LES with BCAA supplementation significantly and rapidly improves liver functioning and CPS in LC patients who have undergone RFA for HCC. Control of blood sugar levels is necessary when calorie-containing BCAA is administrated to LC patients with impaired glucose tolerance.

A 56-year-old man was admitted to our hospital because of consciousness disturbance. Abdominal computed tomography revealed a large low-density tumor in the left lobe of the liver. He presented with marked leukocytosis and hypercalcemia with high levels of serum granulocyte-colony-stimulating factor (G-CSF) and parathyroid hormone-related protein (PTH-rP). A diagnosis of cholangiocellular carcinoma (CCC) of the liver was confirmed by histological examination of an autopsy specimen. The tumor cells showed positivity for both G-CSF and PTH-rP with immunohistochemical staining. These results suggest that the tumor was producing both G-CSF and PTH-rP. This paraneoplastic G-CSF and PTH-rP production caused by CCC is very rare. Such cases must be followed up carefully, since tumors associated with paraneoplastic syndrome progress rapidly, resulting in a poor prognosis.

A 24-year-old man was admitted to our hospital because of liver dysfunction. He had been diagnosed as having psoriasis vulgaris at 18 years of age. Physical examination demonstrated obesity, general erythema, and hepatomegaly. Laboratory data revealed elevated serum levels of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and glucose. A histological examination of the liver revealed macrovesicular fatty change and infiltration of inflammatory cells, including lymphocytes and polymorphonuclear cells, within the liver lobules. Pericentral fibrosis and pericellular fibrosis were also recognized. He was diagnosed as having nonalcoholic steatohepatitis (NASH), based on the fact that he had no habit of drinking alcohol, as well as psoriasis vulgaris and diabetes mellitus. We herein report a very rare case of NASH associated with psoriasis vulgaris.

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Abstract

We demonstrated reduced expression of the LDL receptor in HCC cases with paraneoplastic hypercholesterolemia. LDL receptor genes with genomic disorders may cause decreased expression of the LDL receptor protein, leading to feed-back failure of the cholesterol regulation system, as seen in familial hypercholesterolemia. This is the first report considering the mechanism behind the development of paraneoplastic hypercholesterolemia in HCC.

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