OBJECTIVEThe aim of this study was to investigate the relationship between diabetes and different phenotypes of peripheral vascular disease (lower extremity peripheral artery disease [PAD], carotid artery stenosis [CAS], and abdominal aortic aneurysm [AAA]).RESEARCH DESIGN AND METHODSPrevalence of vascular disease was evaluated in 3,696,778 participants of the Life Line Screening survey between 2003 and 2008. PAD was defined as ankle-brachial pressure index <0.90 or prior revascularization, CAS as ≥50% stenosis or prior revascularization, and AAA as infrarenal aortic diameter ≥3 cm or prior repair. Odds ratios (ORs) and 95% CIs were assessed using logistic regression modeling.RESULTSDiabetes mellitus was present in 10.8% of participants (n = 399,884). Prevalence of PAD, CAS, and AAA was significantly higher (P < 0.0001) in participants with compared with those without diabetes. After multivariate adjustment for baseline demographics and clinical risk factors, a significant interaction existed between diabetes and vascular disease phenotype (P < 0.0001). Diabetes was associated with increased odds of PAD (OR 1.42 [95% CI 1.41–1.4]; P < 0.0001) and CAS (1.45 [1.43–1.47]; P < 0.0001) but decreased odds of AAA (0.86 [0.84–0.88]; P < 0.0001). The strength of association increased with increasing severity of disease in each vascular phenotype, and this association persisted in the population with asymptomatic vascular disease.CONCLUSIONSIn a large population-based study, the association between diabetes and vascular disease differed according to vascular phenotype. Future studies exploring the mechanism for these vascular-specific differences are needed.

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening disease characterized by excessive inflammation and tissue destruction due to a dysregulated immune response. Its secondary form is most commonly triggered by viral infection or malignancy. There have previously been 11 cases of acquired HLH described following liver transplantation in adult transplant recipients, most occurring within the first year following transplantation. Herein, we describe two cases of HLH in liver transplant recipients that both occurred remotely following transplantation. In the first case, HLH was thought to be triggered by the development of a post-transplant lymphoproliferative disorder in a patient who was initially diagnosed with recurrent autoimmune hepatitis.In the second, it was thought to be triggered by a newly acquired human herpesvirus-8 infection. In both cases, the syndrome was not recognized until treatment for the initial putative diagnoses was unsuccessful. Despite treatment, both patients unfortunately died from multiorgan failure. HLH in the post-liver transplant setting is likely under-recognized and has a high mortality; early diagnosis and intervention may lead to improved outcomes. K E Y W O R D Scomplications of liver transplantation, hemophagocytic lymphohistiocytosis, human herpesvirus-8, liver transplantation, post-transplant lymphoproliferative disorder 1 INTRODUCTION Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening syndrome characterized by pathologic macrophage activation, which results in excessive cytokine release, inflammation, tissue destruction, and eventual multi-system organ failure. 1 Primary HLH is an inherited condition caused by autosomal recessive defects in genes triggering macrophage activation, while secondary HLH may be triggered by infection, malignancy, rheumatologic disorders, and immunodeficiencies. 2,3 Regardless of the causative agent, multiorgan failure often results from pervasive organ infiltration of activated monocytes, macrophages, and cytotoxic T-cells. Clinical features are

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