上面是英文，下面是中文
History: Twenty-year-old man.
Shown below are fat-sat T1W enhanced GRE images.
Here now are fat-sat T2W and Dualecho FSPGR images. （5-7）
Findings: There is markedly decread T2 signal intensity within the liver. The liver is normal in size and otherwi normal in appearance. The spleen is surgically abnt. The pancreas and kidneys are normal in size and show normal signal characteristics.
许博文Diagnosis: Secondary hemochromatosis (hemosiderosis).
Discussion
This patient has had hemolytic anemia, thought to be hereditary, since birth. Etiology is uncertain but there is a family history. He has had multiple hospitalizations and blood transfusions and had splenectomy at age 5. Serum iron studies revealed a hemoglobin leve
l of 10.4 gm/dL, a hematocrit of 34%, a markedly elevated ferritin level of 3055 ng/mL, an elevated iron level of 216 mcg/mL, a decread TIBC of 216 mcg/mL, and an elevated iron saturation level of 95%. MRI was ordered to evaluate for iron overload in the liver.
On non-enhanced CT, a liver with incread iron content shows diffuly incread attenuation, usually greater than 75 HU. The contrast between parenchyma and vasculature is incread. The findings can also be prent in glycogen storage dia, patients on amiodarone therapy, gold therapy, and in Wilson dia.
MR is more nsitive and specific for detection of incread hepatic iron deposition. MR imaging of a liver with incread iron content shows a characteristic T2 signal loss due to the magnetic susceptibility artifact of iron which caus spin dephasing. T2-weighted gradient echo images are the most nsitive.
On MR, incread iron accumulation in the liver can be diagnod if the liver demonstrates signal intensity equal to or lower than that of skeletal muscle, such as the paraspinal muscles, on either T2-weighted gradient echo, or T2-weighted spin echo imag
es.
Primary hemochromatosis is an autosomal recessive dia which results in abnormally incread iron absorption from the gut, and subquent deposition into organs including the liver, heart, pancreas, pituitary, joints, and skin. This can result in organ dysfunction including liver cirrhosis and its complications including HCC, skin pigmentation, and type 1 diabetes which generally occur late in the dia.
羊村大门图片Most patients with primary hemochromatosis do not have involvement of the spleen; iron deposition in primary hemochromatosis occurs in the parenchymal cells of the liver (hepatocytes) and not in the reticuloendothelial system (Kupffer cells and spleen). Therefore, splenic signal intensity usually is normal in the patients.
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Patients who receive multiple blood transfusions also develop iron overload, occasionally termed hemosiderosis or condary hemochromatosis. Iron from the transfud erythrocytes is deposited in the reticuloendothelial system in the liver, spleen, and bone marrow. Abnormal iron accumulation in the reticuloendothelial system does not damage t
he affected organs, thus is of little clinical significance.
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In patients who have received more than 40 units of blood, the reticuloendothelial system is typically saturated with iron (10 g), and additional iron deposits are en in the parenchymal cells of the liver, pancreas, and heart. The abnormal parenchymal iron deposition can cau organ dysfunction, similar to that en in primary hemochromatosis. Iron chelation therapy is ud in patients who receive large numbers of transfusions to remove excess iron and prevent organ damage.
怎样可以丰胸Quantitative measurement of hepatic iron content can be performed with MR. Various methods include measuring liver-to-tissue signal-intensity ratios, and utilizing gradient echo quences to correlate the natural logarithm of the ratio of signal intensity of the liver to the standard deviation of the background noi However, to accurately perform quantitative MR, each MR scanner needs to be properly calibrated with patients who have undergone liver biopsy to measure iron content.
病史：21岁男性患者。
以下是饱和脂肪抑制T1W增强梯度回波（GRE）图像。
这是饱和脂肪抑制T2W和双回波观后感英文快速扰相梯度回波（FSPGR）图像。（5-7）
发现：肝脏T2信号强度显著下降。肝脏大小和形态正常。脾已手术切除。胰腺和肾脏大小和信号均正常。
诊断：继发性血色病（含铁血黄素沉着症）。
讨论：
该患者出生后就有溶血性贫血，认为是遗传性的。病因虽不清，但有家族史。他曾多次住院并接受输血治疗，在5岁时进行了脾切除。血清铁检测显示血红素浓度为10.4mg/dl；红细胞压积为34％；铁蛋白浓度为3055 ng/mL，较正常值明显升高；血清铁浓度为216 mcg/mL，较正常值升高；总铁结合力为216 mcg/mL，较正常值下降；铁饱和度为95％，较正常值升高。行MRI检查以评估肝脏铁负荷。
美丽乡村在CT平扫中，肝脏铁含量增加，表现为弥漫性衰减增强，数值一般高于75HU。肝脏实质
和血管对比增强。这些表现还可见于糖原贮积症，接受胺碘酮治疗、金疗法的患者以及Wilson病患者。
MR检测肝脏铁沉积增加的敏感性和特异性更高。铁含量升高的肝脏MR显像表现为特征性T2信号缺失，缺失的原因为铁离子的磁敏感性伪影引起的自旋去相。T2加权梯度回波成像的敏感性最高。
在MR上，无论是T2加权梯度回波还是T2加权自旋回波成像，如果肝脏信号强度和骨骼肌（如椎旁肌）相同或稍低，则可诊断为铁沉积增加。
小学生300字作文原发性血色病是一种常染色体隐性遗传病。此病导致机体从肠道吸收铁异常升高，继而多余的铁沉积于肝脏、心脏、胰腺、垂体、关节和皮肤等器官中。这可导致器官功能异常，如：肝硬化及其并发症（包括原发性肝癌），皮肤色素沉着和通常在疾病后期出现的1型糖尿病。
大多数原发性血色病患者的脾脏不受累；原发性血色病铁沉积于肝脏实质细胞（肝细胞），而不是网状内皮系统（Kupffer细胞和脾）。因此，这些患者的脾脏信号强度往往正常。
