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Acquired pelger–huët anomaly associated with ibuprofen therapy

Clinica Chimica Acta xxx (2009) xxx–xxx j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / c l i n c h i m Acquired Pelger–Huët anomaly associated with ibuprofen therapy and basophils carry chromatin hypercondensation The secondsuggests that pseudo PHA is not actually an abnormality in neutrophilmaturation but represents an apoptotic cell, since ultrastructurally pseudo PHA neutrophils looked like mature cells undergoing apoptosis(compact chromatine moved toward the periphery of the nucleus and Pelger–Huët anomaly (PHA) is a benign inherited condition condensation of the cytoplasm with abnormally shaped organelles) characterized by hyposegmentation of the neutrophils nucleus and The third hypothesis suggests that pseudo PHA is related to 17p excessive chromatin clumping An acquired neutrophils dysplasia similar to PHA has been already described in hematological diseases A careful review of the pertinent literature revealed that almost all and in some clinical conditions, especially under certain drugs reports of pseudo PHA associated to either drugs use or to several effect It has been known as acquired or pseudo Pelger–Huët diseases were described until middle of 1980. To date, almost all anomaly. A previous report of our group showed that the incidence of reported cases are associated to either myelodysplastic syndrome or acquired PHA in kidney transplanted patients under immunosuppres- other hematological diseases as well as to use of immunosuppressive sive therapy in a local Brazilian Hospital was 5.3% (9 out of 170 patients) Curiously, automated hematological procedures including differen- In March 2008, a healthy 7-year old child was punctioned in a small tial leukocytes counting were widely diffused from end of the 1980s.
laboratory in Mateus Leme/MG for a routine hemogram analysis. Her This fact raises an important question “Can automatic cell blood blood cells showed to be normal under quantitative and qualitative counters reveal neutrophils' morphological changes consistent to PHA points of view. Two months later, this child had fever, without other such as abnormal bilobular or monolobular nuclear forms and excessive symptoms and 17 drops of ibuprofen was given to her, from 4 to 4 h chromatin clumping?” PHA whichever its cause, if it is not registered by during 1 day and night. Next day, as the girl's condition became worse, automated counters may constitute a serious problem considering that she was conducted to the same laboratory for another routine blood clinical laboratories do not examine most of stained blood films on the analysis. This dose (510 mg/24 h) was >12 times higher than that recommended (40 mg/24 h). The leukocytes count was 12,500/μL with The contribution of this report is to alert laboratory professionals and 22% band form neutrophils, 50% segmented neutrophils, 20% lympho- clinicians for pseudo PHA diagnosis. Considering previous reports and cytes and 8% monocytes, erythrocyte sedimentation rate (60 min.) was our own experience, in addition to the frequent use of drugs with no 6 mm and Reactive C Protein was negative. However, blood film clinical prescription (automedication), one can admit that other cases revealed that segmented neutrophils nucleus had a poor segmentation, similar to that one reported here due to administration of ibuprofen (or with only bilobular nuclear form or peanut shaped and the chromatin other drugs) in high doses may be occurring frequently. Whether this was excessively clumped a, b, c and d). Later on a more phenomenon has clinical implication remains to be elucidated. At least, experienced observer has diagnosed the child as a carrier of PHA. Since however, when pseudo PHA is described, its possible cause must be there was a normal blood analysis reported 2 months ago, the hypothesis of benign inherited PHA was discharged. The apparent Finally, considering that acquired PHA is a common finding in neutrophils' shift left (22% band forms) was not coherent with the myelodysplastic syndrome a doubt may be about a predisposition child's symptoms, she only had fever once, with no infection symptoms.
for developing bone marrow diseases in individuals who showed these Five days later, a new blood analysis was done and the total leukocytes neutrophils under certain conditions. However, no report regarding this were 5300/μL persisting 21% of band neutrophils. Six months later, the issue was found in the literature and a follow up of these individuals is child had fever again and other blood analysis was required. The essential to elucidate this important question.
leukocytes count was 17,700/μL and 5% band neutrophils (withoutalterations), 54% segmented neutrophils, 32% lymphocytes, 2% mono- cytes and 7% eosinophils ) was found, which confirm thetransitory character of neutrophil abnormalities observed when the The authors thank FAPEMIG and CNPq/Brazil. LMSD and MGC are child was under ibuprofen use. All data are shown in . It was not grateful to CNPq Research Fellowship (PQ).
suspected that this case of transitory neutrophil abnormalities wascaused by ibuprofen, since it was the only drug that the child had received. Only one report on ibuprofen use and pseudo PHA haspreviously been described [1] Johnson CA, Cass DA, Trillo AA, Snyder MS, Dechatelet LR. Functional and metabolic Although some hypotheses were raised to explain this phenomen, studies of polymorphonuclear leukocytes in the congenital Pelger–Huët anomaly.
Blood 1980;55:466–9.
the mechanism of nuclear change is still unclear. The first hyphothesis is [2] Shetty VT, Mundle SD, Raza A. Pseudo anomalia de Pelger–Huët anomaly in related to abnormalities in the sequence of lamin B receptor (LBR) gene myelodysplastic syndrome: hyposegmented or apoptotic neutrophil? Blood resulting in a lack of LBR protein. This protein is essential for chromatin [3] Kuriyama K, Tomonaga M, Matsuo T. Diagnostic significance of detecting pseudo binding to nuclear membrane. In the absence of LBR, neutrophils and Pelger–Huët anomalies and micro-megakaryocytes in myelodysplastic syndrome.
also erythroblasts, monocytes, lymphocytes, plasma cells, eosinophils 0009-8981/$ – see front matter 2009 Elsevier B.V. All rights reserved.
doi: Please cite this article as: Moreira AMB, et al, Acquired Pelger–Huët anomaly associated with ibuprofen therapy, Clin Chim Acta (2009),doi: Fig. 1. Neutrophils with chromatin excessively clumped. a) Segmented neutrophil b, c) band forms neutrophils d) neutrophil with rodlike nucleus. e) Segmented neutrophils with noabnormalities.
[11] Deutsch PH, Mandell GL. Reversible Pelger ibuprofen therapy. Arch Intern Med 1985;145(1):166.
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[12] Best S, Salvati F, Kallo J, Garner C, Height S, Thein SL, et al. Lamin B-receptor mutations in Pelger–Huët anomaly. Br J Haematol 2003;123(3):542–4.
[13] Tomonaga M. Nuclear abnormalities in Pelger cell morphology. Rinsho Byori 2005;52(1):54–60.
[14] Soenen V, Preudhomme C, Roumier C, Daudignon A, Laï JL, Fenaux P. 17p Deletion in acute myeloid leukemia and myelodysplastic syndrome. Analysis of break- points and deleted segments by fluorescence in situ. Blood 1998;91:1008–15.
[15] Cunningham JM, Patnaik MM, Hammerschmidt DE, Vercellotti GM. Historical perspective and clinical implications of the Pelger–Huët cell. Am J Hematol2009;84:116 [4] Daliphard S, Accard F, Delattre C, Toupance D, Guyot C, Méchinaud F, et al. Reversible Clinical and Toxicological Analysis Department, Faculty of Pharmacy, abnormal chromatin clumping in granulocytes from six transplant patients treatedwith mycophenolate mofetil: a rare adverse effect mimicking abnormal chromatin Federal University of Minas Gerais, Brazil clumping syndrome. Br J Haematol 2002;116(3):726–7.
⁎Corresponding author. Faculdade de Farmácia, [5] Gondo H, Okamura C, Osaki K, Asano Y, Okamura T. Acquired Pelger–Hüet anomaly in Universidade Federal de Minas Gerais, Sala 4104-B3, association with concomitant tacrolimus and fluconazol therapy following allogeneicbone marrow transplantation. Bone Marrow Transplant 2000;26:1255–7.
Av. Antônio Carlos, 6627, Campus Pampulha, [6] Juneja SK, Matthews JP, Luzinat R, Fan Y, Michael M, Rischin D, et al. Association of Belo Horizonte/Minas Gerais CEP: 31270-901, Brazil.
acquired Pelger–Huët anomaly with taxoid therapy. Br J Haematol 1996;93:139–41.
Tel.: +55 31 3409 6880; fax: +55 31 3409 6985.
[7] Kaplan JM, Barrett Jr O. Reversible pseudo anomalia de Pelger anomaly related to sulfisoxazole therapy. N Engl J Med 1967;277:421–2.
[8] May RB, Sunder TR. Hematologic manifestations of long-term valproate therapy.
[9] Oka Y, Kameoka J, Hirabayashi Y, Takahashi R, Ishii T, Sasaki T, et al. Reversible bone marrow dysplasia in patients with systemic lupus erythematosus. Inter Med2008;47:737–42.
[10] Dusse LM, Morais RMS, Freitas VM, Medeiros GM, Vieira LM, Carvalho MG. Pseudo Pelger–Huët in transplanted patients. Acta Haematologica 2006;116:272–4.
Please cite this article as: Moreira AMB, et al, Acquired Pelger–Huët anomaly associated with ibuprofen therapy, Clin Chim Acta (2009),do

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