Latest Research News on Thrombocytopenia : Nov 2020
Fetal Thrombocytopenia and Its Relation to Maternal Thrombocytopenia
Neonates with severe thrombocytopenia can have bleeding leading to death or lifelong residual defects. The predictors, frequency, and consequences of fetal thrombocytopenia are not known, nor is it known if there are maternal clinical features that could predict fetal thrombocytopenia.
We conducted a seven-year cross-sectional study in which platelet counts were determined in newborns’ umbilical-cord blood and blood obtained from their mothers at consecutive deliveries in one obstetrical unit. The relations of the umbilical-cord platelet count to maternal risk factors were determined.
Platelet counts were determined in blood samples from 15,471 mothers and 15,932 newborn infants. The cord-blood platelet count was less than 50,000 per cubic millimeter in 19 infants (0.12 percent; 95 percent confidence interval, 0.07 to 0.19 percent), whereas the platelet count was less than 150,000 per cubic millimeter in 6.6 percent of the mothers (95 percent confidence interval, 6.2 to 7.0 percent). One infant among those born to 756 mothers with incidental thrombocytopenia, 5 infants among those born to 1414 mothers with hypertension, and 4 infants among those born to 46 mothers with idiopathic thrombocytopenic purpura had cord-blood platelet counts between 20,000 and 50,000 per cubic millimeter. Only 6 infants (0.04 percent; 95 percent confidence interval, 0.01 to 0.08 percent) had cord-blood platelet counts of less than 20,000 per cubic millimeter; all their mothers were among the 18 whose 19 fetuses were at risk for neonatal alloimmune thrombocytopenia. Two of these infants had in utero intracranial hemorrhage. In addition, 3 infants born to these 18 women had cord-blood platelet counts between 20,000 and 50,000 per cubic millimeter; there was 1 stillbirth due to intracranial hemorrhage.
Moderate-to-severe fetal thrombocytopenia is a rare event. The only severely affected neonates with morbidity or mortality due to this condition are those born to mothers with antiplatelet alloantibodies. 
Temporal Aspects of Heparin-Induced Thrombocytopenia
Heparin-induced thrombocytopenia is a relatively common antibody-mediated drug reaction. We studied the temporal relation between previous or current heparin therapy and the onset of heparin-induced thrombocytopenia.
We examined the time between the start of heparin therapy and the onset of thrombocytopenia in 243 patients with serologically confirmed heparin-induced thrombocytopenia. We also investigated the persistence of circulating heparin-dependent antibodies by performing a platelet serotonin-release assay and an assay for antibodies against platelet factor 4. The outcome in seven patients who had previously had an episode of heparin-induced thrombocytopenia and were later treated again with heparin was also examined.
A fall in the platelet count beginning four or more days after the start of heparin therapy occurred in 170 of the 243 patients (70 percent); in these patients, a history of previous heparin treatment did not influence the timing of the onset of thrombocytopenia. In the remaining 73 patients (30 percent), the onset of thrombocytopenia was rapid (median time of onset, 10.5 hours after the start of heparin administration); all these patients had been treated with heparin within the previous 100 days. During recovery from thrombocytopenia, heparin-dependent antibodies in the serum fell to undetectable levels at a median of 50 to 85 days, depending on the assay performed. In the seven patients who were given heparin again after the disappearance of heparin-dependent antibodies, a new episode of heparin-induced thrombocytopenia did not occur.
Heparin-induced thrombocytopenia can begin rapidly in patients who have received heparin within the previous 100 days. Heparin-dependent antibodies do not invariably reappear with subsequent heparin use. 
Heparin-associated thrombocytopenia is a relatively common complication of heparin therapy occurring in approximately 5% of the patients who receive this drug. The incidence is higher with bovine heparin than with porcine heparin. Onset of heparin-associated thrombocytopenia usually occurs 6 to 12 days after initiation of treatment and by itself has a low morbidity. Heparin-associated thrombocytopenia plus arterial thrombosis can cause major complications including stroke, heart attack, and death. The incidence of heparin-associated thrombocytopenia plus arterial thrombosis is lower than that for heparin-associated thrombocytopenia alone. The diagnosis of heparin-associated thrombocytopenia remains one of exclusion, but testing for the presence of a heparin-dependent platelet-aggregating factor may prove to be useful. Analysis of the time of onset suggests a strategy for prevention. Oral anticoagulants could be started concomitantly with the heparin so that it could be discontinued in several days. This approach may prevent most episodes of heparin-associated thrombocytopenia. 
Etiologic Evaluation of 1012 Patients Admitted with Thrombocytopenia
Introduction: Thrombocytopenia is the situation where the number of thrombocytes is less than 150.000/ µL. This may result due to decreased thrombocyte production, increase in the destruction of thrombocytes and differentiation in distribution of thrombocytes. Hereditary and acquired diseases both contribute to the condition, but the acquired reasons are more common in older patients. In this study we aimed to present the patients’ data with thrombocytopenia in the eastern Turkey and the underlying diseases that cause thrombocytopenia in order to contribute to literature.
Material and Methods: In this study, we retrospectively aimed to evaluate the etiology of thrombocytopenia at 1012 patients who admitted to Inonu University Medical Faculty Turgut Ozal Medical Center Hematology outpatient clinic, hematology service, emergency department and the ones who were consulted from other departments in the hospital. We collected data of patients for whom we searched the aetiology of thrombocytopenia as Department of Hematology.
Results: Total of 1012 patients, of whom 508 were female and 504 were male, were included to the study. The mean age was 51±20 years. The mean number of the thrombocytes was 64.28±43.05 /mL. The mean number of leucocytes was 13.89±32.71 /µL. The mean level of hemoglobin was 11.22±3.03 g/dL. Leukaemia, infections and the immune thrombocytopenias represented most of the cases, and the other reasons of thrombocytopenia were drugs, chronic liver diseases, megaloblastic anemias, pseudothrombocytopenia, thrombotic microangiopathies and other diseases.
Conclusion: The reasons of thrombocytopenia may differ according to geographic distribution and step level of health centers. It’s an expected situation for thrombocytopenia reasons that the high rate of infections can be accused in developing countries and malignant diseases to be the first reason in developed countries. 
Plasma Thrombopoietin Level in Thrombocytopenic Patients with or without Liver Cirrhosis Chronically Infected by the Hepatitis C Virus
Background and Aim: Thrombocytopenia is a frequent problem in patients with post- hepatitis C (HCV) liver cirrhosis and also occurs in chronic HCV-infected patients without liver cirrhosis. The aim of this study was to evaluate the role of plasma thrombopoietin (TPO) in the occurrence of thrombocytopenia in both conditions.
Method: Platelet count and plasma thrombopoietin level and liver function tests were measured in four groups of patients: twenty chronic patients with post-hepatitis C liver cirrhosis and thrombocytopenia (group I), ten chronic HCV-positive patients with liver cirrhosis without thrombocytopenia (group II), ten chronic HCV-positive patients without liver cirrhosis with thrombocytopenia (group III) and chronic ten HCV-positive patients without liver cirrhosis and without thrombocytopenia (group IV). Ten normal healthy individuals were included as a control group.
Results: Plasma levels of albumin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), TPO and platelet counts in the four groups of patients were significantly different from their corresponding levels in the control group (P <0.001). There was a significant positive correlation between plasma TPO levels and platelet counts in group III patients (ρ (Spearman’s [rho]) = 0.661, P= 0 .038). There was no significant correlation between TPO levels and platelet counts in the other three groups of patients. The logistic regression analysis in the three designated models, using dependent variables (chronic HCV infection, liver cirrhosis and thrombocytopenia) and an independent variable (TPO plasma level) revealed that liver cirrhotic patient and the thrombocytopenic patient have equally the best prediction model for the low plasma TPO.
Conclusion: Decreased thrombopoietin production has a role in the pathogenesis of thrombocytopenia in liver cirrhosis. 
 Burrows, R.F. and Kelton, J.G., 1993. Fetal thrombocytopenia and its relation to maternal thrombocytopenia. New England Journal of Medicine, 329(20), pp.1463-1466.
 Warkentin, T.E. and Kelton, J.G., 2001. Temporal aspects of heparin-induced thrombocytopenia. New England Journal of Medicine, 344(17), pp.1286-1292.
 King, D.J. and Kelton, J.G., 1984. Heparin-associated thrombocytopenia. Annals of internal medicine, 100(4), pp.535-540.
 Erkurt, M., Berber, I., Nizam, I., Kaya, E., Koroglu, M., Kuku, I. and Kalayli, O. (2013) “Etiologic Evaluation of 1012 Patients Admitted with Thrombocytopenia”, Journal of Advances in Medicine and Medical Research, 4(1), pp. 104-113. doi: 10.9734/BJMMR/2014/4606.
 Al-Qtaitat, A., Al-Dalaen, S., Mahgoub, S., Alnawaiseh, N., Al-Shuneiqat, J., Al-Sarayreh, S. and Al –Saraireh, Y. (2014) “Plasma Thrombopoietin Level in Thrombocytopenic Patients with or without Liver Cirrhosis Chronically Infected by the Hepatitis C Virus”, Journal of Advances in Medicine and Medical Research, 5(7), pp. 864-871. doi: 10.9734/BJMMR/2015/9860.