Endogenous Endophthalmitis Caused by Isolated Listeria Monocytogenes Infection.

Purpose: The purpose of this report is to present an extremely rare case of endogenous Listeria monocytogenes endophthalmitis.Methods: A 72-year-old woman was diagnosed with endogenous endophthalmitis. Listeria monocytogenes was identified by culture of aqueous humor. Multiple investigations could not reveal any source of infection. An overview of other published cases is presented and a standardized treatment protocol is suggested.Results: Treatment consisted of topical therapy with antibiotics, corticosteroids, cycloplegics, and intraocular pressure-lowering agents, four intravitreal injections of vancomycin, an anterior chamber washout, intravenous amoxicillin, and eventually a pars plana vitrectomy. The inflammation subsided and the patient was discharged with a best-corrected visual acuity of 20/40.Conclusion: Our study emphasizes the importance of adequate microbiological testing and initiating appropriate treatment early in the management of endogenous endophthalmitis.

Adipose tissue lipolytic inhibition enhances the glucoregulatory properties of exercise in type 2 diabetes patients.

AIMS: Exercise combined with adipose tissue lipolytic inhibition augments intramuscular lipid and glycogen use in type 2 diabetes patients. The present study investigates the impact of adipose tissue lipolytic inhibition during exercise on subsequent postprandial glycemic control in type 2 diabetes patients. METHODS: Fourteen male type 2 diabetes patients (age 65 ± 2 years, HbA1c 6.7 ± 0.1% (50 ± 2 mmol/mol)) participated in a double-blind placebo-controlled randomized cross-over study in which subjects performed endurance-type exercise after being administered 250 mg of a nicotinic acid analogue (acipimox; ACP) or a placebo (PLA). A control experiment was included in which no exercise was performed (CON). RESULTS: Sixty minutes of endurance-type exercise (at 45% Wpeak) did not significantly lower circulating plasma glucose and insulin excursions in PLA when compared with CON (P = .300). Acipimox administration strongly reduced circulating plasma FFA concentrations during exercise (P < .001). Circulating plasma glucose and insulin excursions were substantially lower during 7.5 h of recovery from exercise (i.e. postprandial) in ACP when compared with either CON (P = .041 and P = .002, respectively) or PLA (P = .009 and P = .001, respectively). CONCLUSIONS: Collectively, exercise with adipose tissue lipolytic inhibition reduces postprandial blood glucose and insulin excursions and, as such, further improves glycemic control in male type 2 diabetes patients.

Impact of iron deficiency on exercise capacity and outcome in heart failure with reduced, mid-range and preserved ejection fraction.

BACKGROUND: Little information is available about the prevalence and impact on exercise capacity and outcome of iron deficiency in heart failure with mid-range (HFmrEF) and preserved (HFpEF) ejection fraction in comparison to heart failure with reduced ejection-fraction (HFrEF). Furthermore, no data is available about the progression of ID in patients without baseline anaemia. METHODS: We evaluated baseline iron and haemoglobin-status in a single-centre, prospective heart failure database. Baseline functional status, VO2max, echocardiography and clinical-outcome (all-cause mortality and heart failure admissions) were evaluated. ID, anaemia, HFrEF, HFmrEF and HFpEF were defined according to established criteria. RESULTS: A total of 1197 patients (71% male) were evaluated (HFrEF, n = 897; HFmrEF, n = 229; HFpEF, n = 72). The overall prevalence of ID was 53% (50% in HFrEF; 61% in HFmrEF; 64% in HFpEF) and 36% for anaemia. ID was associated with a lower VO2max in patients with HFrEF, HFmrEF and HFpEF (p < .001 in all). Iron status more closely related to a poor VO2max than anaemia status (p < .001). Furthermore, poor clinical-outcome was more strongly associated with iron status than anaemia status. Exposing eight patients without anaemia to iron deficiency for 39 months resulted in one patient developing new-onset anaemia (defined as progression of ID). Patients with progression of ID exhibited a significant higher risk of heart failure hospitalisation and all-cause mortality (HR = 1.4; CI = 1.01-1.94; p = .046) than patients without progression. CONCLUSIONS: Iron deficiency is common in patients with HFrEF, HFmrEF and HFpEF, and negatively affects VO2max and clinical-outcome. Progression of iron deficiency parallels an increased risk for worsening of heart failure.