Immature Platelet Fraction in Different Diagnosis of Thrombocytopenic States: An Approach to Distinguish Idiopathic Thrombocytopenic Purpura from Myelodysplastic Syndrome with Isolated Thrombocytopenia.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1085-1085
Author(s):  
Koji Miyazaki ◽  
Miyako Taira ◽  
Tomiteru Togano ◽  
Manabu Ohsaka ◽  
Yuhko Suzuki ◽  
...  

Abstract It is sometimes confusing to distinguish idiopathic thrombocytopenic purpura (ITP) from thrombocytopenia due to dysmegakaryopoiesis, as seen in myelodysplastic syndrome (MDS) patients, especially MDS with isolated thrombocytopenia. In this study, we investigated the useful parameters for the different diagnosis of thrombocytopenia. The number of reticulated platelets reflects the rate of thrombopoiesis, and this clinical utility has been established in the laboratory diagnosis of thrombocytopenia due to increased peripheral platelet destruction, such as autoimmune thrombocytopenic purpura (AITP). However, the number of reticulated platelets has not been well investigated in the patients with myelodysplatsic syndrome (MDS), while some of them are misdiagnosed as ITP. The aim of this study is to evaluate the diagnostic utility of the measurements of reticulated platelets as well as other parameters of platelets, such as MPV (mean platelet volume), P-LCR (platelet larger cell ratio) and PDW (platelet distribution width). The reticulated platelets, expressed as the immature platelet fraction (IPF) were determined in 108 ITP and 57 MDS patients using the Sysmex XE-2100 blood cell counter with upgraded software (Sysmex, Kobe, Japan). This system enabled rapid, inexpensive, automated, stable measurements of reticulated platelets compared with the flow cytometry system, of which consensus method has not yet been identified to provide acceptable intra- and inter-laboratory results. The platelet counts in ITP and MDS patients were equivalent (ITP, 7.99 ± 0.40 × 104/μL; MDS, 8.05 ± 0.57× 104/μL). The IPF values in ITP patients (10.4 ± 0.61%) were significantly higher than those in MDS (5.82 ± 0.63%), and the inverse correlation between the IPF and the platelet counts was observed among the ITP patients, but not among the MDS. Both MPV and PDW in MDS (10.6 +/− 0.15 fL and 12.2+/−0.41 fL, respectively) were significantly higher than in ITP (7.7 +/− 0.38 fL and 9.4 +/− 0.48 fL, respectively), while P-LCR in MDS (28.7 +/− 1.2%) and ITP (23.6 +/− 1.3%) were not significantly different. Although MPV was correlated with IPF among either group, the correlation between IPF and either PDW or P-LCR was weak among MDS (IPF × PDW, r=0.673; IPF × P-LCR, r=0.660) compared with ITP (IPF × PDW, r=0.779; IPF × P-LCR, r=0.803). Next we precisely investigated the clinical features of the minor population of MDS with higher IPF. Most of these patients revealed the significantly higher values of PAIgG (Platelet-associated IgG) and/or poor response to the blood transfusion, suggesting the possibility of associated autoimmune mechanisms. The patients of MDS in overt leukemic stage also recorded higher IPF even if they had no or few blood transfusion. The IPF would be a useful parameter to distinguish ITP from MDS with isolated thrombocytopenia, which has been shown to have a favorable prognosis.

1981 ◽  
Author(s):  
M J Stuart ◽  
J G Kelton ◽  
J B Allen

Patients with chronic idiopathic thrombocytopenic purpura (CITP) have been described to have bleeding times (B.Ts) that were shorter than would be predicted by their platelet counts. This phenomenon was explained by the presence in CITP of a young platelet population with increased hemostatic competence (NEJM 287:155, ’72). In contradistinction, we have observed patients with CITP to have a bleeding tendency at platelet counts >75,000/cu mm. We therefore evaluated B.Ts and platelet arachidonic acid (AA) metabolism in 7 patients with CITP who demonstrated increased amounts of platelet associated IgG (PAIgG >3fg per platelet) and compared them to 20 healthy controls. 3/7 patients with CITP and platelet counts of >75,000/cu mm demonstrated marked prolongations in their B.Ts. (10’, 12’ and 14’, normal <7’). Marked abnormalities in the metabolism of AA through the cyclo-oxygenase (Thromboxane B2 and HHT) and lipoxygenase (HETE) pathways were also observed in patients with CITP. Platelets in CITP synthesized less amounts (p <0.005) of Thromboxane B2 (10.3 ± 3.1%) in comparison to controls (22.9 ± 1.8). Values for HHT were decreased (23.7 ± 4.9 vs 39.7 ± 1.9; p<0.005), while HETE production was increased (59.5 ± 7.8 vs 30.7 ± 1.8; p<0.001). No correlation was observed between PAIgG and platelet Thromboxane B2 formation. However, an inverse correlation (r=0.81, p<0.05 was observed between the B.T. and platelet Thromboxane B2 formation in patients with chronic ITP. We have demonstrated platelet dysfunction and impaired Thromboxane B2 formation in CITP. This association should be investigated in the individual patient, since the bleeding tendency in these patients is exacerbated by the superimposed impairment in platelet function.


Blood ◽  
1978 ◽  
Vol 51 (3) ◽  
pp. 479-486
Author(s):  
Z Zeigler ◽  
S Murphy ◽  
FH Gardner

Microscopic evaluation of apparent platelet size and morphology was examined in a variety of hematologic disorders. The time of preparation of the blood smear was important. An artifactual increase in platelet size was noted on blood films from 20 normal individuals that were prepared either immediately or 180 min after venipuncture. The clearest differentiation of patient categories was obtained with smears prepared 60 min after venipuncture using blood anticoagulated with K3EDTA. Under these conditions, normal size and morphology values were found in thrombocytopenic patients with aplasia or with increased splenic pooling. In contrast, large size values were a reliable finding in idiopathic thrombocytopenic purpura patients, whose platelet counts were less than 50,000/microleter. Large size values were also noted in patients with infiltrated bone marrows or myeloproliferative syndromes regardless of the platelet count. The last two groups usually showed abnormal platelet morphology with greater than 10% hypogranular platelets. Normal platelet size and morphology were observed in patients with iron-deficiency and megaloblastic anemias and in patients with idiopathic thrombocytopenic purpura and systemic lupus erythematosus who had normal platelet counts.


2014 ◽  
Vol 4 (2) ◽  
pp. 105-107
Author(s):  
Farhana Afroz ◽  
Hasna Fahmima Haque ◽  
Samira Rahat Afroze ◽  
Muhammad Abdur Rahim ◽  
Aparna Rahman ◽  
...  

Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease where low platelet counts predisposeto various bleeding tendencies; intracranial haemorrhageis one of them. It is a rare and devastating complication of ITP, mostly presenting as intracerebral (ICH) or subarachnoid haemorrhage (SAH). Here, we report a 32-year-old splenectomized chronic ITP patient on corticosteroid and azathioprine, in whom spontaneous SAH developed. In this case, conservative management resulted in clinicoradiological improvement and showed eventual favourable out-come.Birdem Med J 2014; 4(2): 105-107


2014 ◽  
Vol 34 (6) ◽  
pp. 466-468
Author(s):  
Jeonghyun Chang ◽  
Chan-Jeoung Park ◽  
Eul-Ju Seo ◽  
Jung-Hee Lee ◽  
Sang Hyuk Park ◽  
...  

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3933-3933
Author(s):  
Yongqiang Zhao ◽  
Baolai Hua ◽  
Nong Zou ◽  
Shujie Wang ◽  
Tienan Zhu

Abstract Thrombopoietin (TPO) is the key regulator of megakaryocytepoiesis and platelet production. TPO binds to its specific receptor, c-Mpl, on the surfaces of megakaryocytes, and may promote the proliferation, differentiation and maturation of megakaryocytes, and finally increase the circulating platelet count. The role of TPO in the pathogenesis of idiopathic thrombocytopenic purpura (ITP) is not certain. Plasma concentrations of TPO in ITP patients were similar to or little lower than that in healthy subjects. Therefore it is possible that supplemental TPO could significantly promote platelet production and increase platelet counts in ITP patients. Here, we report the result of multiple cycles of recombinant human thrombopoietin (rhTPO) therapy in a patient with refractory ITP. The patient, a 42-year-old woman, was admitted to our department on December 30, 2003. She had suffered from chronic ITP for more than 4 years. The patient had been treated with glucocorticosteroids, immunosuppressive agents and splenectomy. No sustained response could be achieved. The diagnosis of chronic refractory ITP was made. There were petechiae and gingival bleeding on admission. Liver and spleen were not palpable. Hemoglobin was 142g/L, white blood cell count 7.6×10 9/L, platelet count 15×10 9/L. Bone marrow aspiration revealed that erythroid and myeloid development were normal, megakaryocytes were increased in number and no dysplastic features. After an informed consent was obtained from the patient, rhTPO (Sunshine Pharmaceutical Corporation, China) was administrated subcutaneously at dosage of 1.0 μg/kg, daily for 14 days or until platelet count sustained more than 50×109/L. Anti-rhTPO antibodies were determined weekly by ELISA. Three cycles of rhTPO therapy was given with 6, 13 and 8 dosing for each cycle. The platelet counts before each cycle were all less than10×109/L and increased above 50×109/L on day 5, 11 and 8 of rhTPO administration, respectively. The peak platelet counts of 456, 130 and 82×109/L were reached on day 9, 15 and 13 for each cycle. Then platelet count decreased gradually. The durations of platelet count more than 50×109/L in 3 cycles were 13, 7 and 10 days respectively. No increase of WBC count and Hb level occurred. No liver and kidney function damage, abnormal coagulation functions or thrombosis developed during the treatment. rhTPO antibodies were not detectable. The result indicated that rhTPO could transiently increase peripheral platelet counts of the patient with chronic refractory ITP. It was uncertain why peak platelet counts declined and durations of platelet count more than 50×109/L shortened when multiple cycles of rhTPO were given.


1996 ◽  
Vol 76 (02) ◽  
pp. 156-160 ◽  
Author(s):  
Naoaki Ichikawa ◽  
Fumihiro Ishida ◽  
Shigetaka Shimodaira ◽  
Tomoyuki Tahara ◽  
Takashi Kato ◽  
...  

SummaryTo clarify the regulatory mechanism of thrombopoietin (TPO, c-Mpl ligand) in chronic thrombocytopenic conditions, we determined TPO levels in the sera of patients with aplastic anaemia (AA; n = 26) and idiopathic thrombocytopenic purpura (ITP; n = 32) by an enzyme-linked immunosorbent assay. Despite a similarity in platelet counts, serum TPO levels in the AA group were markedly higher than those in the ITP group: 20.41 ± 9.71 f mol/ml (mean ± SD) and 1.66 ± 0.55 f mol/ml, respectively, both of which were significantly elevated compared to normal subjects (n = 41; 1.22 ± 0.37). In both groups, serum TPO level showed an inverse correlation with the platelet count. We determined the megakaryocyte volume using bone marrow clot section and found that it was markedly small in the AA group; while in the ITP group it was augmented with a correlation to serum TPO level. Our findings suggest that TPO levels may be regulated not only by platelets but also megakaryocytes in AA and ITP.


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