Enhanced T-cell expression of RANK ligand in acute coronary syndrome: possible role in plaque destabilization.

OBJECTIVE: Based on its role in inflammation and matrix degradation, we hypothesized a role for osteoprotegerin (OPG), RANK, and RANK ligand (RANKL) in coronary artery disease. METHODS AND RESULTS: We examined the expression of various members of the OPG/RANKL/RANK axis in patients with stable and unstable angina and in the atherosclerotic lesions of apolipoprotein E-deficient (apoE(-/-)) mice. Our findings were: (1) Serum levels of OPG were raised in patients with unstable angina (n=40), but not in those with stable angina (n=40), comparing controls (n=20); (2) mRNA levels of RANKL were increased in T-cells in unstable angina patients accompanied by increased expression of RANK in monocytes; (3) strong immunostaining of OPG/RANKL/RANK was seen within thrombus material obtained at the site of plaque rupture during acute myocardial infarction; (4) OPG/RANKL/RANK was expressed in the atherosclerotic plaques of apoE(-/-) mice, with RANKL located specifically to the plaques; and (5) RANKL enhanced the release of monocyte chemoattractant peptide-1 in mononuclear cells from unstable angina patients, and promoted matrix metalloproteinase (MMP) activity in vascular smooth muscle cells. CONCLUSIONS: We show enhanced expression of the OPG/RANKL/RANK system both in clinical and experimental atherosclerosis, with enhanced T-cell expression of RANKL as an important feature of unstable disease.

[Mechanism of spontaneous rupture of hepatocellular carcinoma].

OBJECTIVE: To study the mechanism of spontaneous rupture of hepatocellular carcinoma (HCC). METHODS: The specimens of 30 patients with ruptured HCC and 30 patients with non-ruptured HCC were collected. Immunofluorescence, immunohistochemical and flow cytometry techniques were used to detect the phagocytosis of macrophages and the deposition of immune complex (IC) on vascular wall. RESULTS: In this study, the poor function of macrophage phagocytosis was found in patients with ruptured HCC, which could results in the cumulating of IC and deposition on vascular wall. The IC, which composed of hepatitis B virus e1 antigen (HBeAg/1), complement C1q and immunoglobulins, was found deposited in the elastic membrane of arteries. Likely as a result of IC deposition, vascular injury occurs mainly in the small arteries where the deposition of IC was present. As the small arteries were the blood vessels with predominant injury, they would likely to be the ones to split and cause hemorrhage and rupture of HCC during vascular load increase. CONCLUSIONS: We would conclude that the poor function of macrophage phagocytosis, which lead to the IC deposition and vascular injury may be the factors involved in the pathogenesis of ruptured HCC.

Perforación espontánea del colon en pacientes trasplantados de riñon / Spontaneous perforation of colon in renal transplant patients

Se presenta el caso de un paciente de 50 años de edad con antecedente de trasplante renal de donante vivo relacionado quien despues del segundo ciclo de tratamiento para rechazo agudo del trasplante presenta perforacion espontánea del colon, haciendose evidente la dificultad para el diagnostico temprano de esta patologia en pacientes que reciben algun tipo de inmunosupresion. Al rededor del caso se discute y revisa el tema de la incidencia de los inmunosupresores sobre la integridad del colon.