Kris Bauchmüller

Universitätsklinikum Freiburg, Freiburg an der Elbe, Lower Saxony, Germany

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Publications (6)18.33 Total impact

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    ABSTRACT: More intensive and novel therapy options in multiple myeloma (MM) hold the promise to improve treatment outcome. However, disease evolution, induced with long disease duration and extensive pretreatment, has resulted in changes in the biological behaviour of MM and unusual relapse emergence, such as of extramedullary (EM) disease or a shift in secretion from intact immunoglobulin (Ig) to free-light chains (FLCs) only. We studied ten patients since 2004, thoroughly assessed relevant patient characteristics, prominent similarities, SFLC-changes, therapy response, mode and speed of progression, and the incidence of light-chain escape (LCE)-MM within our entire myeloma patient cohort. Serum FLCs (SFLCs) were determined via Freelite-assay (Dade-Behringer Nephelometer). This report summarizes the to date largest series of ten patients, whose MM appeared stable, as judged by conventional monitoring of intact Ig levels, but developed severe organ dysfunction as a consequence of initially undetected LC-progression. Median number of anti-MM cycles before LCE occurrence was six, including autologous and/or allogeneic stem cell transplants and novel drugs, predominantly thalidomide, in 4/10. Classic diagnostics, such as electrophoresis and quantitative Ig measurement proved futile to detect LC-progression, whereas SFLCs were reliable markers. The LCE-MM prevalence within 407 MM patients treated in our institution between 2004 and 2007 was 2.46%. Our report suggests that early detection of LCE-MM by means of serial SFLC measurements may prevent unnecessary complications, allows to detect unusual relapse manifestations in the era of intensive and biological therapy options and possibly also permits to improve treatment results in LCE-MM.
    Journal of Cancer Research and Clinical Oncology 10/2008; 135(3):477-84. · 2.91 Impact Factor
  • Leukemia and Lymphoma 12/2007; 48(11):2255-60. · 2.30 Impact Factor
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    ABSTRACT: Renal impairment (RI) has been shown to be one major risk factor in a number of diseases and is associated with a dismal clinical outcome. However, the influence of milder degrees of renal disease is less well defined, particularly not in patients with malignant diseases. We analyzed 167 patients with solid tumors and hematological malignancies. Besides disease-specific parameters, serum creatinine, cystatin C and the estimated glomerular filtration rate (eGFR) ['modification of diet in renal disease' equation (MDRD)/Cockcroft-Gault (CG)] were determined. Patients were compared within eGFR, creatinine and cystatin C groups. The median MDRD, CG, creatinine and cystatin C levels of all patients were 88 ml/min/1.73 m2, 89 ml/min, 1 mg/dl and 0.9 mg/l, respectively. Patients with chronic kidney disease stage 2 still showed normal creatinine and cystatin levels of 1 mg/dl and 1.1 mg/l, respectively, although mild RI was frequent. Those cancer patients with decreased eGFR (MDRD) (<60 ml/min/1.73 m2) had increased odds ratios (ORs) to have more concurrent diagnoses [OR 3.4; 95% confidence interval (CI) 1.5-8.1], a body mass index >24 kg/m2 (OR 2.1; 95% CI 1.0-4.5) and an elevated (> 245 pg/ml) pro-brain natriuretic peptide level (proBNP) (OR 9.2; 95% CI 3.0-28.3). These observations suggest that grouping cancer patients according to renal function, especially eGFR, may be one way to determine specific risk groups.
    Annals of Oncology 05/2007; 18(5):950-8. · 7.38 Impact Factor
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    ABSTRACT: m 2 ) in 16 patients (13.1%) and MEL (200 mg/m 2 )i n 89 patients (73.0%). Two patients with concurrent secondary malignancy, one with MM and non-Hodgkin’s lymphoma (NHL) and the other with MM and solid tumor, were conditioned with BEAM (carmustine 300 mg/m 2 ,A raC 1,600 mg/m 2 , etoposide 800 mg/m 2 , MEL 140 mg/m 2 )a nd VIC (etoposide 1,500 mg/m 2 , carboplatin AUC6 d-4–d-2, ifosfamide 12,000 mg/m 2 ), respectively. Statistical analyses were carried out with SPSS software by calculating the median OS from time of PBSCT to death or last follow-up using the Kaplan–Meier method. We compared the patients in the different conditioning subgroups as summarized in Table 1: despite patients in both Bu/Cy and MEL/TBI groups being younger (52 and 50 years of age, respectively) as compared to the MEL group, this did not reach statistical significance. The percentages of stage I vs stage II/III MM were also similar in the Bu/Cy-, MEL/TBI- and MEL-conditioning groups (87%, 100% and 97%, respectively), as well as for stage III (73%, 56% and 73%, respectively). Therefore, despite our limitation of having small patient numbers in both Bu/Cy and MEL/TBI groups, we observed no significant differences between these subgroups. As shown in Fig. 1a, the median OS of all MM patients after auto-PBSCT was 59.5 months, which is comparable to earlier studies [1–4]. These have previously demonstrated a significant benefit for PBSCT as compared to standard Ctx approaches: one recent analysis of 401 patients (
    Annals of Hematology 04/2006; 85(3):191-3. · 2.87 Impact Factor
  • Annals of Hematology 12/2005; 84(12):830-2. · 2.87 Impact Factor
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    Kris Bauchmüller
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    ABSTRACT: Hydrophobe Gallensäuren führen in der cholestatischen Leber zu Zellschädigung und Apoptose. Die vorliegende Arbeit hat zum Ziel, weiteren Einblick in die Mechanismen der durch die quantitativ bedeutendste hydrophobe Gallensäure des Menschen, Chenodeoxycholsäure, induzierten Leberzellschädigung und deren Antagonisierung durch endogene und exogene Stimuli zu verschaffen und somit mögliche Ansatzpunkte neuer Therapiestrategien chronischer cholestatischer Leberkrankheiten aufzuzeigen. Die Ergebnisse zeigen, dass das Taurin- und das Glycin-Konjugat der CDCA in der intakten Leber unterschiedliche Toxizität aufweisen. Diese Beobachtung ist zumindest teilweise über eine unterschiedliche Rolle der PI3-Kinasen in der Signalgebung der beiden Gallensäuren zu erklären. Während TCDCA simultan PI3-Kinasen-abhängige Überlebenssignale zu aktivieren scheint, die ihre schädigende Wirkung antagonisieren, scheint GCDCA die Lipidkinasen an der Vermittlung seiner starken Toxizität über bislang noch unbekannte Mechanismen zu beteiligen. Die Ergebnisse des zweiten Teils der Arbeit zeigen, dass Sulfasalazin in vitro und in der intakten Leber GCDCA-induzierte Apoptose potent hemmen kann. Mögliche Wirkmechanismen dabei sind eine partielle Reduktion der Gallensäurenaufnahme und vor allem die Aktivierung intrazellulärer Überlebenssignale, die u.a. über den Transkriptionsfaktor NF-kB vermittelt werden könnten. Die neuartigen Beobachtungen der vorliegenden Arbeit könnten zum Verständnis der komplexen Signalgebung im Rahmen cholestatischer Leberschädigung und seiner Antagonisierung beitragen und sind somit von potentieller Bedeutung für die Entwicklung zukünftiger Therapiestrategien bei cholestatischen Leberkrankheiten.

Publication Stats

43 Citations
18.33 Total Impact Points

Institutions

  • 2006–2008
    • Universitätsklinikum Freiburg
      Freiburg an der Elbe, Lower Saxony, Germany
  • 2007
    • Freie Universität Berlin
      • Department of Hematology
      Freiburg, Lower Saxony, Germany
  • 2005
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany