• 2018-07
  • 2019-04
  • 2019-05
  • The risk of breast cancer development in


    The risk of breast cancer development in men with Klinefelter syndrome is 20 times that in men without the syndrome. Gynecomastia occurs after puberty in about 85% of male patients with Klinefelter syndrome. These conditions are related to hormonal imbalance with low plasma testosterone and high estradiol levels, leading to feminization in gynecomastia, and causing male breast cancer via the expected carcinogenesis pathway. HCC is a much more common cancer, and is associated with liver cirrhosis in 70%–80% of cases. A risk factor for HCC is chronic infection with hepatitis B virus, which is found in >50% HCC cases in eastern Asia, while hepatitis C virus and alcoholism are the ribosomal s6 kinase risk factors in the USA. Serum AFP level <20 ng/mL is considered clinically normal. AFP levels greater than 200 ng/mL and 400 ng/mL have been shown to have high specificity (both 100%) for the diagnosis of HCC in patients with a liver mass identifiable by imaging techniques, although their sensitivity (36.3% and 20.2%, respectively) remains low. However, AFP levels may be normal in up to 30% of patients at the time of diagnosis of HCC, and remain so throughout the clinical course of the patient, even in the advanced stage. Higher AFP levels (>400 ng/mL) are associated with larger tumor size, portal vein thrombosis, and poorer median survival. Other than in HCC, AFP levels may also be elevated in metastatic disease of the liver (especially adenocarcinoma) and in primary malignancies of other sites, including the stomach, pancreas, colon, prostate, and ovary. Therefore, solely relying on the AFP level as a predictor of HCC is misleading and not recommended. The conditions of the breast tissue in men are different from those in women owing to a lack of estrogen and progesterone stimulation in men. Breast lobular development is rare in men, resulting in the rarity of diseases related to lobular proliferation in men, such as fibroadenoma, cyst, fibrocystic change, adenosis, phyllodes tumor, invasive lobular carcinoma, and lobular carcinoma in situ. On the other hand, diseases caused by ductal and stromal proliferation may occur in men; these include gynecomastia, invasive ductal carcinoma, ductal carcinoma in situ, and papillary neoplasm. The majority of male breast cancer is moderately- or poorly-differentiated infiltrating ductal carcinoma, which is usually observed as a solid mass on US, and is less frequently found as a thick-walled, thick-septated, or mixed cystic mass. Infiltrating ductal carcinoma with predominantly cystic degeneration, as observed in the present case, is very rare. The US findings consist of a cystic, multicystic, or thick-septated mass, with solid components projecting into the cystic part, fluid-debris level, and increased Doppler signal in the soft tissue projections. Contrast-enhanced CT and MRI reveal the enhancement of the cystic wall, septations, and the projections, as seen in our case. The differential diagnoses of other cystic breast cancers include intracystic papillary carcinoma and the less common adenoid cystic carcinoma, which show similar imaging appearances as the infiltrating ductal carcinoma with cystic degeneration. The sonographic patterns of HCC are variable according to size and intratumoral components. Small and well-differentiated HCC tumor (<3 cm) is usually a circumscribed and hypoechoic mass. The sonographic appearance for a larger mass may be hypoechoic (owing to compact cellular components or necrosis) or hyperechoic (owing to hemorrhage, fatty change, or fibrosis). A tumor capsule may show hypoechoic appearance. Color Doppler imaging may demonstrate hypervascularity and arteriovenous shunting inside the tumor. CT is most commonly used for the diagnosis and staging of HCC. Contrast-enhanced, triphasic CT must be used for the evaluation of liver tumors and includes an arterial phase at 20–30 s after machine injection of the contrast medium, at an injection rate of 4–8 mL/s, an early parenchymal phase at 40–55 s, and a portal venous phase at 70–80 s. An HCC tumor appears hypodense on unenhanced CT; it shows rapid enhancement (hyperdensity) on the arterial phase and an early washout pattern (hypodensity) on the portal venous phase. The tumor capsule, when present, appears hypodense on the arterial phase and shows enhancement on delayed images. This CT enhancement pattern is characteristic of HCC, and was observed in the present case. Heterogeneous contrast enhancement may be present owing to tumor necrosis. Portal vein thrombosis by tumor invasion can also be detected if the thrombus shows enhancement.