Kikuchi-Fujimoto disease: the quandary continues.

Kikuchi-Fujimoto disease (KFD) is a rare lymphohistiocytic disorder with an unknown etiopathogenesis. Due to its non-specific lymphadenopathy presentation, treatment is complicated by the frequency by which it is misdiagnosed-for example up to one-third of cases are misdiagnosed as malignant lymphoma, leading to expensive clinical testing and overtreatment of this typically self-limiting illness. KFD has a strong association with SLE, although its transience and rarity make it difficult to investigate. We present a case of KFD to illustrate the variance in presentation and typical outcome of KFD. We want to increase awareness and shed some light on some typical and atypical clinical presentations of KFD to reduce the incidence of misdiagnosis.

Superior gluteal artery pseudoaneurysm after a gunshot wound to the buttock: A case.

INTRODUCTION: Penetrating trauma to the buttock can rarely result into the development of a gluteal artery pseudoaneurysm. Here we present the case of a patient with a superior gluteal pseudoaneurysm after a gunshot wound to the left buttock. PRESENTATION OF CASE: A 48-year-old male presented with fullness and tenderness at the left gluteal wound that resulted from a gunshot 18 days prior. At the time of initial trauma, imaging showed minimal extravasation of contrast at the left superior gluteal artery, but the bleeding stopped and patient was discharged. On his return, examination showed palpable fluctuance but no bleeding. A superior gluteal artery pseudoaneurysm was identified on CT scan. Patient also complained of intermittent subjective fever and new onset of SOB. CT chest demonstrated a pulmonary embolism at the right basilar segmental artery. Coil embolization was performed to treat the pseudoaneurysm and patient was subsequently started on anticoagulation therapy. DISCUSSION: Penetrating wounds to the buttock can result in associated vascular or visceral injuries. Pseudoaneurysms can develop days to years after the initial injury. On exam, presence of pain, swelling, tenderness, bleeding from wound, thrill, bruit or a pulsating mass should raise suspicion for pseudoaneurysm, which can be diagnosed on CT scan and treated with embolization. CONCLUSION: Proper management of traumatic wounds to the buttock with associated vascular injuries, with follow up protocols and patient education is necessary to prevent life-threatening complications such as hemorrhage from pseudoaneurysm.

1,25-Dihydroxyvitamin D promotes negative feedback regulation of TLR signaling via targeting microRNA-155-SOCS1 in macrophages.

The negative feedback mechanism is essential to maintain effective immunity and tissue homeostasis. 1,25-dihydroxyvitamin D (1,25[OH]2D3) modulates innate immune response, but the mechanism remains poorly understood. In this article, we report that vitamin D receptor signaling attenuates TLR-mediated inflammation by enhancing the negative feedback inhibition. Vitamin D receptor inactivation leads to hyperinflammatory response in mice and macrophage cultures when challenged with LPS, because of microRNA-155 (miR-155) overproduction that excessively suppresses suppressor of cytokine signaling 1, a key regulator that enhances the negative feedback loop. Deletion of miR-155 attenuates vitamin D suppression of LPS-induced inflammation, confirming that 1,25(OH)2D3 stimulates suppressor of cytokine signaling 1 by downregulating miR-155. 1,25(OH)2D3 downregulates bic transcription by inhibiting NF-κB activation, which is mediated by a κB cis-DNA element located within the first intron of the bic gene. Together, these data identify a novel regulatory mechanism for vitamin D to control innate immunity.

Vitamin D receptor signaling inhibits atherosclerosis in mice.

Although vitamin D has been implicated in cardiovascular protection, few studies have addressed the role of vitamin D receptor (VDR) in atherosclerosis. Here we investigate the effect of inactivation of the VDR signaling on atherogenesis and the antiatherosclerotic mechanism of vitamin D. Low density lipoprotein receptor (LDLR)(-/-)/VDR(-/-) mice exhibited site-specific accelerated atherogenesis, accompanied by increases in adhesion molecules and proinflammatory cytokines in the aorta and cholesterol influx in macrophages. Macrophages showed marked renin up-regulation in the absence of VDR, and inhibition of renin by aliskiren reduced atherosclerosis in LDLR(-/-)/VDR(-/-) mice, suggesting that the renin-angiotensin system (RAS) promotes atherosclerosis in the absence of VDR. LDLR(-/-) mice receiving LDLR(-/-)/VDR(-/-) BMT developed larger lesions than LDLR(-/-) BMT controls. Moreover, LDLR(-/-) mice receiving Rag-1(-/-)/VDR(-/-) BMT, which were unable to generate functional T and B lymphocytes, still had more severe atherosclerosis than Rag-1(-/-) BMT controls, suggesting a critical role of macrophage VDR signaling in atherosclerotic suppression. Aliskiren treatment eliminated the difference in lesions between Rag-1(-/-)/VDR(-/-) BMT and Rag-1(-/-) BMT recipients, indicating that local RAS activation in macrophages contributes to the enhanced atherogenesis seen in Rag-1(-/-)/VDR(-/-) BMT mice. Taken together, these observations provide evidence that macrophage VDR signaling, in part by suppressing the local RAS, inhibits atherosclerosis in mice.