Rüdiger Pfeifer
University of Jena
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Featured researches published by Rüdiger Pfeifer.
Resuscitation | 2011
Rüdiger Pfeifer; Christian Jung; Sandra Purle; Alexander Lauten; Atilla Yilmaz; Ralf Surber; Markus Ferrari; Hans R. Figulla
BACKGROUND We investigated whether the use of therapeutic hypothermia improves the outcome after cardiac arrest (CA) under routine clinical conditions. METHOD In a retrospective study, data of CA survivors treated from 2003 to 2010 were analysed. Of these, 143 patients were treated with hypothermia at 33 ± 0.5°C for 24h according to predefined inclusion criteria, while 67 who did not fulfil these criteria received comparable therapy without hypothermia. RESULTS 210 patients were included, 143 in the hypothermia group (HG) and 67 in the normothermia group (NG). There was no significant difference in mortality between the groups; 69 (48.2%) in the HG died in the first four weeks, compared to 30 patients (44.8%) in the NG (p=0.659). Patients in the NG were older and more seriously ill, and CA occurred more often in-hospital. Binary logistic regression revealed ventricular fibrillation (p=0.044), NSE serum level < 33 ng ml⁻¹ (p<0.001), age (p=0.035) and witnessed cardiac arrest (p=0.043) as independent factors significantly improving survival after CA, whereas hypothermia was not (p=0.69). The target temperature was maintained for a significantly longer time (19.5h vs. 15.2h; p=0.003) in hypothermia patients with a favourable outcome than in those with an unfavourable outcome. CONCLUSION There was no improvement in survival rates when hypothermia was added to standard therapy in this case series, as compared to standard therapy alone. The time at target temperature may be of relevance. We need better evidence in order to expand the recommendations for hypothermia after CA.
Resuscitation | 2008
Rüdiger Pfeifer; Markus Ferrari; Angelika Börner; Thomas Deufel; Hans R. Figulla
BACKGROUND AND OBJECTIVES Increased serum concentrations of brain-derived proteins neuron-specific enolase (NSE) and protein S-100beta (S-100b) are used as early predictors of long-term outcome in unconscious survivors after cardiopulmonary resuscitation (CPR). We investigated whether use of short-term Left Ventricular Assist Devices (LVAD) in patients undergoing percutaneous coronary intervention (PCI) effect serum concentrations of NSE and S-100b, because use of such devices in resuscitated cardiogenic shock patients increased during the last years. METHOD We analysed data from 80 consecutive non-resuscitated patients who received LVAD support. 43 patients with uncomplicated myocardial infarction (AMI) without LVAD support after PCI formed the reference group. RESULTS 69 patients (86%) with LVAD support survived and were discharged from hospital. We observed an increase in NSE serum levels in 93.6% and in S-100b serum levels in 58.6% of these patients during LVAD support. This increase was significant in comparison to the upper limit of normal (ULN) of both biomarkers and to the reference group. Cardiogenic shock patients showed significantly higher serum concentrations of both neuroproteins than patients after high-risk PCI, and after AMI during LVAD support. The use of axial flow pumps led to significantly higher serum concentrations of NSE compared to patients on IABP, but not of S-100b. Thrombocytes and haemoglobin (Hb) concentrations declined significantly during LVAD support. Surprisingly, we also observed a significant increase in NSE in the reference group. CONCLUSIONS LVAD support after PCI is associated with a significant increase in NSE serum concentration as well as in S-100b. We therefore postulate an overestimation of the extent of hypoxic brain damage in unconscious survivors after CPR if treatment include LVAD support or PCI or both procedures. The increase in NSE can be partly explained by alteration of thrombocytes and other blood cells. However, the increase in S-100b remains unexplained since S-100b does not occur in peripheral blood cells. An additional release of both biomarkers from ischemic myocardium or cerebral microembolism should be drawn into consideration.
Medizinische Klinik | 1997
Rosemarie Thiele; Daniels Wagner; Margitta Gassel; Klaus Winnefeld; Jens Pleißner; Rüdiger Pfeifer
BACKGROUND Previous examinations have demonstrated decreased selenium levels in serum and full blood in patients with myocardial infarction. PATIENTS AND METHOD 28 patients received a selenium treatment additional to the usual treatment of myocardial infarction. 19 patients with myocardial infarction with no supplementary selenium treatment served as a control group. Selenium levels in serum, full blood and urine were measured and the complications of the myocardial infarction documanted. RESULTS There was a significant increase of serum and full blood selenium and glutathione peroxidase levels under i.v. selenium therapy in the acute phase of myocardial infarction (first to third day). Left heart failure more rarely occurred in the selenium group (20%) than in control patients (57%). Acute tachycardial cardiac rhythm disturbances such as ventricular extrasystoles and couplets diminished in both groups; ventricular extrasystoles decreased in the selenium group. CONCLUSIONS Selen should be substituted in patients with acute myocardial infarction and decreased selen levels. It would be useful to carry out a prospective double-blind study.Summary□Background: Previous examinations have demonstrated decreased selenium levels in serum and full blood in patients with myocardial infarction.□Patients and Method: 28 patients received a selenium treatment additional to the usual treatment of myocardial infarction. 19 patients with myocardial infarction with no supplementary selenium treatment served as a control group. Selenium levels in serum, full blood and urine were measured and the complications of the myocardial infarction documanted.□Results: There was a significant increase of serum and full blood selenium and glutathione peroxidase levels under i. v. selenium therapy in the acute phase of myocardial infarction (first to third day). Left heart failure more rarely occured in the selenium group (20%) than in control patients (57%). Acute tachycardial cardiac rhythm disturbances such as ventricular extrasystoles and couplets diminished in both groups; ventricular extrasystoles decreased in the selenium group.□Conclusions: Selen should be substituted in patients with acute myocardial infarction and decreased selen levels. It would be useful to carry out a prospective double-blind study.
Blood Coagulation & Fibrinolysis | 2011
Rudin Pistulli; Volker Oberle; Hans-Reiner Figulla; Atilla Yilmaz; Rüdiger Pfeifer
Heparin-induced thrombocytopenia (HIT) related to fondaparinux has been rarely reported, although the ability of fondaparinux to cross-react with heparin antibodies has been often a subject of debate. A patient previously exposed to unfractionated heparin and low-molecular-weight heparin (LMWH) was diagnosed with HIT. During treatment with fondaparinux for 5 consecutive days, his thrombocytopenia significantly deteriorated. A functional platelet activation test in vitro showed clear platelet activation after serum exposure with fondaparinux. After discontinuation of fondaparinux, the platelet count was rapidly reestablished. Fondaparinux cross-reacted with heparin antibodies in this case of HIT, resulting in a deterioration of thrombocytopenia. The implication of this drug in HIT was observed clinically and demonstrated in vitro using a platelet activation test.
American Journal of Critical Care | 2010
Julia Schumm; Rüdiger Pfeifer; Markus Ferrari; Friedhelm Kuethe; Hans R. Figulla
A 21-year-old man with signs and symptoms of rapidly progressive shock was admitted to the intensive care unit for treatment of suspected sepsis. Levels of inflammatory markers (including procalcitonin) were highly elevated, but no obvious focus of infection was apparent. Initial sepsis therapy included administration of broad-spectrum antibiotics, vasoconstrictors, and drotrecogin alfa. Cultures of blood, sputum, and urine showed no growth, and no viruses were detected. The random (no stimulation with corticotropin) cortisol level at admission was less than 25 nmol/L. Assays for autoantibodies to the adrenal cortex were strongly positive and confirmed the diagnosis of adrenal failure caused by Addison disease. After initiation of steroid therapy, the patient fully recovered. Although increased procalcitonin levels are considered a reliable and specific indicator of severe generalized infections and bacterial sepsis, elevated procalcitonin levels cannot be relied on when trying to differentiate between addisonian crisis and septic shock.
Medizinische Klinik | 2008
Christian Jung; Markus Ferrari; Christoph Rödiger; Philipp Bahrmann; Bjoern Goebel; Alexander Lauten; Jan Hutschenreuther; Michael Fritzenwanger; Rüdiger Pfeifer; Hans-Reiner Figulla
Die Mikrozirkulation, bestehend aus dem Fluss in Widerstandsgefäßen, Arteriolen, Kapillaren und Venolen, ist zuletzt immer mehr in das Interesse von Klinikern und klinisch orientierten Wissenschaftlern gerückt. Einer eingeschränkten Mikrozirkulation wird eine Schlüsselrolle in der Pathophysiologie des (Multi-)Organversagens eingeräumt; diese ist damit auch eine zentrale Determinante der Prognose beim kritisch Kranken [1]. Der eingeschränkte Sauerstofftransport auf Kapillarebene durch eingeschränkten Mikrofluss mit konsekutivem Organversagen konnte insbesondere für den septischen Schock mehrfach gezeigt werden [2]. Das häufigste genutzte Instrument zur Abschätzung der Mikrozirkulation durch den Kliniker ist die Messung des Blutlactats als Surrogatparameter. Daneben stehen aber auch Verfahren zur indirekten Visualisierung zur Verfügung (Kontrastechokardiographie, Magnetresonanztomographie). Die direkte Visualisierung kann beispielsweise durch die Kapillaroskopie erfolgen; Nachteil ist hier die schlechte Korrelation zur systemischen Mikrozirkulation auf Organniveau. Darin liegt der Vorteil beim OPS („orthogonal polarization spectral“), das eine direkte Visualisierung der Mikrozirkulation der Mundschleimhaut in vivo ermöglicht. Hier kann nichtinvasiv und online eine gute Abschätzung des systemischen Mikroflusses erfolgen [1]. OPS ist eine Form der Intravitalmikroskopie, die sich durch polarisiertes Licht die Absorptionseigenschaften von Hämoglobin zunutze macht [3]. Die Eindringtiefe dabei beläuft sich auf ca. 300 μm; der Mikrofluss kann dann nach Aufzeichnung offline semiquantitativ ausgewertet werden. Diese Technik konnte mit der Sidestream-dark-FieldMethode (SDF) durch eine ringförmige Anordnung der Lichtquelle um den Detektor weiterentwickelt und kontrastverbessert werden. Diese OPSund SDF-Technik konnte den eingeschränkten Mikrofluss in verschiedensten Entitäten visualisieren und quantifizieren: Sepsis, kardiogener Schock, schwere Malaria, Ischämie-Reperfusionsschaden nach Transplantationen und andere (Übersicht in [4]). Des Weiteren wurden auch Therapiemaßnahmen evaluiert, die das Ziel haben, die Mikroperfusion und den Organsauerstofftransport zu verbessern. Das Wissen zur Verbesserung des Mikroflusses durch Flüssigkeitssubstitution, Bluttransfusion, die Gabe von Inotropika oder beispielsweise vasoaktiven Substanzen ist aber noch nicht vollständig und gründet sich häufig auf Tierexperimente. Dabei kommt gerade den Erythrozyten eine doppelte Rolle zu.
Medizinische Klinik | 2008
Mandy Seifert; Jens Gerth; Mieczyslaw Gajda; Frank Pester; Rüdiger Pfeifer; Gunter Wolf
BACKGROUND Eosinophilia is not uncommon in clinical practice. The main causes are allergies and parasitic infections. Rarely, eosinophilia is associated with pulmonary affections, malignant tumors, gastroenteritis, and autoimmune diseases. A new classification based on pathophysiological data for the hypereosinophilic syndrome in order to simplify diagnosis and therapy was introduced in 2006. CASE REPORT A 22-year-old man was admitted to another hospital because of acute abdominal pain. An unspecific colitis was diagnosed. Blood counts showed a mild neutrophilic leukocytosis (12.6 Gpt/l) with a severe relative eosinophilia (30%), thrombocytopenia (67 Gpt/l), and an increased C-reactive protein (CRP 122 mg/l). The patient also had a deep venous thrombosis of the left leg. An explorative laparotomy was performed because of a strong suspicion of a presacral abscess. Pulmonary embolism and embolic pneumonia developed after surgery. A macular-cockade exanthema on the trunk and extremities was found. Histological examination revealed perivascular eosinophilic infiltrates. Histological and cytological analysis of bone marrow showed many eosinophilic granulocytes and a hypercellular medulla without increased numbers of blasts. No parasites in the blood and stools were found, and there was no evidence of neoplasm or cardiac involvement. p- and c-ANCAs (antineutrophil cytoplasmic antibodies), ANAs (antinuclear antibodies), and antibody against dsDNA were negative. Further genetic, FISH (fluorescence in situ hybridization), and PCR (polymerase chain reaction) analyses showed no evidence for chromosomal aberrations. An undefined hypereosinophilic syndrome with multiple organ involvement was diagnosed. Shortly after starting an oral prednisolone therapy (1 mg/kg body weight), the eosinophilia normalized. This therapy was stopped after 2 months and the patient is now, 6 months after diagnosis, in normal health. CONCLUSION As demonstrated in this case, eosinophilia requires a broad differential diagnosis. A hypereosinophilic syndrome can involve many organs and mimic other diseases. The new classification of the hypereosinophilic syndrome from 2006, based on pathophysiological insights, may foster better diagnosis and therapy for this rare disease.ZusammenfassungHintergrund:Eine Eosinophilie wird im klinischen Alltag öfter gesehen. Die häufigsten Ursachen sind allergische Erkrankungen und Parasitosen. Seltener ist eine Eosinophilie Ausdruck von Lungenerkrankungen, Malignomen, Gastroenteritiden oder Autoimmunerkrankungen. Aufgrund neuer pathogenetischer Erkenntnisse wurde im Jahr 2006 eine neue Klassifikation des hypereosinophilen Syndroms erstellt, um sowohl die Diagnostik als auch die Therapie zu vereinfachen. Eine Hypereosinophilie erfordert eine breite Differentialdiagnose.Fallbeschreibung:Ein 22-jähriger Patient wurde aufgrund akuter Bauchschmerzen in einem auswärtigen Krankenhaus aufgenommen. Es lagen ein erhöhtes C-reaktives Protein mit 122 mg/l (Norm < 7,5 mg/l), eine gering erhöhte Leukozytenzahl von 12,6 Gpt/l (Norm 4,4–11,3 Gpt/l) mit einer Eosinophilie von 30% und eine Thrombopenie von 67 Gpt/l (Norm 150–360 Gpt/l) vor. Es bestand eine tiefe Beinvenenthrombose. Aufgrund eines Abszessverdachts im präsakralen Bereich wurde eine Probelaparotomie durchgeführt. Postoperativ traten eine Lungenembolie sowie eine Infarktpneumonie mit septischem Krankheitsbild auf. Zugleich fanden sich makulöse kokardenförmige Hauteffloreszenzen am Stamm und an den Extremitäten mit histologischem Nachweis perivaskulärer eosinophiler Infiltrate und einer eosinophilen Vaskulitis. In der Knochenmarkhistologie zeigten sich zahlreiche eosinophile Granulozyten, in der Zytologie eine starke Markeosinophilie von 50% mit einem hyperzellulären Knochenmark. Eine eosinophile Leukämie wurde aufgrund des Fehlens von Blasten ausgeschlossen. Es konnten keine p- und c-ANCAs (antineutrophile zytoplasmatische Antikörper), ANAs (antinukleäre Antikörper) und Antikörper gegen dsDNA nachgewiesen werden. Umfangreiche Untersuchungen auf Parasiten fielen, wie auch die genetische und molekulare Untersuchung (kein Nachweis einer Chromosom-4q12-Deletion, keine BCR-ABL-Translokation), negativ aus. Hinweise auf das Vorliegen eines Tumors sowie einer kardialen Beteiligung ergaben sich nicht. Es wurde daher von einem undefinierten hypereosinophilen Syndrom bei der schweren Form der Eosinophilie mit letztendlich generalisiertem Befall ausgegangen. Nachdem die Therapie mit Prednisolon (1 mg/kg Körpergewicht) begonnen wurde, sanken die eosinophilen Granulozyten innerhalb weniger Tage auf Normwerte. Die Therapie wurde nach 2 Monaten beendet. Der Patient ist jetzt 6 Monate nach Diagnosestellung völlig beschwerdefrei.Schlussfolgerung:Wie dieser Fall zeigt, ist bei Eosinophilie eine breite Differentialdiagnose notwendig. Ein hypereosinophiles Syndrom kann verschiedene Organe befallen und vielfältige andere Erkrankungen vortäuschen. Die neue pathophysiologisch begründete Einteilung des hypereosinophilen Syndroms von 2006 kann zur Diagnose und bei Therapieentscheidungen hilfreich sein.AbstractBackground:Eosinophilia is not uncommon in clinical practice. The main causes are allergies and parasitic infections. Rarely, eosinophilia is associated with pulmonary affections, malignant tumors, gastroenteritis, and autoimmune diseases. A new classification based on pathophysiological data for the hypereosinophilic syndrome in order to simplify diagnosis and therapy was introduced in 2006.Case Report:A 22-year-old man was admitted to another hospital because of acute abdominal pain. An unspecific colitis was diagnosed. Blood counts showed a mild neutrophilic leukocytosis (12.6 Gpt/l) with a severe relative eosinophilia (30%), thrombocytopenia (67 Gpt/l), and an increased C-reactive protein (CRP 122 mg/l). The patient also had a deep venous thrombosis of the left leg. An explorative laparotomy was performed because of a strong suspicion of a presacral abscess. Pulmonary embolism and embolic pneumonia developed after surgery. A macular-cockade exanthema on the trunk and extremities was found. Histological examination revealed perivascular eosinophilic infiltrates. Histological and cytological analysis of bone marrow showed many eosinophilic granulocytes and a hypercellular medulla without increased numbers of blasts. No parasites in the blood and stools were found, and there was no evidence of neoplasm or cardiac involvement. p- and c-ANCAs (antineutrophil cytoplasmic antibodies), ANAs (antinuclear antibodies), and antibody against dsDNA were negative. Further genetic, FISH (fluorescence in situ hybridization), and PCR (polymerase chain reaction) analyses showed no evidence for chromosomal aberrations. An undefined hypereosinophilic syndrome with multiple organ involvement was diagnosed. Shortly after starting an oral prednisolone therapy (1 mg/kg body weight), the eosinophilia normalized. This therapy was stopped after 2 months and the patient is now, 6 months after diagnosis, in normal health.Conclusion:As demonstrated in this case, eosinophilia requires a broad differential diagnosis. A hypereosinophilic syndrome can involve many organs and mimic other diseases. The new classification of the hypereosinophilic syndrome from 2006, based on pathophysiological insights, may foster better diagnosis and therapy for this rare disease.
Medizinische Klinik | 2001
Stefan Teweleit; Marion Hippius; Rüdiger Pfeifer; Annemarie Hoffmann
ZusammenfassungFallbeschreibung: Es wird über einen 73-jährigen Mann mit Rhabdomyolyse im Rahmen einer akuten Theophyllinintoxikation berichtet. Nach unkontrollierter Einnahme einer unbekannten Menge eines retardierten Theophyllinpräparates in Kombination mit Furosemid wurde er mit Tachykardie, Übelkeit und motorischer Unruhe stationär aufgenommen. Der maximale Theophyllinspiegel betrug 66,5 mg/l. Initial lagen eine Hypokaliämie (2,8 mmol/l), Hyponatriämie (123 mmol/l) sowie erhöhte Werte für Myoglobin (3 789 μg/l) und Kreatinkinase (32,29 μmol/l/s) vor. Es erfolgten die unverzügliche orale Gabe von Aktivkohle in Kombination mit Hämodialyse (CVVH) und forcierter Diurese sowie die intravenöse Gabe von Kaliumchlorid, Natriumchlorid und Metoprolol. Die Serumwerte für Theophyllin, Kreatinkinase und Myoglobin normalisierten sich innerhalb kurzer Zeit, ohne dass ein sekundärer Anstieg des Theophyllinspiegels aufgetreten wäre. Schlussfolgerung: Rhabdomyolysen sind seltene Komplikationen einer Theophyllinintoxikation. In der Literatur sind bislang nur wenige Fälle mitgeteilt worden. Der vorliegende Fallbericht unterstreicht die Notwendigkeit einer schnellen Diagnose und konsequenten Therapieeinleitung, um ein akutes Nierenversagen oder einen letalen Verlauf zu vermeiden. Basierend auf Pathogenese und Epidemiologie theophyllininduzierter Rhabdomyolysen werden Risikofaktoren und Therapieprinzipien formuliert und anhand der Literaturübersicht diskutiert.AbstractCase Report: A case of a 73-year-old male with theophylline overdose complicated by rhabdomyolysis is reported. After uncontrolled self-medication with an unknown number of theophylline slow release 350 mg tablets and furosemide 40 mg tablets he was admitted with unspecific clinical signs like tachyarrhythmia, vomiting and restlessness. Maximum theophylline concentration was 66.5 mg/l, other abnormal laboratory findings included hypokalemia (2.8 mmol/l) and hyponatremia (123 mmol/l). The maximum creatinkinase level was measured after admission (32.29 μmol/s/l) accompanied by a serum myoglobin level of 3,789 μg/l. Immediate treatment with oral activated charcoal and continuous veno-venous hemodialysis (CVVH) was instituted, together with intravenous potassium and sodium chloride substitution, forced diuresis and continuous administratin of intravenous metoprolol. The theophylline, creatinkinase and myoglobin levels decreased rapidly and there was no second rise in theophylline found. The patient survived without sequelae. Conclusion: Rhabdomyolysis is a rare complication of theophylline intoxication. In literature only a small number of cases are reported. Our results illustrate the necessity of a purposeful and fast management to successfully prevent renal failure or death. Some pathogenetic mechanisms of theophylline-induced rhabdomyolysis, epidemiologic data, risk factors and therapeutical principles will be demonstrated by a detailed literature survey.
BMC Neurology | 2014
Gustav Pfeiffer; Rüdiger Pfeifer; Stefan Isenmann
BackgroundBilaterally absent N20 components of the sensory evoked potentials (SEP) from the median nerve are regarded as accurately predicting poor outcome after cardiac arrest.Case presentationWe are reporting on a patient, who regained consciousness despite this ominous finding. Early after cardiac arrest, MRI showed signal alterations in diffusion weighted imaging (DWI) bilaterally in the primary visual and sensorimotor cortex and in the basal ganglia. SEP were repeatedly absent. The patient survived shut out form sensory and visual experience and locked in for voluntary movements, but kept her verbal competence in several languages.ConclusionSEP inform about integrity only of a narrow cortical strip. It is unguarded, but common practice, to conclude from absent SEP, that a patient has suffered diffuse cortical damage after cardiac arrest. Cerebral MRI with DWI helps to avoid this prognostic error and furthers understanding of the sometimes very peculiar state of mind after cardiac arrest.
Medizinische Klinik | 2008
Mandy Seifert; Jens Gerth; Mieczyslaw Gajda; Frank Pester; Rüdiger Pfeifer; Gunter Wolf
BACKGROUND Eosinophilia is not uncommon in clinical practice. The main causes are allergies and parasitic infections. Rarely, eosinophilia is associated with pulmonary affections, malignant tumors, gastroenteritis, and autoimmune diseases. A new classification based on pathophysiological data for the hypereosinophilic syndrome in order to simplify diagnosis and therapy was introduced in 2006. CASE REPORT A 22-year-old man was admitted to another hospital because of acute abdominal pain. An unspecific colitis was diagnosed. Blood counts showed a mild neutrophilic leukocytosis (12.6 Gpt/l) with a severe relative eosinophilia (30%), thrombocytopenia (67 Gpt/l), and an increased C-reactive protein (CRP 122 mg/l). The patient also had a deep venous thrombosis of the left leg. An explorative laparotomy was performed because of a strong suspicion of a presacral abscess. Pulmonary embolism and embolic pneumonia developed after surgery. A macular-cockade exanthema on the trunk and extremities was found. Histological examination revealed perivascular eosinophilic infiltrates. Histological and cytological analysis of bone marrow showed many eosinophilic granulocytes and a hypercellular medulla without increased numbers of blasts. No parasites in the blood and stools were found, and there was no evidence of neoplasm or cardiac involvement. p- and c-ANCAs (antineutrophil cytoplasmic antibodies), ANAs (antinuclear antibodies), and antibody against dsDNA were negative. Further genetic, FISH (fluorescence in situ hybridization), and PCR (polymerase chain reaction) analyses showed no evidence for chromosomal aberrations. An undefined hypereosinophilic syndrome with multiple organ involvement was diagnosed. Shortly after starting an oral prednisolone therapy (1 mg/kg body weight), the eosinophilia normalized. This therapy was stopped after 2 months and the patient is now, 6 months after diagnosis, in normal health. CONCLUSION As demonstrated in this case, eosinophilia requires a broad differential diagnosis. A hypereosinophilic syndrome can involve many organs and mimic other diseases. The new classification of the hypereosinophilic syndrome from 2006, based on pathophysiological insights, may foster better diagnosis and therapy for this rare disease.ZusammenfassungHintergrund:Eine Eosinophilie wird im klinischen Alltag öfter gesehen. Die häufigsten Ursachen sind allergische Erkrankungen und Parasitosen. Seltener ist eine Eosinophilie Ausdruck von Lungenerkrankungen, Malignomen, Gastroenteritiden oder Autoimmunerkrankungen. Aufgrund neuer pathogenetischer Erkenntnisse wurde im Jahr 2006 eine neue Klassifikation des hypereosinophilen Syndroms erstellt, um sowohl die Diagnostik als auch die Therapie zu vereinfachen. Eine Hypereosinophilie erfordert eine breite Differentialdiagnose.Fallbeschreibung:Ein 22-jähriger Patient wurde aufgrund akuter Bauchschmerzen in einem auswärtigen Krankenhaus aufgenommen. Es lagen ein erhöhtes C-reaktives Protein mit 122 mg/l (Norm < 7,5 mg/l), eine gering erhöhte Leukozytenzahl von 12,6 Gpt/l (Norm 4,4–11,3 Gpt/l) mit einer Eosinophilie von 30% und eine Thrombopenie von 67 Gpt/l (Norm 150–360 Gpt/l) vor. Es bestand eine tiefe Beinvenenthrombose. Aufgrund eines Abszessverdachts im präsakralen Bereich wurde eine Probelaparotomie durchgeführt. Postoperativ traten eine Lungenembolie sowie eine Infarktpneumonie mit septischem Krankheitsbild auf. Zugleich fanden sich makulöse kokardenförmige Hauteffloreszenzen am Stamm und an den Extremitäten mit histologischem Nachweis perivaskulärer eosinophiler Infiltrate und einer eosinophilen Vaskulitis. In der Knochenmarkhistologie zeigten sich zahlreiche eosinophile Granulozyten, in der Zytologie eine starke Markeosinophilie von 50% mit einem hyperzellulären Knochenmark. Eine eosinophile Leukämie wurde aufgrund des Fehlens von Blasten ausgeschlossen. Es konnten keine p- und c-ANCAs (antineutrophile zytoplasmatische Antikörper), ANAs (antinukleäre Antikörper) und Antikörper gegen dsDNA nachgewiesen werden. Umfangreiche Untersuchungen auf Parasiten fielen, wie auch die genetische und molekulare Untersuchung (kein Nachweis einer Chromosom-4q12-Deletion, keine BCR-ABL-Translokation), negativ aus. Hinweise auf das Vorliegen eines Tumors sowie einer kardialen Beteiligung ergaben sich nicht. Es wurde daher von einem undefinierten hypereosinophilen Syndrom bei der schweren Form der Eosinophilie mit letztendlich generalisiertem Befall ausgegangen. Nachdem die Therapie mit Prednisolon (1 mg/kg Körpergewicht) begonnen wurde, sanken die eosinophilen Granulozyten innerhalb weniger Tage auf Normwerte. Die Therapie wurde nach 2 Monaten beendet. Der Patient ist jetzt 6 Monate nach Diagnosestellung völlig beschwerdefrei.Schlussfolgerung:Wie dieser Fall zeigt, ist bei Eosinophilie eine breite Differentialdiagnose notwendig. Ein hypereosinophiles Syndrom kann verschiedene Organe befallen und vielfältige andere Erkrankungen vortäuschen. Die neue pathophysiologisch begründete Einteilung des hypereosinophilen Syndroms von 2006 kann zur Diagnose und bei Therapieentscheidungen hilfreich sein.AbstractBackground:Eosinophilia is not uncommon in clinical practice. The main causes are allergies and parasitic infections. Rarely, eosinophilia is associated with pulmonary affections, malignant tumors, gastroenteritis, and autoimmune diseases. A new classification based on pathophysiological data for the hypereosinophilic syndrome in order to simplify diagnosis and therapy was introduced in 2006.Case Report:A 22-year-old man was admitted to another hospital because of acute abdominal pain. An unspecific colitis was diagnosed. Blood counts showed a mild neutrophilic leukocytosis (12.6 Gpt/l) with a severe relative eosinophilia (30%), thrombocytopenia (67 Gpt/l), and an increased C-reactive protein (CRP 122 mg/l). The patient also had a deep venous thrombosis of the left leg. An explorative laparotomy was performed because of a strong suspicion of a presacral abscess. Pulmonary embolism and embolic pneumonia developed after surgery. A macular-cockade exanthema on the trunk and extremities was found. Histological examination revealed perivascular eosinophilic infiltrates. Histological and cytological analysis of bone marrow showed many eosinophilic granulocytes and a hypercellular medulla without increased numbers of blasts. No parasites in the blood and stools were found, and there was no evidence of neoplasm or cardiac involvement. p- and c-ANCAs (antineutrophil cytoplasmic antibodies), ANAs (antinuclear antibodies), and antibody against dsDNA were negative. Further genetic, FISH (fluorescence in situ hybridization), and PCR (polymerase chain reaction) analyses showed no evidence for chromosomal aberrations. An undefined hypereosinophilic syndrome with multiple organ involvement was diagnosed. Shortly after starting an oral prednisolone therapy (1 mg/kg body weight), the eosinophilia normalized. This therapy was stopped after 2 months and the patient is now, 6 months after diagnosis, in normal health.Conclusion:As demonstrated in this case, eosinophilia requires a broad differential diagnosis. A hypereosinophilic syndrome can involve many organs and mimic other diseases. The new classification of the hypereosinophilic syndrome from 2006, based on pathophysiological insights, may foster better diagnosis and therapy for this rare disease.