The morphology and application of stem cells in digestive system surgery.

BACKGROUND: Stem cells constitute a group of cells which possess the ability to self-renew as well as the capacity to differentiate into a vast number of different cells within the human organism. Moreover, stem cells are able to undergo a potentially unlimited number of divisions and this characteristic is clinically essential. Specific fields of its application include treatment of diseases mainly in the field of haematology, orthopaedics, surgery, dentistry, and neurology. MATERIALS AND METHODS: In the following work, the current knowledge concerning mechanisms of stem cell treatment in different parts of the digestive system with its diseases as well as adjacent therapy for surgery has been revised. RESULTS: Stem cells therapy may be used in the treatment of various diseases of different parts of the digestive system. This also applies to the end part of the digestive tract (proctological diseases) because stem cells can be used to treat fistulas. Liposuction allows more recovery of mesenchymal stem cells, compared to previous bone marrow harvesting methods. Despite the application of stem cells in the treatment of different diseases used for many years so far, the therapeutic use for the regeneration of the gastrointestinal tract is still rare and unfamiliar. CONCLUSIONS: Regenerative medicine seems to be a promising tool in medical research, especially when insulated cells and designed biomaterials are taken into consideration. Major points of discussion include types of stem cells, their origin or differentiation for the treatment of many diseases.

Recommendations for Lung Ultrasound in Internal Medicine

A growing amount of evidence prompts us to update the first version of recommendations for lung ultrasound in internal medicine (POLLUS-IM) that was published in 2018. The recommendations were established in several stages, consisting of: literature review, assessment of literature data quality (with the application of QUADAS, QUADAS-2 and GRADE criteria) and expert evaluation carried out consistently with the modified Delphi method (three rounds of on-line discussions, followed by a secret ballot by the panel of experts after each completed discussion). Publications to be analyzed were selected from the following databases: Pubmed, Medline, OVID, and Embase. New reports published as of October 2019 were added to the existing POLLUS-IM database used for the original publication of 2018. Altogether, 528 publications were systematically reviewed, including 253 new reports published between September 2017 and October 2019. The new recommendations concern the following conditions and issues: pneumonia, heart failure, monitoring dialyzed patients' hydration status, assessment of pleural effusion, pulmonary embolism and diaphragm function assessment. POLLUS-IM 2020 recommendations were established primarily for clinicians who utilize lung ultrasound in their everyday clinical work.

Pneumothorax in Patients with Pulmonary Langerhans Cell Histiocytosis.

INTRODUCTION: Pneumothorax often develops in pulmonary Langerhans cell histiocytosis (PLCH), but some patients take a long time to be correctly diagnosed. OBJECTIVES: This study assessed the frequency of pneumothorax in PLCH and analysed the role of chest computed tomography (CT) in the prompt diagnosis. PATIENTS AND MATERIAL: Of the 90 patients with PLCH seen from 2000 to 2015, 29 (32%) had pneumothorax as the initial finding. In this group, 18 (62%) patients were diagnosed within 1 month, whereas the diagnosis was delayed for 4-120 months in 11 (38%) patients. RESULTS: Patients who had pneumothorax as the initial sign of PLCH tended to be younger (mean age 27.7 ± 7.92 vs. 39.9 ± 13.21 years; P = 0.0001), male (69% vs. 43%; P = 0.028), smoked less (mean pack/years 8.4 ± 6.85 vs. 19 ± 17.16; P = 0.003), and had a significantly lower mean FVC (77.96 ± 19.62 vs. 89.47 ± 21.86% pred.; P = 0.015) and FEV1 (68.6 ± 19.93 vs. 79.4 ± 21.48% pred.; P = 0.03 than patients who had no pneumothorax. Recurrent pneumothorax was diagnosed more frequently in the group with a delayed diagnosis (82% vs. 39%; P = 0.02). CT was performed in all of the patients who were diagnosed promptly, but in none of the patients with a delayed diagnosis. CONCLUSIONS: Patients who had pneumothorax as the initial sign of PLCH were younger, more frequently men, and had greater respiratory impairment than those who had no pneumothorax. CT in patients with pneumothorax led to a correct diagnosis of this disease.

Cryptogenic Organizing Pneumonia: IL-1ß, IL-6, IL-8, and TGF- ß1 Serum Concentrations and Response to Clarithromycin Treatment.

Cryptogenic organizing pneumonia (COP) is a distinct clinicopathological entity with unknown etiology. Inflammatory cytokines play a role in the development of the disease. The present study was performed to assess the correlation between concentrations of IL-1ß, IL-6, IL-8, and TGF-ß1 in the serum with response to clarithromycin (CAM) treatment in patients with COP. A total of 39 patients with COP were enrolled in to this study. An oral dose of 500 mg CAM was administered to all of the patients twice daily for 3 months. A complete response was noticed in 31 (80 %) of patients, and 8 (20 %) patients failed to respond to treatment. The concentration of cytokines were assessed by ELISAs before and after treatment. CAM treatment was associated with decreases in serum IL-6 (3.8 pg/mL [IQR 0.9-11.8] vs. 1.1 pg/mL [IQR 0.2-3.1]; p = 0.004), IL-8 (13.6 pg/mL [IQR 9.8-17.5] vs. 8.1 pg/mL [IQR 6.2-13.2]; p = 0.004), and TGF-ß1 (37.1 ng/mL [IQR 31.7-46.2] vs. 25.7 ng/mL [IQR 22-41.7];p = 0.0001), which was particularly notable in the responders. We conclude that IL-6, IL-8, and TGF-ß1 may play a role in the pathogenesis of COP, as their decreased concentrations were associated with a positive response to CAM treatment.

[The use of stem cells in some rheumatic diseases]. / Zastosowanie mezenchymalnych komórek macierzystych w wybranych chorobach reumatycznych.

Stem cells (SC) are characterized by the possibility of a potentially unlimited number of divisions, that are, its self-renewal and differentiation pot in all tissues of the body. The term "stem cells" was first used by the Russian histologist Alexander Maksimova in 1908 in relation to the hematopoietic stem cell (HSC - haematopoietic stem cells). SC, because of their ability to self-renewal and proliferation enormous potential, became the subject of numerous research around the world. These studies offer hope for improving the prognosis and optimization methods for the treatment of many types of diseases, including diseases of the developing autoimmune which include rheumatic diseases. Pain associated with the most common rheumatic diseases, like rheumatoid arthritis and osteoarthritis, cause temporary restriction of efficiency, frequent use of sick leave and abuse of painkillers. Rheumatic diseases often have young people in the labor force, have a chronic condition, and despite of the treatment over time lead to permanent disability and even premature death. Therapy with stem cells, can become an effective alternative to standard therapies used so far. The results of the first studies on the use of stem cells are promising and warrant further work on their application not only in rheumatic diseases.

Pulmonary Function Abnormalities in Regard to Age at the Time of Diagnosis of Hypersensitivity Pneumonitis.

Hypersensitivity pneumonitis (HP) is a complex syndrome caused by exaggerated immune response to inhalation of a variety of organic particles in susceptible individuals. In this study we assessed the relationship between age at the time of diagnosis and the degree of functional and radiological changes in HP. The diagnosis of HP was made on the basis of a combination of clinical symptoms, medical history, serological tests, radiologic evidence of diffuse lung disease, and absence of other identifiable causes of lung disease. We reviewed the records of 111 patients (68 women) diagnosed with HP over a period of 18 years (1995-2013). The patients were stratified into 3 age-groups: <30, 30-49, and ≥50 years old. The commonest cause of HP was avian antigens (56.8 %). Dyspnea was present in 97.3 % of patients, weight loss in 54.7 % of patients, and respiratory insufficiency in 24.3 % of patients. Lung fibrosis in chest computed tomography was found in 35.1 % of patients. Lung function was impaired more seriously in the youngest age-group, with lung diffusing capacity for carbon monoxide (DLCO) <40 % in 69.2 % of these patients. Restrictive pattern was present in 92.3 % of patients in this group, as compared with the 41.0 % in the whole cohort. In this group, desaturation in the six minute walk test also was most notable, amounting to a median of 11 %. In conclusion, diagnosis of HP at young age is predictive of a more severe clinical course of disease, with lung fibrosis and higher disturbances in pulmonary function.

Influence of delays in diagnosis and treatment on survival in small cell lung cancer patients.

The purpose of this study was to evaluate the influence on survival of delays in the diagnosis and treatment in an unselected population of small cell lung (SCLC) patients. Demographic and disease data of 3,479 SCLC patients were registered in the National Tuberculosis and Lung Diseases Research Institute in Warsaw, Poland during 1995-1998. In 50 % of patients, treatment started within 78 days from the appearance of first symptom(s). The median delay was 30 days (mean 47 days) and the median referral delay to a specialist was 19 days (mean 36 days). Half of SCLC patients were diagnosed during 34 days (mean 55 days). The mean time elapse from the diagnosis to the onset of therapy was 30 days (median 6 days). The multivariate analysis revealed that male gender-HR (hazard ratio = 1.2), ECOG Performance Status of 2 (HR = 1.5) and 3 + 4 (HR = 2.4), and clinical stage III (HR = 1.3) and IV (HR = 1.9) of the disease were independent negative predictors of survival. The patients treated with surgery and combined modality treatment had a better prognosis than those treated with chemoradiotherapy (HR = 1.6), chemotherapy (HR = 2.5), symptomatically (HR = 4.0), or those who refused therapy (HR = 3.9). The delay in the diagnosis and treatment had no effect on survival. Interestingly, patients who were diagnosed faster (below 42 days) actually had a worse prognosis than those diagnosed later. We conclude that a prolonged workup of SCLC patients and an extended time for treatment onset have a positive influence on survival, which may likely have to do with the determination of disease stage and more targeted treatment.

Influence of sera from interstitial lung disease patients on angiogenic activity of mononuclear cells.

Chronic inflammation stimulates of neovascularization. The aim of this study was to evaluate the effect of sera from interstitial lung diseases (ILD) patients on angiogenic capabilities of different subsets of mononuclear cells. Serum samples were obtained from 22 patients with sarcoidosis, 20 with hypersensitivity pneumonitis, 20 with idiopathic pulmonary fibrosis, 9 with systemic sclerosis, 6 with pulmonary Langerhans cells histiocytosis, and from 20 healthy volunteers. Animal model of leukocyte induced angiogenesis assay was used as an angiogenic test. The pattern of angiogenic reaction was different in different diseases. Sera from systemic sclerosis and pulmonary Langerhans cells histiocytosis patients exerted inhibitory effects on angiogenesis, but sera from sarcoidosis, hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis patients stimulated angiogenesis. Sera from sarcoidosis and pulmonary Langerhans cells histiocytosis primed monocytes for the production of angiogenic factors. The number of microvessels created after incubation of mononuclear cells depleted of monocytes with sera from systemic sclerosis patients significantly decreased. We conclude that the role of monocytes in the modulation of angiogenesis varies depending on the type of ILD. Sera from sarcoidosis stimulate and from pulmonary Langerhans cells histiocytosis patients inhibit neovascularization induced by monocyte mediators. Sera from systemic sclerosis inhibit angiogenesis induced by lymphocyte products.

Angiogenic activity of sera from interstitial lung disease patients in relation to angiotensin-converting enzyme activity.

The role of angiogenesis in the pathogenesis of interstitial lung diseases (ILD) is unknown. Angiotensin-converting enzyme (ACE) is a marker of sarcoidosis activity and may modulate angiogenesis. The aim of this study was to examine the relationship between ACE activity in ILD patients' sera and their effect on microvessels formation in an in vivo model of leukocyte-induced angiogenesis. The study population consisted of 77 sarcoidosis patients, 22 idiopathic pulmonary fibrosis patients, 16 bird fanciers lung patients, eight silicosis patients and 14 healthy donors. Serum ACE activity was assayed by spectrophotometric method. As an angiogenic test, a leukocyte-induced angiogenesis assay in an animal model was used. Sera from interstitial lung disease patients significantly stimulated angiogenic activity of mononuclear cells compared with healthy donors (p < 0.001). The highest ACE serum activity was measured in sera from the silicosis patients, and lowest in sera from the sarcoidosis and IPF patients. A significantly lower serum ACE activity was detected in the bird fanciers lung patients. Serum angiogenic activity of ILD patients measured by angiogenesis index negatively correlated with ACE serum activity (r = ;-0.52; p < 0.01). This correlation was highest in the sarcoidosis group (r = -0.6; p < ). Sera from ILD patient constitute the source of factors modulating angiogenesis.

Angiogenic activity of sera from interstitial lung disease patients in relation to pulmonary function.

OBJECTIVE: Chronic inflammation and fibrosis are characteristic of interstitial lung diseases (ILD) and are accompanied by neovascularisation. The aim of this study was to examine the relationship between the angiogenic activity of sera from ILD patients and pulmonary function tests. MATERIAL AND METHODS: Serum samples were obtained from 225 ILD patients: 83 with sarcoidosis, 31 with idiopathic pulmonary fibrosis, 29 with extrinsic allergic alveolitis, 16 with collagen vascular diseases, 13 with scleroderma with pulmonary manifestations (SCL), 14 with Wegener's granulomatosis (WG), 12 with silicosis, 12 with pulmonary Langerhans cells histiocytosis, 10 with drug-induced pulmonary fibrosis, 5 with cryptogenic organizing pneumonia, and 36 healthy volunteers. An animal model of leukocyte induced angiogenesis assay was used as an angiogenic test. In all patients spirometry, whole body plethysmography, static lung compliance, and single breath diffusing capacity of the lungs for carbon monoxide (DLco) were performed. RESULTS: The angiogenic properties of sera from ILD differed, depending on the disease. In the examined ILD, the most important functional disturbances were decreases in static compliance and DLco. The correlation between DLco and angiogenic activity of sera was observed (P<0.05). CONCLUSIONS: The data show that sera from ILD patients constitute a source of mediators modulating angiogenesis. Angiogenic activity of sera of ILD patients is related to DLco.

Angiogenic activity of sera from interstitial lung disease patients in relation to clinical and radiological changes.

OBJECTIVE: Clinical symptoms and radiological changes are useful in monitoring patients with interstitial lung diseases (ILD). Neovascularization participates in the pathogenesis of idiopathic pulmonary fibrosis and other ILD. The objective of the study was to examine the relationships between angiogenic activity of sera from ILD patients and clinical or radiological status. MATERIAL AND METHODS: Serum samples were obtained from 83 patients with sarcoidosis, 31 with idiopathic pulmonary fibrosis (IPF), 29 with hypersensitivity pneumonitis (HP), 16 with collagen diseases with pulmonary manifestation (CD), 13 with scleroderma (SCL), 14 with Wegener's granulomatosis (WG), 12 with pulmonary Langerhans cell histiocytosis (HIS), 12 with pneumoconiosis (PNC), 10 with drug-induced lung disease (DLD), 5 with cryptogenic organizing pneumonia (COP), and from 36 healthy volunteers. As an angiogenic test we used a cutaneous angiogenesis assay according to Sidky and Auerbach. Clinical status was evaluated using a special questionnaire. In all patients chest radiographs were performed. RESULTS: The angiogenic properties of sera from ILD differed depending on the clinical diagnosis. The strongest proangiogenic effect was induced by sera from patients with HP (mean number of new vessels 16.8), CD (16.6), sarcoidosis (16.3), IPF (16.2), and PNC (15.7). In the case of DLD (13.2), the effect was comparable to healthy controls (13.5). In contrast, sera from SCL (mean number of the vessels 10.5) and HIS patients (10.8) significantly inhibited angiogenesis compared with controls. The angiogenic activity of sera from patients with hilar or mediastinal lymph nodes involvement was higher than that of sera from patients with lung fibrosis. There were also differences in the serum angiogenic activity in relation to the severity of dyspnea. CONCLUSIONS: The data showed that sera from ILD patients constitute a source of mediators modulating angiogenesis, but the pattern of reaction is different in various diseases. Sera from HP, sarcoidosis, IPF, and CD patients demonstrated the strongest proangiogenic activity. However, sera from SCL and HIS inhibit angiogenesis. Angiogenic activity of examined sera was related to the clinical and radiological changes.

Angiogenic activity of sera from silicosis and pulmonary Langerhans cell histiocytosis patients in relation to lung function tests.

Angiogenesis has been implicated in the pathogenesis of interstitial lung diseases. A correlation between serum angiogenic cytokines level of patients with idiopathic pulmonary fibrosis and radiographic manifestations or functional pulmonary changes has been described, but the role of angiogenesis in the pathogenesis of other interstitial lung diseases such as silicosis and pulmonary Langerhans cell histiocytosis remains unclear. The aim of the study was to examine the effect of sera from silicosis and pulmonary Langerhans cell histiocytosis patients on angiogenesis induced by human mononuclear cells (MNC) in relation to pulmonary function. The study population consisted of 12 patients with silicosis, 12 patients with pulmonary Langerhans cell histiocytosis (PLH), and 14 healthy volunteers. Spirometry, whole-body plethysmography, static lung compliance (Cst), and diffusing capacity of the lung for CO (DL(CO)) were performed in all patients. As an angiogenic test, leukocyte induced angiogenesis assay according to Sidky and Auerbach was used. Sera from PLH patients exerted a significant inhibitory effect on angiogenesis (P<0.001). Sera from silicosis patients significantly (P<0.001) stimulated angiogenesis compared with sera from healthy donors. However, sera from healthy donors significantly stimulated the angiogenic activity of MNC compared with the control with PBS. The mean value of DL(CO) was significantly lower in the group of patients with PLH compared with patients with silicosis (P<0.05). A significant correlation between angiogenesis index and DL(CO) was observed (P<0.05). No significant correlation between the angiogenesis index and other functional parameters was found. Sera from interstitial lung diseases patients and healthy donors constitute a source of mediators modulating angiogenesis. Sera from silicosis patients stimulate neovascularization but sera from PLH patients exert an inhibitory effect on angiogenesis. A correlation between serum angiogenic activity and DL(CO) was found.

Angiogenic activity of sera from patients with systemic autoimmune diseases in relation to clinical, radiological, and functional pulmonary status.

Systemic autoimmune diseases, such as vasculitis and collagen diseases, are characterized by chronic inflammation. Mutual interrelationship between angiogenesis and chronic inflammation has already been demonstrated. The aim of the study was to examine the effect of sera from patients with systemic autoimmune diseases on angiogenesis induced by human mononuclear cells. The study population consisted of 43 patients with a systemic autoimmune disease associated with pulmonary manifestations, divided into three groups: 14 with Wegener's granulomatosis (WG), 13 with systemic sclerosis (SS), and 16 with collagen vascular diseases (CVD) such as rheumatoid arthritis, systemic lupus erythematosus, and dermatomyositis. The control group consisted of 15 healthy volunteers. Clinical status was evaluated using a questionnaire. Standard chest radiographs were performed in all patients. Pulmonary function tests were performed according to the ERS standards. An animal model of a leukocyte-induced angiogenesis assay was used as an angiogenic test. Sera from WG and CVD patients significantly stimulated angiogenesis compared with healthy subjects (P<0.001). On the other hand, sera from healthy donors exerted a proangiogenic effect compared with PBS. In contrast, sera from SS patients significantly (P<0.001) inhibited angiogenesis compared with sera from healthy subjects and PBS. Proangiogenic effect of sera from systemic diseases patients depended on radiological changes. No significant correlation between a degree of dyspnea or functional pulmonary tests and the number of new vessels or angiogenesis index was found. Sera from patients with systemic autoimmune diseases and healthy people constitute the source of mediators modulating angiogenesis. These modulatory effects differ depending on the disease entity.

Modulatory effect of sera from sarcoidosis patients on mononuclear cell-induced angiogenesis.

Sarcoidosis (SAR) is a systemic granulomatous inflammatory disease characterized by recruitment and activation of peripheral blood mononuclear cells to the sites of disease. Neovascularisation is a principal vascular response in chronic inflammation and hypoxia. The aim of the study was to evaluate the effect of sera from sarcoidosis patients on angiogenic capability of different subsets of normal peripheral human mononuclear cells (MNC) in relation to IL-6 and IL-8 serum levels, to radiological stages of disease and to the presence of extrapulmonary changes. Serum samples obtained from 42 sarcoidosis patients were examined. There were 12 patients in stage I, 16 patients in stage II, and 14 in stage III. In order to quantify angiogenesis, a leukocyte-induced angiogenesis assay was performed by a method of Sidky and Auerbach. MNC were depleted in monocytes by glass adherence and phagocytosis of iron particles techniques. IL-6 and IL-8 in sera from sarcoidosis patients were evaluated by an ELISA-based assay. Sera from sarcoidosis patients enhanced angiogenic capability of normal MNC significantly stronger than sera from healthy donors (P<0.001). Angiogenic activity of sera in sarcoidosis depended on the stage of disease and appeared most pronounced in stage II (P<0.05). Sera from patients with extrapulmonary changes exerted stronger effect on angiogenesis than sera from patients with thoracic changes only (P<0.001). IL-6 and IL-8 serum level correlated with each other, but no correlation was found between IL-6 and IL-8 serum level and angiogenic activity of the examined sera. Removal of monocytes from MNC eliminated the effect of sera from sarcoidosis patients on angiogenesis compared with the effect of these sera on intact MNC (P<0.001). Sera from sarcoidosis patients and from healthy people constitute a source of mediators participating in angiogenesis. Sera from sarcoidosis patients prime monocytes for production of proangiogenic factors.

Constrictive bronchiolitis obliterans in patient with Castelman's disease.

A 37-year-old woman with hialin- vascular type Castelman's disease (CD) localised in the retroperitoneal region, incompletely resected, developed progressive dyspnoea. The chest radiograph taken 3 months before the operation was normal. The chest CT scan revealed diffused bronchiectases, hyperinflation and air trapping. Pulmonary function tests disclosed severe obstructive impairment with hyperinflation. The bronchoscopic examination of the bronchial tree was normal. Cultures of sputum, bronchial washing and blood were negative. No pemphigus antibodies were found. Mycoplasmal, chlamydial and viral infections were excluded. Histological examination of specimens obtained by open lung biopsy revealed bronchiolar inflammation, submucosal bronchial fibrosis with obliteration of bronchiolar lumen. Constrictive bronchiolitis obliterans (CBO) was diagnosed. Despite slight clinical and spirometric improvements that were achieved due to corticosteroid therapy, one year later she died as a result of respiratory failure. It is widely known that patients with CD develop CBO during the course of paraneoplastic pemphigus. However we present the case of CBO and CD but without any symptoms of this condition.

Organising pneumonia caused by transtuzumab (Herceptin) therapy for breast cancer.

The case of a 49-yr-old female, who developed fever, effort dyspnoea and cough, with patchy migratory bilateral pulmonary infiltrates 6 weeks after starting transtuzumab therapy, following breast-conserving surgery with adjuvant chemoradiotherapy and hormone therapy for breast carcinoma, is reported here. Chest radiograph and thin section computed tomography demonstrated alveolar opacities with air bronchogram in both lungs. A lung biopsy was performed in a nonirradiated area of the contralateral lung and revealed a typical histological pattern of organising pneumonia (previously known as bronchiolitis obliterans organising pneumonia). Transtuzumab therapy was discontinued and subsequent gradual clinical and radiological improvement was observed. After 3 months, complete resolution of symptoms and radiographical abnormalities were noted. This is the first case report that suggests that transtuzumab therapy might induce the development of lung infiltrates with the histological appearance of organising pneumonia.

Lung cancer in women: age, smoking, histology, performance status, stage, initial treatment and survival. Population-based study of 20 561 cases.

BACKGROUND: The community-based cancer registry was set up and results were analysed to assess differences in clinicopathological parameters between women and men. PATIENTS AND METHODS: The Pulmonary Outpatient Departments supplied data on 20 561 lung cancer patients diagnosed in Poland from 1995 to 1998. Data regarding demographics, smoking, histology, treatment and survival were obtained. RESULTS: There were 2875 women and 17 686 men with lung cancer. Women were younger than men (60.02 versus 62.18 years; P <0.001). Age <50 years was more frequent in women than in men (23.3% versus 12%; P <0.001). Women with small-cell lung cancer (SCLC) and adenocarcinoma were significantly younger than women with squamous cancer (58.2 and 58.2 versus 61 years; P = 0.05). Also, men with adenocarcinoma and SCLC were younger than men with squamous cancer (60.6 and 60.2 versus 62.3 years; P = 0.05). Squamous cancer was the predominant type of lung cancer both in women (32.5%) and men (55.2%). However, SCLC (26.6% versus 19.9%: P <0.001) and adenocarcinoma (21.6% versus 9.6%; P <0.001) were more frequent in women than in men. Women were more frequently non-smokers than men (18.8% versus 2.4%; P <0.001). Adenocarcinoma patients smoked less intensively than patients with squamous and SCLC both in women (31.4 versus 35.8 and 33.7 packs/year; P <0.02) and in men (38.2 versus 42 and 41.9 packs/year; P <0.002). In multivariate analysis, bad performance status, advanced stage, non-surgical treatment, age >50 years at diagnosis and male gender were significant independent negative prognostic factors. CONCLUSIONS: Lung cancer was six times more frequent in men than in women. Women with lung cancer were younger than men and smoked less intensively. Over-representation of adenocarcinoma and SCLC was observed in the women. Women with lung cancer had a better prognosis than men.

[Invasive aspergillosis in autopsy material of patients treated at the Institute of Tuberculosis and Chest Diseases during the years 1993-2000]. / Inwazyjna aspergiloza w materiale autopsyjnym u chorych leczonych w Instytucie Gruzlicy i Chorób Pluc w latach 1993-2000.

The aim of this paper is an analysis of clinical documentation and results of autopsy of 21 patients (pts) who died of invasive aspergillosis (IA) in the Institute of Tuberculosis and Chest Diseases in years 1993-2000 and the assessment of predisposing factors for IA. In 17 pts IA was the main and in other 4 only an accessory cause of death. All pts were treated with corticosteroids and/or cytostatic drugs--because of lung cancer (11 pts), cancer in other site (2 pts), haematologic disorders (2 pts), Wegener's granulomatosis (1 pt), polymyositis (1 pt), idiopathic pulmonary fibrosis (1 pt) and other diseases (3 pts). In 15 out of 21 pts granulocytopenia was revealed (from 0.008 x 10(9)/L to 0.82 x 10(9)/L) on an average one month before death. In 15 pts IA was limited to the lungs, in 6 others there were also fungal lesions in brain, kidneys, liver, spleen and heart. Pts with disseminated form of IA had significantly lower granulocyte count and were treated with higher doses of corticosteroids than others. Immunosuppressive drugs and granulocytopenia can be regarded as predisposing factors. Fatal course of IA depended also on the late diagnosis.