Biomedical subjects

G Hoheisel

Publications and source records attributed to G Hoheisel.

At least 19 recordsLinked to original sources

PubMed2006

[Health significance of inhaled particles].

Particulates refer to particles, dust, dirt, soot and aerosol mists that has suspended in the surrounding air. They may consist of solids of various forms including fibres or liquids. Long term exposure to silicon dioxide containing dusts (crystalline silica: quartz, tridymite, cristobalite, coesite, stishovite) may cause pneumoconiosis in the form of acute or/either chronic silicosis. Asbestos refers to a divers family of crystalline hydrated fibrous siliates typically exhibiting a greater tha 3:1 length ot diameter ratio. It is subdivided into serpentine (Chrysotile) and amphibole (crocidolite, amosite, anthophyllite, tremolite, actinolite). Exposure to asbestos fibres may cause lung fibrosis and promote cancer of the lung or the pleura. Besides the induction of malignant diseases dust exposure may result in obstructive as well as restrictive lung diseases which may be compensate in case of the recognition as a occupational diseases. Other occupational exposures leading to pneumoconiosis are caused be talc, or metals including aluminium containing dusts. Also the group of man-made mineral (MMMFs) or vitreous fibres (MMVFs), including glass wool, rock wool, slag wool, glass filaments, microfibres, refractory ceramic fibres are bioactive under certain experimental conditions. Although it has been shown that MMMFs may cause malignancies when injected intraperitoneally in high quantities in rodents, inhalation trials and human studies could not reproduce these results in the same precision. Fine particles (particulate matter = PM) comprise one of the most widespread and harmful air pollutants in the industrialized world. PM may cause worsening of asthma and other respiratory diseases, reduce lung function development in children, potentially increased the risk of premature death in the elderly and enhance mortality from cardiac diseases. Because of the small size PM2.5 is seen to be even more hazardous than PM10.

Administration, Inhalation↗

PubMed2006

[Acute bronchitis: when are antibiotics, and when is symptomatic treatment indicated?].

Acute bronchitis is usually caused by a virus, while the chronic form is due to inhalative noxae (in most cases decades of cigarette smoking). Both varieties are diagnosed on a clinical basis. Treatment of acute bronchitis is symptomatic. A sore throat is treated locally, and a troublesome, in particular nocturnal, cough with antitussive agents applied for a limited period (14 days). If bronchial mucus is viscous and difficult to clear, short-term treatment with a secretolytic or mucolytic substance is justified. Management of chronic bronchitis consists primarily in the elimination of the noxae. Treatment with antibiotics (usually oral) makes good sense only when there is a bacteriological infection of the upper or lower airways in an acute stage, such as infection-driven exacerbation of chronic obstructive bronchitis (COPD).

Adult↗

PubMed2005

[Matrix metalloproteinases and their inhibitors in lung cancer with malignant pleural effusion].

UNLABELLED: Matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) play a crucial role in physiological and pathological matrix turnover. This study aimed to determine the occurrence of MMP and TIMP in lung cancer patients with malignant pleural effusions (CA). METHODS: MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, TIMP-1, and IMP-2 oncentrations were determined by ELISA and zymography in pleural effusions and plasma of 31 CA and 14 congestive heart failure (CHF) patients and in plasma of 18 healthy controls (CON). RESULTS: MMP-2, TIMP-1, and TIMP-2 ELISA-concentrations were increased in CA pleural fluid vs. CA plasma (p < 0.005, p < 0.005, p < 0.05), in contrast to MMP-9 being higher in plasma (p < 0.005). Pleural fluid MMP-1 and MMP-8 were increased in CA vs. CHF (p < 0.05, p < 0.005). MMP and TIMP plasma concentrations were not different in CA vs. CHF, but MMP-9, TIMP-1, and TIMP-2 were increased vs. CON (p < 0.005, each). Gelatine zymography MMP-9/MMP-2 ratios were increased in CA plasma vs. effusion fluid (p < 0.005), in CA vs. CHF plasma, CA vs. CHF effusions (p < 0.005 each), and in CA vs. CON plasma (p < 0.05). CONCLUSIONS: MMP-2, TIMP-1, and TIMP-2 accumulate in the pleural compartment in CA and CHF, probably reflecting an unspecific pleural reaction. MMP-1 and MMP-8 are increased in cellular rich CA pleural effusions only. The determination of MMP-9/MMP-2 ratios in pleural fluid may contribute to differentiate CHF from CA effusions.

Enzyme-Linked Immunosorbent Assay↗

PubMed2005

Vascular endothelial growth factor in pleural effusions of different origin.

This study aimed to determine the diagnostic relevance of vascular endothelial growth factor (VEGF) in the pleural fluid and serum of patients with pleural effusions of different aetiology. VEGF was quantified in the pleural effusion fluid and serum of 96 patients with malignancies (58 lung cancers (CA) and 38 tumours with secondaries to the lung (TM)), 45 with congestive heart failure (CHF), 28 with tuberculosis (TB), 45 with acute infections (INF), and in the serum of 20 healthy controls. VEGF pleural effusion concentrations were significantly different in the main diagnostic groups. VEGF was higher in effusions of patients with malignancies (CA as well as TM) in comparison with INF, TB or CHF. In serum, however, high VEGF concentrations indicated CA, TM or INF, but not TB or CHF. Despite significant differences of VEGF levels in different patient groups, receiver-operating characteristic analysis revealed insufficient diagnostic value of VEGF for differential diagnosis of pleural effusions. In conclusion, vascular endothelial growth factor serum concentration is highly suggestive of the presence of lung disease in general, except for tuberculosis. In effusion fluid, the presence of vascular endothelial growth factor clearly indicates inflammatory or malignant origin. However, for diagnostic use, additional parameters besides vascular endothelial growth factor are mandatory.

Adult↗

PubMed2004

[Pleuritis tuberculosa - therapeutic value of repeated chest tapping].

Tuberculous pleuritis tends to develop fibrosis to a high degree. The use of corticosteroids enhances the absorption of pleural effusions, the residual pleural thickening, however, remains unaffected. Whether repeated chest tapping in patients with persistent effusions in addition to antituberculous therapy favourably influences the outcome is not known. Therefore, patients with tuberculous pleuritis were examined in a prospective, randomized study. After confirmation of the diagnosis patients were randomized in group A with antituberculous treatment (Isoniazid, Rifampicin, Pyrazinamid, and Streptomycin) alone or in group B with additional pleural tapping for four weeks (phase I). In phase II patients in both groups with persistent effusions received oral prednisolone (0,75 mg/kg body weight) tapered over four weeks. The extent of pleural effusions was determined by chest X-ray. Roentgenological changes were evaluated at the end of the observation period. Lung function tests by spirometry were performed after two, four, eight weeks, and at the last follow up visit. At the end of phase I no pleural effusion could be observed roentgenologically in group A in 7 of 16 patients (44 %) and in group B in 10 of 16 patients (63 %) (p = n. s.). At the end of phase II extensive residual thickening was observed in one patient (group B) necessitating pleurectomy six months later. The lung function parameters demonstrated a restrictive pattern, which did not differ significantly at the end of the observation period. After a mean follow-up period of four months none or minimal residual changes could be observed radiologically in the remaining patients. In summary, despite the low number of patients examined, this study shows that in patients with tuberculous pleuritis repeated chest tapping in addition to antituberculous medication does not seem to benefit the patient, as neither the degree of residual pleural thickening nor the restrictive lung function impairment seem to be influenced significantly.

Adult↗

PubMed2004

[Immunohistochemical localization of matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) in tuberculous pleuritis].

Matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) have been found by ELISA and gelatine zymography in different concentrations in pleural fluid in tuberculous (TB) pleuritis. For further differentiation MMP and TIMP were localized in pleural biopsies by immunhistochemical staining with antibodies directed against MMP-1, MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 using the Labelled-Avidin-Biotin (LAB). Immunohistological reactivity of MMP-1 was found in epitheloidcellular histiocytes, Langhans' giant cells, lymphocytes, macrophages, as well as in fibroblasts of granulomatous reactions. MMP-2 was found in a few epitheloid cellular histiocytes, fibroblasts, and inflammatory cells. MMP-3 was weakly positive in a few lymphocytes only. MMP-9 was found in a few fibroblasts, epitheloid cells, and inflammatory cells, foremost, however, in pleural mesothial cells. A few fibroblasts only showed immunoreactivity of TIMP-1 and TIMP-2. The observed inhomogenous staining pattern could be explained by the different state of activation of individual cellular units. In conclusion, the immunohistochemical demonstration of MMP and TIMP in pleural cells and tissue structures indicates their local involvement in fibrosing reactions in TB-pleuritis.

Female↗

PubMed2003

[Nosocomial pneumonias in haematological malignancies in the medical intensive care unit].

30 patients with malignant haematological disorders and nosocomial pneumonia, treated during a three-year period in the medical intensive care unit (ICU) of a university hospital, were studied in retrospect. Twelve patients had received bone marrow or peripheral stem cell transplantations 90 +/- 143 (10 - 546) days prior to ICU admission. Six of these received cyclosporin A. 19 of 30 patients were on corticosteroids and 20 had received courses of chemotherapy within a period of one month prior to ICU admission. Patients presented with signs of pulmonary infection and respiratory failure. In 24 patients the likely causative pathogen for pneumonia could be identified. Gram-negative bacteria (n = 17) were in the majority, lead by Pseudomonas, Enterobacter, and Klebsiella species. Gram-positive bacteria (n = 5) were Streptococcus and Staphylococcus species. Infections with Chlamydiae species were diagnosed in two cases. Fungal infections were caused by Candida (n = 8) or Aspergillus species (n = 3) and viral infections by Cytomegalovirus (n = 6). Infections with more than one pathogen were common. Ten patients had pneumonia associated with signs of diffuse pulmonary parenchymal damage of varying degree. 26 patients received mechanical ventilation for 7 +/- 9 (1 - 32) days. The duration of stay in the ICU was 11 +/- 10 (1 - 43) days. 26 of the 30 patients (87 %) died. Patients with haematological malignancies and nosocomial pneumonias have despite medical intensive care treatment a poor prognosis with substantial mortality.

Adult↗

PubMed2003

[Severe acute respiratory syndrome (SARS)].

The severe acute respiratory syndrome (SARS) is a highly infectious respiratory disease, to the best of our knowledge caused by a hitherto unknown corona virus. The virus has spread from South East Asia to many countries of the world. Three case reports of patients from the Prince of Wales Hospital of The Chinese University of Hong Kong demonstrate typical clinical courses. Fever, cough, in most cases non-productive, myalgia, chills, and rigor are the leading symptoms. Leucopenia and thrombocytopenia are the most prominent laboratory parameters, increased values for lactatedehydrogenase (LDH) reflect a more severe clinical course. Advanced age and coexisting conditions seem to influence the prognosis unfavourably. The chest roentgenogram may be normal initially but at a later stage progressive consolidations in the majority of peripheral parts of the lung are observed, which cannot be differentiated from pneumonias of other origin. Even young patients can enter a stage of respiratory compromise rather fast. A therapy against the cause of the disease is not known. Empirical therapy with ribavirin in combination with high dose corticosteroids have proved successful. The disease may progress into respiratory failure comparable with an acute respiratory distress syndrome (ARDS). Mortality is around five to ten per cent. Stringent hygiene and quarantine measures are mandatory to prevent the further spread of this threatening disease.

Adult↗

PubMed2001

Occurrence of matrix metalloproteinases and tissue inhibitors of metalloproteinases in tuberculous pleuritis.

OBJECTIVE: Matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) have been found in high concentrations in pleural effusions. Because MMP and TIMP may play a part in the causation of the fibrosis seen in tuberculous (TB) pleuritis their occurrence was examined. DESIGN: Pleural effusion fluid and plasma concentrations of MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, TIMP-1 and TIMP-2 were determined by ELISA in 21 patients with TB pleuritis. To adjust for the total protein content, respective ratios were calculated. Activities of MMP-2 and MMP-9 were measured by gelatine zymography and the MMP-9/MMP-2 ratios calculated. Pleural effusions and plasma of 15 patients with congestive heat failure (CHF) and plasma of 15 healthy persons (CON) served as controls. RESULTS: Immunoreactive pleural fluid concentrations of MMP-1, MMP-2, MMP-8, and MMP-9 were higher in TB compared to CHF, but plasma concentrations were not different between the groups. TB pleural fluid concentrations of MMP-1, MMP-2, TIMP-1, and TIMP-2 were higher compared to TB plasma. MMP-3 was found in trace amounts only. The MMP-9/total protein ratios in pleural fluid were higher in TB compared to CHF (0.4492+/-0.1633 vs 0.0364+/-0.0145, P<0.005) but the TIMP-1 ratios were lower (139.0+/-28.7 vs 517.8+/-183.7, P<0.0005). In TB pleural fluid vs TB plasma, the respective MMP-1, MMP-2, TIMP-1, and TIMP-2 ratios were increased (0.46+/-0.10 vs 0.17+/-0.02; 25.2+/-2.8 vs 4.2+/-0.9; 139.0+/-28.7 vs 27.8+/-8.2; 0.67+/-0.13 vs 0.18+/-0.04, P<0.0005 each). Gelatine zymography demonstrated MMP-2 and MMP-9 bands of different brightness in TB effusions but in CHF effusions the MMP-9 band was barely visible. The MMP-9/MMP-2 effusion ratios were therefore higher in TB compared to CHF (0.46+/-0.15 vs 0.05+/-0.04, P<0.0005). CONCLUSION: Compartmentalized MMP-1, MMP-2, TIMP-1, and TIMP-2 and, compared to CHF, a surplus of MMP-1, MMP-2, MMP-8, and MMP-9 in the pleural space obviously contribute to the fibrotic reactions in TB pleuritis.

Adult↗

PubMed2000

Time-of-flight secondary ion mass spectrometry of matrix-diluted oligo- and polypeptides bombarded with slow and fast projectiles: positive and negative matrix and analyte ion yields, background signals, and sample aging.

Human angiotensin II, chain B of bovine insulin, and porcine insulin were determined by time-of-flight secondary ion mass spectrometry under impact of approximately 25 keV Xe+ and SF5+ ion beams and approximately 100 MeV 252Cf fission fragments. Matrix-embedded samples, dissolved in a large surplus of alpha-cyano-4-hydroxycinnamic acid, were prepared by nebulizer spray deposition, neat samples by the droplet technique. It is shown that the status of the sample can be assessed by evaluating the matrix-specific features of the mass spectra. The beneficial effect of matrix isolation was small for angiotensin but large for the insulin samples, which did not show parent peaks from neat material. Negative ion yields under SF5+ impact were up to a factor of 50 higher than with Xe+. For positive secondary ions, the enhancement was much smaller. The mass spectra produced by slow ion beams or fast fission fragments were qualitatively similar. Quantitative differences include the following: with fast projectiles the yields were about 10-30 times higher than with slow ions, but similar for negative ion emission under SF5+ bombardment; the analyte-to-matrix yield ratios were higher with slow ions and up to 250 times higher than the molar analyte concentration; for analyte ions the peak-to-background ratios were higher using slow projectiles; the fraction of carbon-rich collisionally formed molecular ions was much higher with fast projectiles. Sample aging in vacuum for up to five weeks strongly reduced the yield of protonated analyte molecules ejected by slow ion impact, but not of deprotonated species. Hence protonation seems to correlate with sample "wetness" or the presence of volatile proton-donating additives.

Angiotensins↗

PubMed2000

P-Selectin expression, platelet aggregates, and platelet-derived microparticle formation are increased in peripheral arterial disease.

Platelet volume has been reported to be increased in vascular disease. Therefore, we studied the relationship of mean platelet volume and platelet count as well as flow cytometrically measured platelet size and platelet function in 50 patients with peripheral arterial disease and 50 healthy volunteers. Platelet activation was measured by P-selectin expression analysis on resting and on stimulated platelets, and the determination of platelet aggregates and platelet-derived microparticles using flow cytometry. P-Selectin expression on platelets was significantly elevated in patients suffering from peripheral arterial disease (all P<0.0001). Platelet aggregates (P<0.0001) and platelet-derived microparticles (P<0.0001) were significantly higher in the patient group compared with controls, whereas mean platelet volume and platelet count showed no significant differences. Platelet count was inversely related to mean platelet volume in patients and controls (r = -0.43, P<0.001). The present study supports the hypothesis of platelet hyperreactivity and circulating activated platelets in peripheral arterial disease. Mean platelet volume, and platelet count cannot be used as predictive markers for platelet activation in peripheral arterial disease patients.

Adult↗

PubMed1999

[The solitary echinococcal cyst--a rare cause of a round pulmonary focus].

HISTORY AND ADMISSION FINDINGS: A 29-year-old man from Kazakhstan presented with right-sided chest pain, cough, whitish sputum and a temperature up to 38.5 degrees C. He had been working in an animal farm for the previous two years. INVESTIGATIONS: Laboratory tests showed increased inflammatory parameters (WBC 15.9 gpt/l with an increased proportion of band and segmented granulocytes, C-reactive protein (242.3 mg/dl). Chest radiogram showed an infiltration and effusion in the right base judged to be due to pneumonia. In addition there was a round homogeneous mass, 2.5 cm in diameter, at the lateral thoracic wall in the 8th lower lobe segment. Computed tomography (CT) of the lung and mediastinum confirmed these findings. Bronchoscopy, echocardiography, upper abdominal sonography and CT of the skull revealed no other space-occupying lesion. DIAGNOSIS, TREATMENT AND COURSE: The right-sided pneumonia was successfully treated, at first with ceftriaxone (i.v.), later with ofloxacin (by mouth). An echinococcal cyst was considered especially because of the patient's profession in Kazakhstan in the differential diagnosis of the right-sided round mass and confirmed by an indirect haemagglutination test giving an antibody titre of 1:1024. In response a thoracotomy was performed and the mass, histologically an echinococcal cyst (E. granulosa), resected. There were no other cysts. There was no explanation for the right-sided pneumonia. CONCLUSIONS: Even though Echinococcosis is rare in Central Europe, it should be included in the differential diagnosis of a round pulmonary mass. A detailed history, especially with regard to occupation and country of origin, is essential. Serological tests for specific Echinococcus antibodies, together with usual imaging procedures, will usually and quickly provide the diagnosis.

Adult↗

PubMed1998

Compartmentalization of pro-inflammatory cytokines in tuberculous pleurisy.

Increased levels of interleukin-6 (IL-6) and IL-8 are found in various immunologically mediated inflammatory disorders. Concentrations of IL-6, IL-8 and the soluble form of the IL-6 receptor (sIL-6R) were determined in serum and effusion fluid of 25 patients with tuberculous pleurisy utilizing enzyme linked immunosorbent assays (EIA). Serum IL-6 levels were only slightly increased in patients with tuberculous pleurisy in comparison to controls (11.1 +/- 2.1 vs 7.3 +/- 1.0 pg ml-1). IL-8 could not be detected in the serum of tuberculosis patients, but it was detected in the serum of healthy controls (8.0 +/- 1.5 pg ml-1). In comparison to serum, IL-6 and IL-8 were found in high concentrations in pleural effusions (IL-6: 932 +/- 70 vs 11.1 +/- 2.1 pg ml-1, P < 0.0001; IL-8: 450 +/- 85 vs 0 +/- 0 pg ml-1). In contrast, sIL-6R concentrations were much higher in serum compared to pleural effusion levels [30,477 +/- 1905 vs 9881 +/- 1177 pg ml-1, P < 0.0001 (mean +/- SEM)]. The authors conclude that elevated levels of IL-6 and IL-8 in pleural effusions are compartmentalized at the site of active disease. The low levels of sIL-6R in the presence of high levels of IL-6 in pleural effusions, and the high levels of sIL-6R in the presence of low levels of IL-6 in serum suggest that the expression or shedding of sIL-6R may be downregulated in the presence of excessive amounts of IL-6.

Adult↗

PubMed1998

Proinflammatory cytokine levels in patients with lung cancer and carcinomatous pleurisy.

Increased levels of interleukin-6 (IL-6) and interleukin-8 (IL-8) have been reported in various diseases, including lung cancer. The role of the soluble form of the IL-6 receptor (sIL-6R) remains to be explored. We therefore measured IL-6, IL-8 and sIL-6R in effusion fluid and blood serum of 10 lung cancer patients with carcinomatous pleurisy (5 men, 5 women, age 64.3 +/- 4.4 years) by enzyme-linked immunosorbent assays. Serum levels of healthy individuals served as control. Concentrations of sIL-6R were much higher in serum compared to pleural effusion fluids of tumor patients (25,698 +/- 1,993 vs. 9,438 +/- 1,407 pg/ml: p < 0.0001). In contrast, IL-6 and IL-8 were found at high concentrations in carcinomatous pleural effusions in comparison to serum (IL-6: 964 +/- 176 vs. 10.2 +/- 1.3 pg/ml, p < 0.0001; IL-8: 319 +/- 85 vs. 9.6 +/- 9.6 pg/ml, p < 0.0001). The serum concentrations of IL-6 were not significantly increased in lung cancer patients (10.2 +/- 1.3 pg/ml) in comparison to controls (7.3 +/- 1.0 pg/ml). IL-8 was detected in the serum of only 1 patient and in low levels in the serum of controls (8.0 +/- 1.5 pg/ml; all values are mean +/- SEM). We conclude from this study that decreased levels of sIL-6R, but increased levels of IL-6 and IL-8, are found in pleural effusion fluid of patients with lung cancer and carcinomatous pleurisy. The low sIL-6R levels in the presence of high IL-6 levels in pleural effusions and the high sIL-6R levels in the presence of low IL-6 levels in serum may suggest a downregulation of sIL-6R expression of sIL-6R shedding in the presence of excessive amounts of IL-6.

Aged↗

PubMed1998

The effect of corticotropin-releasing hormone (CRH) on the adrenal medulla in hypophysectomized rats.

CRH occurs in the adrenal medulla of rats. We were interested to know whether CRH affects meduallary chromaffin cells in the absence of ACTH. We investigated the morphological changes of the adrenal medulla in Sprague Dawley rats with light and electron microscopy in normal rats, hypophysectomized rats, and hypophysectomized rats following injections of CRH (10 micrograms = 3 nmol for three days). Chromaffin cells were characterized by immunohistochemistry (anti-tyrosine hydroxylase). At light microscopy level chromaffin cells of hypophysectomized rats were reduced in number. On electron microscopy the number of granules and cell organelles were decreased. Following injections of CRH the medulla regained a more compact texture with cell organelles homogenously distributed, but with chromaffin granules still being reduced in number. Immunohistochemistry allowed the identification of chromaffin cells located within the adrenal cortex. In hypophysectomized rats these cells showed fewer signs of alterations compared to cells located within the medulla itself and had recovered better after treatment with CRH. In conclusion, CRH seems to exert a trophic effect on chromaffin cells in the absence of pituitary ACTH. This observation may provide further evidence for a close interaction of the two neuroendocrine stress systems.

Adrenal Medulla↗

PubMed1997

Corticotropin-releasing hormone-binding protein and its possible role in neuroendocrinological research.

Corticotropin-releasing hormone-binding protein (CRH-BP), predominately produced by the liver, is a glycoprotein with a molecular weight of 37 kDa. The mature protein consists of 7 exons and 6 introns, with 5 tandem disulfide bridges which are essential for the binding of corticotropin-releasing hormone (CRH). This binding protein is distributed and expressed differently from corticotropin-releasing hormone receptors (CRH-Rs), as is the ligand requirement. Most CRH in plasma is bound to its binding protein, is therefore inactive and unable to bind to its receptor. Other competitives can reverse the binding, liberating CRH. Together with the CRH neuropeptides and CRH receptors, CRH-binding protein plays a role in the hypothalamic-pituitary-adrenal axis, in immune/inflammatory reactions as an auto/paracrine proinflammatory regulator, in pregnancy, as well as in some pathological conditions.

Adrenocorticotropic Hormone↗

PubMed1997

Procoagulant activity of purified protein derivative-stimulated pleural effusion mononuclear cells in tuberculous pleurisy.

Mononuclear cells (MNC) generate cell-bound procoagulant activity (PCA) which shortens recalcification time after incubation with an antigen to which the donor has been sensitized. PCA has been demonstrated in various lung diseases, including exudative pleural effusions. To determine the value of measuring cell-bound PCA in the diagnosis of tuberculous pleural effusions we examined pleural effusion MNC of patients with tuberculosis (n = 19), congestive heart failure (n = 7), and carcinoma (n = 7). MNC were isolated, incubated in 0 or 10 micrograms/ml purified protein derivative (PPD) for 15 min and for 20 h, and recalcification time determined. Incubation with thromboplastin was used as control. The recalcification times in serum incubated for 15 min varied within a wide range, the mean values were longest for tuberculous effusion MNC, incubation for 20 h increased variation. Incubation of cells for 15 min with thromboplastin led to a decrease of mean recalcification time in tuberculous (p < 0.001) and heart failure (p < 0.05), and with no significance in carcinomatous effusions. Incubation with PPD led to decrease of recalcification time which was not significant. Comparisons of the mean relative recalcification times after PPD incubation showed that tuberculosis differed from lung cancer (p < 0.001), lung cancer from heart failure (p < 0.05), but not heart failure from tuberculosis. We conclude from our study that pleural effusion MNC express spontaneous PCA in vitro which is strongest in carcinomatous pleural effusions. Incubation of MNC with thromboplastin and less discernable with PPD leads to an increase in PCA which is more pronounced in tuberculous pleural effusions. However, due to substantial intersubject variability and overlap between the study groups, this test does not allow reliable differentiation of tuberculous from other MNC rich pleural effusions.

Blood Coagulation↗

PubMed1997

[Surfactant administration and laterally independent positive pressure ventilation in acute lung failure and atelectasis after septic abortion. Case report].

We report the case of a 35 years old female patient suffering from Staphylococcus aureus induced abortion in the 7th/8th week of gestation. Sepsis with acute respiratory failure (ARDS) developed, which could be treated successfully. Pneumonia, caused by Pseudomonas aeruginosa, induced a recurrence of ARDS, complicated by a persistent incomplete atelectasis of the left lung. Independent ventilation of both lungs with increased pressure on the left side combined with bronchoscopy guided instillation of 1 g of bovine surfactant (Alveofact), caused improvement of arterial oxygenation and radiological signs, signalling airation of collapsed lung areas.

Abortion, Septic↗