Thromb Haemost 2004; 91(05): 1047-1049
DOI: 10.1055/s-0037-1614202
Case Report
Schattauer GmbH

Intravenous Iloprost treatment for severe bone pain caused by sickle cell crisis

Alexander Carl Disch
,
Georg Matziolis
,
Petra Reinke
,
Carsten Perka
Further Information

Publication History

Received 18 December 2003

Accepted after revision 18 February 2004

Publication Date:
15 December 2017 (online)

 

 
  • References

  • 1 Longenecker L, Beyers BJ, McMullan E. Red cell endothelial cell adhesion: role and modulation in sickle cell disease. In: Rubanyi GM, Vanhoutte PM. eds: Endothelium-Derived relaxing factors. Karger, Basle; Switzerland: 1990: 281-90.
  • 2 Zimmermann SA, Ware RE. Inherited DNA mutations contributing to thrombotic complications in patients with sickle cell disease. Am J Hematol 1998; 59: 267-77.
  • 3 Powars DR, Hiti A, Ramicone E. et al. Outcome in hemoglobin SC disease: a four decade observational study of clinical, hematologic, and genetic factors. Am J Hematol 2002; 70 (03) 206-15.
  • 4 Atsumi T, Kuroki Y. Role of impairment of blood supply of the femoral head in the pathogenesis of idiopathic osteonecrosis. Clin Orthop 1992; 227: 22-30.
  • 5 Aigner N, Petje G, Steinboeck G. et al. Treatment of bone-marrow oedema of the talus with the prostacyclin analogue iloprost. J Bone Joint Surg (Br) 2001; 83-B: 855-8.
  • 6 Petje G, Radler C, Aigner N. et al. [Aseptic osteonecrosis in childhood: diagnosis and treatment]. Orthopäde 2002; 31: 1027-38.
  • 7 Kim SK, Miller JH. Natural history and distribution of bone and bone marrow infarction in sickle hemoglobinopathies. J Nucl Med 2002; 43 (07) 896-900.
  • 8 Hofmann S, Engel A, Neuhold A. et al. Bone marrow oedema syndrome and transient osteoporosis of the hip: an MRI controlled study of treatment by core decompression. J Bone Joint Surg (Br) 1993; 75-B: 210-6.
  • 9 Schneider T, Drescher W, Becker C. et al. The impact of vasoactive substances on intraosseous pressure and blood flow alterations in the femoral head: a study based on magnetic resonance imaging. Arch Orthop Trauma Surg 1998; 118 (1–2): 45-9.
  • 10 Harris WH. Traumatic arthritis of the hip after dislocation and acetabular fractures: treatment by mold arthroplasty: an end-result study using a new method result evaluation. J Bone Joint Surg (Am) 1969; 51-A: 741.
  • 11 Vander Jagt DJ, Bonnett C, Okolo SN. et al. Assessment of the bone status of nigerian children and the aldolescents with sickle cell disease using calcaneal ultrasound and serum markers of bone metabolism. Calcif Tissue Int 2002; 71 (02) 133-40.
  • 12 Kim YM, Oh HC, Kim JH. The pattern of bone marrow edema on MR in osteonecrosis of the femoral head. J Bone Joint Surgery (Br) 2000; 82-B: 837-41.
  • 13 Krause R, Glas K, Schulz A. et al. Das transitorische Knochenmarködemsyndrom der Hüfte. Z Orthop 141: 286-96.
  • 14 Mont MA, Hungerford DS. Non traumatic avascular necrosis of the femoral head. J Bone Joint Surg (Am) 1995; 77-A: 459-74.
  • 15 Brugnara C, De Franceschi L, Beuzard Y. Erythrocyte-active agents and treatments of sickle cell disease. Semin Hematol 2001; 38 (04) 324-32.
  • 16 Marlowe KF, Chicella MF. Treatment of sickle cell pain. Pharmacotherapy 2002; 22 (04) 484-91.
  • 17 Grant SM, Goa KL. Iloprost: a review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in peripheral vascular disease, myocardial ischaemia and extracorporal circulation procedures. Drugs 1992; 43: 889-24.
  • 18 Setty BN, Chen D, Stuart MJ. Sickle cell vasoocclusive crisis is associated with abnormalities in the ratio of vasoconstrictor to vasodilatator prostanoids. Pediatr Res 1995; 38 (01) 95-102.
  • 19 Sowemimo-Coker SO, Haywood LJ, Meiselman HJ. et al. Effects of normal and sickle cell erythrocytes on prostacylin release by perfused human umbilical cord veins. Am J Hematol 1992; 40 (04) 276-82.
  • 20 Ueno Y, Koike H, Annoh S. et al. Anti-inflammatory effects of beraprost sodium, a stable analogue of PGI2, and its mechanisms. Prostaglandins 1997; 53 (04) 279-89.
  • 21 Shiu YT, McIntire LV, Udden MM. Sickle erythrocytes increase prostacylin and endothelin-1 production by cultured human endothelial cells under flow conditions. Eur J Heamatol 2002; 68 (03) 163-9.
  • 22 Shiu YT, McIntire LV, Udden MM. Sickle erythrocytes increase prostacylin and endothelin-1 production by cultured human endothelial cells under flow conditions. Eur J Heamatol 2002; 68 (03) 163-9.
  • 23 Wautier JL, Pintigny D, Maclouf J. et al. Release of prostacyclin after erythrocyte adhesion to cultures vascular endothelium. J Lab Clin Med 1986; 107 (03) 210-5.
  • 24 Mehta P, Albiol L. Prostacyclin and platelet aggregation in sickle cell disease. Pediatrics 1982; 70 (03) 354-9.
  • 25 Stuart MJ, Sills RH. Deficiency of plasma prostacyclin or PGI2 regenerating ability in sickle cell anemia. Br J Heamatol 1981; 48 (04) 545-50.
  • 26 Longenecker GL, Mankad V. Decreased prostacyclin levels in sickle cell disease. Pediatrics 1983; 71 (05) 860-1.
  • 27 Starzyk D, Korbut R, Gryglewski RJ. Effects of nitric oxide and prostacyclin on deformability and aggregability of red blood cells of rats ex vivo and in vitro . J Physiol Pharmacol 1999; 50 (04) 629-37.