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Antiphospholipid antibodies in patients with sensorineural hearing loss

Authors:
Edgar Bachor at Sykehuset Østfold
Edgar Bachor
Stephan Kremmer
Stephan Kremmer
Stephan Kremmer
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Ernst Kreuzfelder at University Hospital Essen
Ernst Kreuzfelder
Klaus Jahnke
Klaus Jahnke
Klaus Jahnke
  • This person is not on ResearchGate, or hasn't claimed this research yet.
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Abstract

Sensorineural hearing loss can be associated with autoimmune diseases and the presence of antiphospholipid antibodies. Sixty patients (mean age 47 years, range 18-76 years) with sudden sensorineural hearing loss were studied with audiograms, stapedial thresholds, otoacoustic emissions, positional and caloric testing. The serologic testing included antibodies against phosphatidylserine and beta(2)-glycoprotein. Additionally, a group of 34 patients (mean age 65 years, range 31-81 years) with normal tension glaucoma was examined because in a previous study these patients were reported to have elevated concentrations of antiphospholipid antibodies with a coincidence of progressive sensorineural hearing loss. The baseline for antiphospholipid antibody levels was established in a control group of 40 healthy blood donors. In 12 of the 60 patients with sudden sensorineural hearing loss, levels of antiphospholipid antibodies were elevated. Antiphosphatidylserine IgM antibodies were significantly lower compared to controls and patients with the combination of hearing loss and normal tension glaucoma (Fisher's exact two-sided test, P < 0.01). Our data suggest that antibodies against beta2-glycoprotein seem to coincidence with an acute event, such as sudden sensorineural hearing loss, whereas antibodies against phosphatidylserine IgG are detectable in the prolonged sequel, such as in patients with progressive sensorineural hearing loss and normal tension glaucoma.
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Ernst Kreuzfelder
Baltrumweg 11
4519 Essen
Lebenslauf und Ausbildung
Persönliche Daten:
Geburtsdatum: 6. September 1943
Geburtsort: Bad Wörishofen
Staatsangehörigkeit: Deutsch
Familienstand: Verheiratet. Zwei Kinder (ein Junge, ein Mädchen)
Konfession: Römisch-katholisch
Schulbildung:
1950 - 1954: Katholische Volksschule in Essen
1954 - 1960: Realschule in Essen
1963 - 1967: Bischöfliches Abendgymnasium in Essen
Ausbildung und Tätigkeit als Chemielaborant:
1960 - 1963: Lehre beim Technischen Überwachungsverein in Essen
1963 - 1966: Tätigkeit beim Technischen Überwachungsverein in Essen
Hochschulausbildung :
1967 - 1974: Studium der Physiologischen Chemie und Biochemie an der Eberhard-
Karls-Universität in Tübingen
1974: Diplomprüfung in den Fächern Physiologische Chemie und Biochemie,
Organische Chemie, Physiologie
1974 - 1975: Anfertigung der Diplomarbeit am Max-Planck-Institut für Biologie, Abtlg.
Prof. Dr. med. Henning, Tübingen, mit dem Thema "Lipopolysaccharid
und Zellform von Escherichia coli"
Wissenschaftlicher und beruflicher Werdegang
1975 - 1977: Anfertigung der Doktorarbeit am Institut für Physiologische Chemie der
Medizinischen Einrichtungen der Universität -Gesamthochschule- Essen
unter Anleitung von Prof. Dr. med. H. Schriefers. Thema: Wirkung von
Sexualhormonen auf Enzyme des Sexualhormonstoffwechsels der
Rattenleber
1978: Promotion zum Dr. rer nat. im Fachbereich Chemie der Universität -
Gesamthochschule- Essen
1978 - 1991: Tätigkeit als Wissenschaftlicher Angestellter am Institut für Medizinische
Virologie und Immunologie der Medizinischen Einrichtungen der
Universität -Gesamthochschule- Essen bis 30. 9. 1991
26.4.1990: Habilitation und venia legendi für das Fach Immunologie an der
Medizinischen Fakultät der Universität -Gesamthochschule- Essen. Thema
der Habilitationsschrift: Bestimmung von B- und T-Lymphozyten,
Lymphozytenproliferation und Autoantikörper-Konzentrationen im Blut
von Patienten mit Multipler Sklerose und alters- und geschlechtsent-
sprechenden Kontrollpersonen
1991 - jetzt: Tätigkeit als Wissenschaftlicher Angestellter am Institut für Immunologie
der Medizinischen Einrichtungen der Universität-Gesamthochschule-
Essen
Wissenschaftliche Schwerpunkte
Permeabilität: Bearbeitung analytischer Fragestellungen mittels Konzentrations-
von Proteinen bestimmungen in unterschiedlichen Kompartimenten bei verschiedenen
Krankheitsbildern wie z.B. Mammakarzinom, Niereninsuffizienz und
Schocklunge
Immunologie: Bearbeitung methodischer Fragen bei der Messung humoraler und
zellulärer Parameter und Einsatz dieser Methoden bei unterschiedlichen
Erkrankungen wie Autoimmunopathien, insbesondere Multiple Sklerose,
Schocklunge, Tumoren und Virusinfektionen
16 peer-review Originalarbeiten (5mal Erstautor). 5 Buchbeiträge. 15 publizierte
Zusammenfassungen.
Vorträge auf Nationalen und Internationalen Kongressen.
Betreuung von 4 DoktorandInnen, zwei sind promoviert.
Lehre. Akademische Selbstverwaltung.
2
Priv.-Doz. Dr.rer.nat. E. Kreuzfelder Institut für Immunologie
Originalarbeiten (Nach Habilitation)
(peer review)
1. Brockmeyer NH, Mertins L, Kreuzfelder E, Husemann M, Goos M.
Einfluß von Levomethadon aud das Immunsystem bei HIV-1-infizierten i.v.-drogenabhängigen
Patienten.
AIDS-Forschung 5, 482-486 (1990).
2. Kreuzfelder E, Obertacke U, Erhard J, Funk R, Steinen R, Scheiermann N,
Thraenhart O, Eigler FW, Schmit-Neuerburg KP.
Alterations of the immune system following splenectomy in childhood.
J Trauma 31, 358-364 (1991).
3. Eisenhut S, Kreuzfelder E, Scheiermann N, Thraenhart O.
Tumormarker (CEA,CA 15-3)- und Steroidrezeptor-Bestimmungen im Zytosol von
Mammakarzinomen.
Lab med 15, 155-157 (1991).
4. Obertacke U, Joka T, Jochum M, Kreuzfelder E, Schönfeld W, Kirschfink M.
Posttraumatische alveoläre Veränderungen nach Lungenkontusion.
Unfallchirurg 94, 134-138 (1991).
5. Obertacke U, Joka T, Kreuzfelder E.
Alveolokapilläre Albumindurchlässigkeit nach Polytrauma - Monitoring durch
bronchoalveoläre Lavage.
Pneumologie 45, 610-615 (1991).
6. Kreuzfelder E, Shen G, Bittorf M, Scheiermann N, Thraenhart O, Seidel D,
Grosse-Wilde H.
Enumeration of T, B and natural killer peripheral blood cells of patients with multiple sclerosis
and controls.
Europ Neurol 32, 190-194 (1992).
7. Wandl U, Nagel-Hiemke M, May D, Kreuzfelder E, Kloke O, Kranzhoff M, Seeber
S, Niederle N.
Lupus-like autoimmune disease induced by interferon therapy for myeloproliferative disorders.
Clin Immunol Immunopathol 65, 70-74 (1992).
8. Steinberg F, Quabeck K, Rehn B, Kraus R, Mohnke M, Costabel U, Kreuzfelder E,
Molls M, Bruch J, Schaefer U, Streffer C.
Lung effects after total body irradiation of mice and bone marrow transplant patients
comparison of experimental and preliminary clinical data..
Rec Res Cancer Res 130, 133-43 (1993).
3
9. Thraenhart O, Kreuzfelder E, Hillebrandt M, Marcus I, Ramakrishnan K, Fu ZF,
Dietzschold B.
Long-term humoral and cellular immunity after vaccination with cell culture rabies vaccines
in
man.
Clin Immunol Immunopathol 71, 287-92 (1994).
10. Kreuzfelder E, Quabeck K, Braun M, Weber W, Westhoff U, Schaefer UW, Bruch
J, Costabel U, Grosse-Wilde H.
Association of increased bronchoalveolar lavage fluid albumin and serum ß2-microglobulin
in
patients with pulmonary complications after allogeneic bone marrow transplantation.
Bone Marrow Transplant 16, 249-252 (1995).
11. Goepel M, Otto T, Möllhoff S, Hinke A, Kreuzfelder E, Rübben H.
Immunomonitoring in treatment of metastatic renal cell carcinoma with interferon-gamma.
Onkologie 18, 562-566 (1995).
12. Kreuzfelder E, Menne S, Ferencik S, Roggendorf M, Grosse-Wilde H.
Assessment of peripheral blood mononuclear cell proliferation by 2-[3H]Adenine uptake in the
woodchuck model.
Clin Immunol Immunopathol 78, 223-227 (1996).
13. Ratjen F, Kreuzfelder E.
Immunoglobulin and ß-2 microglobulin concentrations in bronchoalveolar lavage of
children and adults.
Lung 174, 383-391 (1996).
14. Menne S, Maschke T, Tolle T, Kreuzfelder E, Grosse-Wilde H, Roggendorf M.
Determination of peripheral blood mononuclear cell response to mitogens and woodchuck
hepatitis virus core antigen in woodchucks by 5-bromo-2`-deoxyuridine or 2[3H]adenine
incorporation.
Archives of Virology 142, 511-521 (1997).
15. Flach R, Flohe S, Laschinski M, Hofmann K, Kreuzfelder E, Schade FU:
Interleukin-10 is downregulated in momonuclear cells from endotoxin tolerant humans.
J Endotoxin Res 4, 189-195 (1997).
16. Kreuzfelder E, Scheiber G, Quabeck K, Schaefer UW, Bruch J, Costabel U, Grosse-
Wilde H.
Alveolo-capillary protein permeability and lung function in patients with late
complications after allogeneic bone marrow transplantation.
Lung. Im Druck.
Priv.-Doz. Dr.rer. nat. E. Kreuzfelder Institut für Immunologie
4
Buchbeiträge (Nach Habilitation)
1. Kreuzfelder E, Obertacke U, Neumann B, Thraenhart O.
Adult respiratiory distress syndrome as a manifestation of a general permeability defect.
In: Adult respiratory distress syndrome. Ed: Sturm JA. Springer-Verlag. Berlin,
Heidelberg. 1991. p 257-264.
2. Kreuzfelder E, Maghsudi M, Funk R, Thraenhart O.
CD3+, CD4+, CD8+, and B lymphocyte numbers in blood and bronchoalveolar lavage
fluid from trauma patients with and without ARDS.
In: Adult respiratory distress syndrome. Ed: Sturm JA. Springer-Verlag. Berlin,
Heidelberg. 1991. p 168-173.
3. Kaffenberger W, Kreuzfelder E, Peter RU.
Immunological abnormalities in Chernobyl accident patients with cutaneous radiation damage.
Effects of low-dose treatment with interferon-gamma. Results of a long-term follow-up study.
Advances Biosci 94, 249-259 (1994).
4. Thraenhart O, Marcus I, Kreuzfelder E.
Current and future immunoprophylaxis against human rabies: reduction of treatment
failures and errors.
Current Topics Microbiol Immunol 187, 173-193 (1994).
5. Schade FU, Flach R, Flohe S, Majetschak M, Kreuzfelder E, Dominguez E, Börgermann J,
Obertacke U.
Endotoxin tolerance.
Endotoxins in health and disease. Eds. Morrison C, Brade H, Vogel SN, Gauldy. Marcel
Dekker. Im Druck.
Priv.-Doz. Dr.rer.nat. E. Kreuzfelder Institut für Immunologie
5
Publizierte Abstracts (Nach Habilitation)
1. Moritz T, Kreuzfelder E, Nagel-Hiemke M, Nowrousian M, Niederle N, Seeber S.
Induktion von Akutphase-Proteinen unter Therapie mit Tumornekrosefaktor- (TNF-)
and Interferon- (IFN-).
Klin Wschr 69 (S XXIII), 243 (1991).
2. Joka T, Obertacke U, Kreuzfelder E, Kirschfink M, Rumler F.
Prediction model of posttraumatic lung failure by C3a and alpha-2-MG levels in
bronchoalveolar lavage fluid.
Circulatory Shock 34, 41-42 (1991).
3. Obertacke U, Joka T, Jochum M, Kreuzfelder E, Schmit-Neuerburg KP.
Biochemical monitoring of alveolar-capillary permeability for serum proteins and
prediction model of lung failure by means of serial bronchoalveolar lavage in trauma
patients.
Europ Respir Rev 1 (Suppl), 13 (1991).
4. Moritz T, Kreuzfelder E, Nagel-Hiemke M, Thraenhart O, Niederle N, Seeber S.
Widespread induction of acute phase parameters in chronic myelogenous leukemia
patients treated with repetitive TNF alpha infusions and interferon.
Ann Hematol 62, A 123 (1991).
5. Kreuzfelder E, Thraenhart O, Marcus I, Dietzschold B.
Alterations of the rhesus monkeys immune system following rabies virus infection and
monoclonal antibody treatment.
Immunobiol 183, 167 (1991).
6. Obertacke U, Joka T, Kreuzfelder E, Schmit-Neuerburg KP.
Verlaufsmessungen der alveolären Proteindurchlässigkeit nach Polytrauma durch serielle
bronchoalveoläre Lavage
Hefte zur Unfallheilkunde 220, 265-266 (1991).
7. Wandl UB, Nagel-Hiemke M, May D, Kreuzfelder E, Kloke O, Moritz T, Kranzhoff M,
Anders C, Seeber S, Niederle N.
Antinuclear antibodies (ANA) before and during interferon (Ifn) treatment in patients
(pts) with myeloproliferative disease.
Blood 78 (Suppl 1): 31a (1991).
8. Cissewski K, Rzepka A, Kreuzfelder E, Reihart W, Wagner R, Olbricht T, Reinwein D.
Transient immunodeficiency in cushing's disease - a longitudinal study.
Exp Clin Endocrinol 101 (Suppl 1), 152 (1993).
9. Kreuzfelder E, Siemes P, Wandl UB, Grosse-Wilde H. Interferon did not change
ANA specificity of antinuclear antibodies in patients with chronic myelogenous l
leukemia.
Immunobiology189, 119 (1993).
6
10. Kreuzfelder E, Grosse-Wilde H, Majetschak M, Obertacke U, Schade FU.
Alterations of HLA-DR expression on monocytes, T and B cell count after
lipopolysaccharide application and polytrauma.
Shock 6 (Suppl), 20 (1996).
11. Ditschkowski M, Kreuzfelder E, Grosse-Wilde H, Majetschak M, Schade FU.
Prediction of sepsis after trauma through measurement of HLA-DR expression on T
lymphocytes.
Immunobiology 196, 154 (1996).
12. Maschke J, Menne S, Kreuzfelder E, Roggendorf M, Grosse-Wilde H.
First evidence of low thymidine kinase activity in the woodchuck.
Immunobiology 196, 128 (1996).
13. Ditschkowski M, Kreuzfelder E, Grosse-Wilde H, Majetschak M, Schade F.
HLA-DR expression on T-cells during gram-positive sepsis after trauma.
Shock 7 (Suppl), 139 (1997).
14. Rebmann V, Kreuzfelder E, Majetschak M, Obertacke U, Schade F, Grosse-Wilde H.
Plasma levels of soluble HLA molecules in patients after polytrauma.
Shock 7 (Suppl), 105 (1997).
15. Kreuzfelder E, Ditschkowski M, Flach R, F.U. Schade, Grosse-Wilde H.
T and B cell inhibitory factors in human endotoxin tolerance.
Shock 7 (Suppl), 23 (1997).
Priv.-Doz. Dr.rer.nat. E. Kreuzfelder Institut für Immunologie
Wissenschaftliche Vorträge (Nach Habilitation)
1. Kreuzfelder E, Dietzschold B, Lücking H, Marcus I, Thraenhart O.
Long-term B and T cell immunity after rabies vaccination with tissue culture vaccines.
VIIIth International Congress of Virology. Berlin, 26.-31. August 1990.
2. Kreuzfelder E, Dietzschold B, Lücking H, Marcus I, Thraenhart O.
Langzeit B- und T-Zellreaktivität nach Tollwut-Schutzimpfung.
7
18. Tagung des Arbeitskreises für Klinische Immunologie.Frankfurt/Main, 26.-27.
Oktober 1990.
3. Kreuzfelder E, Thraenhart O, Marcus I, Dietzschold B.
CD2-Lymphozyten-Defizienz bei Rhesusaffen nach Infektion mit Tollwut-Strassenvirus
aus Thailand.
Frühjahrstagung der Gesellschaft für Virologie. Potsdam, 19.-23. März 1991.
4. Mertins L, Brockmeyer NH, Mock M, Malessa R, Kreuzfelder E, Goos M.
Clinical and immunological effects of levomethadone maintenance therapy.
Seventh International Conference on AIDS. Florenz, 16.-21. Juni 1991.
5. Kreuzfelder E, Thraenhart O, Hillebrandt M, Marcus I, Dietzschold B.
Analysis of T and B cell reactivity of rabies virus vaccinees.
8. Frühjahrstagung der Gesellschaft für Immunologie. München, 9.-11. März 1992.
6. Kreuzfelder E, Westhoff U, Grosse-Wilde H, Graben N.
Serumkonzentrationen des Beta2-Mikroglobulins und löslichen HLA Klasse I bei "high
flux"- oder "low flux"-hämodialysierten Patienten.
XX. Tagung des Arbeitskreises für klinische Immunologie. Frankfurt/Main, 6.-7.
November 1992.
7. Kreuzfelder E, Rebmann V, Westhoff U, Grosse-Wilde H.
Immundefizienz bei Strahlen-exponierten Mitarbeitern des Kernkraftwerkes Tschernobyl.
Med. A-Schutz-Tagung des BMVg. München, 24.-25. Februar 1993.
8. Kreuzfelder E., Kubens B.
Das menschliche HLA-System
Graduiertenkolleg "Zell- und Molekularbiologie normaler und maligner Zellsysteme".
Essen, 7. Juni 1993.
9. Kreuzfelder E, Quabeck K, Braun M, Schaefer UW, Grosse-Wilde H.
Bronchoalveolar lavage fluid albumin and serum ß2-microglobulin as risk factors for
developing pulmonary complications following bone marrow transplantation for
hematologic malignancy.
10th Spring Meeting of the Gesellschaft für Immunologie. Heidelberg, 9.-12. März
1994.
10. Kreuzfelder E, Quabeck K, Braun M, Weber W, Westhoff U, Schaefer UW, Bruch J,
Costabel U, Grosse-Wilde H.
Assoziation erhöhter Albumin-Konzentrationen in der Lavageflüssigkeit und ß2-
Mikroglobulin-Konzentration im Serum mit frühen und späten Lungenkomplikationen
nach allogener KMT.
XXII. Tagung des Arbeitskreises Klinische Immunologie. Frankfurt/Main, 4.-5.
November 1994.
11. Ratjen F, Kreuzfelder E.
8
Differences in BAL immunoglobulin and ß2-microglobulin levels between normal
children and adults.
5th International Conference on Bronchoalveolar lavage. Dublin, 29. Juni - 1. Juli
1995.
12. Kreuzfelder E, Menne S, Ferencik S, Roggendorf M, Grosse-Wilde H.
Messung der Proliferation mononukleärer Zellen mittels 3H-Adenin beim Woodchuck
(Hepatitismodell).
XXIII. Tagung des Arbeitskreises Klinische Immunologie. Frankfurt/Main, 3.-4.
November 1995.
13. Thraenhart O, Kreuzfelder E, Dietzschold B, Baer G.
Post-exposure treatment with a monoclonal anti-rabies virus cocktail in rhesus monkeys.
VII Annual International Meeting on Research Advances & Rabies Control in the
Americas. Atlanta. 9.-13. Dezember 1996.
14. Rebmann V, Kreuzfelder E, Majetschak M, Obertacke U, Schade F, Grosse-Wilde H.
Plasma levels of soluble HLA molecules in patients after polytrauma.
European Immunology Meeting. Amsterdam. 22.-25. Juni 1997.
15. Rebmann V, Plewa S, Kreuzfelder E, Majetschak M, Obertacke U, Schade F, Grosse-
Wilde H.
Lösliche HLA Plasmaspiegel in Patienten mit Polytrauma
5. Jahrestagung der Deutschen Gesellschaft für Immungenetik.
Priv.-Doz. Dr.rer.nat. E. Kreuzfelder Institut für Immunologie
Wissenschaftliche Poster (Nach Habilitation)
1. Kreuzfelder E, Dietzschold B, Luecking H, Marcus I, Thraenhart O.
Long-term B and T cell immunity after rabies vaccination with tissue culture vaccines
(HDCS, PCEC).
VIIIth International Congress of Virology. Berlin, 24.-31. August 1990.
2. Thraenhart O, Süss J, Kreuzfelder E, Amelung I, Müller H, Schrader A, Schiller GW.
Dosisabhängige Immunogenität des Hühnerfibroblasten-Impfstoffes (PCEC) bei
Anwendung des Essen-WHO- und des 3-1-Schemas der post-expositionellen
9
Tollwutherapie beim Menschen.
Frühjahrstagung der Gesellschaft für Virologie. Potsdam, 19.-23. März 1991.
3. Kreuzfelder E., Westhoff U, Graben N, Grosse-Wilde H.
Soluble HLA and ß2-microglobulin in patients on long-term dialysis.
25. Jahrestagung der Arbeitsgemeinschaft für Histokompatibilitätstestung. 1. Kongress
der Deutschen Gesellschaft für Immungenetik. München, 28.-30. Oktober 1993.
4. Menne S, Maschke J, Kreuzfelder E, Grosse-Wilde H, Roggendorf M.
Messung der zellulären Immunantwort im Woodchuck-Tiermodell auf der Grundlage
alternativer Thymidylat-Synthesewege.
Jahrestagung der Gesellschaft für Virologie. Jena, 6.-9. März 1996.
5. Maschke J, Menne S, Kreuzfelder E, Roggendorf M, Grosse-Wilde H.
Estimation of lymphocyte proliferation by alternative DNA synthesis pathways after
stimulation with mitogens and viral proteins.
Cold Spring Harbor Laboratory. Molecular Biology of Hepatitis B Viruses. New York,
18.-22. September 1996.
6. Maschke J, Menne S, Kreuzfelder E, Roggendorf M, Grosse-Wilde H.
Thymidin-Kinase-Aktivität peripherer Blutlymphozyten von Woodchuck und Mensch
als limitierender Faktor für dei Verwendung von [3H]Thymidin zur in-vitro Messung
der zellulären Immunantwort.
Jahrestagung der Gesellschaft für Virologie. Hamburg. 10.-13- März 1997
Lehrtätigkeit (Nach Habilitation)
a. Pflichtveranstaltungen
Praktikum der Mikrobiologie und Immunologie WS 90/91 bis jetzt
Anteil 1,2 Semesterwochenstunden (SWS)
b. Wahlpflichtveranstaltungen
Vorlesung Medizinische Mikrobiologie WS 90/91 bis jetzt
Anteil wechselnd durchschnittlich 0,4 SWS
10
WS 90/91 bis WS 91/92
Konzepte der Viruspathogenese und Virusabwehr 0,2 SWS
Virologische Labordiagnose 0,2 SWS
Virusinfektionen in den Tropen 0,2 SWS
Doktorandenkolloquium 0,1 SWS
SS 92 bis WS 94/95
Immunbiologie der Organtransplantation 0,4 SWS
Immunologische Toleranz und Autoaggression 0,4 SWS
SS 95 bis jetzt
Immunologische Toleranz und Autoaggression 0,4 SWS
c. Betreuung von Doktoranden
Mathias Heribert Hillebrandt
Humorale und zelluläre Langzeitimmunität nach Tollwutschutzimpfung.
Essen, 1994
Petra Siemes
Spezifizierung antinukleärer Antikörper bei myeloproliferativen Erkrankungen und
Interferon-Therapie.
Essen, 1996
Z. Zt. betreue ich cand.med. J.E. Maschke (Proliferationsmessungen beim Woodchuck)
und cand.med. M. Ditschkowski (Immunologie der Sepsis bei Schwerverletzten). Die
Experimente sind fast abgeschlossen. Ein Manuskript (Maschke) ist beim J. Biol. Chem.
eingereicht und es bestehen begründete Aussichten, daß es publiziert wird. Herr Ditschkowski
hat ebenfalls ein Manuskript erstellt, das beim J. Clin. Invest. eingereicht
wird.
Bei weiteren 17 Promotions-Verfahren war ich 2. Gutachter; bei insgesamt 7 Verfahren
führte ich den Vorsitz.
d. Sonstige
Seit 1991 erteile ich Unterricht im Fach Immunologie in der Lehranstalt für Technische
Assistenten in der Medizin des Universitätsklinikums Essen
Akademische Selbstverwaltung (Nach Habilitation)
a.) Fachbereichsrat:
Vom 1.7.1996 bis zum 30.6.1998 bin ich als Ersatzkandidat gewählt worden.
Vom 1.7.1994 bis zum 30.6.1996 war ich Mitglied des Fachbereichsrat, der
Kommission zur Verleihung der Bezeichnung "außerplanmäßiger Professor".
b) Kommissionen
11
Ich war Mitglied der Berufungskommission zur Wiederbesetzung der Universitätsprofessur
(C3) "Biochemische Pharmakologie" (Nachfolge Prof. Dr. K.
Aktories).
Forschungsprojekte mit Mitteln Dritter
Deutsche Forschungsgemeinschaft; Sachbeihilfe; Kr 844; 1984 - 1988
Deutsche Krebshilfe; Sachbeihilfe; Thraenhart, Marcus, Kreuzfelder; 1990 - 1994
Deutsche Forschungsgemeinschaft; Sachbeihilfe; Grosse-Wilde und Kreuzfelder; Gr 608;
1994-1996
12
Mitgliedschaften
Member of the European Society of Shock
Mitglied der Deutschen Gesellschaft für Immungenetik
Mitglied der Deutschen Gesellschaft für Immunologie
Mitglied der Gesellschaft für Virologie
13
Gutachter:
Prof. Dr. H.H. Peter
Medizinische Klinik
Abt. für Rheumatologie/Klinische Immunologie
Albert-Ludwigs-Universität
Hugstetter Str. 55
79106 Freiburg
T: 0761-270-3448
FAX: 0761-270-3446
Prof. Dr. H. Redl
Abt. für Biochemie
Ludwig Boltzmann Institut für Experimentelle und Klinische Traumatologie
Donaueschingenstr. 13
A-1200 Wien
T: 0043-1-331-10-489
FAX: 0043-1-331-10-460
14
... Regarding the potential correlation between NTG and progressive SNHL, some authors focused on the role of autoantibodies against antigens in the inner ear [91,92]. ...
... Both Kremmer S. and Bachor E. evaluated the role of autoimmunity in NTG and SNHL by measuring the serum levels of antiphosphatidylserine antibodies (APSA), one of the hallmarks of the antiphospholipid syndrome [91,92]. Kremmer et al. showed that patients with NTG had significantly higher concentrations of IgG APSA compared to controls (p < 0.05), and elevated APSA concentrations showed significantly higher concentrations in NTG with progressive SNHL compared to NTG patients with normal hearing (p< 0.01) [92]. ...
... Kremmer et al. showed that patients with NTG had significantly higher concentrations of IgG APSA compared to controls (p < 0.05), and elevated APSA concentrations showed significantly higher concentrations in NTG with progressive SNHL compared to NTG patients with normal hearing (p< 0.01) [92]. Significantly higher concentrations of IgG APSA in NTG with progressive SNHL compared to normal hearing and controls were also found by Bachor et al., who additionally found the concentrations of IgM APSA were significantly elevated in all subgroups of NTG patients, as well as in in NTG patients with normoacusis, compared to controls [91]. The exact mechanisms underlying the association between APSA levels and NTG are not fully understood; however, higher levels of APSA in patients with NTG could be indicative of an underlying autoimmune or vascular mechanism contributing to the pathogenesis of NTG. ...
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Full-text available
  • Feb 2024
Purpose: To investigate the relationship between glaucoma, pseudoexfoliation and hearing loss (HL). Methods: A systematic literature search following PRISMA guidelines was conducted using the PubMed, Embase, Scopus and Cochrane databases from 1995 up to 28 August 2023. Results: Thirty studies out of the 520 records screened met the inclusion criteria and were included. Most articles (n = 20) analysed the association between pseudoexfoliation syndrome (XFS) and HL, showing XFS patients to have higher prevalence of sensorineural hearing loss (SNHL) at both speech frequencies (0.25, 0.5, 1 and 2 kHz), and higher frequencies (4 and 8 kHz) compared to controls in most cases. No significant differences in prevalence or level of HL between XFS and pseudoexfoliative glaucoma (XFG) were detected in most studies. Eight articles analysed the relationship between primary open-angle glaucoma (POAG) and HL. Overall, a positive association between the two conditions was highlighted across all studies except for two cases. Similarly, articles focusing on NTG and HL (n = 4) showed a positive association in most cases. The role of autoimmunity and, in particular, the presence of antiphosphatidylserine antibodies (APSA) in patients with NTG and HL suggested an underlying autoimmune or vascular mechanism contributing to their pathogenesis. Only one study analysed the relationship between angle-closure glaucoma (ACG) and HL, showing higher incidence of ACG in patients with SNHL compared to normal hearing controls. Conclusions: Most studies detected an association between XFS and HL as well as POAG/NTG/ACG and HL, suggesting the presence of a similar pathophysiology of neurodegeneration. However, given the strength of the association of XFS with HL, it remains unclear whether the presence of XFG is further associated with SNHL. Further research specifically targeted to assess the correlation between glaucoma, XFS and HL is warranted to provide a more comprehensive understanding of this association.
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... Similar percentages were seen in patients with Meniere's syndrome or SSNHL [9]. In these two disorders, anti-b2 glycoprotein-I antibody would play a major role in their physiopathogenesis [10]. ...
Sudden sensorineural hearing loss in Systemic Lupus Erythematosus and Antiphospholipid Syndrome. An Update
Article
  • Oct 2019
Background: Sudden sensorineural hearing loss (SSNHL) is defined as a sudden loss of hearing, usually unilateral, of more than 30 dB in 3 contiguous frequencies of the tonal audiometry. SSNHL estimates an incidence ranging from 5 to 20 per 100.000 people per year. In approximately 75% of cases, a cause cannot be identified. However, it could be a clinical manifestation of Systemic lupus erythematosus (SLE) and Antiphospholipid Syndrome (APS). Objective: This review will focus on the clinical presentation, diagnosis, and management of the SLE and APS associated SSNHL. Methods: We searched in PubMed, Scopus, Lilacs, and Cochrane reviewing reports of Sudden sensorineural hearing loss in SLE and/or APS. Articles written in English and Spanish, and were available in full text, were included. Results: In patients with SLE, bilateral involvement was frequent. Antiphospholipid antibodies were positive in the majority of the patients. Corticosteroids were the mainstay of the treatment. The auditory prognosis was poor with total hearing loss recovery reached in only 22% of patients. On the other hand, most of the patients with SSNHL and APS were males and presented associated symptoms such as vertigo, tinnitus and/or headache, 75% had bilateral disease. Lupus anticoagulant and aCL were found in equal proportions, all patients were anticoagulated, and aspirin was associated in 25% of the cases. Complete resolution or improvement of symptoms was observed in 25% of the patients. Conclusion: Sudden sensorineural hearing loss, can be a clinical feature of SLE and APS. Treating physicians should be aware of this devastating complication, especially when bilateral involvement occurs.
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... Immunological disorders including autoimmune conditions (e.g. Cogan's syndrome) may be another possible cause ( Bachor et al., 2005) Goodhill V et al., 1976). Blood flow change in the inner ear is considered one of the pathophysiological mechanisms in SSHL. ...
Sudden sensorineural hearing loss (SSHL) following a local anesthetic dental procedure
Article
Full-text available
  • May 2019
Acute sensorineural hearing loss is an uncommon phenomenon in dentistry. We describe the case of a 79-year-old male who presented with acute sensorineural hearing loss occurring 2 days after a tooth extraction procedure under local anesthesia. Possible mechanisms are discussed. He was treated with vasodilators (Ginaton and Alprostadil Injection) and Mecobalamin injection with benefit. High dose oral steroids (1 mg/kg) and low molecular weight dextran were used. Keywords: Sudden sensorineural hearing loss, Dental procedure, Acute hearing loss
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... Antiphosphatidylserine IgM antibodies were significantly lower compared to controls and patients with the combination of hearing loss and normal-tension glaucoma (Fisher's exact two-sided test, P \ 0.01). The antibodies against beta2-glycoprotein seem to coincidence with an acute event, such as sudden sensorineural hearing loss, whereas antibodies against phosphatidylserine IgG are detectable in the prolonged sequel, such as in patients with progressive sensorineural hearing loss and normal-tension glaucoma [73]. ...
Glaucoma: recent advances in the involvement of autoimmunity:
Article
Full-text available
  • Feb 2017
Glaucomatous optic neuropathy is the most commonly acquired optic neuropathy encountered in clinical practice. It is the second leading cause of blindness globally, after cataracts, but it presents a greater public health challenge than cataracts, because the blindness it causes is irreversible. It has pathogenesis still largely unknown and no established cure. Alterations in serum antibody profiles, upregulation, and downregulation have been described, but it still remains elusive if the autoantibodies seen in glaucoma are an epiphenomenon or causative. Hypertension, diabetes, and hearing disorders also are associated. This review is a glaucoma update with focus about the recent advances in the last 15 years.
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... This is mainly because a direct investigation of labyrinthine tissue in a living patient is not yet possible without permanent damage of the inner ear and postmortem histopathology is rarely available. Therefore, animal models that mimic the disease entity have been developed, as well as indirect diagnostic tools, such as serologic testing for different agents, in order to unravel the pathogenesis of ISSNHL [Satoh et al., 2003;Bachor et al., 2005;Solares and Tuohy, 2005;Merchant et al., 2008]. The central nervous system, and the inner ear by extension, were originally thought to be immunoprivileged sites due to the presence of the blood-brain and the blood-labyrinthine barriers, respectively [Bodmer et al., 2002]. ...
The Expression of TNFα, IL-6, IL-2 and IL-8 in the Serum of Patients with Idiopathic Sudden Sensorineural Hearing Loss: Possible Prognostic Factors of Response to Corticosteroid Treatment
Article
Full-text available
  • Apr 2016
Introduction: Idiopathic sudden sensorineural hearing loss (ISSNHL) remains one of the major unsolved otologic emergencies. A viral infection, a systemic inflammatory disorder, as well as physical, mental and metabolic stress can trigger an innate immune response in the inner ear resulting in ISSNHL. Proinflammatory cytokines play a central role in this cochlear immunological cascade. Objective: To examine the expression of proinflammatory cytokines in the serum of patients with ISSNHL in correlation with the therapeutic outcome of intravenous administration of corticosteroids. Method: Forty-three patients primarily diagnosed with ISSNHL underwent intravenous corticosteroid treatment for 8 days. The expression of tumor necrosis factor-α (TNFα), interleukin-6 (IL-6), interleukin-2 (IL-2) and interleukin-8 (IL-8) was detected with the use of enzyme-linked immunosorbent assay in serum specimens on the 1st and 8th day of treatment and it was correlated with the treatment outcome. Results: TNFα reduction and IL-6 increase strongly correlate with a good therapeutic result [χ2(2) = 13.12, p = 0.001 and χ2(2) = 16.78, p = 0.0001]. IL-8 increase reflects negatively on the outcome, however, not in a statistically significant way. No association was established between IL-2 variations and the therapeutic outcome. Conclusions: TNFα and IL-6 can be used as prognostic factors for the treatment outcome, whereas the prognostic value of IL-8 requires further statistical confirmation.
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Sudden Sensorineural Hearing Loss During Pregnancy and the Postpartum Period
Chapter
  • Aug 2022
Sudden sensorineural hearing loss (SSNHL) is defined as a hearing loss of at least 30 dB that occurs within 72 h at three contiguous frequencies. Although this is the general acceptance, there is no consensus regarding the degree of hearing loss and the duration of its occurrence [1]. Bilateral involvement is rare. Accompanying symptoms may include fullness in the affected ear, varying degrees of tinnitus, dizziness, and impaired balance [2, 3]KeywordsSudden hearing lossInner earOtolaryngologyPregnancyPostpartum period
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Open-angle Glaucoma and Sensorineural Hearing Impairment in the Korean Population
Article
  • Jan 2020
Purpose: This study identifies the prevalence and risk factors of sensorineural hearing loss and primary open-angle glaucoma (POAG). Materials and methods: Patients aged 19 years or older who had undergone both ophthalmologic examination and audiometry as part of the Korea National Health and Nutrition Examination Survey V (2010-2012) were analyzed. Hearing loss was defined as the pure-tone average over 40 decibels based on the automatic hearing test to determine the threshold of airway hearing for each frequency. We investigated the prevalence of glaucoma and hearing loss when they occurred alone or simultaneously. The risk factors for concurrent glaucoma and hearing loss were examined. Result: Among the participants, 6.6% had hearing loss alone, 2.3% had glaucoma alone, and 0.5% had both glaucoma and hearing loss. The weighted prevalence of glaucoma in patients with hearing loss was 7.5%; however, the weighted prevalence of glaucoma was 3.2% among patients without hearing loss, with a significant difference (P <0.001). Multivariable logistic regression analysis revealed that the risk factors associated with concurrent glaucoma and hearing loss were age (3.786 times per 10 years, P <0.001) and triglyceride level (1.002 times per 1 mg/dL, P = 0.028). Conclusion: Sensorineural hearing loss and POAG are relevant. If hearing impairment and visual impairment occur together, the quality of life of the patient is worsened and the social burden is greater. Therefore, care should be taken when treating elderly patients with glaucoma.
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Deep capillary retinal ischemia and high-titer prothrombin-associated antiphospholipid antibodies: A case series of three patients
Article
Full-text available
  • Apr 2019
Purpose: Acute macular neuroretinopathy has been shown to be due to ischemia of the deep capillary retinal plexus and most cases occur in young women; we hypothesized that there may be an association with antiphospholipid antibodies. Observations: We identified three patients who were diagnosed with deep capillary retinal ischemia after presenting with sudden onset of focal paracentral scotoma who tested persistently positive for antiphospholipid antibodies. All patients had high-titer prothrombin-associated antibodies and two of the three also had low-titer anticardiolipin antibodies. In all patients, the diagnosis was missed at the initial presentation. All patients experienced involvement of both eyes over time with permanent visual deficits and all were female with an average age at symptom onset of 34 years. All patients were using exogenous estrogen and had additional but previously undiagnosed symptoms or signs that may be seen in the antiphospholipid syndrome. One patient was ANA positive with a titer of 1:320, but none had lupus-specific antibodies or clinical features of lupus. Conclusions and importance: The persistent presence of high-titer prothrombin-associated antiphospholipid antibodies in three women with deep capillary retinal ischemia suggests this may be an important association. Prothrombin-associated antibodies (anti-prothrombin IgG and anti-phosphatidylserine-prothrombin IgG and IgM) as well as the traditional antiphospholipid antibodies (anticardiolipin IgG, IgM and IgA; anti-beta 2 glycoprotein I IgG, IgM and IgA; and the lupus anticoagulant) should be included in the diagnostic work-up of patients diagnosed with deep capillary retinal ischemia. Because of the broader health and treatment implications of high-titer antiphospholipid antibodies, further investigation into this suspected association is warranted.
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Emerging Concepts in Glaucoma and Review of the Literature
Article
  • Apr 2016
Glaucoma is the most commonly acquired optic neuropathy. It represents a public health challenge because it causes an irreversible blindness. Emerging evidence indicates that the pathogenesis of glaucoma depends on several interacting pathogenetic mechanisms, which include mechanical effects by an increased intraocular pressure, decreased neutrophine-supply, hypoxia, excitotoxicity, oxidative stress and the involvement of autoimmune processes. In particular, alterations in serum antibody profiles have been described. However, it is still unclear wether the autoantibodies seen in glaucoma are an epiphenomenon or causative. Oxidative stress appears to be a critical factor in the neurodestructive consequences of mitochondrial dysfunction, glial activation response, and uncontrolled activity of the immune system during glaucomatous neurodegeneration. In addition, hearing loss has been identified in association with glaucoma. A higher prevalence of antiphosphatidylserine antibodies of the IgG class was seen in normal-tension-glaucoma patients with hearing loss in comparison to normal-tension glaucoma patients with normacusia. This finding suggests a similar pathological pathway as a sign for generalised disease.
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Inner Ear Autoantibodies and their Targets in Patients with Autoimmune Inner Ear Diseases
Article
  • Jan 2001
Immunological mechanisms are thought to play an important role in the pathogenesis of some cochleo-vestibular diseases. This study attempts to present further evidence of autoantibodies reactive against guinea pig inner ear proteins found in patients with autoimmune inner ear diseases (AIED) and specifically identifies the main target antigens of these antibodies. Sera from 110 patients with a clinical diagnosis of either rapidly progressive sensorineural hearing loss (n = 32). Meniere's disease (n = 41), sudden deafness (n = 6) or other aetiologies of hearing loss (n = 11) were screened by the Western blot technique. Forty-four percent of the patients' sera had antibodies to several inner ear proteins, of which the 30, 42 and 68 kDa proteins were found to be the most reactive. These highly reactive proteins were identified by gas-phase micro sequencing after digestion with trypsin and separation of peptide fragments by high-performance liquid chromatography. A partial sequence of each protein was determined. These data, together with those obtained from 2-dimensional gel electrophoresis followed by Western blotting, demonstrated that the 30 and 42 kDa inner ear proteins are the major peripheral myelin protein P0 and the beta-actin protein, respectively, while sequence analysis indicated that the 68 kDa protein is novel. These findings further support the hypothesis that several populations of antibodies may contribute to the enhanced immunological activity of AIED patients. They also add a new dimension to our knowledge of AIED and may open new avenues in the development of simple serological assays, which are easier to perform and more rapid than Western blotting.
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Platelet-Endothelial Interactions: Sepsis, HIT, and Antiphospholipid Syndrome
Article
  • Jan 2003
Acquired abnormalities in platelets, endothelium, and their interaction occur in sepsis, immune heparin-induced thrombocytopenia (HIT), and the antiphospholipid syndrome. Although of distinct pathogeneses, these three disorders have several clinical features in common, including thrombocytopenia and the potential for life- and limb-threatening thrombotic events, ranging from microvascular (sepsis > antiphospholipid > HIT) to macrovascular (HIT > antiphospholipid > sepsis) thrombosis, both venous and arterial. In Section I, Dr. William Aird reviews basic aspects of endothelial-platelet interactions as a springboard to considering the common problem of thrombocytopenia (and its mechanism) in sepsis. The relationship between thrombocytopenia and other aspects of the host response in sepsis, including activation of coagulation/inflammation pathways and the development of organ dysfunction, is discussed. Practical issues of platelet count triggers and targeted use of activated protein C concentrates are reviewed. In Section II, Dr. Theodore Warkentin describes HIT as a clinicopathologic syndrome, i.e., the diagnosis should be based on the concurrence of an appropriate clinical picture together with detection of platelet-activating and/or platelet factor 4-dependent antibodies (usually in high levels). HIT is a profound prothrombotic state (odds ratio for thrombosis, 20–40), and the risk for thrombosis persists for a time even when heparin is stopped. Thus, pharmacologic control of thrombin (or its generation), and postponing oral anticoagulation pending substantial resolution of thrombocytopenia, is appropriate. Indeed, coumarin-associated protein C depletion during uncontrolled thrombin generation of HIT can explain limb loss (coumarin-associated venous limb gangrene) or skin necrosis syndromes in some patients. In Section III, Dr. Jacob Rand presents the most recent concepts on the mechanisms of thrombosis in the antiphospholipid syndrome, and focuses on the role of β2-glycoprotein I as a major antigenic target in this condition. Diagnosis of the syndrome is often complicated because the clinical laboratory tests to identify this condition have been empirically derived. Dr. Rand addresses the practical aspects of current testing for the syndrome and current recommendations for treating patients with thrombosis and with spontaneous pregnancy losses.
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Sicca-Symptomatik und Hörverlust beim Behçet-Syndrom
Article
  • May 1998
Anamnese und klinischer Befund: Eine 39jährige Patientin erlitt einen irreversiblen Hörverlust des linken Ohres, ein halbes Jahr später eine Fazialisparese links. Im Mund traten immer wieder Aphthen auf, gleichzeitig Fieber bis 39,5.°C. Der Allgemeinzustand der relativ jungen Frau war deutlich reduziert. Untersuchungen: Auf eine Entzündung wiesen die erhöhte Blutsenkungsgeschwindigkeit (70/100 mm), die Leukozytenzahl (18 500/µl), der Hämoglobinspiegel (10,2 g/l) und eine Linksverschiebung der neutrophilen Granulozyten hin. Diagnostische Maßnahmen zum Ausschluß infektiöser, autoimmunologischer oder hämato-onkologischer Krankheit blieben ohne wegweisende Ergebnisse. Therapie und Verlauf: Eine antibiotische und antimykotische Therapie brachten keine durchschlagende Besserung. Im weiteren Verlauf traten Thrombophlebitiden bzw. venöse Thrombosen an beiden oberen Extremitäten sowie eine akute Episkleritis (Skleritis) des linken Auges auf. Nach Diagnose eines Behçet-Syndroms mit oraler, okulärer, neurologischer, kutaner und vaskulärer Beteiligung wurde eine Therapie mit Chlorambucil (variabel, um 7 mg/d oral) durchgeführt, unter der sich die Symptome rasch zurückbildeten. Ein Vierteljahr später traten Gelenkschmerzen auf, weitere 18 Monate später eine okuläre Sicca-Symptomatik. Beides ließ sich durch symptomatische Maßnahmen beherrschen. Folgerung: Die Kombination eines Hörverlustes und einer Sicca-Symptomatik bei Behçet-Syndrom wurde bisher noch nicht beschrieben.
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Immunologic and Serologic Testing in Patients with M??ni??re's Disease
Article
  • Jul 2002
Objective: To establish the value of immunologic and serologic testing in patients with Ménière's disease. Study Design: Prospective cohort. Setting: University-based, tertiary care balance center. Intervention: Patients with active unilateral or bilateral Ménière's disease underwent testing, including antinuclear antibodies, anti-DNA antibodies, rheumatoid factor, complement levels, anti-Sjögren syndrome A and B antibodies, sedimentation rate, antiphospholipid antibodies, Western blot for anticochlear antibodies (anti-heat shock protein 70), microhemagglutination test for Treponema pallidum, and Lyme titers. Outcome Measures: Results of laboratory tests. Results: In patients with unilateral Ménière's disease (n = 40), 27% demonstrated elevated antiphospholipid antibody titers (population norm, 6–9%). The majority of these patients manifested negative assays on the other tests listed above. In patients with bilateral Ménière's disease (n = 18), elevations in antinuclear antibody titers (38%) were the most notable finding. As part of a broader study of patients with progressive hearing loss, four patients with positive syphilis titers were identified; however, none of these patients complained of vertigo. Conclusion: In general, the results of this study do not support the hypothesis that immune or infectious pathologies are involved in the pathogenesis of unilateral Ménière's disease. In particular, Lyme disease does not seem to cause labyrinthine disease. However, the potential role of the thrombogenic antiphospholipid antibodies must be further investigated. Patients with bilateral Ménière's disease may be more likely to have a systemic autoimmune process.
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The Antiphospholipid Syndrome
Article
  • Nov 2003
The antiphospholipid (aPL) antibody syndrome is an autoimmune condition in which vascular thrombosis and/or recurrent pregnancy losses occur in patients with laboratory evidence for antibodies that bind to phospholipids. There have been significant advances in the recognition of the role of phospholipid-binding cofactors, primarily β2GPI, as the true immunologic targets of the antibodies. Recent evidence suggests that the antibodies disrupt phospholipid-dependent anticoagulant mechanisms and/or that aPL antibodies induce the expression of procoagulant and proadhesive molecules on endothelial cells. Current diagnosis is based on clinical findings and empirically derived tests, such as assays for antibodies that bind to phospholipids or putative cofactors and coagulation assays that detect inhibition of phospholipid-dependent coagulation reactions. Current treatment relies primarily on anticoagulant therapy. Research advances are expected to bring mechanistically based diagnostic tests and improved therapy ...
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Sudden sensorineural hearing loss in patients with systemic lupus erythematosus or lupus-like syndromes and antiphospholipid antibodies
Article
  • Mar 1998
Although the pathogenesis of sudden sensorineural hearing loss (SNHL) in patients with systemic lupus erythematosus (SLE) is not clear, several reports suggest an association with the antiphospholipid antibody (aPL). We describe 6 patients with SLE or a lupus-like syndrome, who had sudden SNHL and had elevated levels of anticardiolipin antibodies (aCL) or the lupus anticoagulant. In a literature search, of 5 additional reported cases, 2 were not tested for aPL; the remaining 3 had elevated aCL levels. Thus, acute SNHL in patients with SLE who have aPL may be a manifestation of the antiphospholipid syndrome. We recommend anticoagulation treatment of these patients.
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Sensorineural Hearing Loss Associated With Systemic Lupus Erythematosus
Article
  • Mar 1986
Because our recent clinical experiences suggested a possible association between hearing loss and systemic lupus erythematosus (SLE), we prospectively studied the hearing of 30 patients hospitalized because of exacerbation of SLE. Twenty-nine of the 30 patients were receiving immunosuppressive therapy at the time of testing. We found an 8% incidence of substantial, previously undetected hearing loss without attributable cause. Hearing loss could not be correlated to age, sex, disease activity, organ-system involvement, laboratory test abnormalities, or duration of symptoms of SLE. Otolaryngologists treating patients with unexplainable hearing loss--particularly if it is sudden, fluctuating, or rapidly progressive--are alerted to the possibility of underlying systemic autoimmunity. We advise physicians who frequently treat patients with SLE to include questions on hearing in the review of systems and to refer the patient with hearing complaints for thorough otologic evaluation.
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Sensorineural Hearing Loss in Lupus Erythematosus
Article
  • Jun 1986
  • Am J Otol
A 51-year-old woman had sudden profound sensorineural hearing loss (SNHL) in her right ear, followed by profound SNHL in her left ear three weeks later. On subsequent work-up, a diagnosis of systemic lupus erythematosus (SLE) was made on the basis of an antinuclear antibody titer of 1:500 and immunofluorescence below the dermis on skin and muscle biopsy specimens. Treatment with prednisone and cyclophosphamide did not improve the hearing loss. To our knowledge, this is the second reported case of SLE occurring with SNHL and the first reported case of bilateral hearing loss.
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Sudden Hearing Loss: Eight Years' Experience and Suggested Prognostic Table
Article
  • Jun 1984
The etiology, incidence, acute and late prognosis, and treatment of sudden hearing loss (SHL) are described variously in the literature. In an 8-year prospective study of 225 SHL patients, initiated in July 1973, overall, normal, or complete recovery occurred in 45% of patients and late otologic complications in 28%. Important prognostic indicators were severity of initial hearing loss and vertigo, time to initial audiogram, and elevated erythrocyte sedimentation rate; other indicators were age greater than 60 and less than 15 years, midfrequency audiogram configuration, and hearing status of the opposite ear. A common inflammatory cause is suggested for all degrees of severity in SHL, and a prognostic table is provided to aid the practitioner in predicting recovery. There is still no evidence that treatment achieves a result better than expected with spontaneous recovery.
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