showed the disappearance of respiratory events and an evident improvement in oxymetric records. Twenty two patients showed an AHI < 5. Nine patients could not be classified and other diagnostic method were deemed necessary. CONCLUSION: A previously validated cardiorrespiratory portable polygraphic device was useful in most cases for taking diagnostic decisions in OSAS.

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The toxic oil syndrome is a new multisystemic disease, caused by ingestion of adulterated olive oil; this oil had a part of rapeseed oil, which was denatured with aniline for industrial use, and then re-refined. It is estimated that 20,000 people were more or less affected, the mortality being 1.7%. There is no clear pathogenetic mechanism, but the most probable is the generation of free radicals, caused by anilides. The clinical picture began with fever, acute interstitial pneumonia, pruritus, exanthems, myalgias and eosinophilia. The main pathological findings were generalized endothelial lesions, septal oedema, mild inflammatory mononuclear infiltrates and hydropic degeneration of type I and II pneumocytes with desquamation of type I. The pneumonic syndrome had a favourable evolution, except in 5% of the patients who went into acute respiratory distress and suffered an important mortality. In 10% of the patients, a moderate hypoxaemia remained with normal chest film; in these cases, a transbronchial biopsy showed more severe endothelial lesions and, in some of these patients, it was possible to find clinical signs of pulmonary hypertension, which was moderate and did not improve with oxygen or vasoactive agents. The neurological symptomatology was progressive, leading to very severe muscular atrophy and, in some cases, to alveolar hypoventilation. The neuromyopathy, as the other clinical manifestations, improved slowly during the following months. A year after the onset, a pulmonary restriction with a low transfer factor of CO remained, and some patients had residual neuromyopathy and severe scleroderma-like lesions of the skin. (ABSTRACT TRUNCATED AT 250 WORDS)

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