Journals / Turkish Journal of Hematology / 2000 / Cilt: 17 - Sayı: 3

Natural inhibitors and lipids in patients with sickle cell disease

Pages
119–122
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In conclusion, PC, PS and AT-IIII deficiencies in patients with SCD are certain.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Microvascular occlusion in sickle cell disease (SCD) is a multifactorial process.
📊
Key Findings & Data:A total of 18 patients with SCD were included in this study at the Antalya State Hospital, Thalassemia Center.
💡
Conclusion & Impact:In conclusion, PC, PS and AT-IIII deficiencies in patients with SCD are certain.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Osteonekroz · Lipidler · Bacak ülseri

Özet

Microvascular occlusion in sickle cell disease (SCD) is a multifactorial process. Disordered coagulation may play a role in the pathogenesis of vaso occlusive crisis (VOC). The aim of this study was to evaluate the patients and to investigate their Protein C (PC), Protein S (PS) and AT-III levels during normal and crisis periods. A total of 18 patients with SCD were included in this study at the Antalya State Hospital, Thalassemia Center. The mean number of VOC episodes of the patients per year was 4.1 ± 3.2. Complications in patients included 4 cases of osteonecrosis (23.5%), 2 cases of cholealithiasis (11.7%), 2 cases of leg ulcers (11.7%), and 3 splenectomies (17.6%). The patients during noncrisis periods have lower cholesterol and higher triglycerides levels than the controls (p< 0.001). Hepatic and renal functions were normal in all patients. The mean totals of the PS, PC and AT-III levels were statistically lower both in non crisis and in crisis periods than the control (p< 0.001), but there was no statistical difference between the levels durining noncrisis and crisis periods. In conclusion, PC, PS and AT-IIII deficiencies in patients with SCD are certain. However, these deficiencies do not change during noncrisis and crisis situations and does not play a role on the period of crisis. Abnormal lipid patterns may be a predisposing condition for a crisis.

🔖

Cite This Article

CANATAN, D., OĞUZ, N., ÖZSANCAK, A., ASLAN, İ., BENGÜ, A., GÜRMAN, A., SARICA, B. (2000). Natural inhibitors and lipids in patients with sickle cell disease. Turkish Journal of Hematology, Cilt: 17 - Sayı: 3, 119–122. https://ajindex.com/articles/413446

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (10)

  1. Powars D. Sickle cell anemia and major organ failure. Hemoglobin 1990;14(6):573-98
  2. Francis RB. Platelet coagulation and fibrinolysis in sickle cell disease: Their possible role in vascular occlusion. Blood Coagul Fibrinolysis 1992;2:341-53
  3. Hagger D, Wolff S, Owen J and Samson D. Changes in coagulation and fibrinolysis in patients with sickle cell disease compared with helathy black controls. Blood Coagul Fibrindysis 1995;6(2):93-9
  4. Nsiri B, Gritli N, Bayoudh F, Messaoud T, Fattoum S and Machghoul S. Abnormalities of coagulation and fibrinolysis in homozygous sickle cell disease. Hematol Cell Ther 1996;38(3):279-84
  5. Francis RB. Protein S deficiency in sickle cell anemia, J Lab Clin Med 1988;111(5):571-6
  6. El-Hazmi MA, Wrasy AS, Bahakim H. Blood protein C and S in sickle cell disease. Acta Haematol 1993;90(3):114-9
  7. Marfaing-Koka A, Boyer-Neumann C, Wolf M, Leroy Matheron C, Cynober T, Tchernia G. Decreased protein S activity in sickle cell disease. Nouv Rev Fr Hematol 1993;35(4):425-30
  8. MacCallum PK, Cooper JA, Mart n J, Howarth DJ, Meade TW and Miller GJ. Associations of protein C and protein S with serum lipid concentrations. Br J Haematol 1998;102:609-15
  9. Wright JG, Malia R, Cooper P, Thomas P, Preston FE and Serjeant GR. Protein C and S in homozygous sickle cell disease: Does hepatic dysfunction contribute to low levels? Br J Haematol 1997;98:627-31
  10. Borgna Pignatti C,Carnelli V,Caruso V, Dore F, De Mattia D, Di Palma A, Di Gregorio F, Romeo MA, Longhi R, Mangiagli A, Melevendi C, Pizarelli G, Musumeci S. Thromboembolic events in beta thalassemia major: An Italian Multicenter Study. Acta Haematol 1998;99:76-9.