ABSTRACT
OBJECTIVES: To evaluate the prevalence and therapeutic relevance of drug resistance among isolates from ART-experienced HIV-1-infected patients over the past two decades in Italy. METHODS: Dynamics of resistance to one, two and three or more antiretroviral classes were evaluated from 1999-2018. Virological success (VS) after the latest therapy switch was evaluated according to cumulative class resistance and cumulative genotypic susceptibility score (Stanford HIV_DB algorithm). RESULTS: Among 13 663 isolates (from 6739 patients), resistance to at least one drug class decreased sharply from 1999 to 2010 (≤2001, 84.6%; 2010, 43.6%; P < 0.001), then remained relatively constant at â¼40% during 2010-18, with the proportion of resistance to three or more classes also stable (â¼5%). After 2008, integrase inhibitor resistance slightly increased from 5.6% to 9.7% in 2018 and contributed to resistance, particularly in isolates with resistance to three or more classes (one class, 8.4%; two classes, 15.3%; three or more classes, 34.7%, P < 0.001). Among 1827 failing patients with an available follow-up, by 1 year after genotype-guided therapy start the probability of VS was 87.6%. Patients with cumulative resistance to three or more classes and receiving a poorly active regimen showed the lowest probability (62.6%) of VS (P < 0.001) compared with all other patients (≥81.8%). By Cox regression analysis, cumulative MDR and receiving poorly active antiretroviral regimens were associated with a lower hazard of VS compared with those without resistance. CONCLUSIONS: A dramatic drop of HIV-1 drug resistance at failure has been achieved over the last two decades in Italy; resistance to three or more classes is low but present among currently failing patients. Its management still requires a rational and careful diagnostic and therapeutic approach.
Subject(s)
Anti-HIV Agents , HIV Infections , HIV-1 , Anti-HIV Agents/pharmacology , Anti-HIV Agents/therapeutic use , Antiretroviral Therapy, Highly Active , Drug Resistance, Viral/genetics , Genotype , HIV Infections/drug therapy , HIV Infections/epidemiology , HIV-1/genetics , Humans , Italy/epidemiology , Treatment FailureABSTRACT
BACKGROUND: As in non-infected subjects, statins and aspirin have a pivotal preventive role in reducing the cardiovascular related morbidity and mortality in HIV infected patients. The persistence of immune activation in these subjects, could contribute to accelerate atherosclerosis, therefore, these treatments that reduce inflammation could provide additional cardiovascular protection. However the current guidelines for the use of these drugs in general population are dissimilar, with important differences between American and European ones. Aim of the present position paper is to provide recommendations aimed to overcome the actual differences and limitations among the current ones and to adapt them to the needs of HIV infected patients. RESULTS: We propose to adopt the new ACC/AHA guidelines, simple to use and cost effective, to use the ASCVD score that seems to estimate more accurately the cardiovascular risk among these patients. We suggest to start statin therapy in all patients with a calculated 10-year risk of a cardiovascular event of 10% or greater. Rosuvastatin and atorvastatin should be preferred. LDL-C target may be adopted. Aspirin should be always associated with a statin, in secondary prevention, while in primary prevention it should be reserved only to patients with ≥ 20% 10-year risk particularly adherent to treatments, and with low risk of bleeding. We suggest to start with a dose of 100 mg/day. Finally, management of antiplatelet agents or novel oral anticoagulants may include selecting antiretrovirals with a lower potential for drug interactions or choosing agents least likely to interact with antiretrovirals. CONCLUSIONS: As demonstrated in surveys, HIV physicians are generally highly committed regarding CVD and autonomous in prescribing statins and ASA. Consequently, in the light of the previously discussed discrepancies among the different guidelines and of the incomplete indications regarding HIV-positive persons, the present suggestions could overcome the actual differences and limitations among the current ones.
Subject(s)
Aspirin/administration & dosage , Cardiovascular Diseases/prevention & control , HIV Infections/complications , Hydroxymethylglutaryl-CoA Reductase Inhibitors/administration & dosage , Primary Prevention/standards , Adult , Aged , Humans , Middle Aged , Practice Guidelines as Topic , Risk Factors , United StatesABSTRACT
OBJECTIVES: Only a few studies have addressed liver stiffness dynamics after hepatitis C virus (HCV) treatment in patients with HIV/HCV coinfection. The aim was to evaluate the variation in liver stiffness and in serum liver fibrosis scores in HIV/HCV-coinfected patients before and after treatment with direct-acting antivirals (DAAs). METHODS: Liver stiffness measured using transient elastography as well as serum liver fibrosis scores [fibrosis-4 (FIB-4) score and the aspartate aminotransferase to platelet ratio index (APRI)] were evaluated before and at 6-12 months after DAA treatment. Variation in the outcome variables was evaluated using the Wilcoxon nonparametric test. Univariate analysis and multivariate regression models were used. RESULTS: A total of 78 HIV/HCV-coinfected subjects were included in the study. Median values of hepatic stiffness significantly decreased after DAA treatment compared with baseline [16.8 (interquartile range (IQR) 10.2-27.0) kPa at baseline vs. 9.4 (IQR 6.7-15.0) kPa after DAA treatment; P < 0.01). Further, a decrease in median FIB-4 score [2.8 (IQR 1.5-4.8) vs. 2.0 (IQR 1.3-3.2), respectively; P < 0.01] and APRI [0.9 (IQR 0.5-2.2) vs. 0.4 (IQR 0.2-0.7), respectively; P < 0.01] was found. In univariate analysis, liver stiffness decrease was associated with increasing age, 'other' HCV genotype (vs. G1), the presence of cirrhosis, higher pre-DAA liver stiffness, sofosbuvir-based regimens and longer DAA treatment (all P < 0.05). Multivariate regression confirmed the significance of the association only with higher baseline liver stiffness (P < 0.01). Greater FIB-4 and APRI reductions were associated with higher respective baseline values, while the presence of hepatic steatosis correlated with lower score reduction after DAA. CONCLUSIONS: A reduction in liver stiffness and an improvement in fibrosis scores were observed in HIV/HCV-coinfected patients soon after DAA treatment. The clinical implications of these observations need to be evaluated in larger populations with longer follow-up.
ABSTRACT
Objectives: To evaluate the maintenance of virological suppression (VS) in antiretroviral-treated HIV-1-suppressed patients switching to a tenofovir/emtricitabine/rilpivirine (TDF/FTC/RPV) single-tablet regimen, by considering pre-existent resistance (pRes). Methods: pRes was evaluated according to resistance on all previous plasma genotypic resistance tests. Probability and predictors of virological rebound (VR) were evaluated. Results: Three hundred and nine patients were analysed; 5.8% of them showed resistance to both NRTIs and NNRTIs, while 12.6% showed resistance to only one of these drug classes. By 72 weeks, the probability of VR was 11.3%. A higher probability of VR was found in the following groups: (i) patients with NRTI + NNRTI pRes compared with those harbouring NRTI or NNRTI pRes and with those without reverse transcriptase inhibitor pRes (39.2% versus 11.5% versus 9.4%, P < 0.0001); (ii) patients with a virus with full/intermediate resistance to both tenofovir/emtricitabine and rilpivirine compared with those having a virus with full/intermediate resistance to tenofovir/emtricitabine or rilpivirine and those having a virus fully susceptible to TDF/FTC/RPV (36.4% versus 17.8% versus 9.7%, P < 0.001); and (iii) patients with pre-therapy viraemia >500 000 copies/mL compared with those with lower viraemia levels (>500 000: 16.0%; 100 000-500 000: 9.3%; <100 000 copies/mL: 4.8%, P = 0.009). pRes and pre-therapy viraemia >500 000 copies/mL were independent predictors of VR by multivariable Cox regression. Conclusions: TDF/FTC/RPV as a treatment simplification strategy shows a very high rate of VS maintenance. The presence of pRes to both NRTIs and NNRTIs and a pre-therapy viraemia >500 000 copies/mL are associated with an increased risk of VR, highlighting the need for an accurate selection of patients before simplification.
Subject(s)
Anti-HIV Agents/therapeutic use , Emtricitabine/therapeutic use , HIV Infections/drug therapy , Rilpivirine/therapeutic use , Tenofovir/therapeutic use , Viral Load/drug effects , Adult , Anti-HIV Agents/administration & dosage , Deoxycytidine/therapeutic use , Drug Combinations , Emtricitabine/administration & dosage , Female , HIV Infections/virology , HIV-1/drug effects , HIV-1/genetics , Humans , Male , Middle Aged , RNA, Viral/blood , Reverse Transcriptase Inhibitors/therapeutic use , Rilpivirine/administration & dosage , Tablets , Tenofovir/administration & dosageABSTRACT
OBJECTIVES: We evaluated the virological response in patients starting a regimen based on darunavir/ritonavir (DRV/r), which is currently the most widely used ritonavir-boosted protease inhibitor. METHODS: Data from 206 drug-naïve and 327 PI-experienced patients starting DRV/r 600/100 mg twice daily (DRV600) or 800/100 mg once daily (DRV800) were examined. The probabilities of virological success (VS) and virological rebound (VR) were evaluated in survival analyses. Baseline DRV/r resistance and its evolution at failure were also examined. RESULTS: DRV600 was preferentially administered in patients with complex requirements (older age, higher viraemia, lower CD4 cell count and DRV/PI resistance) compared with DRV800. By 12 months, the probability of achieving VS was 93.2% and 84.3% in drug-naïve and PI-experienced patients, respectively. The higher the baseline viraemia, the longer was the time required to achieve VS, both in drug-naïve patients [>500 000 HIV-1 RNA copies/mL: median [interquartile range (IQR)] 6.1 (5.1-10.3) months; 100 000-500 000 copies/mL: median (IQR) 4.9 (3.8-6.1) months; <100 000 copies/mL: median (IQR) 3.9 (3.5-4.8) months; P < 0.001] and in PI-experienced patients [≥100 000 copies/mL: median (IQR) 7.2 (5.7-11.6) months; <100 000 copies/mL: median (IQR) 2.8 (2.4-3.3) months; P < 0.001]. In PI-experienced patients, the probability of VR was higher for higher viraemia levels (22.3% for ≥100 000 copies/ml vs. 9.7% for <100 000 copies/mL; P = 0.007). Baseline resistance did not affect the virological response. At failure, a high percentage of patients maintained virus susceptible to all PIs (drug-naïve: 95%; PI-experienced: 80%). Despite being used more often in patients with more complex requirements, DRV600 performed as well as DRV800. CONCLUSIONS: In clinical practice, use of DRV/r (with its flexible dosage) results in high rates of virological response. These data support the use of PI/r in patients whose characteristics require potent drugs with a high genetic barrier.
Subject(s)
Anti-HIV Agents/administration & dosage , Darunavir/administration & dosage , Drug Resistance, Viral , HIV Infections/drug therapy , HIV-1/drug effects , HIV-1/isolation & purification , Viral Load , Adolescent , Adult , Female , HIV Infections/virology , Humans , Male , Middle Aged , Ritonavir/administration & dosage , Treatment Failure , Young AdultABSTRACT
BACKGROUND: We aimed at evaluating the temporal trend of drug-resistance and APOBEC editing from HIV-DNA genotypic resistance tests (GRT) in virologically suppressed individuals. MATERIAL AND METHODS: Major resistance mutations (MRM), genotypic susceptibility score (GSS) for the current regimen and APOBEC-related mutations (APO-M) were evaluated. Potential changes in trends of MRM and APO-M over-time were assessed and predictors of MRM detection or sub-optimal GSS (GSS<2) at HIV-DNA-GRT were estimated through logistic regression analyses. RESULTS: Among the 1126 individuals included, 396 (35.2%) harboured at least one MRM (23.4% to NRTI, 18.8% to NNRTI, 7.7% to PI and 1.4% to INSTI [N=724]); 132 (12.3%) individuals showed a GSS <2. APO-M and stop codons were found in 229 (20.3%) and 105 (9.3%) individuals, respectively. APO-DRMs were found in 16.8% of individuals and were more likely observed in those individuals with stop codons (40.0%) compared to those without (14.4%, P<0.001). From 2010 to 2021 no significant changes of resistance or APO-M were found. Positive predictors of MRM detection at HIV-DNA GRT were drug abuse, subtype B infection, and a prolonged and complex treatment history. Perinatal infection and having at least 2 stop codons were associated with a current suboptimal regimen. CONCLUSIONS: In virologically suppressed individuals, resistance in HIV-DNA and the extent of APOBEC editing were generally stable in the last decade. A careful evaluation of APOBEC editing might be helpful to improve the reliability of HIV-DNA GRT. Further investigations are required to understand how to apply the estimation of APOBEC editing in refining genotypic evaluation.
ABSTRACT
PURPOSE: This study evaluated with ultrasonography (US) the presence of epiaortic vessel lesions in HIV-positive individuals receiving highly active antiretroviral therapy (HAART) and compared them with naïve patients and healthy individuals to highlight the differences among the different vascular damage patterns. MATERIALS AND METHODS: A total of 222 HIV-infected patients receiving HAART, 64 HIV-infected patients naïve to antiretroviral therapy and 135 HIV-negative control patients underwent US of the carotid vessels. The morphological examination included grey-scale and colour and power Doppler imaging to better characterise lesions and intima media thickness. An automated computerised software package (Q LAB) was used to determine intima media thickness values. Independent risk factors for the development of carotid lesions and, in particular, cholesterolaemia and triglyceridaemia were considered. Atherosclerotic plaques and inflammatory-type lesions were reported. Statistical analysis included the chi-square test, the Fisher exact test for qualitative variables and the Kruskal-Wallis test to compare continuous variables. RESULTS: We observed a higher prevalence of carotid lesions in HIV-positive patients receiving HAART compared with HIV-positive naïve patients (p<0.0000001) and HIV-negative patients (p<0.0001). Findings consistent with inflammatory-type lesions rather than classic atheroma were depicted only in five patients receiving HAART (0.02%). CONCLUSIONS: Our study confirms a higher prevalence of carotid lesions in HAART-treated HIV patients. In agreement with other authors, we identified carotid lesions that were consistent with arteritis rather than with classic atheroma, but the percentage was too small to suggest any robust hypothesis. Further studies are warranted to define the mechanism of onset of carotid lesions in HIV-positive individuals.
Subject(s)
Antiretroviral Therapy, Highly Active , Carotid Artery Diseases/diagnostic imaging , Carotid Artery Diseases/etiology , HIV Infections/complications , HIV Infections/drug therapy , Adolescent , Adult , Aged , Case-Control Studies , Chi-Square Distribution , Female , Humans , Male , Middle Aged , Risk Factors , Software , Tunica Intima/pathology , Tunica Media/pathology , Ultrasonography, DopplerABSTRACT
We report two cases of HIV positive patients with SARS-CoV-2 infection and a recent diagnosis of opportunistic infections of central nervous system (CNS). We investigated the potential impact of coinfection with SARS-CoV-2 on HIV replication in CNS.
Subject(s)
COVID-19/virology , Central Nervous System/virology , Coinfection/virology , HIV Infections/virology , SARS-CoV-2 , Viral Load , Adult , HIV Infections/drug therapy , Humans , Male , Middle AgedSubject(s)
Lung/pathology , Papilloma/complications , Papilloma/diagnosis , Papillomavirus Infections/diagnosis , Papillomavirus Infections/pathology , Respiratory Sounds/etiology , Trachea/pathology , Endoscopy , HIV Infections/complications , Histocytochemistry , Humans , Male , Microscopy , Middle Aged , Radiography, Thoracic , Tomography, X-Ray ComputedABSTRACT
Extra-intestinal cryptosporidiosis, especially of the biliary and respiratory tract, is likely in the course of an intestinal involvement, whereas it is rare without such a localization. We report a case of pulmonary cryptosporidiosis without apparent intestinal involvement in an AIDS patient, with favourable outcome after antimicrobial combination therapy with paromomycin plus azithromycin. The successful response to antimicrobial treatment was subsequently maintained by effective highly active antiretroviral therapy (HAART). We suggest that respiratory cryptosporidiosis should be investigated in HIV-infected patients with pulmonary symptoms and low CD4 cell count, and, if detected, treatment should include HAART plus the combination of paromomycin and azithromycin.
Subject(s)
AIDS-Related Opportunistic Infections/drug therapy , Azithromycin/therapeutic use , Cryptosporidiosis/drug therapy , Cryptosporidium parvum/drug effects , Lung Diseases, Parasitic/drug therapy , Paromomycin/therapeutic use , AIDS-Related Opportunistic Infections/parasitology , Animals , Antiretroviral Therapy, Highly Active , Cryptosporidiosis/parasitology , Drug Therapy, Combination , HIV Infections/complications , HIV Infections/drug therapy , Humans , Lung Diseases, Parasitic/parasitology , Male , Middle Aged , Treatment OutcomeABSTRACT
Exposure prevention is the primary strategy to reduce the risk of occupational bloodborne pathogen infections in healthcare workers (HCW). HCWs should be made aware of the medicolegal and clinical relevance of reporting an exposure, and have ready access to expert consultants to receive appropriate counselling, treatment and follow-up. Vaccination against hepatitis B virus (HBV), and demonstration of immunisation before employment are strongly recommended. HCWs with postvaccinal anti-HBs levels, 1-2 months after vaccine completion, >or=10 mIU/mL are considered as responders. Responders are protected against HBV infection: booster doses of vaccine or periodic antibody concentration testing are not recommended. Alternative strategies to overcome non-response should be adopted. Isolated anti-HBc positive HCWs should be tested for anti-HBc IgM and HBV-DNA: if negative, anti-HBs response to vaccination can distinguish between infection (anti-HBs >or=50 mUI/ml 30 days after 1st vaccination: anamnestic response) and false positive results(anti-HBs >or=10 mUI/ml 30 days after 3rd vaccination: primary response); true positive subjects have resistance to re-infection. and do not need vaccination The management of an occupational exposure to HBV differs according to the susceptibility of the exposed HCW and the serostatus of the source. When indicated, post-exposure prophylaxis with HBV vaccine, hepatitis B immunoglobulin or both must be started as soon as possible (within 1-7 days). In the absence of prophylaxis against hepatitis C virus (HCV) infection, follow-up management of HCV exposures depends on whether antiviral treatment during the acute phase is chosen. Test the HCW for HCV-Ab at baseline and after 6 months; up to 12 for HIV-HCV co-infected sources. If treatment is recommended, perform ALT (amino alanine transferase) activity at baseline and monthly for 4 months after exposure, and qualitative HCV-RNA when an increase is detected.
Subject(s)
Health Personnel , Hepacivirus , Hepatitis B virus , Occupational Exposure , Antiviral Agents/therapeutic use , Europe , Hepatitis B/drug therapy , Hepatitis B/prevention & control , Hepatitis C/drug therapy , Hepatitis C/prevention & control , Humans , Occupational Exposure/prevention & controlABSTRACT
Exposure prevention is the primary strategy to reduce the risk of occupational bloodborne pathogen infections in healthcare workers (HCW). HCWs should be made aware of the medicolegal and clinical relevance of reporting an exposure, and have ready access to expert consultants to receive appropriate counselling, treatment and follow-up. Vaccination against hepatitis B virus (HBV), and demonstration of immunisation before employment are strongly recommended. HCWs with postvaccinal anti-HBs levels, 1-2 months after vaccine completion, >10 mIU/mL are considered as responders. Responders are protected against HBV infection: booster doses of vaccine or periodic antibody concentration testing are not recommended. Alternative strategies to overcome non-response should be adopted. Isolated anti-HBc positive HCWs should be tested for anti-HBc IgM and HBV-DNA: if negative, anti-HBs response to vaccination can distinguish between infection (anti-HBs >50 mUI/ml 30 days after 1st vaccination: anamnestic response) and false positive results(anti-HBs >10 mUI/ml 30 days after 3rd vaccination: primary response); true positive subjects have resistance to re-infection. and do not need vaccination The management of an occupational exposure to HBV differs according to the susceptibility of the exposed HCW and the serostatus of the source. When indicated, post-exposure prophylaxis with HBV vaccine, hepatitis B immunoglobulin or both must be started as soon as possible (within 1-7 days). In the absence of prophylaxis against hepatitis C virus (HCV) infection, follow-up management of HCV exposures depends on whether antiviral treatment during the acute phase is chosen. Test the HCW for HCV-Ab at baseline and after 6 months; up to 12 for HIV-HCV co-infected sources. If treatment is recommended, perform ALT (amino alanine transferase) activity at baseline and monthly for 4 months after exposure, and qualitative HCV-RNA when an increase is detected.
ABSTRACT
Human immunodeficiency virus (HIV)-related pulmonary hypertension (HRPR) is a cardiovascular complication of HIV infection that has been recognized in the last years with increasing frequency. The etiology of HRPH is unknown. All the attempts to isolate HIV on pulmonary vessels in HRPH patients failed, and an indirect role for HIV in this disease has been hypothesized. Current theories on the pathogenesis focus on abnormalities of endothelial and smooth muscle cells of pulmonary vasculature. Endothelial and smooth muscle cell injury could be due to a high production or to a reduced clearance of cytokines in these patients. In fact, in several studies high levels of ET-1, IL-1alpha, IL-6 and PDGF in primary pulmonary hypertension (PPH) and in HRPH have been found. HIV gp 120 could induce the production of these cytokines by a stimulation of monocytes/macrophages. A high alpha1-adrenoreceptors stimulation of pulmonary vessels could be also implicated in the pathogenesis of HRPH. Chronic hypoxia is observed with increased frequency in HIV patients, and this could induce a chronic stimulation of alpha1-receptors of pulmonary vasculature with typical pathological changes. However, only a small percentage of HIV- patients develop HRPH. This observation suggests the existence of an idiosyncratic susceptibility to the development of vascular disease. This susceptibility could have a genetic basis, and might be determined by particular major histocompatibility complex alleles.
Subject(s)
HIV Infections/complications , Hypertension, Pulmonary/etiology , Autoimmune Diseases/etiology , HIV Infections/pathology , Humans , Hypertension, Pulmonary/pathology , Liver Diseases/etiology , Receptors, Adrenergic, alpha/physiologyABSTRACT
OBJECTIVES: To determine the clinical features, sites of involvement, bacteriological findings, and outcome of infective endocarditis (IE) in patients with HIV infection. PATIENTS AND METHODS: All patients with diagnosis of IE admitted to 54 infectious disease centres in Italy over a 15-year period (1984-1999) were reviewed, and 895 cases fulfilled the Duke criteria for definite diagnosis of IE. Data were collected with regard to the clinical, laboratory, and demographic characteristics of patients, as well as results of blood cultures and data on clinical outcome. RESULTS: There were 108 episodes of IE in 105 HIV-infected patients. The mean age of patients was 30.1 years, and the commonest predisposing condition was intravenous drug use (94.3%). Staphylococci were the predominant organisms (60.2%), and the tricuspid valve was the most frequently involved site of infection (51.9%). Left-sided heart involvement (45.4%) and multivalvular involvement (17.6%) were also frequently observed. The greater frequency of S. aureus affecting the tricuspid valve vs. other valves was statistically significant (P<0.001). Six patients (5.9%) underwent surgery, and one (16.7%) of them died. Ninety-five (94.1%) patients were treated medically, and 17 (17.9%) of them died. Overall mortality rate was 17.8%. Any left-sided heart involvement was predictive of an increased risk of death if compared with any right-sided heart involvement (P< 0.004). The mortality rate among HIV-infected patients was higher in those with CD4 cell counts below 200/mm(3). CONCLUSIONS: IE in HIV-infected patients, for the most part intravenous drug users, is more commonly localized to the right side of the heart; however, mixed or left-side valvular infections are frequent. Severe immunosuppression and left-side valvular involvement are associated with a greater risk for mortality.
Subject(s)
AIDS-Related Opportunistic Infections/diagnosis , AIDS-Related Opportunistic Infections/microbiology , Endocarditis, Bacterial/diagnosis , Endocarditis, Bacterial/microbiology , Adult , CD4 Lymphocyte Count , Candida albicans/isolation & purification , Diagnosis, Differential , Endocarditis/diagnosis , Endocarditis/microbiology , Female , Humans , Immunocompromised Host , Male , Middle Aged , Prognosis , Risk Factors , Staphylococcus aureus/isolation & purification , Streptococcus/isolation & purificationABSTRACT
A 34-year-old woman presented with a 10-year history of recurrent oral and genital ulcerations and recurrent episodes of bilateral conjunctivitis associated with HIV infection. A diagnosis of Behçet's disease (BD) in association with keratoconjunctivitis sicca (KCS) was made after exclusion of other viral and autoimmune diseases according to the international criteria for BD. This is the first reported case of a combination of BD and KCS in a patient with HIV infection in which a complete resolution was observed as a result of successful highly active antiretroviral therapy. The likelihood that a direct viral effect or HIV-induced autoimmune mechanisms act in the pathogenesis of both BD and KCS in HIV-infected patients is discussed.
Subject(s)
Antiretroviral Therapy, Highly Active , Behcet Syndrome/diagnosis , HIV Infections/drug therapy , Keratoconjunctivitis Sicca/diagnosis , Adult , Behcet Syndrome/complications , Behcet Syndrome/pathology , Diagnosis, Differential , Female , HIV Infections/complications , Humans , Keratoconjunctivitis Sicca/complications , Keratoconjunctivitis Sicca/pathologyABSTRACT
Antiretroviral prophylaxis (PEP) after occupational exposure to HIV in healthcare workers (HCWs) is used across Europe, but not in a consistent manner. A panel of experts, funded by the European Commission, formulated a set of recommendations. When it has been decided that the characteristics of the exposure indicate the initiation of PEP, PEP should be started as soon as possible; initiation is discouraged after 72 hours. PEP should be initiated routinely with any triple combination of antiretrovirals approved for the treatment of HIV-infected patients; a two class regimen is to be preferred. The source patient's treatment history should be sought. Counselling, psychological support, HIV testing and clinical evaluation should be performed at baseline, at 6-8 weeks, and at least 6 months post exposure. Additional clinical and laboratory monitoring at one and two weeks should be considered, as adherence with and tolerance of the regimen can highlight adverse reactions and potential toxicity. Routine HIV resistance tests in the source patient, and direct virus assays in the exposed HCW are not recommended.
ABSTRACT
Antiretroviral prophylaxis (PEP) after occupational exposure to HIV in healthcare workers (HCWs) is used across Europe, but not in a consistent manner. A panel of experts, funded by the European Commission, formulated a set of recommendations. When it has been decided that the characteristics of the exposure indicate the initiation of PEP, PEP should be started as soon as possible; initiation is discouraged after 72 hours. PEP should be initiated routinely with any triple combination of antiretrovirals approved for the treatment of HIV-infected patients; a two class regimen is to be preferred. The source patient's treatment history should be sought. Counselling, psychological support, HIV testing and clinical evaluation should be performed at baseline, at 6-8 weeks, and at least 6 months post exposure. Additional clinical and laboratory monitoring at one and two weeks should be considered, as adherence with and tolerance of the regimen can highlight adverse reactions and potential toxicity. Routine HIV resistance tests in the source patient, and direct virus assays in the exposed HCW are not recommended.
Subject(s)
Anti-HIV Agents/administration & dosage , HIV Infections/prevention & control , Health Personnel , Occupational Exposure/prevention & control , Practice Guidelines as Topic , Preventive Medicine/standards , Risk Assessment/standards , Europe/epidemiology , European Union , HIV Infections/epidemiology , Humans , Risk FactorsABSTRACT
The use of central vascular catheters (CVC) is associated with a substantial number of complications, amongst which infections predominate. A diagnosis of CVC-related infection usually requires catheter removal for culture. Semiquantitative (roll-plate method) and quantitative methods (flush, vortex, centrifugation or sonication methods) are the most reliable diagnostic methodologies requiring catheter removal, because of their greater specificity. The roll-plate method is the simplest and most commonly used technique. This method only samples the external surface of the catheter, and is particularly indicated for recently inserted catheters in which extraluminal colonisation is the primary mechanism of infection. Luminal culture techniques, such as the quantitative methods, may be more relevant for catheters that have been in place for a long period of time. However, in up to 85% of removed CVC the culture is negative, and other diagnostic techniques that do not require catheter removal have been proposed, including paired quantitative blood cultures, endoluminal brushing, and differential time to positivity (DTP) of paired blood cultures. DTP, that compares the time to positivity for qualitative cultures of blood samples simultaneously drawn from the CVC and a peripheral vein, appears to be the most reliable in the routine clinical practice since many hospitals use automatic devices for qualitative blood culture positivity detection. More recently catheter-sparing direct diagnostic methods, which include Gram stain and acridin-orange leucocyte cytospin (AOLC) test, appeared to be especially useful because of the rapidity of results and the ability to distinguish different microorganisms, allowing early targeted antimicrobial therapy.
ABSTRACT
In recent years, the pathogenic role of human immunodeficiency virus (HIV) and the clinical manifestations of HIV-associated pulmonary arterial hypertension (HIV-PAH), which currently represents one of the most severe complications of HIV infection, have received more attention HIV-PAH occurs at all stages of the disease, and does not seem to be related to the degree of immune deficiency. Many of the symptoms in HIV-PAH result from right ventricular dysfunction: the first clinical manifestation is effort intolerance and exertional dyspnoea that will progress to the point of breathlessness at rest. Echocardiography is an extremely useful tool for the diagnosis of HIV-PAH, and Doppler echocardiography can be used to estimate systolic pulmonary artery pressure. Assessment of haemodynamic measures by catheterization remains, however, the best test for evaluating the response to therapy. Cardiac catheterization is mandatory to definitively diagnose the disease and exclude any underlying cardiac shunt as the aetiology. Recently, effective therapies for pulmonary arterial hypertension (PAH) have been available, including prostanoids, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors, allowing amelioration of symptoms and a better prognosis. However, HIV-PAH remains a progressive disease for which treatment is often unsatisfactory and there is no cure. As new efficient antiretroviral treatment is introduced, clinicians should expect to encounter an increasing number of cases of PAH in HIV-infected patients in the future.