Impact of Coffee Consumption on Cardiovascular Health.

Background: Coffee is a widely available beverage that is enjoyed by individuals of many cultures. The publication of new studies prompts a review of the clinical updates regarding the association between coffee consumption and cardiovascular disease. Methods: We present a narrative review of the literature related to coffee consumption and cardiovascular disease. Results: Recent (2000-2021) studies have shown that regular coffee consumption is associated with a decreased risk of developing hypertension, heart failure, and atrial fibrillation. However, results are inconsistent with regard to coffee consumption and risk of developing coronary heart disease. Most studies show a J-shaped association, wherein moderate coffee consumption resulted in decreased risk of coronary heart disease and heavy coffee consumption resulted in increased risk. In addition, boiled or unfiltered coffee is more atherogenic than filtered coffee because of its rich diterpene content that inhibits bile acid synthesis and ultimately affects lipid metabolism. On the other hand, filtered coffee, which is essentially devoid of the aforementioned compounds, exerts antiatherogenic properties by increasing high-density lipoprotein-mediated cholesterol efflux from macrophages through the influence of plasma phenolic acid. As such, cholesterol levels are principally influenced by the manner of coffee preparation (boiled vs filtered). Conclusion: Our findings suggest that moderate coffee consumption leads to a decrease in all-cause and cardiovascular-related mortality, hypertension, cholesterol, heart failure, and atrial fibrillation. However, no conclusive relationship between coffee and coronary heart disease risk has been consistently identified.

Lupus pathogenesis and autoimmunity are exacerbated by high fat diet-induced obesity in MRL/lpr mice.

OBJECTIVE: SLE is an autoimmune disease characterised by persistent inflammation and autoantibody production. Genetic predisposition and environmental factors such as a high-fat diet (HFD) may contribute to lupus development. However, the immune cell profile and gender difference in response to HFD in lupus have not been reported. Here we investigated the impact of HFD on lupus pathogenesis and autoimmunity using lupus-prone mice. METHODS: Thirty male and 30 female MRL/lymphoproliferation (lpr) mice were fed with regular diet (RD) or HFD. Body weights were recorded weekly. SLE progression was monitored by skin lesion, urine protein, titres of antidouble-strand DNA (dsDNA) and ANA. At week 14, kidney and skin tissue sections were stained with H&E and periodic acid-Schiff to detect histological kidney index and skin score. Splenocytes were identified by immunofluorescence staining and flow cytometry. RESULTS: HFD significantly increased body weight and lipid levels compared with RD (p<0.01). Skin lesions were observed in 55.6% of the HFD group compared with 11.1% of the RD group, with greater histopathological skin scores in the female HFD group (p<0.01). Although both male and female mice had higher serum IgG in the HFD group than in the RD group, only the male HFD group showed an increased trend in anti-dsDNA Ab and ANA titres. Kidney pathological changes in the HFD group were more severe in male mice than in female mice (p<0.05), detected by proteinuria, kidney index and glomerular cell proliferation. Significant increases of germinal centre B cells and T follicular helper cells were observed in the spleens of HFD mice (p<0.05). CONCLUSION: HFD induced an accelerated and exacerbated lupus development and autoimmunity in MRL/lpr mice. Our results parallel many known clinical lupus phenotypes and sexual dimorphism in which male patients are likelier to have a severe disease (nephritis) than female lupus patients who may have a broader range of lupus symptoms.

Etiologies and management of haemophagocytic lymphohistiocytosis: is it time for an updated protocol and targeted treatments?

OBJECTIVE: The objective of this study was to analyse the features, therapeutic approaches, and outcomes for adult patients with haemophagocytic lymphohistiocytosis (HLH) at a single centre. METHODS: This study was a retrospective chart review of all patients >18 years of age diagnosed with HLH according to HLH-2004 or H-score criteria at Ochsner Medical Center-New Orleans between 2013 and 2019. RESULTS: A total of 29 patients with HLH met inclusion criteria. A total of 7 patients had an underlying malignancy, 12 had an autoimmune disease, 2 were transplant patients, and 2 had a combination of malignancy, autoimmune disease, or immunodeficiency. A total of 6 patients developed HLH precipitated by infection alone. All 29 patients presented with fever. A total of 28 (97%) patients met H-score criteria, and only 20 (67%) met HLH-2004 criteria. Fifteen patients were treated with the HLH-2004 protocol. Of those treated with the HLH-2004 protocol, 73% (11/15) died, 8% (1/15) had recurrence of HLH, and 20% (3/15) had resolution of HLH. A total of 14 patients were treated with targeted therapy. Of those treated with targeted therapy, 93% (13/14) had resolution of HLH and 1 died. Targeted therapy included pulse steroids, tocilizumab, anakinra, IVIG, CSA, rituximab, and/or CYC in addition to antiviral or antibiotic therapy. CONCLUSION: Our findings suggested that the rheumatologic patient population responded well to a targeted therapeutic approach and poorly to the HLH-2004 protocol. Whether the poor outcomes found with the use of the HLH-2004 protocol are secondary to the protocol itself or the aggressive nature of malignancy-associated HLH is unclear. Further studies are needed to develop tailored therapeutic regimens.

Rheumatoid Arthritis and Cardiac Compression Caused by a Large Fibrotic Intrapericardial Mass and Effusion: A Case Report.

BACKGROUND Pericarditis is common in rheumatoid arthritis, mostly occurring as an extra-articular manifestation of the disease. We describe a patient with stable rheumatoid arthritis who presented with a large pericardial effusion and a compressive fibrotic pericardial mass. The patient had recently started treatment with a tumor necrosis factor-alpha (TNF-alpha) antagonist. CASE REPORT The patient was a 58-year-old woman with rheumatoid arthritis who presented with right ventricular compression caused by a pericardial fibrotic mass and a large pericardial effusion. The patient did not have active arthritis at the time of presentation. She had been started on treatment with a tumor necrosis factor-alpha (TNF-alpha) antagonist 4 months prior to this presentation. She was successfully treated with surgical pericardiectomy and resection of the pericardial mass. Pathologic analysis of the pericardial mass demonstrated fibrosis and no evidence of active inflammation, rheumatoid arthritis, opportunistic infection, or malignancy. CONCLUSIONS We describe a patient with stable rheumatoid arthritis who developed subacute right heart compression syndrome secondary to pericardial effusion and fibrous pericardial mass. The exact cause of pericarditis and the pericardial mass remain uncertain. There is a need for increased awareness of the association between use of TNF-alpha antagonists and the possible development of an intrapericardial fibrotic mass and effusion.

Adult Onset Henoch-Schonlein Purpura associated with a Metastatic Malignancy of Unknown Primary Origin.

The cause of Henoch-Schonlein purpura, or IgA vasculitis, is largely unknown. It has been associated with infections, other rheumatologic triggers, and adverse drug reactions. Rarely, adult Henoch-Schonlein purpura is also associated with solid-tumor malignancies. We present the case of a 66 year-old woman who presented with Henoch-Schonlein purpura associated with a metastatic malignancy of unknown primary origin. We recommend that adult patients presenting with Henoch-Schonlein purpura, especially those with no identifiable trigger, receive age-appropriate work-up for potential malignancy.