Atipik İzoenzim Paternli Benign Geçici Hiperfosfatazemi Olgu Sunumu

Yıl 2019, Cilt: 3 Sayı: 3, 114 - 118, 31.12.2019

Ahmet Girgeç

Öz

Alkalen fosfataz özellikle ergenlik döneminde artmış büyüme hızı nedeniyle ve gebelik döneminde ise fetal ve plesental yapıların üretimindeki artıştan dolayı 2- 3 kat artabilir.  Fakat hayatın hiçbir döneminde benign geçici hiperfosfatazemideki kadar artmaz. Benign geçici hiperfosfatazemi (BGH), sıklıkla 5 yaşından küçük çocuklarda serum alkalen fosfataz düzeyinin (ALP) normal değerlerin 3–50 kata kadar yüksekliği ile seyreden ve ALP’nin haftalar veya aylar içinde normale döndüğü benign bir klinik durumdur. Bu hastalıkta genellikle karaciğer ve kemik kaynaklı ALP izoenzimleri yükselir, ince barsak izoenzimlerin yükseldiği daha az görülmüştür. ALP yüksekliği ile başvuran hastalarda karaciğer, kemik hastalıkları ve maligniteler ekarte edildikten sonra benign geçici hiperfosfatazemi tanıda akla gelmelidir. Bu yazıda bulantı kusma nedeniyle takip edilen ve bakılan tetkiklerinde rastlantısal olarak ALP düzeyinin normalin 20 katı kadar yüksek olan ve diğer hastalıklar ekarte edilerek BGH tanısı konulan15 aylık kız hastayı literatürdeki bilgiler eşliğinde paylaşmak istedik. 

Anahtar Kelimeler

Çocukluk çağında Alkalen Fosfataz Yüksekliği, Benign geçici hiperfosfatazemi

Benign Transient Hyperphosphatasemia with Atypical İsoenzyme Pattern: A Case Report

Öz

Alkaline phosphatase (ALP) can increase by 2-3 times due to the increase in the production of fetal and plasental structures during pregrancy, especially due to the increased growth rate during adolescence. But in any period of life it never increases as much as Benign Transient Hyperphosphatasemia (BTH). BTH is a benign clinical condition in which serum alkaline phosphatase  elevates 3-50 times higher than the normal rates in children under 5 years old. In this disease liver and bone derived ALP izoenzymes usually rise, small intestines’ rise less. For patients with elevated ALP, after excluding liver and bone diseases and malignancies, for diagnosis and differantial diagnosis benign transient hyperphosphatasemia should be taken into consideration.In this article, we would like to present that; 15 month-old girl patient who is followed up nuasea and vomiting, incedentally during the follow up ALP value was found 20 times higher than the normal value of a patient in the same age group  with in information of literatüre.

Kaynakça

• KAYNAKLAR: Referans1. Huh SY, Feldman HA, Cox JE, Gordon CM. Prevalence of transient hyperphosphatasemiaamonghealthyinfantsandtoddlers. Pediatrics 2009;124:703-9.
• 2.Teitelbaum JE, Laskowski A, Barrows FP. Benign transient hyperphosphatasemia in infantsandchildren: A prospectivecohort. J Pediatr EndocrinolMetab 2011;24:93-5.
• Referans3. Candemir M, Özdemir MA, Ergin H. Bir vaka nedeniyle selim ge¬çici hiperfosfatazemi. Fırat Tıp Derg 2008;13:74-6.
• Referans4. Tolaymat N, de Melo MC. Benigntransienthyperphosphatasemia of infancyandchildhood. South Med J 2000;93:1162-4.
• Referans5. Eymann A, Cacchiarelli N, Alonso G, Llera J. Benigntransient hyperphosphatasemia of infancy. A commonbenignscenario, abigconcernfor a pediatrician. J Pediatr EndocrinolMetab2010;23:927-30
• Referans6.Arıkan Ç, Arslan M, Tümgör G, Çakır M, Aydoğdu S. Çocukluk çağı benign geçici hiperfostazemisi. Güncel Pediat 2007;5:96-8. Referans7. Posen S, Lee C, Vines R, et al. Transienthyperphosphatasemia of infancy--an insufficientlyrecognizedsyndrome. ClinChem 1977;23:292-4.
• Referans8. Kraut JR, Metrick M, Maxwell NR, Kaplan MM. Isoenzymestudies in transienthyperphosphatasemia of infancy. Ten newcasesand a review of theliterature. Am J Dis Child 1985;139:736-40.
• Referans9. Kutilek S, Cervickova B, Bebova P, Kmonickova M, Nemec V. Nor¬mal bone turnover in transienthyperphosphatasemi. J ClinRes Pediatr En docrinol 2012;4:154-6.
• Referans10. Eboriadou M, Skouli G, Panagopoulou P, Haidopoulou K, MakedouA, Varlamis G. Acute laryngotracheobronchitis and associated transienthyperphosphatasemia: A newcase of transient hyperphosphatasemia in earlychildhood. J Paediatr Child Health2006;42:149-50.
• Referans11. Suzuki M, Okazaki T, Nagai T, Törõ K, Sétonyi P. Viralinfection of infantsandchildren with benign transien thyperphosphatasemia.FEMS ImmunolMedMicrobiol 2002;33:215-8.
• Referans12. Crofton PM. What is thecause of benigntransienthyperphosphatasemia? A study of 35 cases. ClinChem 1988;34:335-40.
• Referans13. Asanti R, Hultin H, Visakorpi JK. Serum alkaline, phosphatase in healthyinfants. Occurrence of abnormallyhighvalueswithoutknowncause. AnnPaediatrFenn 1966;12:139-42.
• Referans14. Carrol AJ andCoakley JC. Transienthyperphosphatasaemia: An important condition torecognize. J Paediatr Child Health2001;37:359-362.
• Referans15. Behulova D, Bzduch V, Holesova D, Vasilenkova A, Ponec J.Transient hyperphosphatasemia of infancyandchildhood:study of 194 cases. ClinChem2000;46:1868-1869.
• Referans16. Otero JL, Gonzalez-Peralta RP, Andres JM, et al. Elevated Alkali¬ne Phosphatase in Children: An AlgorithmtoDetermineWhen a “WaitandSee” Approach is Optimal. ClinMedInsights Pediatr 2011;5:15-8.
• Referans17. Antoniades K, Karakasis D, Kapetanos G, Lasaridis N,Tzarou V. Chronic idiopathic hyperphosphatasemia. Case report. Oral Surg Oral Med Oral Pathol1993;76:200-204.
• Referans18. Dundar B, Turedi A, Comak E. Selim gecicihiperfosfatazemili bir vaka. Çocuk Dergisi 2005;5:66-67.
• Referans19. Siraganian PA, Mulvihill JJ, Mulivor RA, Miller RW. Benign familialhyperphosphatasemia. JAMA 1989;261:1310-1312.