Thrombopoietin serum levels do not correlate with thrombocytopenia in hepatic schistosomiasis

Souza, MRa; Aguiar, Lak; Goto, JM; Carvente, CT; Cf, Toledo; Borges,; Souza, Mo^ônica R. A.; Aguiar, Luciano F.; Goto, Janaína Midori; Carvente, Cla ́áudia T.; Toledo, Carlos Fischer de; Borges, Durval Rosa

doi:10.1034/j.1600-0676.2002.01574.x

Cited by 11 publications

(4 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Section: Introductioncontrasting

confidence: 73%

“…Portal hypertension in schistosomiasis may progress with variable degrees of pancytopenia, with thrombocytopenia as the main and earliest presentation. However, this thrombocytopenia is not explained by thrombopoietin serum concentrations (Souza et al, 2002), which differs from that reported in severe forms of cirrhosis (Peck-Radosavljevic et al, 1997). The aim of the present study was to evaluate reticulated platelets and thrombopoietin serum levels in patients with chronic and isolated forms of schistosomiasis in order to better interpret the thrombocytopenia present in these patients.…”

Section: S U M M a R Ymentioning

confidence: 64%

See 1 more Smart Citation

Reticulated platelets and thrombopoietin in schistosomiasis patients

Kopke-Aguiar

Léon

Shigueoka

et al. 2009

Int J Lab Hematology

View full text Add to dashboard Cite

Schistosomiasis mansoni is a non-cirrhotic liver disease. In cirrhosis patients with portal hypertension, a decreased number of reticulated platelets associated with increased thrombopoietin serum levels were reported. We previously reported a 120/nl platelet cutoff level as a marker of clinically significant portal hypertension in schistosomiasis patients. To evaluate reticulated platelet counts and thrombopoietin serum levels (TPO) in schistosomiasis patients and correlate them with portal hypertension markers. Thirty-three schistosomiasis patients without co-morbidities were endoscopically classified as those with (n = 19) or without (n = 14) clinically significant portal hypertension. Flow cytometric determination of reticulated platelets was performed using CD41 antibody and thiazol orange. Ultrasonographic examinations were performed according to the Niamey protocol. TPO and hyaluronic acid serum levels were determined in duplicate using ELISA methods. The platelet number of 120/nl discriminates the two groups with 100% accuracy and 100% positive and negative predictive values, and correlates with spleen length and portal and splenic vein diameters. Differences in reticulated platelets and hyaluronic acid serum levels between both groups were significant (P = 0.025 and 0.012, respectively), but thrombopoietin serum levels were not (P = 0.769). Schistosomiasis patients with portal hypertension have increased reticulated platelets associated with normal TPO serum levels.

show abstract

Section: Introductioncontrasting

confidence: 73%

Section: S U M M a R Ymentioning

confidence: 64%

Reticulated platelets and thrombopoietin in schistosomiasis patients

Kopke-Aguiar

Léon

Shigueoka

et al. 2009

Int J Lab Hematology

View full text Add to dashboard Cite

show abstract

“…For example, the blood of many, if not most, patients with myeloproliferative thrombocytosis display higher than expected TPO levels [15,16]. The same is true for reactive thrombocytosis associated with inflammation, or infection; the opposite is true for the thrombocytopenia of various states of liver disease, in which the hepatic source of TPO should be reduced, yet blood levels are occasionally higher than expected [8,9,17]. Several investigators have now demonstrated that marrow stromal cell production of TPO can rise in many of these states [18,19,20] and that the inflammatory mediator interleukin‐6 can increase TPO production from hepatocytes [21].…”

Section: The Regulation Of Thrombopoietin Productionmentioning

confidence: 99%

Thrombopoietin: a tool for understanding thrombopoiesis

Kaushansky

2003

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

Summary. Although first proposed to be the primary regulator of platelet production 45 years ago, the gene for thrombopoietin was cloned only within the last decade. Since then, our understanding of megakaryocyte and platelet production has increased substantially, and it is now appreciated that in addition to its critical role in regulating thrombopoiesis, the hormone affects multiple aspects of hematopoiesis, including playing a non-redundant role in stem cell survival, self-renewal and expansion. In addition to this greater physiological understanding of thrombopoietin biology, the molecular mechanisms by which the hormone affects cell survival and proliferation are coming under increased scrutiny. At least four signaling pathways have been identified that play important and non-overlapping roles in stem cell and megakaryocyte growth and development, potentially providing new strategies to therapeutically intervene in hematopoiesis. This review will focus on our current understanding of these processes.

show abstract

“…For the form without portal hypertension, lesion markers and hepatic function are within normal limits. Patients with portal hypertension are characterized by the extent of preservation of hepatic function in relation to the degree of portal hypertension, although some laboratory alterations have been found that characterize organ dysfunction from an early stage [2][3][4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%