scholarly journals Cancer incidence following a high-normal platelet count: cohort study using electronic healthcare records from English primary care

2020 ◽  
Vol 70 (698) ◽  
pp. e622-e628
Author(s):  
Luke TA Mounce ◽  
Willie Hamilton ◽  
Sarah ER Bailey

BackgroundA raised platelet count (thrombocytosis) measuring >400 × 109/l is associated with high cancer incidence. It is uncertain whether platelet counts at the upper end of the normal range (high-normal: 326–400 × 109/l) are also associated with cancer.AimTo investigate cancer incidence following a normal platelet count in primary care.Design and settingA prospective cohort study was undertaken using data from the Clinical Practice Research Datalink and National Cancer Registration and Analysis Service, dating from 1 May 2005 to 30 April 2014.MethodOne-year cancer incidence was estimated for 295 312 patients with normal platelet counts (150–400 × 109/l). Patients with platelet counts >325 × 109/l were oversampled to maximise precision of estimates of cancer incidence. All patients were aged ≥40 years with no prior cancer diagnoses. The effects of age, sex, and smoking were explored. Non-melanoma skin cancers were omitted from exclusions and incidence.ResultsOne-year cancer incidence increased greatly with age, male sex, and higher platelet count. Males aged ≥60 years with a high-normal count had an incidence of 4.2% (95% confidence interval [CI] = 4.0 to 4.4). The highest incidence of 6.7% (95% CI = 5.3 to 8.4) was found in males aged ≥80 years, who had platelets in the range of 376–400 × 109/l; this was 3.1 percentage points higher than the incidence for patients in the same age group with lower-normal counts of 150–325 × 109/l. Risks for all female subgroups were <3%. Patients with high-normal platelet counts were most at risk of lung and colorectal cancers and, in general, had advanced-stage cancer at diagnosis.ConclusionPlatelet counts at the high-normal range in males aged ≥60 years may be indicative of an underlying malignancy, and referral for further investigation should be considered.

2018 ◽  
Vol 35 (6) ◽  
pp. 671-675 ◽  
Author(s):  
Emily Ankus ◽  
Sarah J Price ◽  
Obioha C Ukoumunne ◽  
William Hamilton ◽  
Sarah E R Bailey

2020 ◽  
Vol 70 (701) ◽  
pp. e852-e857
Author(s):  
Cansu Clarke ◽  
Willie Hamilton ◽  
Sarah Price ◽  
Sarah ER Bailey

BackgroundThrombocytosis is an excess of platelets, which is diagnosed as a platelet count >400 × 109/l. An association of thrombocytosis with undiagnosed cancer has recently been established, but the association with non-malignant disease has not been studied in primary care.AimTo examine, in English primary care, the 1-year incidence of non-malignant diseases in patients with new thrombocytosis and the incidence of pre-existing non-malignant diseases in patients who develop new thrombocytosis.Design and settingProspective cohort study using English Clinical Practice Research Datalink data from 2000 to 2013.MethodNewly incident and pre-existing rates of non-malignant diseases associated with thrombocytosis were compared between patients with thrombocytosis and age- and sex-matched patients with a normal platelet count. Fifteen candidate non-malignant diseases were identified from literature searches.ResultsIn the thrombocytosis cohort of 39 850 patients, 4579 (11.5%) were newly diagnosed with any one of the candidate diseases, compared with 443 out of 9684 patients (4.6%) in the normal platelet count cohort (relative risk [RR] 2.5, 95% confidence intervals [CI] = 2.3 to 2.8); iron-deficiency anaemia was the most common new diagnosis (4.5% of patients with thrombocytosis, RR 4.9, 95% CI = 4.0 to 6.1). A total of 22 612 (57.0%) patients with thrombocytosis had a pre-existing non-malignant diagnosis compared with 4846 patients (50%) in the normal platelet count cohort (odds ratio 1.3, 95% CI = 1.2 to 1.4). There was no statistically significant difference in cancer diagnoses between patients with and without pre-existing disease in the thrombocytosis cohort.ConclusionThrombocytosis is associated with several non-malignant diseases. Clinicians can use these findings as part of their holistic diagnostic approach to help guide further investigations and management of patients with thrombocytosis.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2160-2160
Author(s):  
Swee Lay Thein ◽  
Steve Best ◽  
Stephan Menzel ◽  
Helen Rooks ◽  
Tim D. Spector ◽  
...  

Abstract Although the ’normal’ range of platelet count in a healthy person is quite broad (150 to 400 ×109/L), an individual’s platelet count is maintained within a much narrower range, constantly balanced between thrombopoiesis and senescence. Platelet counts within the normal range have been shown to be largely determined by genetic factors with heritability estimates from twin studies ranging from 0.57 to 0.80. A genome-wide linkage analysis was carried out in a large Asian Indian kindred with β thalassemia to search for genes influencing variation in normal platelet count. Significant linkage is shown at two locations on chromosome 3q with age, sex and β thalassemia adjusted platelet counts. Linkage analysis showed one marker (D3S1309) on chromosome 3q with a lod score of 3.26 and another marker (D3S1282) approximately 30 cM centromeric, with a lod score of 2.52. Multipoint linkage analysis across 90 cM of chromosome 3q identified two peaks across the region with maximum multipoint lod scores of 3.52 and 4.11 under markers D3S1309 and D3S1282, respectively. Two strong candidate genes for platelet variation were identified in the linked region; thrombopoietin (THPO) and glycoprotein IX (GPIX). Resequencing of four individuals revealed five single nucleotide polymorphisms (SNPs) in THPO and one mutation in the transmembrane region of GPIX. Analysis of variance showed that the GPIX mutation and one THPO SNP accounted for 6% and 4% of the variation in platelet count in the kindred, respectively. The THPO SNP lies in the 3′ untranslated region (3′ UTR) of the gene and has not been previously reported. Although no function could be attributed to the THPO SNP it could potentially influence post-transcriptional control of gene expression. The G to A transition in nucleotide 653 (Ref seq NM_000174) resulted in an Ala 156 (GCC) to Thr (ACC) replacement in the GPIX protein. The GPIX mutation was recently identified in a Chinese patient with Bernard-Soulier syndrome (BSS), a rare bleeding disorder characterized by severe thrombocytopenia and giant platelets. The Chinese patient was homozygous for the mutation; however, heterozygous relatives did not show the characteristic BSS symptoms, leading the authors to conclude that the mutation acted under a recessive model of inheritance. Transient transfection studies by the same group confirmed that the mutation prevents GP Ib/IX complex insertion in the cytoplasmic membrane of platelets, and suppresses GPIbα and GPIX expression, but does not cause its intracellular degradation. One copy of the GPIX mutation was found in 300 European individuals with platelet counts within the normal clinical range. Conclusion: Although the genetic determinants of many thrombocythemias and congenital thrombocytopenias have been identified, very little is known about the genetic determinants of normal platelet count variation. The results suggest that two QTLs on chromosome 3q influence platelet count variation in the Asian Indian kindred, with the GPIX transmembrane mutation and the 3′ UTR SNP in THPO, being strong candidates.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e18531-e18531
Author(s):  
Jiwen Wang ◽  
Min Luo ◽  
Hanmo Wu ◽  
Liming Sheng ◽  
Dan Su ◽  
...  

e18531 Background: Activated platelet is thought to promote cancer cells growth and metastasis, playing an important role in progression of cancer. However, the association between platelet counts and prognosis of patient with non small cell lung cancer (NSCLC) had not been fully elucidated. The aim of this study is to investigate the prognostic value of platelet counts in resectable NSCLC. Methods: A total of 636 primary NSCLC patients who had curatively resected surgery in Zhejiang Cancer Hospital from November 2006 to January 2011 were retrospectively analyzed. Preoperative platelet counts and clinicopathological factors were collected from the medical record database. Patients were followed up for disease progression free survival (PDS) and overall survival (OS) until January 20, 2013. The association between platelet counts and patients’ outcome were evaluated. Results: In all patients, 13.8% (88/636) had increased platelet count (>300 × 109/L), referred to as thrombocytosis. The proportion of thrombocytosis was significantly higher in male, squamous-cell carcinoma and stage III than that in female, other histological types and early stage NSCLC. Moreover, thrombocytosis was associated with significantly shortened survival. Multivariate Cox analysis showed patient with thrombocytosis not only had a 1.66 time elevated risk for disease progression (95% CI, 1.14-2.41, p=0.009), but also had and a 1.47 time risk for death (95% CI, 1.04-2.08, P=0.029), compared with that in those having normal platelet count. More interestingly, the risk for replase was increased to 3.19 times (95% CI, 1.41-7.23, p=0.006) in stage I NSCLC with thrombocytosis than that in patients with normal platelet count after stratified analysis by stage. Conclusions: Preoperative platelet count is an independent prognostic predictor in operable NSCLC, especially in early stage I NSCLC. Platelet count may serve as a useful indicator and potential target for personalized treatment with antiplatelet reagent.


2020 ◽  
pp. bjgp20X713981
Author(s):  
Fergus W Hamilton ◽  
Rupert Payne ◽  
David T Arnold

Abstract Background: Lymphopenia (reduced lymphocyte count) during infections such as pneumonia is common and is associated with increased mortality. Little is known about the relationship between lymphocyte count prior to developing infections and mortality risk. Aim: To identify whether patients with lymphopenia who develop pneumonia have increased risk of death. Design and Setting: A cohort study in the Clinical Practice Research Datalink (CPRD), linked to national death records. This database is representative of the UK population, and is extracted from routine records. Methods: Patients aged >50 years with a pneumonia diagnosis were included. We measured the relationship between lymphocyte count and mortality, using a time-to-event (multivariable Cox regression) approach, adjusted for age, sex, social factors, and potential causes of lymphopenia. Our primary analysis used the most recent test prior to pneumonia. The primary outcome was 28 day, all-cause mortality. Results: 40,909 participants with pneumonia were included from 1998 until 2019, with 28,556 having had a lymphocyte test prior to pneumonia (median time between test and diagnosis 677 days). When lymphocyte count was categorised (0-1×109/L, 1-2×109/L, 2-3×109/L, >3×109/L, never tested), both 28-day and one-year mortality varied significantly: 14%, 9.2%, 6.5%, 6.1% and 25% respectively for 28-day mortality, and 41%, 29%, 22%, 20% and 52% for one-year mortality. In multivariable Cox regression, lower lymphocyte count was consistently associated with increased hazard of death. Conclusion: Lymphopenia is an independent predictor of mortality in primary care pneumonia. Even low-normal lymphopenia (1-2×109/L) is associated with an increase in short- and long-term mortality compared with higher counts.


2004 ◽  
Vol 91 (02) ◽  
pp. 367-372 ◽  
Author(s):  
Jing Yang ◽  
Xiaojun Lu ◽  
Tokuhiro Okada ◽  
Tamiaki Kondo ◽  
Changgeng Ruan ◽  
...  

SummaryThe effects of biological variations on platelet counts were investigated in 694 healthy subjects aged 18 to 60 years living in three cities including Chengdu (Sichuan Province), Suzhou (Jiangsu Province) and Harbin (Heilongjang Province) in China. Platelet counts in healthy subjects were significantly lower in Chengdu (52∼202 X 109/L) and Suzhou (60∼259 X 109/L) than in Harbin (154∼348 X 109/L)(p <0.0001), but the mean platelet volume (MPV) determined concurrently was negatively correlated with platelet count, the MPV values were significantly higher in Chengdu (11.8∼15.6 fl) and Suzhou (10.9∼15.8 fl) than in Harbin (9.5∼12.9 fl) (p < 0.0001). Platelet counts were significantly higher in summer (73∼289 X 109/L) than in winter (52∼202 X 109/L) (p <0.0001), but the MPV values were lower in summer (11.2∼14.7 fl) than in winter (11.8∼15.6 fl) (p <0.05) in Chengdu. Platelet associated immunoglobulin (PA-IgG) in Chengdu was revealed to be significantly higher in the low platelet count group (<150 X 109/L, 13.5 ± 7.1 ng/107 PLT) than in the normal platelet count group (≥150 X 109/L, 8.3 ± 2.7 ng/107 PLT)(p <0.0001). Similar results were observed in Suzhou for the reticulated platelet ratio, which was significantly higher in the low platelet count group (19.5 ± 7.1%) than in the normal platelet count group (11.6 ± 2.7%)(p <0.01). The bleeding time in Chengdu showed a significantly longer time in the low platelet count group (8.6 ± 2.3 min) than in the normal platelet count group (6.0 ± 1.2 min)(p <0.01). With regard to the effects of lipids on platelet counts, the HDL values were significantly higher in the normal platelet count group (1.60 ± 0.76 mmol/L) than the low platelet count group (1.23 ± 0.31 mmol/L) (p <0.01); but no significant differences in cholesterol and triglycerides values between the normal and low platelet count groups (p >0.05) were recorded. These findings suggest that the platelet counts could be greatly influenced in healthy subjects by biological variations such as geographical, seasonal, and lipid variations.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1111-1111
Author(s):  
Patrizia Noris ◽  
Iride F. Ceresa ◽  
Chiara Ambaglio ◽  
Luca M. Dezzani ◽  
Carlo L. Balduini

Abstract TPO, the primary regulator of megakaryopoiesis, is produced at a constant rate and is removed from the circulation by adsorption to specific receptors on platelet and megakaryocyte surfaces. An inverse relationship between platelet count and TPO therefore exists in healthy subjects. However, a few studies in patients with reactive thrombocytosis identified levels of the hormone higher than expected, and suggested that TPO behaves as an acute-phase protein and was responsible for increased platelet count. At the opposite, other studies did not find any significant rise of the hormone in patients who similarly developed reactive thrombocytosis. To gain further information on this topic, we compared TPO levels and platelet counts in two series of hospitalized patients: one (53 patients aged 73 ± 17 years) with strong elevation of both erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and the other (28 age-matched control patients) with normal values. All subjects had been admitted to hospital for acute illnesses: infections, cancer, heart failure or ischemia, stroke, deep vein thrombosis or pancreatitis. Within the group of subjects with high ESR and CRP, 38 had normal platelet counts, while 15 had thrombocytosis at the admittance (n=9) or developed it during their stay (n=6). No thrombocytosis was observed in control patients. Patients with high acute phase indexes had significantly higher TPO levels (R&D Systems, Minneapolis, USA) and platelet counts than control patients (TPO 189.55pg/ml ± 139 vs 62.04pg/ml ± 83, p<0.0001; platelets 310×109/L ± 98 vs 242×109/L ± 67, p=0.0016). Since similar TPO and platelet values were found in patients grouped according to their disorders, we assumed that the acute phase, but not the basic illness, was responsible for the increase of TPO and platelets. We identified strong, positive correlations between ESRc (ESR corrected for Hct) and CRP (r=0.809, p<0.0001), but only weak correlations between TPO and CRP (r=0.584, p<0.0001). Interestingly, no significant relationship between platelet counts and TPO levels (r=0.180, p=NS) was find. When we grouped patients with acute-phase reaction according to absence (platelets 280×109/L ± 61) or presence (platelets 516×109/L ± 105) of thrombocytosis, we found similar TPO values (184pg/ml ± 146 vs 203.4pg/ml ± 126, p=NS). By measuring plasma glycocalicin (GC, Takara Bio Inc. Shiga, Japan) and estimating the glycocalicin index (GCI, by normalizing GC levels for the individual platelet count), which reflects platelet turnover, we excluded that shortened platelet survival masked increased platelet production in subjects with inflammatory conditions and normal platelet count. In fact, identical values of GCI were found in patients with normal platelet count or thrombocytosis (2.434 ± 1.4 vs 2.496 ± 2.5). Finally, no correlation was detected between TPO and GCI (r=0.003, p=NS). Conversely, a strong positive correlation between IL-6 (R&D Systems) and CRP (r=0.692, p<0.0001), and a trend towards correlation between platelet count and IL-6 (r=0.493, p<0.0001) and between TPO and IL-6 (r=0.484, p<0.0001) have been identified. All together our results confirm that TPO acts as an acute phase protein but exclude the possibility that it is uniquely responsible for thrombocytosis of inflammatory disorders, which might recognize in IL-6 a credible candidate as a cooperating factor.


Blood ◽  
1985 ◽  
Vol 66 (6) ◽  
pp. 1362-1370 ◽  
Author(s):  
MA Bitter ◽  
ME Neilly ◽  
MM Le Beau ◽  
MG Pearson ◽  
JD Rowley

Abstract Fourteen patients with acute nonlymphocytic leukemia (ANLL) or dysmyelopoietic syndromes were found to have abnormalities involving the long arm of chromosome 3. In eight patients, the structural rearrangements involved both bands 3q21 and 3q26 and included t(3;3) (four patients), inv(3) (three patients), and ins(5;3) (one patient). Before treatment, seven of these eight patients had platelet counts above 100,000 per microliter, five had normal or elevated platelet counts, and four had significantly elevated platelet counts (600,000 to 1,731,000 per microliter). In each of the eight cases, normal or elevated platelet counts were associated with marked abnormalities of megakaryocytopoiesis, including increased numbers of megakaryocytes and numerous micromegakaryocytes. Classification within the French-American- British system was difficult in most of these cases; however, the leukemia in five of the eight patients with abnormalities of chromosome 3 that involved both bands 3q21 and 3q26 was classified as M4. The remaining six of the 14 patients had translocations between chromosome 3 and another chromosome. None involved both bands 3q21 and 3q26, and a break in either q21 or q26 was noted in only two patients. One of the six, who had ANLL (M4) with a normal platelet count, had a 3;5 translocation which involved band 3q25. These data suggest that in patients with ANLL, abnormalities of chromosome 3 which simultaneously involve bands 3q21 and 3q26 are associated with unusually high platelet counts.


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1118-1118 ◽  
Author(s):  
Douglas B. Cines ◽  
Tatiana Lebedeva ◽  
M. Anna Kowalska ◽  
Mortimer Poncz ◽  
Lubica Rauova ◽  
...  

Abstract Abstract 1118 There are no currently available tests to rapidly assess and reliably identify both impaired hemostasis and hypercoagulable states, in part because of difficulties in measuring integrated reactions in whole blood using a single sensitive and clinically useful platform. Methods like T2 magnetic resonance (T2MR) can provide rich information from complex samples, such as changes in the blood during hemostasis, by measuring signals emanating from the hydrogen nuclei within the sample, primarily in water. We used a 14”x6”x7” portable instrument to measure changes in T2MR that provide a continuous report on the dynamically changing microscopic environment of water during coagulation of whole blood (WB), platelet-poor or platelet-rich plasma (PRP). In these initial foundational studies, we measured T2MR continuously over 20 mins using 34 μL blood samples from consented normal adult donors. We tested clotting of WB initiated by the addition of thrombin or kaolin + calcium. Platelet activation was achieved in WB by addition of ADP or arachidonic acid in the presence of reptilase and factor XIIIa with and without addition of the platelet inhibitors aspirin or 2-methylthioadenosine 5'-monophosphate (2-MeSAMP) and results were confirmed by standard platelet aggregometry. At normal platelet counts from 1.5–3×105/μL and normal hematocrit (HCT) from 38%-48%, T2MR gave two curves corresponding to: (1) water trapped within a retracted clot and (2) water in the surrounding liquid, i.e. serum (Fig. 1a). Platelet counts <1×105/μL or addition of aspirin or 2-MeSAMP eliminated the signal originating from clot retraction (Fig. 1b). High platelet counts (3–13×105/μL) and high thrombin concentrations (10 u/mL) led to a third, even more highly ordered signal (Fig. 1c). The signal also revealed the influence of hematocrit on clot formation/retraction over a wide range of values (20%-73%). Platelet inhibition by aspirin or 2-MeSAMP decreased or eliminated the signal originating from clot retraction (Fig. 1d). Our proof-of-principle studies show that T2MR technology can be applied to measurement of blood clotting across a range of hemostatic conditions. This single technology may be applicable to the study, diagnosis, and management of a spectrum of disorders that range from impaired hemostasis to hypercoagulable states. These T2MR studies represent the first application of this technology to hemostasis and thrombosis. Additional studies will be needed to develop a more complete understanding of the biochemical events measured by T2MR and to more fully explore its clinical utility. Figure 1. Examples of T2MR 3D surfaces for 34 μL of citrated whole blood mixed activated by adding a dried formulation of CaCl2 (11 mM) and kaolin (<0.25%) for (a) a normal platelet count (2.82×105 platelets/μL); (b) thrombocytopenia (9.0×104 platelets/μL); and (c) thrombocytosis (1.0×106 platelets/μL). All samples were reconstituted blood in the same way. (d) Citrated whole blood activated by ADP in the presence of 2-MeSAMP. Figure 1. Examples of T2MR 3D surfaces for 34 μL of citrated whole blood mixed activated by adding a dried formulation of CaCl2 (11 mM) and kaolin (<0.25%) for (a) a normal platelet count (2.82×105 platelets/μL); (b) thrombocytopenia (9.0×104 platelets/μL); and (c) thrombocytosis (1.0×106 platelets/μL). All samples were reconstituted blood in the same way. (d) Citrated whole blood activated by ADP in the presence of 2-MeSAMP. Disclosures: Cines: T2 Biosystems: Research Funding. Lebedeva:T2 Biosystems: Research Funding. Massefski:T2 Biosystems: Employment. Papkov:T2 Biosystems: Employment. Thayer:T2 Biosystems: Employment. Lowery:T2 Biosystems: Employment.


Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 41-41
Author(s):  
Charles Schlappi ◽  
David McCall ◽  
Prasannalaxmi Palabindela ◽  
Christy Bemrich Stolz ◽  
Lee Hilliard ◽  
...  

Abstract Thrombocytopenia is a common reason for referral to a Pediatric Hematologist Oncologist. However, the need for acute intervention in patients with mild or moderate thrombocytopenia is likely a rare event. Because mild and moderate thrombocytopenia is less likely to need intervention and could resolve, the potentially stressful impact of referral to an Oncology center needs consideration. But with minimal literature to support the hypothesis that mild to moderate thrombocytopenia is unlikely associated with severe or progressive hematologic diseases, our ability to provide evidence based recommendations for need for referral is limited. To better understand the course for patients with mild and moderate thrombocytopenia, we conducted a retrospective chart review to assess the prevalence, outcomes, and need for intervention among patients referred for thrombocytopenia. Methods: We conducted a retrospective chart review of 1,140 patients referred to a large Pediatric Hematology Oncology program over a three year period (2012-2014). The diagnosis and demographics were recorded for every patient. Platelet counts at time of referral, lowest platelet count, and current platelet count were recorded and categorized as mild (plt: 100-149x103/mL), moderate (plt: 50-99 x103/mL), severe (plt: 20-49 x103/mL), and very severe (plt: <20 x103/mL). Therapeutic interventions and reason for intervention were recorded. Finally, ANA, platelet antibody and IgG levels were recorded. Descriptive statistics and univariate analysis were conducted using JMP10. Results: In a three year period (2012-2014), 1140 patients were referred to Pediatric Hematology Oncology, 902 of these patients for hematologic diagnoses. One hundred and three (11.4%) of 902 Hematology patients were referred for thrombocytopenia. The mean age of patients with thrombocytopenia was 9.2 years (s.d. 5.8yrs) and 58% were male. At the time of referral, 29% were categorized as mild, 33% were moderate, 17% severe and 21% very severe. The mean platelet count was 68 x103/mL (range 3-143). Younger patients had lower platelet counts (p<0.001), but no differences in mean platelet count were identified by gender (F:M 59 vs. 75 x103/mL, p=0.06). Thirty patients were categorized as mild thrombocytopenia at the time of referral. Only 2 (6%) patients needed eventual treatment (Crohn's disease and SLE treated by subspecialist) and 7 (23%) patients had at least one episode of moderate thrombocytopenia. On their most recent platelet count, 17 (57%) patients remained categorized as mild, 1 (3%) was moderate, and 12 (40%) had a normal platelet count. Thirty four patients were categorized as moderate thrombocytopenia at the time of referral. Only 5 (15%) patients needed eventual treatment (3 ITP patients for QOL/bruising/petechiae, one for SLE and one for NAIT) and 4 (12%) patients had at least one episode categorized as severe thrombocytopenia. On their most recent platelet count, 9 (26%) patients remained categorized as moderate, 10 (29%) were mild, and 15 (44%) had a normal platelet count. At time of diagnosis, 9 of 17 (53%) patients with severe thrombocytopenia and 19 of 22 (86%) of patients with very severe thrombocytopenia required interventions. Currently, 19 of the 39 (49%) patients have normal platelet counts. Other known diagnoses for the 103 patients include: rheumatologic diagnoses (n=5), drug induced (n=5), NAIT (n=3), ADP deficiency (n=1), X-linked thrombocytopenia (n=1), HSP (n=1), HIV (n=1), and Crohn's (n=1) Conclusion: Mild and moderate thrombocytopenia does not often progress or require interventions. Pediatricians should evaluate for Rheumatologic disorders in their initial work-up for mild to moderate thrombocytopenia as well as consider medication-induced thrombocytopenia. A safe and cost-effective approach to a patient with mild to moderate thrombocytopenia could be to observe repeat laboratory data (including ANA) in lieu of any other co-morbid condition. This approach could save families time, money, effort, and emotional stress in making appointments at large referral institutions. Disclosures No relevant conflicts of interest to declare.


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