Abstract:Key Points
One in 7 patients suspected of having primary ITP was misdiagnosed at some point during their disease course; 56.1% had grade 2 bleeding. The McMaster ITP Registry is a useful tool to improve the diagnosis of ITP and identify unique subgroups of patients.
“…Patients were identified from the McMaster ITP Registry, a prospective, longitudinal observation study of consecutive adults referred for thrombocytopenia. 10 ITP was defined per established guidelines. 11 We identified all ITP patients with platelet counts ,50 3 10 9 /L who were receiving anticoagulation for any indication.…”
“…Patients were identified from the McMaster ITP Registry, a prospective, longitudinal observation study of consecutive adults referred for thrombocytopenia. 10 ITP was defined per established guidelines. 11 We identified all ITP patients with platelet counts ,50 3 10 9 /L who were receiving anticoagulation for any indication.…”
“…The rate of secondary ITP in adults in our survey is consistent with those of other studies (18-25.7%). 2,23,24 However, the distribution of causes of secondary ITP in children and adults significantly differed from that reported in France. 2 The findings of higher HCV and HBV and lower human immunodeficiency virus as causes of secondary ITP in Taiwan compared with France are consistent with variations in prevalence rates of these infectious diseases in these two regions.…”
BACKGROUND
The incidence of immune thrombocytopenia (ITP) is not well known in Asians. The aims of this study were to survey incidences and clinical features of ITP in Taiwan.
STUDY DESIGN AND METHODS
This study identified 4855 incident ITP cases from the population‐based National Health Insurance Research Database from mid‐2006 to mid‐2013, and compared incidences, patient characteristics, and clinical manifestations of ITP by age.
RESULTS
Respective ITP incidence rates among those aged <15, 15 to 59, and ≥60 years were 4.0, 2.0, and 5.4 per 100,000 person‐years. A male predominance was noted in children, and a female predominance was found in adults. The most common causes of secondary ITP were systemic lupus erythematosus (21.8%), viral hepatitis C (16.9%), and viral hepatitis B (13.4%). The rate of secondary ITP in children was less than one fifth that in adults (4.2% vs. 23.8%). Rates of central nervous system (1.1%) and gastrointestinal tract bleeding (3.3%) were rare, with variations by age. The rate of splenectomies in children (0.4%) was only one tenth that in adults (4.1%). The disease in 25% of children and 30% of adults became persistent or chronic. A decreasing trend in the ITP incidence was found (annual percentage change, −4.9%), and it was confined to those aged >15 years.
CONCLUSION
Incidence estimates of ITP in Taiwan were close to those of Western countries, with age‐specific variations in sex ratio, comorbidity, splenectomy, secondary causes, and incidence trends. The results suggest no racial variations in ITP incidences, but a geographical difference in causes of secondary ITP.
“…One recent study estimated that nearly one in seven patients who are initially diagnosed with ITP are later found to have another cause for their thrombocytopenia, indicating that a high index of suspicion for other diagnoses should be maintained. 17 In the pediatric population, genetic causes of thrombocytopenia should be considered, especially if there is a positive family history of thrombocytopenia and/or accompanying laboratory abnormalities that are not fully explained by ITP. For example, isolated thrombocytopenia is sometimes the initial presenting symptom in patients with inherited bone marrow failure syndromes, such as Fanconi anemia or congenital amegakaryocytic thrombocytopenia.…”
Growth factor‐independent 1B (GFI1B) variants are a rare cause of thrombocytopenia. We report on a male child who was initially diagnosed with immune thrombocytopenia. However, subtle clinical signs led to suspicion of a genetic cause of thrombocytopenia. Gene panel sequencing revealed a rare variant in GFI1B (C168F), which has recently been reported in several families with thrombocytopenia. We demonstrate that this variant significantly alters platelet parameters in population studies. This case highlights how diagnoses of exclusion, such as immune thrombocytopenia, can be confounded by genetic variation. Our understanding of blood disorders will undoubtedly evolve from an increased knowledge of human genetic variation.
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