Zusammenfassung
Wir berichteten über eine junge Fußballspielerin, die im Alter von 21 Jahren zunächst eine transitorisch ischämische Attacke und ein halbes Jahr später einen akuten Myokardinfarkt bei zugleich bestehender Thrombozytopenie erlitt. Ursache hierfür war ein Antiphospholipidsyndrom. Dieses Erkrankungsbild wird durch eine sehr heterogene Gruppe von Antiphospholipidantikörpern ausgelöst. Diese greifen an verschiedenen Stellen der plasmatischen Gerinnung ein und vermögen Thrombozyten, Endothelzellen wie auch Monozyten zu aktivieren. Dies führt zu einem thrombophilen Zustand, welcher sich klinisch durch das rezidivierende Auftreten von venösen Thrombosen, arteriellen Embolien oder Frühgeburten bzw. Aborten manifestiert. Therapeutisch stehen deshalb orale Antikoagulation, Heparine und Aspirin im Vordergrund. Bei ausgeprägten Thrombozytopenien werden Steroide und bei deren Versagen auch Immunsuppressiva empfohlen.
Gerade bei jungen Patienten mit thromboembolischen Ereignissen sollte an das Antiphospholipidsyndrom gedacht werden, da sich innerhalb dieser Patientengruppe zu 10–20% Antiphospholipidantikörper nachweisen lassen und eine effektive Therapie nach Diagnosestellung das Rezidivrisiko senkt.
Abstract
We report on a case of a young female soccer player who first experienced a transient ischemic attack at the age of 21 and then suffered an acute myocardial infarction accompanied by thrombocytopenia 6 months later. The underlying cause was antiphospholipid syndrome. This clinical picture is caused by a very heterogeneous group of antiphospholipid antibodies, which interfere with plasmatic coagulation at various sites and are able to activate thrombocytes, endothelial cells, and monocytes. This leads to a thrombophilic condition with clinical manifestation of recurrent venous thromboses, arterial embolisms, or premature birth or miscarriage. The main therapeutic options are thus anticoagulation, heparins, and aspirin. Steroids are recommended for cases of pronounced thrombocytopenias; if treatment fails, immunosuppressants are also advisable.
The antiphospholipid syndrome should be kept in mind especially in cases of young patients with thromboembolic events since the presence of antiphospholipid antibodies can be detected in 10–20% of this patient group and effective therapy after diagnosis lowers the rate of recurrence.
Literatur
Thiagarajan P, Pengo V, Shapiro SS (1986) The use of dilute Russel viper venom time for the diagnosis of lupus anticoagulant. Blood 68: 869–874
Vila P, Hernandez MC, Lopes-Fernandes MF, Battle J (1994) Prevalence, follow-up and clinical significance of the anticardiolipin antibodies in normal subjects. Thromb Haemost 72: 209–213
Shi W, Krilis SA, Chong BH, Gordon S, Chesterman CN (1990) Prevalence of lupus antikoagulant and anticardiolipin antibodies in a healthy population. Aust N Z J Med 20: 231–236
Fianzzi B, Brancaccio V, Moia M et al. (1996) Natural history and risk factors for thrombosis in 360 patients with antiphospholipid antibodies: A four year prospective study from Italian registry. Am J Med 100: 530
Martinuzzo ME, Maclouf J, Carreras LO, Levy-Toledano S (1993) Antiphospholipid antibodies enhance thrombin-induced platelet activation and thromboxane formation. Thromb Haemost 70: 667–671
Campbell AL, Pierangeli SS, Wellhausen S, Harris EN (1995) Comparison of the effects of anticardiolipin antibodies from patients with the antiphospholipid syndrome and syphilis on platelet activation and aggregation. Thromb Haemost 73: 529–534
McNeil HP, Simpson RJ, Chesterman CN et al. (1990) Antiphospholipid antibodies are directed against a complex antigen that includes a lipid binding inhibitor of coagulation: ß2-G lykoprotein I (apolipoprotein H). Proc Natl Acad Sci U S A 87: 4120–4124
Nimpf J, Wurm H, Kostner GM (1987) ß2-Glykoprotein I (apo-H) inhibits the release reaction of human platelets during ADP-induced aggregation. Atherosclerosis 63: 109–114
Arvieux J, Darnige L, Caron C et al. (1995) Development of an ELISA for autoantibodies to prothrombin showing their prevalence in patients with lupus anticoagulants. Thromb Haemost 74: 1120–1125
Wilson WA, Gharavi AE, KoikeT et al. (1999) International consensus statement on preliminary classification criteria for definite antiphospholipid syndrome. Arthritis Rheum 42: 1309–1311
Hamsten A, Norberg R, Bjorkholm M, de Faire U, Holm G (1986) Antibodies to cardiolipin in young survivors of myocardial infarction: an association with recurrent cardiovascular events. Lancet 8473: 113–116
Nencini P, Baruffi MC, Abbate R, Massai G, Amaducci L, Inzitari D (1992) Lupus anticoagulant and anticardiolipin antibodies in young adults with cerebral ischemia. Stroke 23: 189–193
Asherson RA, McKee PH, Farrant JM (1990) Primary antiphospholipid syndrome. Clin Exp Dermatol 15: 234
Lynch A, Marlar R, Murphy J, Davila G, Santos M, Rutledge J, Emlen W (1994) Antiphospholipid antibodies in predicting adverse pregnancy outcome. Ann Intern Med 120: 470–475
Khamashta MA, Cuadrado MJ, Mujic F et al. (1995) The management of thrombosis in the antiphospholipid-antibody syndrome. N Engl J Med 332: 993
Schmidt R, Scheuemann EH, Viertel I et al. (1999) Antiphospholipidantikörpersyndrom. Med Klin 94: 93–100
Maddison PJ, Isenberg DA, Woo P, Glass DN (2001) The antiphospholipid antibodysyndrome. In: Oxford Textbook of Rheumatology, 2nd edn, vol 2. Oxford Medical Publications, pp 1202–1215
Brunner HI, Chan WS, Ginsberg JS, Feldman BM (2002) Longterm anticoagualtion is preferable for patients with antiphospholipid antibody syndrome. J Rheumatol 29: 490–501
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Rank, A., Lindner, L. & Hiller, E. 21-jährige Patientin mit Myokardinfarkt, TIA und Thrombozytopenie. Internist 44, 349–353 (2003). https://doi.org/10.1007/s00108-002-0811-6
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00108-002-0811-6
Schlüsselwörter
- Antiphospholipidsyndrom
- Myokardinfarkt
- Thrombozytopenie
- Thromboembolie
- Transitorisch ischämische Attacke