Intermittent hypoxia increases exercise tolerance in patients at risk for or with mild COPD.

The effects of repeated short-term hypoxia on exercise tolerance in patients at risk for, or with mild COPD were investigated. Eighteen patients (10 males, 8 females; 33-72 years) were randomly assigned in a double-blind fashion to receive 15 sessions of intermittent hypoxia (FiO(2): 0.15-0.12) or normoxia within 3 weeks. Three weeks of intermittent hypoxia increased total haemoglobin mass (+4% vs. 0%, p<0.05), total exercise time (+9.7% vs. 0%, p<0.05) and the exercise time to the anaerobic threshold (+13% vs. -7.8%, p<0.05) compared to controls. Changes in the total exercise time were positively related to the changes in total haemoglobin mass (r=0.59, p<0.05) and changes in the time to the anaerobic threshold were positively related to the changes in the lung diffusion capacity for carbon monoxide (r=0.48, p<0.05). Intermittent hypoxia treatment may be a valuable addition to therapy designed to improve exercise tolerance in patients at risk for, or with mild COPD.

Chronic obstructive pulmonary disease and oxidative stress.

The respiratory tract as the main entrance for various inhalative substances has great potential to generate reactive species directly or indirectly in excess. Thus, heavy smokers are at high risk for development, impairment and failed response to treatment of chronic obstructive pulmonary disease (COPD). The article is an update regarding the influence of reactive oxygen (ROS) and nitrogen (RNS) species on COPD; however, we do not intend to describe ROS and RNS actions on the entire lung tissue. Here, we focus on the airways, because in human most of the described effects of ROS and RNS species are measured on respiratory epithelial cells obtained by bronchoscopy. ROS and RNS species are physiological compounds in cells and risk factors for several respiratory diseases. In general, both kinds of species are thermodynamically stabile, but their reaction behaviors in cellular environments are very different. For example, the life times of the superoxide anion radical range from micro/milliseconds up to minutes and even hours in in-vitro model systems. Oxidative stress by cigarette smoke was investigated in detail by the authors of this article. In addition, original studies by the authors on the amount of fine particulate matter and trace elements in lung biopsies after defined inhalation indicate a distortion of the equilibrium between oxidants and antioxidants. We also try to present some modern views with respect to genomic medicine for future therapeutic perspectives, although this is an upcoming sector of COPD therapy.

Bone loss in patients with untreated chronic obstructive pulmonary disease is mediated by an increase in bone resorption associated with hypercapnia.

This study sought to determine whether the bone loss in untreated chronic obstructive pulmonary disease (COPD) is associated with hypercapnia and/or respiratory acidosis. Bone mineral density (BMD) measured at the distal forearm of the nondominant arm (with peripheral quantitative computed tomography [pQCT]) and serum markers of bone turnover were determined in 71 male patients with untreated COPD and 40 healthy male subjects who matched the patients in age, weight, and body mass index (BMI). The COPD patients, compared with controls, had reduced pulmonary functions, lower arterial pH, and elevated arterial partial pressure of CO2 (PCO2) The BMD (in T score) was significantly lower in COPD patients than that in control subjects (-1.628 +/- 0.168 vs. -0.058 +/- 0.157; p < 0.001). The BMD of COPD patients correlated positively with arterial pH (r = 0.582; p < 0.001), negatively with PCO2 (r = -0.442; p < 0.001), and negatively with serum cross-linked telopeptide of type I collagen (ICTP), a bone resorption marker (r = -0.444; p < 0.001) but not with serum osteocalcin, a bone formation marker. Serum ICTP, but not osteocalcin, correlated with PCO2 (r = 0.593; p < 0.001) and arterial pH (r = -0.415; p < 0.001). To assess the role of hypercapnia, COPD patients were divided into the hypercapnic (PCO2 > 45 mm Hg; n = 35) and eucapnic (PCO2 = 35-45 mm Hg) group (n = 36). Patients with hypercapnia had lower BMD, lower arterial pH, and higher serum ICTP than did patients with eucapnia. Arterial pH and serum ICTP of eucapnic patients were not different from those of controls. To evaluate the role of uncompensated respiratory acidosis, COPD patients with hypercapnia were subdivided into those with compensatory respiratory acidosis (pH > or = 7.35; n = 20) and those with uncompensated respiratory acidosis (pH < 7.35; n = 15). The BMD and serum ICTP were not different among the two subgroups. In conclusion, this study presents the first associative evidence that the bone loss in COPD is at least in part attributed to an increased bone resorption that is associated primarily with hypercapnia rather than uncompensated respiratory acidosis.

Increased immune activation during and after physical exercise.

The present study has been performed to examine the pattern of immune response during and following a long-duration of physical exercise. We have measured plasma concentrations of serum soluble immune activation markers namely soluble interleukin-2 receptor (sIL-2R), soluble CD8 (sCD8), soluble intercellular adhesion molecule 1 (sICAM-1), soluble CD23 (sCD23), soluble tumor necrosis factor receptor (sTNF-R) and neopterin in 18 individuals before, during (ascent: 3 h, descent: 2 h) and after an alpine tour. Compared to baseline levels, all the parameters were significantly increased on top of the mountain and/or after descent. Within 36 hours after the tour sIL-2R, sCD8 and sICAM-1 decreased. In contrast, sTNF-R and neopterin levels remained higher than baseline throughout the study, only partially decreasing 24 and 36 hours from start. These data show immune system activation induced by physical exercise. The increase of parameters sTNF-R and neopterin, reflecting activation of macrophages, was sustained. The data suggest that immune activation phenomena may be involved in the pathogenesis of impaired immune function after exercise and the exercise-induced asthma.

Relapse of pulmonary Mycobacterium kansasii disease associated with large-cell cancer of the lung: a case report.

A 43-year-old caucasian male diabetic presented with purulent cough and a history of weight-loss, elevated temperature, night-sweat and dyspnea. Four years previously, the patient had undergone a 12-month antimycobacterial regimen because of pulmonary mycobacterium kansasii (MK) disease of the left upper lobe (LUL). Treatment had led to complete recovery with the exception of minor fibrous residuals in the involved pulmonary segments. Chest radiograph and computed tomography (CT), performed on recent admission, revealed a dense infiltration of these residual-containing segments. Microbiological evaluation of bronchial brushings, aspirates and histology of the transbronchial biopsies indicated a relapse of pulmonary MK disease. Although antimycobacterial treatment was started immediately, therapeutic effects were only minimal and remained to be limited to the initial phase of the treatment. After four weeks of treatment, the patient's general condition worsened again. Follow-up CT of the lung showed a marked increase of the infiltration in the left apicoposterior lobe and re-bronchoscopy showed a tumorous protrusion of the bronchial wall involving the apicoposterior segment ostium, a finding which was not seen in the previous bronchoscopy. Histology of the transbronchial biopsies revealed a carcinoma mainly from large-cell type.

Local and systemic treatment in small cell carcinoma of the esophagus.

Primary small cell carcinoma of the esophagus is a rare and aggressive disease. We report on our experience with two patients having a small cell cancer of the esophagus, being treated with photodynamic therapy combined with irradiation and induction-chemotherapy as well as a review of literature. Both patients were admitted with severe dysphagia, weight loss and a Karnovsky performance status of 90. Diagnostic work-up revealed tumor-stenosis in the proximal third in one and in the distal third in the other case. Clinical staging showed T4N2M0 and T3N2M0, pure small cell carcinoma. Due to dysphagia and lymph node enlargement, local and systemic therapy were considered as first-line treatment. Restaging after three cycles of induction-chemotherapy revealed partial response in both cases. Esophagectomy as a second-line treatment was considered. However, in the preoperative period, one patient developed motorical aphasia. The CT-scan of the brain showed multiple brain metastases. External beam irradiation and further chemotherapy was initiated. The patient died 12 months after admission. The other patient revealed anatomical inoperability at the staging laparoscopy. External beam irradiation and a second session of PDT was performed. The patient is still alive, 12 months after his first admission. The biological behavior of this aggressive disease and metastases in about 50% of patients at admission, as well as significant dysphagia makes combined systemic and local treatment necessary. Nevertheless, after reviewing the literature, esophagectomy and adjuvant chemotherapy may have an advantage pertaining to survival time when anatomical and functional operability is given.

Trace elements in pleural effusions.

When the secretion of pleural fluids exceeds their resorption, liquid (pleural effusion ) will accumulate between the visceral and parietal pleura. Pleural effusions derived from the liquid components of blood are expected to contain trace elements and may, as a sink for trace elements, deprive the body of needed essential elements upon their removal by medical intervention. Consequently, patients may be at risk of drifting into trace-element deficiencies. Because the literature is almost devoid of data about trace elements in effusions, the concentrations of 14 trace elements (Ba, Ca, Cd, Co, Cs, Cu, Mg, Mn, Mo, Pb, Rb, Sn, Sr, Zn) were determined simultaneously by inductively-coupled argon-plasma mass spectrometry (ICP-MS) in effusions from 17 patients. The median values for the concentrations of Rb (209 microgram/kg, range 104-334 microgram/kg) and Cs (1.5 micrograms/kg, range 0.8-2.4 microgram/kg) in the effusions were almost the same as in the sera. The concentrations of Mg (range 15-22 mg/kg), Ca range 52-91 mg/kg), Sr (range 12-37 micrograms/kg), and Ba (range 1.4-18.2 micrograms/kg) were consistently lower in the effusions than in the sera by 18% for Mg, 26% Ca 14% for Sr, and 88% for Ba (percentages based on median in serum as 100%). The concentrations of the essential trace elements Co (range 0.16-0.5 microgram/kg), Cu (130-902 micrograms/kg), Mn (0.2-2.2 micrograms/kg), Mo (0.4-1.5 micrograms/kg), Sn (0.4-1.2 micrograms/kg), and Zn (27-1931 micrograms/kg) in the effusions are generally lower (25-55% based on median) than in the corresponding sera, although a few effusions have higher concentrations of Co, Mn Mo, or Zn than in the sera. The concentrations of Cd (range 0.2-0.5 microgram/kg) in the effusions were approximately the same as in the sera for three patients, considerably lower than in the sera for four patients, and considerably higher for three patients. The concentrations for lead (range 0.6-45 micrograms/kg) in the effusions were generally much higher than in the sera. The effusions were not significantly contaminated with lead-rich erythrocytes. The concentrations of Ca, Cu, and Zn in the effusions correlated positively with the protein concentrations in the effusions. One kilogram of the effusions contain from 10-30% of the trace elements present in the entire volume of serum in circulation.

Clinical laboratory parameters in osteoarthritic knee-joint effusions correlated to trace element concentrations.

Interactions of clinical laboratory parameters with trace elements in knee-joint effusions might turn out to be potential diagnostic tool, increasing our pathophysiological understanding and knowledge on knee-joint effusions. Thus, the 11 clinical laboratory parameters, total protein, albumin, glucose, lactate dehydrogenase, uric acid, pH, rheumatoid factor, antistreptolysin, C-reactive protein, leukocyte, and erythrocyte counts were determined in 39 osteoarthritic knee-joint effusions and in corresponding sera. Additionally, concentrations of the 17 trace elements barium, beryllium, calcium, cadmium, cesium, copper, lanthanum, lithium, magnesium, molybdenum, lead, rubidium, antimony, tin, strontium, thallium, and zinc in both effusions and corresponding sera were quantified by inductively coupled plasma-mass spectrometry. Concentrations of most laboratory parameters in synovial fluid were within the normal ranges for serum. However, concentrations of total protein and albumin in effusions were distinctly lower than in sera of healthy adults. Results for rheumatoid factor, antistreptolysin, and C-reactive protein in the effusions were below their corresponding threshold values for serum. An indicator for inflammation, the leukocyte count had a median < 6.3 G/L. The erythrocyte count (median: < 0.06 T/L) revealed a very low presence of red blood cells in the effusions. Total protein concentrations and lactate dehydrogenase activity in the effusions correlated positively with effusion copper (r = 0.61 and 0.66) and effusion zinc (r = 0.71 and 0.49). For cesium, a negative correlation in both sera (r = -0.44) and effusions (r = -0.44) with LDH activity could be established. Concentrations of rubidium, strontium, and cesium responded to albumin concentrations in sera and in effusions, establishing an inverse correlation. All other trace elements showed no or only weak associations with the clinical laboratory parameters determined. Although distinct relationships between trace element concentrations and clinical laboratory parameters in knee-joint effusions exist, the clinical relevance of these findings needs to be further elucidated.

Concentrations of trace elements in osteoarthritic knee-joint effusions.

Concentrations of the 18 elements, barium (Ba), beryllium (Be), bismuth (Bi), calcium (Ca), cadmium (Cd), cesium (Cs), copper (Cu), lanthanum (La), lithium (Li), magnesium (Mg), molybdenum (Mo), lead (Pb), rubidium (Rb), antimony (Sb), tin (Sn), strontium (Sr), thallium (Tl), and zinc (Zn), were determined in the synovial fluids of osteoarthritic knee joints and in the corresponding sera of 16 patients by inductively coupled plasma-mass spectrometry. Knee-joint effusions have lower elemental concentrations than their corresponding sera. For the essential elements Ca, Cu, Mg, and Zn and for the nonessential and toxic elements Ba, Be, Bi, La, and Sb, this difference was highly significant. Strong positive correlations between concentrations in effusions and sera for the essential elements Cu and Mg and for the nonessential elements Cs, Li, Rb, and Sr could be established. The grade of localized hyperperfusion of the knee region in the blood pool phase of 99mTc HDP bone scan indicating inflammation did not correlate with any elemental concentration determined.

Pleural effusions and sera from patients with benign or malignant diseases.

In pleural effusions and sera from 66 patients copper and zinc were quantified by inductively coupled argon plasma-mass spectrometry after mineralizations in a closed-pressurized microwave unit with a mixture of concentrated nitric acid and 30% hydrogen peroxide. Total protein, pH, leukocyte count, lactate dehydrogenase, glucose, C-reactive protein, ceruloplasmin, and alpha1-antitrypsin were determined in many of the effusions. All but four effusions had concentrations of copper (range 58-1720 microg/kg) and zinc (range 27-1001 microg/kg) that were lower than the concentrations in the corresponding sera. Very high concentrations of zinc (1930-6470 microg/kg) were characteristic for thoracic empyemata. In the scatterplots of serum copper versus effusion copper, serum zinc versus effusion zinc, and serum copper/effusion copper versus serum zinc/effusion zinc no clearly delineated regions were noticeably useful for identifying malignant effusions. Similar plots of the concentrations of copper or zinc versus the eight clinical laboratory parameters or plots of clinical parameter versus clinical parameter failed to be of diagnostic value. Statistically highly significant correlations (p < or = 0.05, n > 45, r2 > 0.25) were observed for 9 of 28 pairs of the clinical parameters, for total protein and copper in the effusions and zinc in the effusions and for ceruloplasmin and copper in the effusions. Among the patients suffering from benign or malignant effusions, 52% had zinc concentrations in the sera below the low limit of the normal range (600 microg/kg). Supplementation of such patients with zinc should be considered.

Concentrations of copper, zinc, manganese, rubidium, and magnesium in thoracic empyemata and corresponding sera.

In this study, a number of selected trace elements and clinically relevant parameters were compared between thoracic empyemata and the corresponding sera for a better understanding of the trace element distribution between these two compartments. Serumempyema pairs were obtained from 13 patients and quantified for selected and essential trace elements, namely copper (Cu), zinc (Zn), manganese (Mn), rubidium (Rb), and magnesium (Mg), by inductively coupled plasma-mass spectrometry (ICP-MS). In addition, the concentrations of the following clinical laboratory parameters were analyzed by standard methods: total protein, leukocyte count, lactate dehydrogenase, glucose, pH, and the C-reactive protein. Individual concentrations of the elements determined in the empyemata were frequently higher than in pleural effusions of any other benign or malignant condition except for Cu. Serum Cu exceeded the normal range (600-1400 microg/kg) in 6 out of 13 patients (median 1410 microg/kg). In the empyemata, Zn concentrations (median 2000 microg/kg) were characteristically higher than in the sera (median 450 microg/kg) and exceeded the upper limit for serum (1200 microg/kg) in 8 of the 13 patients. Manganese concentrations in the empyemata (median 2.7 microg/kg) were also higher compared to corresponding sera, although they stayed within the limits considered normal for serum of healthy adults (upper limit 2.9 microg/kg). Rubidium was also moderately higher in most empyemata (median 290 microg/kg) and exceeded the upper limit for serum (560 microg/kg) in two patients. The median concentration of the essential element magnesium was higher in the empyemata (23 mg/kg) than in the sera (21 mg/kg). However, all serum Mg concentrations except three remained within the normal range (17-22 mg/kg). Removal of large amounts of empyematous fluid may deprive the body of trace elements and can cause suboptimal or deficient trace element status and homeostasis. Recuperation will be accelerated by compensatory supplementation of trace elements. Therefore, selective medication with adequate trace element compounds in patients with thoracic empyema can be generally recommended for zinc. The other elements need not necessarily be monitored or substituted, because of their stable concentrations in the serum. Rb may have a biological impact, but deficiency symptoms in man are not clearly defined.

[Fetal alcohol syndrome and malignant tumors]. / Alkoholembryopathie und maligner Tumor.

This paper presents the case report of a 2 year-old boy in whom a grade II fetal alcohol syndrome was diagnosed at 17 months. At 21 months, an embryonal rhabdomyosarcoma of the urinary bladder trigone was found, and the tumour excised. Polychemotherapy was initiated, but bone-marrow depression and death in septicaemic shock followed. The main autopsy findings included the demonstration of tumour remnants in the urinary bladder and prostate, and a severe acute purulent pyelonephritis. This is the fifth case of fetal alcohol syndrome in conjunction with a malignant tumour to be reported in the international literature. These cases do not show any uniformity as to tumour type. No conclusion can as yet be drawn as to whether there is a pathogenetic connection between the fetal alcohol syndrome and the occurrence of malignant tumours (as is the case with the fetal hydantoin syndrome and neuroblastoma), or whether these findings are purely coincidental. Clinicians and pathologists should, however, be advised to look more closely for even minimally pronounced forms of the fetal alcohol syndrome in children with embryonic tumours.

Unilateral high-altitude pulmonary edema (HAPE): a case report and discussion of pathophysiology.

High-altitude pulmonary edema (HAPE), a potentially life-threatening altitude adaptation disorder, is considered to be caused by an exaggerated increase in pulmonary blood pressure and a non-cardiogenic rise in pulmonary vascular permeability subsequent to alveolar hypoxia. A 40-year-old male mountaineer was affected by an advanced stage of HAPE at high altitude (Monte Rosa plateau, 4000 m). The symptoms abated immediately after the patient descended from the altitude. However, six hours after the symptoms had resolved, radiographic signs of pulmonary edema, confined to the right lung, were seen. This rarely described unilateral radiological pattern of HAPE resolved completely within two days. We suggest that aspiration events of nasal secretion, the right sleeping position at night and an elevated right diaphragm reduced the patient's compensatory hyperventilation capacity of the right lung. The resulting increased alveolar hypoxia in the right lung was responsible for unilateral edema. The pathophysiological mechanism underlying unilateral HAPE is discussed.

[Sense and nonsense in antibiotic therapy for respiratory tract infections]. / Sinn und Unsinn der Antibiotikatherapie respiratorischer Infekte.

Whether an antibiotic successfully eradicates pathogens depends on the pathogens involved, on pharmacokinetics and bioavailability in the target tissue, and on the antimicrobial resistance of the pathogen. Other determinants are drug interactions, individual risk factors, age and compliance with respect to correct dosage and duration of therapy. In many cases, antimicrobial therapy is begun on an empirical basis, because the responsible pathogen can be identified in only half of all respiratory infections. The eradication of the pathogen has to be the first aim if treatment is to be curative and the development of resistance prevented. Long-term prevention of antimicrobial resistance will require a more critical prospective evaluation of the prescription of antibiotics. This paper considers rational and irrational measures in the antimicrobial therapy of respiratory infections.

[Respiratory adaptation to altitude and risk factors due to respiratory illnesses]. / Höhenanpassung der respiratorischen Funktion und Risikofaktoren durch Atemwegserkrankungen.

Adaptation to altitude is a complex ability of the organism which involves primarily the cardiovascular and respiratory system in order to increase the oxygen supply for body tissues. Cardiovascular adaptations to rapid altitude challenge are regulated sympathetically and manifest themselves first of all as variations of cardiac output, systolic blood pressure and heart rate at rest. However, respiration plays an important role in compensating hypobaric hypoxia at altitude. The hypoxic ventilatory response (HVR) to alveolar hypoxia expressed as alveolar hyperventilation happens within a very short period of exposure to hypoxic conditions. This immediate adaptation response is followed by the acclimatization period, which encompasses longer lasting compensation processes such as the increase of blood hemoglobin concentration improving the arterial oxygen content. This final stage of adaptation is reached within days or weeks of persisting exposure and will vary somewhat depending on the degree of altitude. For healthy, acclimatized individuals the oxygen supply to the organism does not limit the exercise performance at moderate altitudes and higher. However, above 5000 meters (15,000 ft) long term adaptation cannot occur because oxygen-diffusion becomes a limiting factor to physical exercise capacity. Altitude-related disorders are contributing significantly to the morbidity and mortality of non-acclimatized individuals. Subjects already suffering from symptomatic underlying respiratory disease and hypoxemia at rest have a higher risk and incidence of altitude adaptation disorders even at lower altitudes. Therefore, several diseases with impaired respiratory function are contraindicated for any stay at altitude.

Rheumatoid arthritis with extensive lung lesions.

A man of 74 who had had seropositive rheumatoid arthritis for 10 years presented with dyspnoea and reticular striation in both lung fields. At necropsy two years later there was pulmonary fibrosis with multiple rheumatoid nodules and non-specific granulomas.

[Function and repertoire of the immune system in body's defense]. / Funktion und Repertoire des Immunsystems bei körpereigener Abwehr.

This is a minireview on the organisation and activity of the human immune system with special reference to sport and--more precisely--stress by mountaineering. The activation of the immune system under physical exercise is shown and the immune depression after the sport documented. Hence the conclusion of increased susceptibility to diseases in the post activation phase--a sort of depression after alpine sport.

[Physical exercise impairs the acute stage of adaptation to moderate altitude]. / Körperliche Belastung beeinträchtigt die akute Anpassung in mittlerer Höhenlage.

UNLABELLED: A recent study has reported the impairment of high altitude adaptation capacity by physical exercise in a decompression chamber. The aim of our protocol was to evaluate if physical exercise at moderate altitude in the Alps would show a similar effect. 8 alpinists were examined in a randomised cross-over trial at 171 m and at 3000 m altitude under sedentary and under exercise condition (50% maximal workload on the bicycle ergometer four times 30 minutes during the first 6 hours of an 8 hour observation period at each altitude). At the beginning and at the end of each observation period AMS scores and arterial oxygen saturation SaO2 were measured. The differences of the AMS scores and the differences of SaO2 at both test conditions were compared at both altitudes. RESULTS: In comparison to sedentary condition, the differences between initial and final AMS scores at 3000 m altitude were significantly higher (-0.38 +/- 0.52 vs. -1.25 +/- 0.46, diff 0.88, 95% CI 0.58 to 1.17, p < 0.01), as well as the difference between initial and final SaO2 (-0.25 +/- 0.71% vs. 2.25 +/- 1.04%, diff. -2.5%, 95% CI for the diff. -3.59 to -1.41, p < 0.01). AMS score and SaO2 did not change after exercise at 171 m altitude. CONCLUSION: Physical exercise impairs the acute stage of adaptation to moderate altitude. This is mainly due to the exercise-induced exaggeration of arterial hypoxaemia.

[Smoking behavior of Styrian physicians--results of a 1995 questionnaire survey]. / Rauchverhalten steirischer Arzte--Ergebnisse einer Fragebogenaktion 1995.

Tobacco use among all physicians registered in the state of Styria was investigated at the beginning of the year 1995 using an anonymous questionnaire. In addition to the smoking prevalence among different specialties in medicine the main interest was focused on motives for smoking as well as for stopping it. Nearly all physicians were aware of the associated health risks. The overall prevalence of smoking was 14% which lay markedly below the Austrian average of 36%. 52% started smoking before the age of 18. In addition 70% of smoking doctors wanted to reduce or stop smoking within the next 6 months. The early start of smoking during adolescence emphasizes the importance of educational and special teaching programs because even in the medical profession there is a big difference between the intention to stop smoking and the actual success in doing so.

[Differential diagnostic considerations in eosinophilia with reference to a 19-year-old patients with Löffler endocarditis]. / Differentialdiagnostische Uberlegungen zur Eosinophilie anhand einer 19jährigen Patientin mit Löfflerscher Endokarditis.

In this case report a 19-year-old girl suffering from hypereosinophilia with 3500 cells/mm3 and involvement of the right lung, lymph nodes, skin, serosa and heart is described. Within 10 days of admission an infiltration of the right upper lung lobe disappeared spontaneously and was diagnosed as transient eosinophilic lung infiltration according to Löffler. Both lymph node needle biopsy and several skin biopsies revealed merely general reactive changes whereas a bronchial lavage produced a significant number of eosinophilic granulocytes. Autoimmunologic or infectious-toxic disorders were ruled out as etiologic causes. Within 4 weeks after admission severe mitral and tricuspidal insufficiency as well as AV-block second grade and protodiastolic galloping rhythm developed in addition to progressing polyserositis. The echocardiographic pattern was in accordance with restrictive endocarditis. Due to the greatly reduced left ventricular ejection fraction cortisone (125 mg prednison equivalent) was tentatively administered as therapy. Within 2 weeks heart-, serosa- and lymph-node-findings became normal as well as the eosinophilic count, the scaling skin rash being only partly improved. After 10 months of continuous cortisone therapy (10 mg prednison equivalent) the patient was without evidence of disease. However in conclusion, it may be said that such pattern of findings suggests a hypereosinophilic syndrome with Löffler endocarditis with an unknown future course of disease although generally survival prognosis may not be too high.