Bacteroides fragilis Bacteremia Complicated by Spondylodiscitis, Spinal Epidural Abscess, and Sepsis: A Case Report.

BACKGROUND Pyogenic spondylitis comprises several clinical entities, including native vertebral osteomyelitis, septic discitis, pyogenic spondylodiscitis, and epidural abscess. The lumbar spine is most often infected, followed by the thoracic and cervical areas. It mainly develops (i) after spine surgery; (ii) from history of blunt trauma to the spinal column; (iii) from infections in adjacent structures (such as soft tissues); (iv) from iatrogenic inoculation after invasive procedures (such as lumbar puncture); and (v) from hematogenous bacterial spread to the vertebra (mainly through the venous route). Any delay in diagnosis and treatment can lead to significant spinal cord injury, permanent neurological damage, septicemia, and death. CASE REPORT We describe a 63-year-old man with no significant past medical history who presented with fever and an altered level of consciousness. Significant thoracic spine pain was also reported during the last 3 months. The final diagnosis was vertebral spondylodiscitis, contiguous spinal epidural abscess, and sepsis due to Bacteroides fragilis bacteremia. Clinical recovery was achieved after surgical decompressive therapy with abscess drainage combined with appropriate antibiotic therapy for 12 weeks. The primary focus of the infection was not clarified, despite all the investigations that were performed. CONCLUSIONS Spondylodiscitis, spinal epidural abscess, and sepsis as complications of Bacteroides fragilis bacteremia are rare in a patient without any previously known predisposing conditions and without an obvious primary focus. Early diagnosis and proper treatment of anaerobic spondylodiscitis, especially if epidural abscess and sepsis are present, are of great importance to reduce mortality and avoid long-term complications.

Lipomatous Hypertrophy of the Interatrial Septum in a Patient with Chronic Dyspnea and Episodes of Paroxysmal Atrial Fibrillation: A Case Report.

Lipomatous Hypertrophy of the Interatrial Septum (LHIS) is an unusual condition usually found as an incidental finding on echocardiography. It can create a mass-like bulge typically sparing the fossa ovalis. We describe a 73-year-old overweight Cypriot woman, who visited our clinic in November 2018 and was complaining of dyspnea on exertion, chest tightness, and two episodes of paroxysmal atrial fibrillation for the last eight months. A big sessile mass was detected in the interatrial septum measuring 3.7×4.7 cm during transoesophageal echocardiography. The patient underwent resection of the mass and pericardial patch reconstruction of the defect with significant improvement of her clinical status during the follow-up period. The histopathological analysis suggested LHIS. In patients with persistent cardiac symptoms, a prompt resection is a useful option, although surgery is generally considered unnecessary in this clinical setting. Preprint of this article is available on: https://www.authorea.com/users/380290/articles/496351-a-patient-with-chronic-dyspnea-and-episodes-of-paroxysmal-atrial-fibrillation-in-the-presence-of-a-right-atrial-mass.

Spontaneous Rupture of a Bicuspid Aortic Valve in a Middle-Aged Weightlifter.

We describe a 58-year-old Caucasian male weightlifter who presented with acute shortness of breath after finishing his extensive exercise routine. Acute aortic valve regurgitation, due to spontaneous rupture of a bicuspid aortic valve, was diagnosed. Urgent surgical intervention was carried out, during which the bicuspid aortic valve was resected and replaced with an On-X bileaflet mechanical valve. The patient remains asymptomatic and is treated with warfarin, being in excellent physical condition 4 years after aortic valve replacement. LEARNING POINTS: Spontaneous rupture of a bicuspid aortic valve, after heavy weightlifting, is a very rare cause of acute aortic valve regurgitation.Echocardiography is of vital importance to distinguish the reason for this medical emergency from other possible causes.Prompt diagnosis and surgical treatment can achieve excellent long-term results.

Anti-tumor necrosis factor therapy improves insulin resistance, beta cell function and insulin signaling in active rheumatoid arthritis patients with high insulin resistance.

INTRODUCTION: Prevalence of insulin resistance and the metabolic syndrome has been reported to be high in rheumatoid arthritis (RA) patients. Tumor necrosis factor (TNF), a pro-inflammatory cytokine with a major pathogenetic role in RA, may promote insulin resistance by inducing Ser312 phosphorylation (p-Ser312) of insulin receptor substrate (IRS)-1 and downregulating phosphorylated (p-)AKT. We examined whether anti-TNF therapy improves insulin resistance in RA patients and assessed changes in the insulin signaling cascade. METHODS: Prospective study of RA patients receiving anti-TNF agents (infliximab, n = 49, adalimumab, n = 11, or etanercept, n = 1) due to high disease activity score in 28 joints (DAS28 > 5.1). A complete biochemical profile was obtained at weeks 0 and 12 of treatment. Insulin resistance, insulin sensitivity and pancreatic beta cell function were measured by the Homeostasis Model Assessment (HOMA-IR), the Quantitative Insulin Sensitivity Check Index (QUICKI) and the HOMA-B respectively. Protein extracts from peripheral blood mononuclear cells were assayed by western blot for p-Ser312 IRS-1 and p-AKT. RA patients treated with abatacept (CTLA4.Ig) were used as a control group for insulin signaling studies. RESULTS: At study entry, RA patients with high insulin resistance (HOMA-IR above median) had significantly higher mean DAS28 (P = 0.011), serum triglycerides (P = 0.015), and systolic blood pressure levels (P = 0.024) than patients with low insulin resistance. After 12 weeks of anti-TNF therapy, patients with high insulin resistance demonstrated significant reduction in HOMA-IR (P < 0.001), HOMA-B (P = 0.001), serum triglycerides (P = 0.039), and increase in QUICKI (P < 0.001) and serum HDL-C (P = 0.022). Western blot analysis in seven active RA patients with high insulin resistance showed reduction in p-Ser312 IRS-1 (P = 0.043) and increase in p-AKT (P = 0.001) over the study period. In contrast, the effect of CTLA4.Ig on p-Ser312 IRS-1 and p-AKT levels was variable. CONCLUSIONS: Anti-TNF therapy improved insulin sensitivity and reversed defects in the insulin signaling cascade in RA patients with active disease and high insulin resistance. The impact of these biochemical changes in modifying cardiovascular disease burden in active RA patients remains to be seen.

Metabolic syndrome in rheumatic diseases: epidemiology, pathophysiology, and clinical implications.

Subjects with metabolic syndrome--a constellation of cardiovascular risk factors of which central obesity and insulin resistance are the most characteristic--are at increased risk for developing diabetes mellitus and cardiovascular disease. In these subjects, abdominal adipose tissue is a source of inflammatory cytokines such as tumor necrosis factor-alpha, known to promote insulin resistance. The presence of inflammatory cytokines together with the well-documented increased risk for cardiovascular diseases in patients with inflammatory arthritides and systemic lupus erythematosus has prompted studies to examine the prevalence of the metabolic syndrome in an effort to identify subjects at risk in addition to that conferred by traditional cardiovascular risk factors. These studies have documented a high prevalence of metabolic syndrome which correlates with disease activity and markers of atherosclerosis. The correlation of inflammatory disease activity with metabolic syndrome provides additional evidence for a link between inflammation and metabolic disturbances/vascular morbidity.

Modest but sustained increase of serum high density lipoprotein cholesterol levels in patients with inflammatory arthritides treated with infliximab.

OBJECTIVE: Tumor necrosis factor-a (TNF-a) is a key cytokine in the pathogenesis of chronic inflammatory arthritides, has proatherogenic effects, and may be positively correlated with impairment of the action of insulin. Patients with chronic inflammatory arthritides have an increased risk for cardiovascular diseases. We assessed whether anti-TNF-a treatment modifies the unfavorable lipid profile induced by chronic inflammatory arthritides. METHODS: Sixty patients (24 with rheumatoid arthritis, 26 ankylosing spondylitis, and 10 psoriatic arthritis) receiving infliximab because of ongoing disease activity despite disease modifying drugs (DMARD) were prospectively studied for 6 months. Lipid profile, total cholesterol/high density lipoprotein cholesterol (TC/HDL-C), and low density lipoprotein cholesterol (LDL-C)/HDL-C ratios, as well as disease activity indices (DAS28 and BASDAI), were assessed. RESULTS: A sustained increase of serum HDL-C was observed [mean increase (95% CI)] 5 (3-7) mg/dl, 3.5 (1-6) mg/dl, and 3 (1-5) mg/dl at 1, 3, and 6 months, respectively (p < 0.01). Compared to nonresponders, HDL-C increased significantly more in EULAR or BASDAI responders (0.8 vs 5.8 mg/dl; p = 0.05). Serum TC was significantly increased [11 (4-8) mg/dl; p = 0.001] only after the first month of treatment. TC/HDL-C and LDL-C/HDL-C decreased only after the first month [0.3 (0.1-0.4), p < 0.01, and 0.2 (0.1-0.4), p < 0.01, respectively]. For patients with baseline LDL-C > 130 mg/dl, LDL-C/HDL-C decreased (p < 0.05) during the whole study period and TC/HDL-C decreased (p < 0.05) at 1 and 3 months. CONCLUSION: Anti-TNF-a treatment in patients with chronic inflammatory arthritides induces a modest, but sustained, increase in serum HDL-C levels, which may have a favorable effect in reducing the cardiovascular risk in these patients.