Bakır Eksiklliği ile Subakut Kombine Dejenerasyonun Birllikte Görüldüğü Atipik Bir Vaka
Giriş: Subakut kombine dejenerasyon (SKD) kobalamin eksikliğinden kaynaklanan nörodejeneratif bir hastalıktır. B12 vitamini eksikliğine bağlı olarak diğer nörolojik, psikiyatrik, hematolojik ve gastrointestinal semptomlar eşlik edebilir. Bu yazıda vitamin b12 eksikliğinin yanında bakır eksikliği de bulunan atipik subakut kombine dejenerasyon olgusunu sunmaktayız. Vaka Sunumu: 74 yaşında kadın hasta fiziksel tıp ve rehabilitasyon departmanına her iki bacakta güçsüzlük ve yürüyememe şikayeti ile başvurdu. Her iki alt ekstremitede belirgin güçsüzlüğü vardı ve sol yanlı dismetrisi ve disdiadokokinezisi mevcuttu. Alt ekstremitelerde vibrasyon, pozisyon duyusu kaybı, iki nokta ayrımı bozulmuştur. Kliniğimize başvurmadan önce B12 vitamini replase edilmişti. Hastanın semptomları replasmana rağmen progrese olmaya devam etti. Spinal MR görüntülemede spinal kord kompresyonuna veya miyelopatiye rastlanmadı. İğne EMG de motor ünite rekrütmanında azalmaa saptandı. Üst gastrointestinal siste endoskopisinde B12 eksikliği ile uyumlu olarak kronik atrofik gastrit saptandı. Hastanın bakır düzeyi düşüktü. Tedaviye oral bakır eklendi. Hasta 6 ve 9. aylarda değerlendirildi. Fonksiyonel durumu bir önceki vizitle aynıydı. Sonuç: B12 vitamini tedavisine yanıtsız miyelopatide bakır eksikliğini göz önünde bulundurmak öneml
An Atypical Case of Subacute Combined Degeneration With Concomitant Copper Deficiency
Background: Subacute combined degeneration (SCD) is aneurodegenerative disease caused by cobalamin deficiency. Itis can be accompanied by other neurological, psychiatric,hematological and gastrointestinal symptoms. Here wedescribe a patient with subacute combined degeneration whohas vitamin B12 and copper deficiency.Case Description: 74-year-old woman was admitted to ourphysical medicine and rehabilitation department complainingof weakness in both legs and inability to walk. She had markedloss of strength in both lower extremities also dysmetria anddysdiadochokinesia tests were positive on left-side. Vibration,position sense, two-point discrimination were impaired in thelower extremities. Her vitamin B12 was replaced beforeadmission to our department. Patient’s symptoms keptprogressing despite the vitamin replacement. Her spinal MRIshowed no compression of spinal cord or myelopathy.Theneedle EMG findings revealed a decrease in motor unitrecruitment.Upper gastrointestinal endoscopy revealed chronicatrophic gastritis which is compatible with B12 deficiency. Herblood copper level was low. Oral copper was added to thetreatment. Patient evaluated on 6th and 9th months afterdischarge. Her functional state was similar with previous visit.Conclusion: It is important to consider copper deficiency inpatients with myelopathy who are unresponsive to vitamin B12treatment
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