Subcutaneous Human Dirofilariosis By D. Repens In South Italy: A Case Report.

Human dirofilariosis is a zoonosis caused by different Dirofilaria species: D. repens, D. immitis, D. tenuis and D. ursi, thin nematodes belonging to the Onchocercidae family, whose larval stages are generally found in the natural (felines and canids) or accidental (human) definitive host. In Europe, human infection is rare, even in areas considered endemic such as Spain or Italy. In this paper we describe the case of an 82-year-old woman living in Modugno (Bari municipality), who came to our observation for a subcutaneous nodule on her right thigh that had appeared in the previous two weeks and gradually became necrotic. The woman lived in an apartment with a dog. An adult worm, white, thin, about 140 mm long, came out of the necrotic area spontaneously. After microscopic examination, the worm was identified as D. repens. In Apulia, a South-Italy region, human dirofilariosis is a rare disease and since 1885 only 11 cases have been reported. In recent years we have witnessed an increase in the number of diseases transmitted by vectors at all latitudes, and in our region an increase in the Aedes albopticus population has been reported, so it is reasonable to expect an increase in dirofilariosis cases in humans.

HIV-1 coreceptor tropism: A syllogistic connection with The Veterans Aging Cohort Study Index and the CD4/CD8 ratio.

BACKGROUND: The association between X4 virus and an increased risk of non-AIDS-events has been reported. Morbidity/mortality due to non-AIDS events, which are properly predicted by the CD4/CD8 ratio and VACS index, have become particularly remarkable in HIV-infected patients receiving effective combined antiretroviral therapy (cART). METHODS: We verified the validity of the syllogism: as HIV-tropism (CRT) contributes to the onset of non-AIDS events which are successfully predicted by the CD4/CD8 ratio and VACS index, then CRT correlates with these two variables. The CD4/CD8 ratio and VACS index at baseline and overtime were analyzed according to CRT tested before the first successful cART regimen in newly-diagnosed patients. RESULTS: Patients with R5 variants had a significantly lower baseline VACS percentage risk [mean (95%CI):18.2%(16.1-20.3) vs 24.3%(18.2-22.5), p = 0.002] and higher baseline CD4/CD8 ratio [mean (95%CI):0.43 (0.38-0.47) vs 0.28 (0.19-0.36), p = 0.002] than non-R5 patients. After an initial drop, VACS increased again in R5 and non-R5 patients and the two trend curves almost overlapped. The CD4/CD8 ratio had an increasing trend in both R5 and non-R5 patients; however, even though non-R5 patients had a greater gain of CD4+, they maintained a lower CD4/CD8 ratio at any time point. CONCLUSION: Our study confirms an association between pre-therapy CRT, CD4/CD8 ratio and VACS. A successful cART regimen positively affects the CD4/CD8 ratio; however, the disadvantage conferred by a non-R5 CRT is maintained overtime. The restoration of VACS in all patients could be directly due to variables included in the VACS calculation and to factors that adversely influence these variables.

Cardiovascular risk in advanced naïve HIV-infected patients starting antiretroviral therapy: Comparison of three different regimens - PREVALEAT II cohort.

BACKGROUND AND AIMS: PREVALEAT (PREmature VAscular LEsions and Antiretroviral Therapy) II is a multicenter, longitudinal cohort study aimed at the evaluation of cardiovascular risk among advanced HIV-positive, treatment-naïve patients starting their first therapy. We hypothesized that these patients, present a higher cardiovascular (CV) risk. METHODS: The study included all consecutive naïve patients with less than 200 CD4 cells/ml starting antiretroviral therapy. Our primary objective was to evaluate changes in carotid intima- media thickness (IMT). Secondary endpoints included changes in flow mediated vasodilation (FMD), inflammatory markers, triglycerides and cholesterol. Patients were evaluated at time 0, and after 3, 6 and 12 months. RESULTS: We enrolled 119 patients, stratified into three different groups: patients receiving atazanavir/ritonavir boosted (ATV/r) based regimens, efavirenz (EFV) based regimens and darunavir/ritonavir boosted (DRV/r) based regimens. At baseline, advanced naïve patients showed a relevant deterioration of CV conditions in terms of traditional CV risk factors, endothelial dysfunction and serum biomarkers. During the 12-month follow up period, mean blood lipids significantly increased: total cholesterol from 159 to 190 mg/dL, HDL-C from 31 to 41 mg/dL, and LDL-C from 99 to 117 mg/dL. D-dimers steadily decreased (median level 624 at baseline and 214 at T3), whereas ICAM and VCAM consistently raised. DRV/r and ATV/r determined a more marked decrease of D-dimers as compared to EFV. Regarding the epi-aortic changes (IMT >1 mm or presence of atherosclerotic plaques), patients in the DRV/r group were at risk of developing pathological IMT during the study (OR 6.0, 95% CI 0.9-36.9), as compared to EFV ones. CONCLUSIONS: CV risk was elevated in advanced naïve patients and tended to remain high in the first year of therapy.

Long-term efficacy and safety of switching from lamivudine+adefovir to tenofovir disoproxil fumarate in virologically suppressed patients.

BACKGROUND AND AIM: Tenofovir disoproxil fumarate (TDF) is recommended as first-line monotherapy for nucleos(t)ide (NA)-naïve chronic hepatitis B (CHB) patients and as a second-line rescue therapy for NA-experienced patients with a previous treatment failure. However, data regarding the efficacy of TDF monotherapy in patients with lamivudine resistance (LAM-R) successfully treated with LAM+adefovir (ADV) are limited. Herein, the efficacy and safety of switching from LAM+ADV to TDF monotherapy in clinical practice have been evaluated. METHODS: Sixty LAM-R HBeAg-negative CHB patients treated with ADV add-on therapy and stable viral suppression, were switched to TDF monotherapy and prospectively evaluated for virological response, liver and renal function, and bone mineral density. RESULTS: During a median period of 57 months of TDF monotherapy, all patients maintained a virological response, four of whom cleared HBsAg (6.6%) and discontinued treatment. Monitoring of renal function showed no case of the Fanconi syndrome, no significant alterations of median serum creatinine, eGFR and phosphate levels, although a reduction of TDF dosage was required in five patients (8.3%). Despite the stable virological suppression, five cirrhotic patients and one CHB patient developed hepatocellular carcinoma. CONCLUSIONS: Our results demonstrate the efficacy of switching to TDF monotherapy in virologically suppressed CHB patients receiving long-term LAM+ADV therapy, with a low rate of adverse events.

Prevalence and Risk Factors for Significant Liver Fibrosis in Patients with HIV Infection.

AIM: The aim of the present study was the evaluation of liver fibrosis in a population of patients monoinfected with HIV using the transient liver elastography (FibroScan) method. PATIENTS AND METHODS: A total of 228 consecutive patients with HIV were evaluated: 80 (35.09%) were HIV-1 monoinfected and 148 (64.91%) (HIV)/hepatitis C virus (HCV) co-infected. Echoic liver diagnosis was also performed. RESULTS: F2 Metavir-score fibrosis or higher was found to be associated with drug addiction, alanine aminotransferase >80 UI/l, cluster of differentiation 4 (CD4(+)) T lymphocytes nadir <200 copies/ml, therapy duration, protease inhibitor (PI)-based antiretroviral regimen, HCV infection and AIDS diagnosis. Multivariate analysis highlighted a significant association with drug addiction, AIDS diagnosis, therapy duration and HCV co-infection. Echoic liver diagnosis showed signs of damage among 43.75% of monoinfected patients vs. 62.84% among co-infected. CONCLUSION: Monoinfected patients showed pathological signs both at liver ultrasonography and at FibroScan. In the onset of these changes, a significant role by HIV disease and duration of therapy is observed.

Bone and kidney toxicity induced by nucleotide analogues in patients affected by HBV-related chronic hepatitis: a longitudinal study.

OBJECTIVES: Nucleotide analogues may promote renal and bone toxicity. The aim of the present study was to evaluate markers of osteorenal toxicity in patients affected by hepatitis B virus-related chronic hepatitis treated with lamivudine plus adefovir who were switched to tenofovir. PATIENTS AND METHODS: We evaluated 60 consecutive patients at the time of the switch of treatment and after 1, 3, 6, 9 and 12 months. The mean baseline estimated glomerular filtration rate (eGFR) was 89.3 ± 19.0 mL/min/1.73 m(2). RESULTS: During the study period we observed a reduction in mean eGFR up to 6 months after switching to tenofovir, and this remained stable for the last two timepoints. At the end of study, the mean eGFR was 82.6 ± 21.5 mL/min/1.73 m(2), a reduction of 7.5%. The mean baseline proteinuria was 202.6 ± 237.6 mg/24 h. Microhaematuria was observed in 22.6% of patients and hypophosphataemia in 18.6%. After 1 month of tenofovir, we observed a worsening of serum phosphate and parathyroid hormone levels, haemoglobinuria and 24 h proteinuria. After 3 and 12 months of tenofovir, these data tended to recover to baseline levels. A total of 92.6% of patients at baseline had hypovitaminosis D. After supplementation with cholecalciferol, this percentage decreased significantly. We observed a reduced bone mineral density (BMD) in 52.7% of patients at baseline; this increased to 77.8% after 6 months of tenofovir, but at the last timepoint the percentage of patients with a reduced BMD had fallen to a level above the baseline. CONCLUSIONS: In conclusion, patients exposed to lamivudine plus adefovir showed relevant osteorenal damage. The switch to tenofovir provoked a slight reduction in eGFR that stabilized after 6 months. The reduced BMD at baseline did not worsen under tenofovir treatment.

Fatal fulminant hepatitis following administration of clarithromycin in a patient chronically treated with antipsycotic drugs.

BACKGROUND: Clarithromycin is a widely used antibiotic, especially prescribed for the treatment of respiratory tract infections, The drug is generally well tolerated. It is described as a very rare cause of fulminant liver failure. CASE PRESENTATION: Herein we report a case of fatal fulminant hepatitis in a young patient. In his past history the patient presented documented episodes of hypertransaminasemia. CONCLUSIONS: This case confirms that clarithromycin although very rarely, can be a cause of fulminant hepatitis, especially in patients with pre-existing liver damage. Although the presumption that clarithromycin hepatotoxicity is dose related is reasonable, an immune-toxicologic hypothesis cannot be excluded.