Kardiyomiyopatinin Tedavi Edilebilir Bir Nedeni: Vitamin D Eksikliği

Dilate kardiyomiyopati KMP çocuklarda kalp yetmezliğinin önemli bir nedenidir. Çoğunlukla transplantasyon ihtiyacı duyulan bu hastalıkta nadiren medikal tedavi ile tam iyileşme sağlanabilir. Burada KMP ve rikets tanılarıyla izlenen bir olgu sunulmuştur. Olgu Sunumu: Üç aylık olgu çocuk endokrin polikliniğine kalsiyum Ca düşüklüğü nedeniyle yönlendirilmişti. Fizik muayenede el bileklerinde genişleme, geniş ön fontanel dikkati çekiyordu. Laboratuvar değerlendirmede, Ca 6,8 mg/dl, fosfor 4,9 mg/dl, alkalin fosfataz 1637 U/L, paratiroid hormon 191,2 pg/ml, 25 hidroksi vitamin D düzeyi 5,7 ng/ml saptandı. El bilek grafisinde raşitizmle uyumlu bulgular vardı. Ekokardiyogramda geniş sol ventrikül, hipokinetik kalp kası, ejeksiyon fraksiyonu %42, fraksiyonel kısalma %20 idi. Vitamin D eksikliği tanısıyla önce Ca laktat tedavisi ardından D vitamin tedavisi başlandı. Tedavinin 3. ayında radyolojik bulguların düzeldi ve rikets bulguları kayboldu. Ekokardiyogram bulguları normale döndü. Tedaviden sonra kardiyak fonksiyonların düzelmeye başlaması nedeniyle olguda vitamin D eksikliğine bağlı dilate KMP düşünüldü. Nutrisyonel riketsin endemik olduğu bölgelerde dilate KMP’nin etyolojik değerlendirmesinde vitamin D eksikliği tanısı düşünülmeli, tedavinin dramatik iyileşme sağlayabileceği akılda tutulmalıdır

A Treatable Cause of Cardiomyopathy: Vitamin D Deficiency

Dilated cardiomyopathy is an important cause of heart failure in children. Medical therapy rarely results in complete improvement of the disease, treatment of which usually requires transplantation. Herein, we present a patient with cardiomyopathy and rickets. Case report: A 3-month-old boy was referred to Pediatric Endocrinology Clinic due to low calcium level. On his physical examination, enlarged wrists and large anterior fontanel were remarkable. Results of laboratory analyses revealed a calcium level of 6.8 mg/dL, phosphorus level of 4.9 mg/dL, alkaline phosphatase level of 1637 U/L, parathyroid hormone level of 191.2 pg/mL, and 25-hydroxyvitamin D level of 5.7 ng/mL. Hand-wrist radiograph revealed signs consistent with rickets. Echocardiogram revealed dilated left ventricle, hypokinetic myocardium, an ejection fraction of 42%, and fractional shortening by 20%. Oral calcium lactate was started and then vitamin D treatment was added. At the 3rd month of the therapy, laboratory tests completely returned to normal and signs of rickets disappeared. Echocardiogram findings returned to normal. Since cardiac functions began to improve after the therapy, dilated cardiomyopathy associated with vitamin D deficiency was considered. Vitamin D deficiency should be considered while evaluating dilated cardiomyopathy in the regions that are endemic for nutritional rickets and it should be kept in mind that the therapy may provide dramatic improvement

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