Case A 14 year old male patient presented to our emergency deparment with complaints of bruises on the feet and gingival bleeding Hepatomegaly and diffuse ecyhmoses and petechiae were present on physical examination Laboratory findings were as follows: WBC: 307 800 mm3 hemoglobin: 7 9 g dL platalet count: 46 000 mm3 Abundant blasts were observed on the peripheral smear and bone marrow examination Central nervous system involvement was present at the time of diagnosis Phenotyping revealed a diagnosis of T cell acute lymphoblastic leukemia ALL Translocation studies revealed negative t 9;22 t 4;11 t 12;21 and 1;19 With these findings the patient was classified into the moderate risk group according to the modified BFM 95 risk classification TRALL BFM 2000 protokol induction treatment was started On the 8th day no blast was observed on the peripheral blood smear On the 15th day 4 blast was found on bone marrox examination but the patient was classified into the high risk group since minimal residual disease was found to be 31 39 normal value: lt;1x10 4 as a result of flow cytometry On the 33trd day 4 blast was observed on bone marrow examination Sinus tachycardia observed in the patient from the first days of induction treatment was initially associated with anemia but apical heart rates were intermittantly found to be 100 140 min although hemoglobin values were kept in the normal limits with transfusions Familial history did not include any known thyroid disease or autoimmune disease No murmur was heard and peripheral pulses were palpable on physical examination Thyroid examination was found to be normal Antibiotic treeatment was given because of febrile neutropenia Tachycardia did not resolve in the period when the patients had no fever and infection Electrocardiography did not reveal any pathology except for sinus tachycardia Telecardiography echocardiography and cardiac enzymes were found to be normal Diagnosis: primary hyperthyroidism Thyroid function tests were ordered in terms of thyroid pathology Free T3 4 76 pg ml and free T4 2 15 pg ml levels were found to be high and TSH level was found to be low 0 6 mIU L Anti thyroglobulin 14 81 IU mL n=0 40 anti thyroid peroxidase 7 72 IU mL n=0 35 and TSH receptor 0 45 IU mL n=0 1 1 autoantibodies were found to be negative Thyroid ultrasonography and Doppler ultrasonography were found to be normal Sine the peripheral blood and bone marrow were in remission in this period and no pathology was found on thyroid ultrasonography and Doppler ultrasonography biopsy was not considered necessary in terms of thyroid involvement The patient was evaluated as primary hyperthroidism and propranolol and methimazole treatment was started Thyroid function tests repeated in the first month of treatment were found to be normal His complaint did not recur and tachycardia resolved in the follow up Discussion Acute lymphoblastic leukemia is the cause of approximately 25 30 of childhood cancers and 75 of childhood leukemias Tachycardia may ocur beacuse of different causes during treatment of leukemia Although infection fluid loss and enamia are frequently found as the cause thyroid pthologies should also be considered in the etiology Hyperthroidism is a disease which should be considered primarily in the differential diagnosis of tachycardia in individuals who are healthy otherwise Tachycardia due to increased sympathetic activity is frequently observed in hyperthroidism Different thyroid pathologies amy accompany leukemia; hypothyroidsm and hyperthyroidism due to different causes may be observed in the patients and sick euthyroid syndrome may be found 1 2 3 In the course of severe diseases including leukemia changes in thyroid hormon levels may ocur in the absence of thyroid disease and this is called sick euthyroid syndrome The most commonly observed among these changes is decreased T3 concentration alone or incombination with decreased T4 concentration 2 It is thought that thyroid hormon levels change with the effect of the tumor chemotherapy and impairment in the emotional and physical condition in children with cancer but the mechanism has not been fully elucidated 4 5 These changes in thyroid hormones may be briefly an adaptation of the body to morbidity but the physiological effects of this condition are not known In children the negative effects of low levels of a hormone which has been shown to be important for growth and development and brain development may be observed in the long term In a prospective study performed in children receiving cancer treatment changes in thyroid hormon levels were found in 90 of the patients 1 In this study it was shown that the variable which had the greatest effect on hormon change was dexamethasone treatment It is known that dexamethasone suprsses the release of TSH T3 and prolactin Corticosteroids additionally decrease TBG binding capacity and inhibit peripheral transformation of T4 to T3 6 7 8 Corticosteroids are one of the most important drugs in ALL treatment and are used with high doses for a long period Thyroid involvement can be rarely observed in patients with leukemia 9 10 11 12 Thyroid functions generally do not change but hypothyroidism is observed more frequently and hyperthroidism has been found in some patients It is thought that hyperthroidism develops as a result of rapid release of thyroid hormone into the blood due to destruction of thyroid follicles with malignency Ultrasonography Doppler ultrasonography computarized tomography and fine needle biopsy are recommended in clinically suspicious patients even though thyroid function tests are normal We found primary hyperthroidism in our patient who had unresolved tachycardia from the first days of treatment during leukemia treatment Low thyroid autoantibodies and normal parenchymal appearance on thyroid ultrasonography suggested that autoimmunity was not the cause of hyperthyroidism The fact that the patient was in remission and thyroid Doppler ultrasonographic examination was normal excluded thyroid involvement for the time being Hoever long term follow up of this patient will allow better differential diagnosis for autoimmune thyroiditis or thyroid involvement In this article we aimed to emphasize that hyperthyroidism should be considered as a cause in presence of tachycardia observed during leukemia treatment though it is not a frequent cause and to discuss thyroid pathologies in patients with leukemia References
Olgu On dört yaşında erkek hasta ayaklarda morluk ve diş etlerinde kanama yakınması ile acil servisimize başvurdu Fizik bakısında; karaciğer büyüklüğü yaygın ekimoz ve peteşileri vardı Laboratuvar tetkiklerinde lökosit sayısı 307 800 mm3 hemoglobini 7 9 g dL trombosit sayısı 46 000 mm3 saptandı Periferik yayma ve kemik iliği aspirasyonunda silme blast görüldü Tanı anında merkezi sinir sistemi tutulumu vardı T hücreli akut lenfoblastik lösemi ALL olarak fenotiplendi Translokasyon çalışmalarında; t 9;22 t 4;11 t 12;21 ve t 1;19 negatif bulundu Hasta bu bulgularla orta risk grubuna alındı ve TRALL BFM 2000 protokolü indüksiyon tedavisi başlandı Sekizinci gün periferik yaymada blast görülmedi On beşinci gün kemik iliği aspirasyonunda 4 blast saptandı ancak akım sitometrisi ile değerlendirme sonucu minimal kalıntı hastalık 31 39 normali lt;1x10 4 bulunduğundan hasta yüksek risk grubuna geçirildi Otuz üçüncü gün kemik iliği aspirasyonunda 4 blast belirlendi Hastanın indüksiyon tedavisinin ilk günlerinden itibaren olan sinüs taşikardisi başlangıçta anemisi ile ilişkilendirilmişti ancak hemoglobin değeri transfüzyonlarla normal sınırlarda tutulmasına rağmen aralıklı olarak kalp tepe atımları dinlenirken 100 140 dk arasında bulundu Soygeçmişinde bilinen tiroid hastalığı veya otoimmün bir hastalık yoktu Fizik bakısında üfürümü yoktu periferik nabızları alınıyordu Tiroid muayenesi doğaldı Ateşli nötropeni nedeniyle antibiyotik tedavisi verildi ateşi düştüğü dönemde enfeksiyonu yokken de taşikardisi düzelmedi Elektrokardiyografisinde sinüs taşikardisi dışında özellik belirlenmedi Teleradyografi ekokardiyografi ve kalp enzimlerinde patoloji saptanmadı Tanı: Primer hipertiroidi Tiroid patolojileri açısından tiroid işlev testleri istendi Serbest T3 4 76 pg mL ve serbest T4 2 15 pg mL düzeyleri yüksek TSH düzeyi düşük 0 6 mIU L saptandı Anti tiroglobulin 14 81 IU mL n= 0 40 anti tiroid peroksidaz 7 72 IU mL n= 0 35 ve TSH almaç 0 45 IU mL n= 0 1 1 otoantikorları negatif tiroid ultrasonografisi ve Doppler ultrasonografisi normal olarak saptandı Bu dönemde periferik yayma ve kemik iliği remisyonda olduğundan tiroid ultrasonografisi ve Doppler ultrasonografisinde de patolojik özellik belirlenmediğinden tiroid tutulumu açısından biyopsi yapılması gerekli görülmedi Hasta birincil hipertiroidi olarak değerlendirilerek propranolol ve metimazol tedavilerine başlandı Tedavinin birinci ayında tekrarlanan tiroid işlev testleri normal düzeylerde bulundu İzleminde yakınması tekrarlamadı ve taşikardisi düzeldi.
Primary Language | Turkish |
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Subjects | Health Care Administration |
Journal Section | Case of the Month |
Authors | |
Publication Date | June 1, 2013 |
Published in Issue | Year 2013 Volume: 48 Issue: 2 |