Altered placental macrophage numbers and subsets in pregnancies complicated with intrahepatic cholestasis of pregnancy (ICP) compared to healthy pregnancies.

INTRODUCTION: Intrahepatic cholestasis of pregnancy (ICP) can result in adverse outcomes for both mother and fetus. Inflammatory (M1 subset) or anti-inflammatory (M2 subset) macrophage polarisation is associated with various complications of pregnancy. However, the influence of ICP on macrophage numbers and polarisation remains unknown. This study analyses macrophage density and distribution in placentas of patients with ICP compared to controls. Clinical parameters were correlated to macrophage distribution and ursodeoxycholic acid use (UDCA). METHODS: This study included routinely collected placental tissue samples of 42 women diagnosed with ICP and of 50 control pregnancies. Immunohistochemical staining was performed on placental tissue using CD68 antibody as a pan-macrophage marker, CD206 antibody as an M2 and HLA-DR antibody as an M1 macrophage marker. Macrophage density (cells/mm2) and distribution (CD206+/CD68+ or CD206+/CD68+HLA-DR+) in both decidua (maternal tissue) and villous parenchyma (fetal tissue) were compared between groups. Macrophage density and distribution were correlated to clinical parameters for ICP patients. RESULTS: The density of CD68+ macrophages differed significantly between groups in villous parenchyma. In both decidua and villous parenchyma, CD206+/CD68+ ratio was significantly lower in ICP patients compared to controls (p = 0.003 and p=<0.001, respectively). No difference was found based on UDCA use or in CD68+HLA-DR+ cell density. Significant correlations were found between macrophage density and peak serum bile acids and liver enzymes. DISCUSSION: In ICP patients, an immune shift was observed in both decidual and villous tissue, indicated by a lower CD206+/CD68+ ratio. ICP seems to affect placental tissue, however more research is required to understand its consequences.

A rare cause of acute ST-elevation myocardial infarction: case report of native aortic valve thrombosis.

BACKGROUND: One to 13% of all patients with the clinical diagnosis of an acute coronary syndrome (ACS) show no evidence of significant obstructive coronary artery disease on angiography. Less common causes should be considered in those situations. A very rare cause of ACS is native aortic valve thrombosis. CASE SUMMARY: A 69-year-old previously healthy woman presented with acute chest pain. The electrocardiogram showed an anterolateral ST-elevation myocardial infarction (STEMI). She was immediately transferred for primary percutaneous coronary intervention. Shortly after arriving in hospital her condition deteriorated, with development of cardiogenic shock necessitating cardiopulmonary resuscitation. A coronary angiogram was performed during resuscitation that did not reveal any obstructive coronary artery disease. Echocardiography showed no pericardial effusion, no significant left-sided valve pathology, no signs of an aortic dissection or pulmonary embolism. She died of cardiogenic shock of unknown cause. Permission for autopsy was obtained. Pathologic examination revealed a large anterolateral myocardial infarction caused by a mass attached to the bottom of the left coronary cusp of the native aortic valve, which was large enough to occlude the ostium of the left main coronary artery. Microscopic analysis showed a thrombus of unknown origin. The aortic valve itself showed no signs of pathology. DISCUSSION: An ST-elevation myocardial infarction due to native aortic valve thrombosis is a rare condition, especially when there are no significant valvular abnormalities. This case demonstrates that thrombosis can develop in an apparently healthy middle-aged woman without any history of thrombotic disease.