acute problems in pediatric hematology...acute problems in pediatric hematology machiel van den...
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Acute problems in Pediatric Hematology
Machiel van den AkkerPediatric Hematology Oncology
Queen Paola Children's Hospital/UZ BrusselHerfst symposium – Koningin Paola Kinderziekenhuis
8 October 2016
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Contents
Pediatric Hematology
• Marrow Failure Syndromes
• Red Cell Disorders
• Granulocyte Disorders
• Lymphocyte Disorders
• Platelet Disorders
• Coagulation Disorders
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Contents
Pediatric Hematology
• Marrow Failure Syndromes
• Red Cell Disorders
• Granulocyte Disorders
• Lymphocyte Disorders
• Platelet Disorders
• Coagulation Disorders
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Case 1
• two year old, previously fit girl
• two weeks ago viral URTI
• pale, sleeps a lot
• PE: pale, small cervical lnn, no HSM, morfological normal
• Labo: -Hb 5,5 MCV 78, Reti 0,1%, Plt 386, WBC 8,5 ANC 1500
-LDH/bili/hapto normal
• ?
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Case 1
Bone marrow aspirate smear illustrates a marked decrease in the erythroid lineage with only rare erythroblasts and no maturing forms. Granulocytic lineage is normal.
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Transient Erythroblastopenia of Childhood
• expectative
• RBC transfusion as needed
• DD Parvo virus infection, Diamond Blackfan Anemie
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Contents
Pediatric Hematology
• Marrow Failure Syndromes
• Red Cell Disorders
• Granulocyte Disorders
• Lymphocyte Disorders
• Platelet Disorders
• Coagulation Disorders
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Case 2
• 5 years old girl was referred for jaundice and fatigue
• new immigrants, first of three children of healthy, non-consanguineous Iraqi parents
• language barrier
• PE: tachycardia, anemic sclera and mild jaundice
• Labo: Hb 5.4 g/dl, MCV 82 fl, reticulocytes 104/1000 RBC, schistocytes and bite cells, LDH 912 U/l, total bilirubin 1.4 mg/dl, haptoglobin 10.4 mg/dl
• ?
•
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G6PD deficiency
• additional information: jaundice and fatigue after eating fava beans; family history revealed a paternal aunt who was not allowed to eat fava beans
• spectrophotometric analysis revealed: G6PD 0.1 U/g Hb
• although her father and her 6 year old sister never had symptoms of hemolysis, G6PD respectively 0.1 U/g Hb and 0.0 U/g Hb, normal range on this age 4.1-7.9 U/g Hb)
• the girl recovered after red blood cell transfusion; no further hemolytic episode occurred
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G6PD deficiency
Family tree: Father: G6PD-Mediterranean variant (c.563C>T (p.Ser188Phe)) in hemizygosity. Mother: G6PD-Chatham variant (c.1003G>A (p.Ala335Thr)) in heterozygosity. Both girls had both mutations in compound heterozygosity.
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G6PD deficiency
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G6PD deficiency
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Contents
Pediatric Hematology
• Marrow Failure Syndromes
• Red Cell Disorders
• Granulocyte Disorders
• Lymphocyte Disorders
• Platelet Disorders
• Coagulation Disorders
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Case 3
• 11 month old boy
• ER: high fever, silent infant, exophthalmos
• history: recurrent seborrheic dermatitis all over the skin, bilateral otorrhea
• PE: seborrheic dermatitis all over the skin
bilateral otorrhea
soft mass (about 1.5 cm in diameter) in the right parietal region
exophthalmos of both eyes (particularly in the left eye)
splenomegaly
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Case 3
• CT skelet: round-shaped osteolytic lesion of the right parietal bone and erosion of the right scapula
• CT head: soft tissue mass in the left posterior orbit
• CT thorax and abdomen: increased interstitial markings, with reticular patterns in the lungs and enlargement of spleen
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Case 3
• Labo: CBC: Hb 112 g/l, WBC 6.1×109/l, Plt 456×109/l
ALK, liver and kidney function tests: normal
• multisytem disease?
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Langerhans Cell Histiocytosis
• diagnosis based on histopathological examination:
characterized by multinucleated Langerhans' cells, histiocytesand eosinophils
EM examination: Birbeck granules (gold standard)
Immunohistochemistry: diagnosis can be established with the use of CD1a, S100, CD45, and/or Langerin immunostaining on histopathological specimens
S100 positivity
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Langerhans Cell Histiocytosis
• wide spectrum of presenting symptoms and variable clinical behavior and prognosis
• previously, the disease was separated into three classifications: eosinophilic granuloma, Hand-Schüller-Christian and Letterer-Siwe
• in 1990 LCH Study Group classification: single system LCH (unifocal bone, skin or lymph node, multifocal bone
or lymph nodes)
multisystem LCH (low-risk and high-risk (liver, lungs, spleen and hematopoietic system) forms)
• etiology: characterized by a clonal proliferation of histiocyte-like cells, is
controversial: neoplastic or inflammatory?
number of findings with regard to the molecular aspects of the disease suggested the possibility that LCH may be the result of an immune dysregulation
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Langerhans Cell Histiocytosis
• treatment: for multisystem LCH controversial, systemic multiagent chemotherapy
is recommended (most common chemotherapeutic agents are vinblastine, prednisone, etoposide and methotrexate)
severe and refractory LCH patients, particularly those with a life-threatening disease, may benefit from other therapies, including monoclonal antibodies that target CD1a, CD207 or CD52, specific cytokine inhibitors, 2-chlorodeoxyadenosine, BRAF V600E inhibition and bone marrow transplantation
• our patient: VEP/VCP regimens applied for a year, after which the patient received
vincristine every two weeks for a year;
following one cycle of chemotherapy, the patient's temperature returned to normal, with rapid improvement observed with regard to the dermatitis and otorrhea.
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Contents
Pediatric Hematology
• Marrow Failure Syndromes
• Red Cell Disorders
• Granulocyte Disorders
• Lymphocyte Disorders
• Platelet Disorders
• Coagulation Disorders
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Case 4
• three and half year old boy
• ER: fever, cough, shortness of breath
• history: several admission for bronchiolitis, pneumonia, arthritis, coxsackievirus meningitis, many antibiotic treatments for AOM
• PE: Weight 9.5 kg, RR 44, Sat 85% (at room air), no cervical lnn, no tonsils, air entry diminished on the right side
• ?
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Case 4
• many infections – why?
• Labo: WBC 22x109/L, ANC 94%, CRP 265
IgG, IgM and IgA ↓↓↓↓
Flow cytometry: absence B-cell markers CD 19 and 20
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X-linked Agammaglobulinemia
• affects males only
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X-linked Agammaglobulinemia
• B cells do not differentiate. Mutation in Bruton’s tyrosine kinase (Btk) required for B cell development.
- B cells absent in peripheral blood.- T cell numbers and function are normal
• no antibodies are produced, thus no antibody-mediated immunity
• cell-mediated immunity is normal
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X-linked Agammaglobulinemia
• treat with intravenous immunoglobulin (IVIG)
• still infections esp. giardiasis and chronic conjunctivitis
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Contents
Pediatric Hematology
• Marrow Failure Syndromes
• Red Cell Disorders
• Granulocyte Disorders
• Lymphocyte Disorders
• Platelet Disorders
• Coagulation Disorders
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Case 5
• previous healthy two year old girl
• ER: many small red spots, not sick
• PE: petechial rash and some hematomas, otherwise normal
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Case 5
• Labo:
CBC: WBC 6x109/L, Hb 11.5 g/dL, MCV 74, Plt 4x109/L
large platelets on smear
CRP 6, LDH 450
• ?
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ITP
• Antiplatelet antibody testing: not recommended
• Consider: ANA, viral serology, H. pylori Ab
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ITP
• when PE doesn’t fit ITP, no response to therapy, or duration 6 months: Bone Marrow Aspiration for further investigation
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ITP
• Treatment: observation only IV immunoglobulin (IVIG, Privigen, Nanogam etc) IV Rho immunoglobulin (RhIG) for Rh(D)-positive patients with
intact spleens, but difficult to get in Belgium oral prednisone, IV methylprednisolone, or high-dose
dexamethasone may be used
• Third line: Rituximab (anti-CD20) splenectomy thrombopoietin receptor agonists (ie, eltrombopag,
romiplostim) may maintain platelet counts at safe levels (still in research setting in children)
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Contents
Pediatric Hematology
• Marrow Failure Syndromes
• Red Cell Disorders
• Granulocyte Disorders
• Lymphocyte Disorders
• Platelet Disorders
• Coagulation Disorders
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Case 6• one and a half-year-old boy
• ER: right-sided hemiparesis since 1 day
• VG: no problems in personal or family history were noted, besides a varicella infection 8 months before admission
• Labo: normal CBC, CRP, kidney and liver function
• MRI brain: (sub)acute ischemic lesion in the left corona radiata and nucleus lentiformis compatible with the deep arteria cerebri media territorium
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Case 6
• echocardiography was normal
• extensive coagulation investigation [APTT, prothrombin time, fibrinogen, d-dimers, prothrombin G20210A mutation, antithrombin III, protein C activity, activated protein C resistance, protein S activity, platelet function tests and homocysteine] was normal
• lupus anticoagulans: negative
• metabolic screening for amino acids and organic acids: normal
• PCR for varicella on CSF was weakly positive. Anti-VZV IgG in serum was positive
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Varicella cerebral vasculopathy
• treatment with ceftriaxone (100 mg/kg/d until negative cultures were reported), acyclovir (30 mg/kg/d for 2 weeks) and methylprednisolone (1 mg/kg/d for 5 days) was immediately started
• because of the severity of the neurologic deficit, in anticipation of the results, subcutaneous enoxaparin (2mg/kg/d until discharge) was added to the therapy
• symptoms slowly improved during hospitalization
• the patient was discharged to receive aspirin for a total period of 2 years
• MRI angiography, performed a month after discharge, showed the ischemic injury without residual stenosis
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References-Vascular Complications of Varicella: Description of 4 Cases and a Review of Literature. Driesen
Y, Verweij M, De Maeseneer M, De Dooy J, Wojciechowski M, Van Den Akker M. Pediatr Infect Dis
J. 2015 Jul 29.
-Transient erythroblastopenia of childhood is an underdiagnosed and self-limiting disease. van
den Akker M, Dror Y, Odame I. Acta Paediatr. 2014 Jul;103(7):e288-94
-Langerhans cell histiocytosis with multisystem involvement in an infant: A case report. Bi L, Sun
B, Lu Z, Shi Z, Wang D, Zhu Z. Exp Ther Med. 2015 Jun;9(6):2137-2140
-Glucose-6-phosphate dehydrogenase deficiency: not exclusively in males. Leonie van den Broek,
Evelien Heylen, Machiel van den Akker. Clin Case Reports 2016
-Current Management of Primary Immune Thrombocytopenia. Provan D, Newland AC. Adv Ther.
2015 Oct;32(10):875-87.
-Langerhans cell histiocytosis is a neoplasm and consequently its recurrence is a relapse: In
memory of Bob Arceci. Egeler RM, Katewa S, Leenen PJ, Beverley P, Collin M, Ginhoux F, Arceci RJ,
Rollins BJ; Steering Committee of the Nikolas Symposium. Pediatr Blood Cancer. 2016
Oct;63(10):1704-12
-X-Linked Agammaglobulinemia. Smith CIE, Berglöf A. In: Pagon RA, Adam MP, Ardinger HH, Wallace SE, Amemiya A, Bean LJH, Bird TD, Fong CT, Mefford HC, Smith RJH, Stephens K, editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2016. 2001 Apr 5 [updated 2016 Aug 4]
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