scholarly journals Immune Thrombocytopenia: A Rare Presentation of Pulmonary Sarcoidosis

2021 ◽  
Author(s):  
Mariana da Silva Leal ◽  
Carolina Amado ◽  
Bárbara Paracana ◽  
Flávio Pereira ◽  
Mariana Sousa ◽  
...  
Keyword(s):  
Immunosuppressive Therapy ◽  
Major Bleeding ◽  
Immune Thrombocytopenia ◽  
Pulmonary Sarcoidosis ◽  
Severe Thrombocytopenia ◽  
Rare Presentation ◽  
Emergency Situations ◽  
Gingival Bleeding ◽  
Granulomatous Disorder ◽  
Current Guidelines

Thrombocytopenia may be the initial presentation of sarcoidosis, which is a systemic granulomatous disorder. Various pathophysiological mechanisms have been identified. Immune thrombocytopenia often has a severe presentation but may respond favourably to immunosuppressive therapy. There are no guidelines for the treatment of thrombocytopenia in sarcoidosis. However, in emergency situations with major bleeding, it seems reasonable to apply the current guidelines recommended for immune thrombocytopenia. The authors report a case of sarcoidosis presenting with severe thrombocytopenia, petechial rash, and nasal and gingival bleeding.

scholarly journals Cefazolin Induced Thrombocytopenia: A Rare Presentation

2020 ◽  
Vol 7 (4) ◽  
Author(s):  
Prakash A ◽  
◽  
Symaco E ◽  
Dalmacion DLV ◽  
Reyes D ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Immune Thrombocytopenia ◽  
First Generation ◽  
Generation Cephalosporin ◽  
Hospitalized Patients ◽  
Severe Thrombocytopenia ◽  
Drug Induced ◽  
Rare Presentation ◽  
Multiple Conditions

Drug-induced immune thrombocytopenia is a frequent condition among hospitalized patients and is hard to diagnose because of the ambiguity of etiologies. It can lead to severe complications. We present a case of a 35-yearold male who was recently treated for infective endocarditis, now presenting with cellulitis. He was treated with cefazolin, a first-generation cephalosporin and later on developed severe thrombocytopenia. The diagnosis was difficult since our patient had multiple conditions that could explain his thrombocytopenia. This is one of the few reported cases of cefazolin-induced thrombocytopenia where we also discuss etiology, workup, and treatment in detail.

scholarly journals Urgent Management of Bleeding in Immune Thrombocytopenia: Towards a Standardized Protocol in the Emergency Department

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 3517-3517
Author(s):  
Siraj Mithoowani ◽  
Andrea Cervi ◽  
Nishwa Shah ◽  
Resham Ejaz ◽  
Rebecca Barty ◽  
...  
Keyword(s):  
Emergency Department ◽  
Platelet Count ◽  
Major Bleeding ◽  
Research Funding ◽  
Immune Thrombocytopenia ◽  
Severe Thrombocytopenia ◽  
Minor Bleeding ◽  
Standardized Protocol ◽  
Ed Visits ◽  
Platelet Transfusions

Abstract Background Severe bleeding is a rare but serious complication of immune thrombocytopenia (ITP). A standard approach to treatment is lacking and the delivery of emergency care is often disjointed. The objective of this study was to describe 1) the treatments and outcomes of ITP patients who present to the emergency department (ED) with severe thrombocytopenia and bleeding; and 2) predictors of worsening bleeding or death among ITP patients presenting to the ED. Methods We did a retrospective cohort study of all patients with ITP who presented to the ED with severe thrombocytopenia (platelet count <20 x109/L) and bleeding in 4 academic hospitals affiliated with McMaster University in Hamilton, Canada between January 2008 and April 2016. Patients were followed from arrival to the ED until 10 days after hospital admission, discharge or death. We extracted demographic data, bleeding symptoms at presentation, all ITP treatments administered, new or worsening bleeding, thrombosis and mortality. Bleeding was graded using the ITP Bleeding Score. We defined major bleeding as intracranial hemorrhage (ICH), pulmonary bleeding, or gross gastrointestinal bleeding (GIB). We summarized the results descriptively by frequencies (percentage), and medians (interquartile range [IQR]). Ethics approval was obtained from the Hamilton Integrated Research Ethics Board. Funding was provided by the Platelet Disorder Support Association. Results We identified 110 patients who presented to the ED (n=139 ED visits) with platelets <20 x109/L and bleeding. Median age was 59 years (IQR: 38-74) and 57% were female. For 63 patients (57%), this was their initial presentation of ITP; for the remaining 47 patients, 36% had previously been treated for ITP and had received a median of 3 (IQR: 2-4) ITP therapies. Twenty-eight patients presented to the ED with major bleeding; the remaining 82 patients had ED visits with minor bleeding only. There were 31 ED visits with major bleeding at presentation including GIB (n=23 visits), ICH (n=4), pulmonary hemorrhage (n=3) and GIB plus ICH (n=1). Median platelet count among patients with major bleeding was 3 x109/L (IQR: 3-8 x109/L). Patients received a median of 3 ITP therapies (IQR: 2-4) after presentation to the ED, including intravenous immune globulin (IVIG; 90% of visits), corticosteroids (77% of visits), platelet transfusions (74% of visits), and romiplostim (3% of visits). Median time from ED presentation to first treatment was 7.6 (4.5-9.5) hours. Treatment for bleeding was initiated by Internal Medicine or Hematology consultants in 19/31 visits (61%) or Emergency Department physicians in 12/31 visits (39%). One patient developed arterial thrombosis and 2 patients died, both from bleeding. There were 6 patients who initially presented to the ED with minor bleeding but who subsequently developed major bleeding after a median of 2 days (range: 1-7). All 6 patients had oral purpura and 4 had frank hematuria before or coincident with the development of major bleeding. Conclusions Management of ITP-associated bleeding in the ED consisted mostly of IVIG, corticosteroids and platelet transfusions. Time to first ITP treatment was greater than 7 hours from ED presentation. Oral purpura and hematuria were associated with the development of new or worsening bleeding. A standardized protocol for the management of ITP bleeding in the ED would help identify patients at risk for new or worsening bleeding, and improve health care delivery by making appropriate treatments available in a timely manner. Disclosures Arnold: Amgen: Consultancy, Research Funding; UCB: Consultancy; UCB: Consultancy; Amgen: Consultancy, Research Funding; Bristol Myers Squibb: Research Funding; Novartis: Consultancy, Research Funding; Bristol Myers Squibb: Research Funding; Novartis: Consultancy, Research Funding.

scholarly journals Sarcoidosis Causing Complete Nasal Obstruction

2021 ◽  
pp. 014556132110038
Author(s):  
Margaret K. Mills ◽  
M. Melinda Sanders ◽  
Todd E. Falcone
Keyword(s):  
Nasal Obstruction ◽  
Pulmonary Sarcoidosis ◽  
Prior History ◽  
Rare Presentation ◽  
History Of ◽  
Sinonasal Involvement

Our case demonstrates the rare presentation of sinonasal sarcoidosis causing severe nasal obstruction. While the patient had a remote history of pulmonary sarcoidosis, she was in remission and had no prior history of sinonasal involvement. Sarcoidosis should be considered in a patient with nasal obstruction especially when there is a history of systemic sarcoid disease.

scholarly journals Regulation of thrombopoiesis: effects of the degree of thrombocytopenia on megakaryocyte ploidy and platelet volume

Blood ◽  
1987 ◽  
Vol 70 (1) ◽  
pp. 177-185 ◽  
Author(s):  
L Corash ◽  
HY Chen ◽  
J Levin ◽  
G Baker ◽  
H Lu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Platelet Count ◽  
Immune Thrombocytopenia ◽  
Temporal Relationship ◽  
Recovery Phase ◽  
Severe Thrombocytopenia ◽  
Detectable Change ◽  
Platelet Volume ◽  
Murine Bone Marrow ◽  
Ploidy Class

Abstract We have established a murine model and techniques with which to serially study thrombocytopoiesis after induction of experimental immune thrombocytopenia of variable severity and duration. Bone marrow megakaryocyte ploidy distribution was determined by using unfractionated bone marrow, a polyclonal megakaryocyte-specific probe, and two-color, fluorescence-activated flow cytometry. With these techniques, the modal megakaryocyte ploidy class in normal murine bone marrow was 16N. Serial studies of bone marrow megakaryocyte ploidy after the induction of acute, severe thrombocytopenia (platelet count, less than 0.05 X 10(6) microL) demonstrated no detectable change in the ploidy distribution at 12, 24, and 36 hours after the onset of thrombocytopenia. At 48 hours, the modal ploidy class shifted from 16N to 32N, and the 64N class increased significantly (P less than .001). The ploidy distribution returned to normal 120 hours after the onset of thrombocytopenia. A lesser degree of thrombocytopenia (platelet count reduction to 0.100 to 0.200 X 10(6)/microL) delayed the modal ploidy class shift from 16N to 32N until 72 hours after the onset of thrombocytopenia. Chronic, severe thrombocytopenia (platelet count, less than 0.05 X 10(6)/microL for seven days) resulted in a modal ploidy class shift from 16N to 32N during the thrombocytopenic phase and an enhanced increase in the 64N megakaryocyte class during the recovery phase. Mean platelet volume (MPV) was simultaneously measured on isolated total platelet populations after induction of thrombocytopenia. MPV was significantly increased (P less than .001) as early as eight hours after the onset of acute, severe thrombocytopenia, 40 hours before a shift in the ploidy distribution. Mild thrombocytopenia (platelet count reduction to 0.400 X 10(6)/microL) was not associated with a ploidy shift but did result in a significantly increased MPV (P less than .001). These studies demonstrate that the temporal relationship and magnitude of the effects of thrombocytopenia upon megakaryocyte ploidy distribution are dependent upon the degree and the duration of the thrombocytopenic stimulus and that the effects of experimental thrombocytopenia on platelet volume and megakaryocyte ploidy are dissociated.

scholarly journals Immune Thrombocytopenia Induced by Immune Checkpoint Inhibitors in Solid Cancer: Case Report and Literature Review

2020 ◽  
Vol 10 ◽  
Author(s):  
Xiaolin Liu ◽  
Xiuju Liang ◽  
Jing Liang ◽  
Yan Li ◽  
Jun Wang
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Checkpoint ◽  
Immune Thrombocytopenia ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Cancer Case ◽  
Solid Cancer ◽  
Severe Thrombocytopenia ◽  
Advanced Cancer Patients

Immune checkpoint inhibitors, including antibodies targeting programmed cell death protein-1 (PD-1) and its receptor programmed cell death ligand-1 (PD-L1), represent promising therapeutic strategies for advanced human malignancies. However, a subgroup of patients experiences various autoimmune toxicities, termed immune-related adverse events (irAEs), that occur as a result of on-target and off-tumor autoimmune responses. Although irAEs are generally confirmed to be less severe than toxicities caused by conventional chemotherapy and targeted therapy, uncommon irAEs, such as immune thrombocytopenia, may occur with a very low incidence and sometimes be severe or fatal. This review focuses on the epidemiology, clinical presentation, and prognosis of immune thrombocytopenia occurring in advanced cancer patients induced by immune checkpoint inhibitors, especially in those with PD-1 or PD-L1 inhibitor treatment. We also first present one patient with non-small cell lung cancer who received the PD-L1 inhibitor durvalumab and developed severe thrombocytopenia.

Intramuscular anti-D in chronic immune thrombocytopenia children with severe thrombocytopenia

2013 ◽  
Vol 55 (6) ◽  
pp. e146-e148 ◽  
Author(s):  
Nongnuch Sirachainan ◽  
Usanarat Anurathapan ◽  
Ampaiwan Chuansumrit ◽  
Duantida Songdej ◽  
Pakawan Wongwerawattanakoon ◽  
...  
Keyword(s):  
Immune Thrombocytopenia ◽  
Severe Thrombocytopenia ◽  
Chronic Immune Thrombocytopenia

Pulmonary Sarcoidosis

2017 ◽  
Vol 38 (04) ◽  
pp. 437-449 ◽  
Author(s):  
Martina Bonifazi ◽  
Stefano Gasparini ◽  
Veronica Alfieri ◽  
Elisabetta Renzoni
Keyword(s):  
Tissue Characterization ◽  
Wide Spectrum ◽  
Diagnostic Techniques ◽  
Pulmonary Sarcoidosis ◽  
Unknown Etiology ◽  
Local Resources ◽  
Clinical Scenarios ◽  
Risk Of Progression ◽  
Prognostic Implications ◽  
Granulomatous Disorder

AbstractSarcoidosis is a systemic granulomatous disorder of unknown etiology, with a predilection for the respiratory system, involved in more than 90% of cases, with considerable variability in terms of patterns and prognostic implications. A protean interplay between genetic susceptibility and antigen exposure in selected environmental contexts is likely to define not only the risk for disease but also the different clinical phenotypes. Advances in imaging and functional tests over the past decades have increasingly broadened the awareness of the wide spectrum of features potentially occurring in pulmonary sarcoidosis, while the evolution of diagnostic techniques in interventional pulmonology has increased the possibility of obtaining tissue characterization more easily, by means of ultrasound-guided tools and cryotechnology. However, histological proof is not always needed, as, in selected scenarios with compatible clinical and imaging picture, a confirmatory biopsy is perceived as redundant. The diagnostic workup should be tailored on a case-by-case basis, according to an integrated assessment of clinical features, local resources, and expertise availability. Owing to the heterogeneity of possible clinical scenarios and the paucity of evidence-based data on treatments, a standardized clinical management has yet to be established, and general approach usually reflects expert opinion from accumulated clinical data. Key elements of decision-making process are to assess the baseline severity of disease, to stratify the risk of progression, and to define the goals of treatment.

A Multi-Centre Prospective Observational Study of Platelet Transfusion Practice in Neonates with Severe Thrombocytopenia.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 961-961 ◽  
Author(s):  
Neil Murray ◽  
Sally Ballard ◽  
Angela Casbard ◽  
Mike Murphy ◽  
Irene Roberts ◽  
...  
Keyword(s):  
Observational Study ◽  
Major Bleeding ◽  
Platelet Transfusion ◽  
Transfusion Practice ◽  
Major Haemorrhage ◽  
Study Entry ◽  
Severe Thrombocytopenia ◽  
Minor Bleeding ◽  
Grade 3 ◽  
Platelet Transfusions

Abstract Background: Platelet transfusion practice in neonates is not evidence-based and there is a lack of data relating transfusion to clinical outcome. To inform the design of clinical trials, we conducted a prospective multicentre observational study of platelet transfusion in thombocytopenic neonates to describe: transfusion practice, including reason for transfusion; clinically-related outcomes, including minor and major bleeding and mortality. Methods: Neonates with platelets &lt;60x109/l were studied at 7 UK neonatal intensive care units Mar 05-Jun 06. With parental consent, daily data were collected on minor bleeding (blood staining of oral/nasogastric/endotracheal secretions and stool; microscopic haematuria; petechial rash; oozing from puncture sites - scored 0–7), and major bleeding (intraventricular (IVH), intra-abdominal, pulmonary or renal). Surviving neonates were studied for 7 days or until platelets were ≥60x109/l. Blood counts and all transfusions were directed by the attending neonatologist, with reason for transfusion and its effect on bleeding prospectively documented. Results: 145 of 167 (87%) eligible neonates were enrolled; 123 (85%) were &lt; 37 weeks gestational age (GA), 89 (61%) were male. The study documented 186 episodes of thrombocytopenia (1606 study days) and 309 platelet transfusions given to 91 (63%) neonates. GA, birth weight and age at thrombocytopenic episode were: 27 (24–32) weeks; 825 (675–1370) grams; 5 (2–16) days, respectively [all data median (IQR)]. 21/145 babies (14%) had major IVH (Grade 3/4) at study entry. Platelets (x 109/l) at study entry, and at platelet nadir, and duration of count &lt;60x109/l were: 44 (33–54); 31 (19–42); 2 (1–5) days respectively. In transfused neonates, platelets (x109/l) pre- and post-transfusion, and number of transfusions were: 27 (19–36); 84 (46–138); 2 (1–4) respectively. The principal indications for transfusion were:- platelet count below threshold of unit guideline: 265/309 (86%); deteriorating clinical condition: 17/309 (6%); and significant bleeding: 7/309 (2%). At least 1 episode of minor bleeding was recorded on 622/1606 (39%) of study days. Minor bleeding scores recorded for 12 hours pre- and post each transfusion were [median (IQR)]: 1 (0–2) and 0 (0–1) respectively. New or extension of IVH bleeding to Grade 3/4 occurred in 7 neonates and other major haemorrhage in 9 neonates (4 pulmonary, 3 GI). A total of 20/145 (14%) neonates died, 13 with major IVH bleeding (of which 10 had Grade 3/4 IVH at study entry); all received platelet transfusions [total 87; median 3 (2 to 7). Conclusion: This study confirms that most neonates with severe thrombocytopenia are preterm, most episodes develop after 72 hours of life (median 5 days) and are of short duration (median 2 days). Minor haemorrhage is common and may be reduced by platelet transfusion. Major haemorrhage is uncommon (11%), is associated with mortality (82%) and affected patients receive a large number of platelet transfusions. There is a clear distinction between the majority of thrombocytopenic neonates who receive one or two transfusions as prophylaxis with a good outcome, and the minority who suffer adverse outcomes despite transfusion. Many neonates are transfused with platelets at thresholds below those suggested in guidelines without apparent clinical detriment. These data will be invaluable for planning the randomised trials necessary for rationalising platelet transfusion in these vulnerable patients.

Association of Interleukin-18 Gene Polymorphism with Severity of Chronic Immune Thrombocytopenia (ITP).

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3693-3693
Author(s):  
Takayuki Saitoh ◽  
Norihiko Moriyama ◽  
Tomonori Takani ◽  
Takeki Mitsui ◽  
Takumi Hoshino ◽  
...  
Keyword(s):  
Platelet Count ◽  
Immune Thrombocytopenia ◽  
Initial Diagnosis ◽  
Severe Thrombocytopenia ◽  
Interleukin 18 ◽  
Single Nucleotide ◽  
Chronic Itp ◽  
Significant Difference ◽  
Haplotype Frequencies ◽  
And Control

Abstract Abstract 3693 Introduction: Immune thrombocytopenia (ITP) is a chronic acquired organ-specific autoimmune disorder characterized by the production of antibodies against antigens on the membranes of platelets. Several cytokine studies have shown Th1 polarization in ITP patients. Interleukin-18 (IL-18) plays an important role in Th1 and Th2 immune response. Recent studies showed that single-nucleotide promoter polymorphisms influence the transcriptions of IL-18 mRNA. IL-18 polymorphism has been implicated in autoimmunity, including Crohn's disease, rheumatoid arthritis, and asthma. We examined the single nucleotide polymorphisms (SNPs) in the promoter regions of the IL-18 genes in patients with ITP, and analyzed the relationship between IL-18 SNPs and clinical features. Patients and Methods: One hundred patients (male/female; 22/78, median age; 54.5) diagnosed as chronic ITP and 151 healthy controls were included. Chronic ITP was defined as thrombocytopenia (platelet count < 100×109/L) persisting greater than 12 months, normal or increased marrow megakaryocytes, and no secondary immune or non-immune abnormality that could account for the thrombocytopenic state. ITP with severe thrombocytopenia was defined as thrombocytopenia (platelet count < 10×109/L) at presentation of ITP. The response criteria of the ITP International Working Group was used. A complete response (CR) is defined as any platelet count of at least 100×109/L, and a response (R) was defined as any platelet count between 30 and 100×109/L and at least doubling of the baseline count. Allparticipants gave written informed consent about the study. Genomic DNA was isolated from peripheral blood using the DNA Kit (QIAGEN, Hilden, Germany). An allele-specific polymerase chain reaction was used to analyze polymorphism in IL-18 –607A/C and -137G/C. Genotype and allele frequencies were compared between the study groups using Χ2-test. The characteristics and laboratory features of the ITP patients with each IL-10 promoter polymorphism were compared using X2-tests and student t-tests. Probability values <0.05 were considered statistically significant. Results: The platelet count was at an initial diagnosis ranged from 1×109/L to 98 ×109/L, with a median of platelet count of 15×109/L. Thirty-five patients (35%) had severe thrombocytopenia. Steroid treatment was given to 68 patients (68%), while splenectomy was used in 11 patients (11%).The frequencies of the genotypes were as follows: AA (34%), AC (57%), and CC (9%) for -607; GG (77%), GC (21%), and CC (2%) for -137 loci. The frequencies of each haplotype were as follows: C-G/C-G haplotype (9%), A-G/C-G haplotype (47%), A-C/C-G haplotype (10%), A-G/A-G haplotype (21%), A-G/A-C haplotype (11%) and A-C/A-C haplotype (2%). No significant differences in the genotype or haplotype frequencies demonstrated between chronic ITP patients and control group. However, patients with -137CC genotypes showed severe thrombocytopenia at initial diagnosis compared to those with -137GG/GC genotypes (5×109/L vs. 22×109/L, p=0.002). Furthermore, patients with A-C/A-C haplotype showed severe thrombocytopenic state (5×109/L vs. 22×109/L, p=0.002) compared to those without A-C/A-C haplotype. No significant difference of treatment response was observed according to IL-18 polymorphism. Conclusion: No significant differences in the genotype or haplotype frequencies demonstrated between chronic ITP patients and control. However, -137CC genotypes or AA/CC haplotype was associated with severity of chronic ITP. Our data suggest that the group with low IL-18 inducibility (i.e. -137CC genotype, A-C/A-C haplotype) may have more severe thrombocytopenia. Disclosures: No relevant conflicts of interest to declare.

The Cytokine Polymorphisms Affect the Severity of Thrombocytopenia at Diagnosis in Chronic Immune Thrombocytopenia.

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2194-2194
Author(s):  
Takayuki Saitoh ◽  
Chiaki Ushie ◽  
Atsushi Iwasaki ◽  
Norihiko Moriyama ◽  
Tomonori Takani ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Platelet Count ◽  
Clinical Features ◽  
Immune Thrombocytopenia ◽  
Steroid Treatment ◽  
Severe Thrombocytopenia ◽  
Bleeding Tendency ◽  
Chain Reaction ◽  
Chronic Itp ◽  
Polymerase Chain

Abstract Abstract 2194 Introduction: The severity of immune thrombocytopenia (ITP) depends on the degree of the thrombocytopenia and the extent of bleeding. Some investigators have reported the association between the thrombocytopenia and cytokine dysregulation in ITP. We investigated the association between the severity of thrombocytopenia at diagnosis in ITP patients and several cytokine polymorphisms, including IL-10-1082A/G, -819T/C, -592A/C, IL-17F-7488T/C and IL-18-607A/C, −137G/C. Patients and methods: We examined 102 patients (male/female, 24/78; median age, 42) diagnosed with chronic ITP. The definition, response criteria, including complete response (CR)and response (R), loss of CR,and “corticosteroid-dependence” were assessed according to the criteria of the ITP International Working Group. ITP with severe thrombocytopenia (ST group)was defined as thrombocytopenia (platelet count < 10×109/L) at the initial diagnosis of ITP. Genotyping of IL-10 (rs1800870 − 1082 A/G, rs1800871 − 819 T/C, and rs1800872 − 592 A/C) and IL-17F (rs763780, 7488 T/C) polymorphisms were determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and the genotyping of the IL-18 polymorphism (rs187238 −137G/C and rs1946518−607 A/C) was determined by the allelic specific polymerase chain reaction technique. To confirm the accuracy of the assay, amplification products of several individuals were sequenced using an ABI Prism Genetic Analyzer. Genotype and allele frequencies were compared between the study groups using χ2-test. The characteristics and laboratory features of ITP patients with each polymorphisms were compared using χ2-tests and student t-tests. Odds ratios (OR) and 95% confidence intervals (CIs) were estimated for each study. All patients were provided written information about the study. This study was approved by the Institutional Research Board of Gunma University Hospital. Results: Clinical features of chronic ITP: The platelet count ranged from 1×109/L to 98×109/L with a mean of platelet count of 32×109/L at the initial diagnosis. Fifty seven patients (49%) had bleeding tendency. Steroid treatment was given to 68 patients (66.7%) and eradication of Helicobacter pylori (H. pylori) was performed in 32 patients (31.4%), while splenectomy was performed in only 11 patients (10.8%). Clinical features of ST group vs. non-ST group in chronic ITP: Of these 102 patients, 17 (16.7%) had severe thrombocytopenia (platelet count < 10×109/L) (ST group). ST group were significantly older (ST group: median 59 years vs. non-ST group: 41 years, p<0.01) and had more severe bleeding tendency (ST group: 100% vs. non-ST group: 54%, p<0.0001). Steroid treatment was frequently given to ST group than to non-ST group (ST group: 100% vs. non-ST group: 59.5%, p<0.001). Though the response to corticosteroids treatment was not significantly different between ST group and non-ST group (CR rate, ST group: 50% vs. non-ST group: 51.0%, p=0.94), corticosteroid-dependent patients in ST group was significantly higher than in non-ST group (76.9% vs. 25.3%, p<0.005). Polymorphism study of ST group vs. non-ST group in chronic ITP: The frequencies of genotypes of cytokines in patients with chronic ITP according to the definition of criteria of ST were as follows: AA (93.3% vs. 97.1%) and AG (6.7% vs. 2.9%, p=0.48) for IL-10–1082; TT (46.7% vs. 33.3%), TC (33.3% vs.55 %) and CC (20% vs. 11.7%) for IL-10–819; AA (46.7% vs. 33.3%), AC (33.3% vs.55 %) and CC (12.2% vs. 11.5%) for IL-10–592; TT (100% vs. 81%) and TC (0% vs. 19%) for IL-17F; GG (82.4% vs. 74.4%), GC (17.6% vs. 23.2%) and CC (0% vs. 2.4%) for IL-18–137; AA (35.3% vs. 34.1%), AC (58.8% vs. 53.7%) and CC (5.9% vs 12.2%) for IL-18–607 loci (ST group vs. non-ST group, respectively). No significant difference was observed between ST group and non-ST group according to IL-10–1082A/G, −819T/C, −592A/C, and IL-18–607A/C, −137G/C polymorphism. However, the numbers of IL-17F 7488TT genotype (higher function type) in ST group were significantly higher than in non-ST group (ST group: 100% vs. non-ST group: 81% p<0.05). Conclusion: These findings suggest that severe thrombocytopenia at diagnosis have an impact of bleeding tendency and corticosteroid-dependency of chronic ITP. Furthermore, IL-17F polymorphism may affect the severity of thrombocytopenia of chronic ITP. Disclosures: No relevant conflicts of interest to declare.

Sign in / Sign up

Export Citation Format

Share Document