Donor‐derived strongyloidiasis after organ transplantation in Norway

Strongyloides stercoralis is an intestinal helminth which in humans can cause asymptomatic chronic infection maintained for decades through its auto‐infective cycle. During solid organ transplantation, recipients may unintentionally receive an organ infected with strongyloides. This is a very rare complication but may have deadly outcome if not detected. We hereby report two transplant recipients whom developed Strongyloides hyperinfection syndrome after organ transplantation from the same deceased donor. Recipient 1 was kidney transplanted and presented at day 65 post engraftment with diarrhea and subsequent septicemia and gastric retention. Larvae were detected in gastric aspirate. Recipient 2 was simultaneously kidney and pancreas transplanted and presented at day 90 post engraftment also with gastric retention and septicemia. Larvae were demonstrated on duodenal biopsy and stool sample. The clinical course was complicated with severe duodenal bleedings, gastric retention, meningitis, and prolonged hospitalization. Retrospective testing of pre‐transplant donor serum was positive for Strongyloides stercoralis antibodies. As a result of disease severity and gastric retention albenazole was administered via a jejunal tube and ivermectin subcutaneously in both recipients. S stercoralis was successfully eradicated and the transplants ended up with unaffected graft function. Following these two cases, we started systematic screening of all deceased donors for serum Strongyloides IgG in October 2016. After having screened 150 utilized donors one tested positive for Strongyloides, which initiated prophylactic ivermectin treatment to organ recipients. No symptoms or disease developed. Our center will continue to screen all donors as prophylactic treatment may avert this potentially lethal complication in cases of donor‐derived Strongyloides infection.     

Undiagnosed dysglycaemia and inflammation in cardiovascular disease

BACKGROUND: Cardiovascular (CV) disease is associated with increased levels of glucose, but the prevalence of dysglycaemia in CV diseases is not fully known. The study examined the prevalence of unknown dysglycaemia and its association with inflammation in Caucasian patients with ischaemic vascular complications, i.e. coronary artery disease (CAD), cerebrovascular disease (CVD) and peripheral artery disease (PAD). MATERIALS AND METHODS: This case-controlled study involved 149 patients (mean age 68 years) hospitalized for CAD, PAD or CVD and 59 control-subjects (CTR) free from CV-disease. The prevalence of dysglycaemia according to WHO/ADA criteria (impaired fasting glycaemia, impaired glucose tolerance or diabetes mellitus) was assessed by a 75-g oral glucose tolerance test. Inflammatory parameters were analyzed in fasting samples. RESULTS: Dysglycaemia was found in 49%, 55% and 57% of patients with CAD, CVD and PAD, respectively; all were significantly higher than among the controls (29%). The odds ratio (95% CI) for being dysglycaemic were 1.7 (1.04-2.77), 1.9 (1.19-3.06) and 2.0 (1.25-3.19) for CAD, CVD and PAD, respectively. Inflammatory markers (the total leucocyte count, soluble tumour necrosis factor-receptor type I, C-reactive protein) were elevated in patient groups and tended to increase with increasing blood glucose levels in all groups. The levels of the anti-inflammatory cytokine transforming growth factor-beta1 and insulin-like growth factor binding protein 3 were lowered in patients with CAD and, in patients with PAD, the former was inversely related to the levels of the blood glucose. CONCLUSIONS: Undiagnosed dysglycaemia was common in patients with ischaemic CV manifestations regardless of vascular bed involved. Inflammation was associated in a dosage-related manner to glucose levels.     

Blood glucose lowering by means of lifestyle intervention has different effects on adipokines as compared with insulin treatment in subjects with type 2 diabetes

Aims/hypothesis Adipokines may be important in mediating signals from adipocytes to insulin-sensitive tissue and vasculature. We studied the effect of different glucose-lowering therapies on serum levels of plasminogen activator inhibitor-1 (PAI-1), high-sensitivity C-reactive protein (hs-CRP), TNF-α, leptin, adiponectin and ghrelin in patients with type 2 diabetes.Subjects and methods Twenty-eight patients with poorly controlled type 2 diabetes who were receiving oral hypoglycaemic agents were allocated to one of the following groups, and treated for 1 year: (1) lifestyle intervention (L); (2) insulin treatment (I); and (3) combined treatment (L+I).Results Similar improvements in glycaemic control occurred in all three groups. There was a reduction in body weight of 3.0 kg (median) (95% CI −5.9 to −2.0) in group L, whereas in groups L+I and I body weight increased by 3.5 kg (95% CI 1.5–4.9) and 4.9 kg (95% CI −3.1 to 8.2), respectively. By trend analyses, group L had reduced levels of PAI-1 (p=0.002), hs-CRP (p<0.0001) and TNF-α (p=0.006), while no significant changes were observed in the levels of leptin or adiponectin. In group I, the median levels of PAI-1 (p=0.008), TNF-α (p=0.058) and leptin (p=0.004) increased. In the L+I group there was a reduction in PAI-1 levels (p=0.014) and an increase in levels of leptin (p<0.001). The differences in changes in the levels of PAI-1, hs-CRP, TNF-α and leptin between groups were also significant (all p<0.01).Conclusions/interpretation Improvement of glycaemic control through lifestyle intervention in type 2 diabetes had more beneficial effects on adipokine levels than when the same lowering of HbA_1c was achieved with insulin treatment.Electronic Supplementary Material Supplementary material on this article is available at     

Important differences in components of the metabolic syndrome between HIV-patients with and without highly active antiretroviral therapy and healthy controls

The aim of this study was to compare the prevalence of metabolic syndrome and insulin resistance in HIV-positive patients with and without HAART and healthy HIV-negative controls. In total 357 subjects were examined: 56 HIV-positive HAART-na?ve, 207 HIV-positive on HAART treatment and 94 HIV-negative controls. We measured blood pressure, abdominal circumference, weight and height, and fasting serum levels of glucose, insulin and lipids in all the subjects. The presence of lipodystrophy was assessed in the HAART-treated patients. In non-overweight subjects the prevalence of the metabolic syndrome was 15% (25 of 162) in HAART-treated patients, 2% (1 of 44) in HAART-na?ve (p=0.019) and 2% (1 of 45) in controls (p=0.020). The prevalence of insulin resistance in non-overweight subjects was also higher in HAART-treated than in controls, 39% vs 18% (p=0.012) but similar to HAART-na?ve, 32% (p = 0.48 vs HAART, p = 0.22 vs controls). In non-overweight patients with lipodystrophy the metabolic syndrome was diagnosed in 21% and insulin resistance in 49%. In the entire HAART group 25% had the metabolic syndrome and/or insulin resistance without having lipodystrophy. We conclude that fasting glucose, HDL-cholesterol, triglycerides and blood pressure should be closely monitored in all HAART-treated patients, not only in overweighed or lipodystrophic individuals.     

Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2

BACKGROUND/AIMS: To elucidate the role of systemic inflammation in nonalcoholic fatty liver disease (NAFLD). METHODS: Serum samples in 47 patients with histologically verified NAFLD (22 with simple steatosis and 25 with nonalcoholic steatohepatitis [NASH]), and in 30 age-, sex- and ethnicity-matched healthy controls, were assessed for (i) general markers of inflammation (C-reactive protein [CRP], tumor necrosis factor [TNF]-alpha, and interleukin [IL]-6), (ii) chemokines (CC-chemokine ligand [CCL] 2/monocyte chemoattractant protein [MCP]-1, CCL19 and CCL21), (iii) adipocytokines related to insulin resistance and inflammation (adiponectin and leptin) and (iv) a marker of oxidative stress (8-isoprostane-F2alpha). RESULTS: Serum levels of several inflammatory cytokines were increased in NAFLD as compared to controls, and IL-6 (P=0.017), CCL2/MCP-1 (P=0.008) and CCL19 (P=0.001), but not CRP (P=0.199), remained elevated also after correction for sex, body mass index (BMI) and age. Comparing NASH with simple steatosis, levels of TNF-alpha (P=0.024) and CCL2/MCP-1 (P=0.012) were elevated and adiponectin (in women) (P=0.001) were decreased also after adjustment for sex, BMI and presence of the metabolic syndrome. CONCLUSIONS: Our results indicate that patients with NAFLD are characterized by a low-grade systemic inflammation. The high CCL2/MCP-1 levels in NASH might be of importance for the conversion from simple steatosis to NASH.     

Inflammation and coronary angiography in asymptomatic type 2 diabetic subjects

Objective. Coronary artery disease (CAD) is prevalent in patients with type 2 diabetes mellitus (T2DM) and because it is often asymptomatic and extensive in comparison with CAD in subjects without diabetes, it represents a diagnostic challenge. The objective of the study was to investigate the prevalence of CAD in asymptomatic T2DM patients utilizing angiography and to investigate its association with cardiovascular (CV) risk factors, the metabolic syndrome and markers of inflammation. Material and methods. Eighty‐two patients with T2DM without symptoms of CAD, and with ?1 CV risk factor (hypertension, dyslipidaemia, premature familial CAD, smoking or microalbuminuria) underwent a diagnostic stress test and coronary angiography irrespective of stress test results. Stenosis detected in the main coronary arteries ?50% of lumen diameter was categorized as one‐, two‐ or three‐vessel disease. Inflammatory markers were analysed in fasting samples. Results. Fifteen men and two women had significant CAD (21%) (1‐vessel disease, n = 10; 2‐ or 3‐vessel disease, n = 7). Patients with 2‐ or 3‐vessel disease were significantly older and had a longer duration of diabetes, but the prevalence of other traditional CV risk factors or the metabolic syndrome was similar among those with 1‐vessel and those with 2‐ or 3‐vessel disease. Sensitivity for CAD of the stress test was low (0.35). The mean level of the pro‐inflammatory marker interleukin‐6 was elevated in patients with 2‐ to 3‐vessel CAD as compared to patients with no or 1‐vessel CAD (p<0.05). Conclusions. Significant CAD was found in 21% of asymptomatic patients with T2DM with ?1 CV risk factor. Inflammatory markers may be helpful in identifying patients that are likely to have significant CAD, but larger studies are warranted.