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Biomedical subjects

N Konietzko

Publications and source records attributed to N Konietzko.

At least 19 recordsLinked to original sources
PubMed1992

BOOP in Europe.

Explore the source record for details and available documents.

Adult↗
PubMed1992

[The current role of thoracoplasty in treatment of chronic pleural empyema].

To demonstrate the indication for surgery, the preoperative and postoperative course, and to assess the influence of thoracoplasty on respiratory physiology, the data of patients subjected to thoracoplasty during the past 30 years at our hospital were evaluated. Final assessment was performed separately for patients with and without preceding pulmonary resection. In 21 cases there was an unspecific empyema of the pleura and in 6 cases a specific one; in 14 cases there was also a concomitant bronchopleural fistula. After a washing-out period of 92 days (24-283) and after surgery had been unsuccessful in 9 patients, standard thoracoplasty was performed, complemented by a "jalousie" ("Venetian blind") plasty after Heller. Postoperative lethality was 11.1%. 5 patients developed pleuro-cutaneous fistulas that healed by local treatment; in one patient, a small residual cavity remained that required an additional plasty for correction. In 94% of the patients who had been operated upon, scoliosis occurred convex to the thoracoplasty; this was more marked in patients in whom lung resection had been performed than in patients without resection. Restrictive ventilatory disorders were seen in the lung function of 55% of the patients, whereas mixed restrictive-obstructive disorders occurred in 45%. Ergospirometry resulted under load besides in an increased respiratory minute volume (AMV), in a proportionate dead space of the AMV which was significantly higher than preoperatively. Despite the considerable functional and aesthetic consequences resulting therefrom, thoracoplasty still has its justification in refractory pleura empyemas as an ultimate means of cleaning up.

Adenocarcinoma↗
PubMed1992

[Esophago-thoracic fistula after pneumonectomy and long-term main bronchus stump fistula].

A woman patient admitted for treatment, who had reached the age of 65 years, had a previous history of an open pulmonary tuberculosis in 1946 that had been treated at that time by means of collapsotherapy and phrenico-exeresis. Pleuropneumonectomy was performed in 1976 because of a residual cavity of a thoracic empyema. Since 1978 the patient suffered from a fistula of the bronchus treated by postural therapy without achieving a cure. In 1989 a fistula formed between oesophagus and pneumonectomy cavity. Clinically this was associated with an increasing reduction of performance and a suddenly ineffective postural drainage, resulting in triphasic and eventually fatal aspiration. Histology revealed a suppurative inflammation in the fistular channel and a slight superficial Candida colonisation of the pneumonectomy cavity, of the fistular channel and of adjacent mucous glands of the oesophagus. Formation of the fistula was probably due to a small traction diverticulum followed by perforation because of obstructed oesophageal passage due to scarified distortions.

Aged↗
PubMed1991

[Asbestos content in bronchoalveolar lavage fluid].

The concentration and size distribution of bronchoalveolar lavage (BAL) asbestos fibers (AF) longer than 2 microns was determined by analytical transmission electron microscopy (TEM). The concentration of asbestos bodies (AB) was measured by TEM and light microscopy (LM). The study group consisted of 110 patients. 27 patients had no occupational asbestos exposure, 44 patients had occupational exposure to asbestos but no asbestos related disease and 39 patients had asbestos related diseases, either asbestosis (n = 34) or malignant mesothelioma of the pleura (n = 5) following long time asbestos exposure at the working place. Occupational asbestos exposure was reflected by increased asbestos fiber concentration in the BAL samples. Mean fiber concentration and size was different between the groups, but the scatter was large.

Asbestos↗
PubMed1990

[Clinical and functional disorders in side effects of drugs on the lung].

Although, at 5% of all drug-related adverse reactions in the human organism, drug-associated injuries to the lungs are not very common, their consequences can be substantial: the disordering of the organ, often detected late, can lead to irreversible fibrosis. The detection of a drug-induced adverse reaction in the lungs is difficult on account of the usually complex situation presenting: specific pathological signs are lacking, the underlying disease being treated may itself mimic adverse drug reactions, and often several drugs or forms of treatment are being employed simultaneously, so that the causal drug is difficult to identify. In principle, a differentiation must be made between cytotoxic drugs that "follow" a dose-effect curve, and idiosyncratic, sporadic effects, together with dose that involve the lung via drug-induced erythematodes. In contrast, undesired adverse effects manifesting in the airways, pulmonary vessels, pleura or respiratory muscles are usually easier to diagnose and treat. In the daily application of potentially pulmotoxic drugs, the decisive point is monitoring by means of pulmonary function parameters, which may preceded clinical manifestation by weeks. In this manner, irreversible damage can be avoided.

Antineoplastic Agents↗
PubMed1990

[Procollagen-III-peptide in bronchoalveolar lavage fluid as an index of fibrosis in sarcoidosis and idiopathic lung fibrosis?].

In order to answer the question whether in sarcoidosis and idiopathic pulmonary fibrosis there is a relationship between the activity of alveolitis (T4/T8 ratio in sarcoidosis, number of granulocytes in idiopathic pulmonary fibrosis) and the activity of connective tissue formation (type III procollagen peptide in the BAL fluid) BAL was performed in 12 healthy subjects, 33 patients with type II sarcoidosis, and 26 patients with idiopathic pulmonary fibrosis. In the unconcentrated BAL fluid of the healthy subjects, P3P was not measurable. On the basis of the T4/T8 ratio and P3P in type II sarcoidosis, three groups of patients with possibly different risks of progression were found: 1) T4/T8 normal and P3P not or only mildly elevated, 2) T4/T8 elevated and P3P normal or only mildly elevated, 3) T4/T8 elevated and P3P greatly increased. In patients with idiopathic pulmonary fibrosis, the concentration of P3P correlated significantly with the number of granulocytes and the clinical activity parameters. On the basis of these results, we conclude that P3P levels in the BAL fluid, as a direct measure of connective tissue neogenesis, may be a valuable addition to cellular and immunocytological BAL findings.

Bronchoalveolar Lavage Fluid↗
PubMed1990

[Detection of the activation of alveolar lymphocytes in alveolar proteinosis].

In 7 patients with pulmonary alveolar proteinosis, differential cytology and lymphocyte subsets in BAL fluid were investigated. The study showed that pulmonary alveolar proteinosis is another disorder characterized by a lymphocytic alveolitis and activation of T-lymphocytes (expression of HLA-DR antigens and IL-2 receptors). Our data indicate that immunological mechanisms involving T-cell activation may contribute to be pathogenesis of pulmonary alveolar proteinosis.

Adult↗
PubMed1989

[Use of microcomputers in polysomnography].

Constantly falling prices and increasing power combine to make the personal computer an attractive alternative to established recording devices for use in polysomnography. Apart from its price advantage, digital recording of psychophysiological signals offers the possibility of selective display (compression and zooming to parts of special interest), and also semi-automatic evaluation. In order to be able to feed the data acquired in the sleep laboratory into the computer, an interface for signal matching, an analog/digital converter, and suitable software, are required. In order to reduce the wealth of data to the clinically relevant (and, in the last resort, also manageable) amount, preprocessing hardware, such as EEG filters, snore detectors, etc., are required. The system we recommend comprises individual hardware, modules for the pickup of physiological signals, and flexibly combinable software routines that permit adaptation to any future expansions of changing medical problems.

Humans↗
PubMed1988

Replacement therapy for alpha-1-protease inhibitor deficiency in PiZ subjects with chronic obstructive lung disease.

In a six-month multicenter feasibility and safety study, 20 patients, who all had a congenital deficiency of alpha-1-protease inhibitor (A1PI) of the PiZ phenotype accompanied by a chronic obstructive lung disease, were treated with human-plasma-derived A1PI. A weekly dose of 60 mg/kg, administered intravenously, was shown to be sufficient to maintain patient serum levels above the threshold limit of 35 percent, the serum level of healthy persons of the MZ phenotype. This is supposed to be the minimal effective level for protection against the elastolytic attack of the lung and, therefore, satisfies one of the most important criteria of feasibility of long-term replacement therapy. The global concentration in serum or bronchiolar lavage fluid A1PI including active and inactivated A1PI was measured immunologically by rate nephelometry and radial immunodiffusion. The functional activity of A1PI, expressed as free inhibitor activity against trypsin and leukocyte elastase, confirmed that the infused A1PI remained mostly in its active form in the circulation. Reported adverse reactions were moderate and did not require alteration to the schedule of the infusions and/or the dose and rate of administration. Antibodies to A1PI as measured by the Ouchterlony method did not develop. Laboratory and physical signs of possible hepatitis virus contamination were not observed. The long-term replacement therapy, therefore, appears to be safe.

Adult↗
PubMed1988

[Mucociliary transport and bronchial inflammation].

The system of mucociliary clearance has the important task to remove from the airways inhaled substances and locally formed secretions. Inborn disorders of the mucociliary transport are the result of ciliary dysfunction (primary ciliary dyskinesia) or of increased viscosity of the bronchial secretions (mucoviscidosis). By far more frequency however are acquired disturbances. Inflammation of the airways results nearly always in disorder of the mucociliary transport which in early stages is reversible. With morphologic lesions, the disturbance may become irreversible. Infectious inflammations, especially those by rhinoviruses and mycoplasma, are causing ciliostatic and ciliotoxic alterations which may disturb the mucociliary clearance up to one year following the infection. Noninfectious inflammation is at first accelerating the transport of mucus through the action of cells of the body itself, especially granulocytes and eosinophiles and mediators liberated from them. Probably, these are causing a cilioexcitation which is later followed by a long-lasting depression of the mucociliary transport caused by production of mucus with high viscosity. Therapeutic measures consist in an early anti-infectious treatment and in the stimulation of the frequency of ciliary beating by beta-adrenergic drugs.

Bronchi↗