ABSTRACT
Lung cancer (LC) is the most common cancer among the non AIDS-defining malignancies in the highly active antiretroviral therapy (HAART) era. We described 23 HIV infected patients with a LC diagnosis followed in the Clinic of Tropical and Infectious Diseases of Brescia during the period of 1999-2009. All of these patients except two (n = 21, 91.3%) were cigarette smokers and all had at least one risk factor for developing cancer of the lung, or predisposing comorbidities, such as a COPD (chronic obstructive pulmonary disease) or a previous pneumonia. The median age at LC diagnosis was 53.6 years (range 21.2-71.4 years). Adenocarcinoma and squamous cell carcinoma were diagnosed in 10 cases (43.5%) respectively. In 21 subjects (91.3%) cancer was detected at stage IV with metastases. The median survival was 5.95 months. Greater intervention focused on the cessation of smoking is necessary, as well as the implementation of closer screening policies, especially in HIV-positive subjects with LC risk factors.
Subject(s)
HIV Infections/complications , Lung Neoplasms/virology , Adult , Antiretroviral Therapy, Highly Active , Female , HIV Infections/drug therapy , HIV Infections/epidemiology , HIV Infections/virology , Humans , Incidence , Italy/epidemiology , Lung Neoplasms/epidemiology , Male , Middle Aged , Retrospective Studies , Risk Factors , Smoking/epidemiology , Viral LoadABSTRACT
OBJECTIVES: The aim of the study was to estimate the burden and direct costs of diseases in HIV-infected patients (either opportunistic illnesses or other chronic diseases) with respect to the HIV-uninfected population. These estimates will be useful for the projection of future direct costs of HIV care. PATIENTS AND METHODS: A population-based study was conducted in the Brescia Local Health Agency in northern Italy. An administrative database recorded diagnoses, deaths, drug prescriptions and health resource utilization for all medical and surgical patients in the region from 2003 to 2007. The study estimated the prevalence of HIV infection as well as HIV-related mortality and annual cost per patient, and compared mortality and costs related to HIV infection with those for a set of 15 other chronic diseases. The standardized hazard ratio (SHR) and standardized mortality ratio (SMR) were obtained using an indirect standardization method. RESULTS: The prevalence of HIV infection increased from 218 per 100,000 inhabitants in 2003 to 263 per 100,000 in 2007. Although mortality rates decreased markedly (from 24 per 1000 HIV-infected patients in 2003 to 16 per 1000 in 2007), the data show that mortality was still higher in HIV-infected patients compared with the general population in the most recent years (SMR 8.8 in 2007). In each year included in the study, HIV-infected patients had higher rates of care-seeking for chronic diseases, including liver diseases (SHR>8), neuropathy, oesophagus-gastro-duodenum diseases, serious psychiatric disorders and renal failure (SHR approximately 3 for each). Also, the rate of medical attendance for neoplasias, chronic pulmonary disease, diabetes, and cardiovascular disease increased over time in HIV-infected patients compared with the general population. Ranking diseases in order of their total cost to the health system, HIV infection ranked 12th, with total costs of 28.6 million in 2007. Ranking in order of cost per patient, HIV infection ranked third, with a cost per patient of 9894 in 2007. HIV-infected patients with concomitant chronic diseases had higher average costs. The cost per patient in 2007 was 8104 for HIV-infected patients without other chronic diseases, 9908 for HIV infection plus cardiovascular disease, 11,370 for HIV infection plus chronic liver disease and 12,013 for HIV infection plus neoplasias. CONCLUSIONS: The prevalence and population cost of people living with HIV are likely to increase as a result of prolonged survival, aging of HIV-infected patients and increased risk of other chronic diseases. In the near future, HIV infection will rank as one of the most costly chronic diseases. Prevention strategies need to be more widely adopted to control the growing burden of the HIV epidemic and other chronic diseases affecting HIV-infected patients.
Subject(s)
HIV Infections/economics , Health Care Costs , Adult , Aged , Antiretroviral Therapy, Highly Active/economics , Chronic Disease , Costs and Cost Analysis , Female , HIV Infections/mortality , Health Resources/economics , Health Resources/statistics & numerical data , Humans , Italy/epidemiology , Male , Middle Aged , Prevalence , Proportional Hazards ModelsABSTRACT
This study assessed changes in prevalence and distribution of HIV-1 non-subtype B viruses in Italian and immigrant patients over two decades in a province in Italy. All HIV-positive patients who underwent genotypic resistance testing were selected. Prevalence of non-subtype B viruses in 3-year periods was calculated. All sequences of non-subtype B and those provided by REGA as unassigned were analysed for phylogenetic relationships. In total, 250/1563 (16%) individuals were infected with a non-subtype B virus. Prevalence increased over time, reaching a peak (31.5%) in 2004-2006. In Italian patients, the most frequent subtypes were B (92.5%) and F1 (4%). F1 subtype was also prevalent in patients from South America (13.6%); in patients of African origin, CRF02_AG (54.9%) and G (12.3%) were the most frequent. HIV-1 non-subtype B infections in Italians were mostly found in patients who acquired HIV sexually. A phylogenetic relationship between F subtypes in Italian and representative HIV-1 sequences from Brazil was found. C subtypes in Italians were phylogenetically related to subtypes circulating in Brazil. Inter-subtype recombinants were also found in the latest years. The HIV-1 epidemic in Brescia province evolved to the point where about 1/3 patients recently diagnosed harboured non-B HIV subtypes. The distribution of HIV-1 non-B subtypes in Italian patients resembled that in South American patients and phylogenetic relatedness between some Italian and South American HIV-1 strains was found. The possible epidemiological link between these two populations would have been missed by looking only at risk factors for HIV acquisition declared by patients. The evidence of inter-subtype recombinants points to significant genetic assortment. Overall our results support phylogenetic analysis as a tool for epidemiological investigation in order to guide targeted prevention strategies.
Subject(s)
HIV Infections/epidemiology , HIV Infections/virology , HIV-1/classification , Adult , Chi-Square Distribution , Female , Genotype , HIV Infections/ethnology , HIV Infections/genetics , HIV-1/genetics , Humans , Italy/epidemiology , Logistic Models , Male , Molecular Epidemiology , Phylogeny , Prevalence , Sequence Analysis, DNAABSTRACT
BACKGROUND: Although the mechanism of atazanavir (ATV)-related hyperbilirubinemia is well identified, its prevalence, risk factors, and association with transaminase flares have rarely been assessed in a large population from the "real life" setting. METHODS: Prospectively collected data on 2,404 patients from the Italian MASTER Cohort and the Italian ATV expanded access program database were examined. Uni- and multivariable Cox proportional hazards regression models were conducted to identify risk factors for grade >or= III hyperbilirubinemia during the administration of ATV. The risk of increased levels of serum alanine aminotransferase (ALT) was compared between patients with or without grade >or= III hyperbilirubinemia in a Cox regression analysis stratified by hepatitis C virus (HCV) serostatus. RESULTS: Grade III and IV hyperbilirubinemia were observed in 1,072 (44.6%) and 174 (7.2%) of the patients, respectively. Higher CD4+ T-cell counts, abnormal bilirubinemia at baseline, and ritonavir co-administration were associated with a higher risk of developing grade >or= III hyperbilirubinemia. In contrast, female gender, clinical class C, and non-nucleoside reverse transcriptase co-administration appeared to be protective. Higher bilirubinemia at baseline and the use of ritonavir were associated with a higher risk of grade IV hyperbilirubinemia. The occurrence of grade >or= III hyperbilirubinemia was not associated with severe hepatotoxicity (hazard ratio 1.00, 95% confidence interval 0.64-1.57; p = 0.997). CONCLUSIONS: Hyperbilirubinemia is a common side effect of an ATV pharmacotherapeutic regimen. However, grade IV increase in bilirubin was rarely found. In most cases, ATV hyperbilirubinemia appeared to be an innocent phenomenon as far as the risk of a subsequent increase in liver enzyme level is concerned.
Subject(s)
Alanine Transaminase/blood , Anti-HIV Agents/adverse effects , HIV Infections/drug therapy , Hyperbilirubinemia/chemically induced , Liver/drug effects , Oligopeptides/adverse effects , Pyridines/adverse effects , Adult , Alanine Transaminase/metabolism , Analysis of Variance , Antiretroviral Therapy, Highly Active , Atazanavir Sulfate , CD4 Lymphocyte Count , Cohort Studies , Female , HIV Infections/complications , HIV Infections/pathology , Hepatitis C/complications , Hepatitis C/drug therapy , Humans , Hyperbilirubinemia/epidemiology , Hyperbilirubinemia/pathology , Liver/enzymology , Male , Multivariate Analysis , Prevalence , Proportional Hazards Models , Risk Factors , Ritonavir/therapeutic use , Severity of Illness IndexABSTRACT
BACKGROUND: There is very less information on the use of antiretroviral (ARV) drugs and viro-immunological outcome over calendar years in Italy. PATIENTS AND METHODS: We performed an analysis of a prospective observational cohort (MASTER) to assess antiretroviral drug use in first line HAART and explore whether initial treatment response changed over the years. RESULTS: 3,648 ARV-naive patients with available HIV-RNA and CD4+ T cell count at baseline who started their first HAART between 1997 and 2004 were studied. Mean age was 37.7 years; they were mostly males (72.3%) and Italians (81.4%). Prescription of non-nucleoside reverse transcriptase inhibitors and protease inhibitors boosted with ritonavir rose from 0.3% in 1997 to 58% in 2004 and from 0.3%in 1997 to 33.4% in 2004, respectively. Virological failures decreased over calendar years: from 42.9% in 1997 to 8.1%in 2004 after 6 months of HAART (p<0.001); from 42.1%(1997) to 10.7% (2004) after 12 months (p<0.001) and; from 39.5% (1997) to 8.2% (2004) after 18 months (p<0.001). The same trend, but less striking, was found for immunological failure rates. CONCLUSIONS: In the general Italian population of HIV-positive patients, evolution of treatment prescription correlated with improved viro-immunological outcome.
Subject(s)
Anti-HIV Agents/therapeutic use , Drug Administration Schedule , HIV Infections/drug therapy , Reverse Transcriptase Inhibitors/therapeutic use , Adult , Anti-HIV Agents/administration & dosage , Antiretroviral Therapy, Highly Active , CD4 Lymphocyte Count , Cohort Studies , Drug Therapy, Combination , Female , HIV Infections/immunology , HIV Infections/virology , Humans , Italy , Longitudinal Studies , Male , RNA, Viral/blood , Reverse Transcriptase Inhibitors/administration & dosage , Treatment Failure , Treatment OutcomeABSTRACT
A 45-year-old woman was admitted to the hospital because of cholestatic liver disease and severe thrombocytopenia following a 4-day history of fever and malaise. In her childhood the patient suffered from acute rheumatic fever with secondary mitral stenosis. Three years before admission, an atrial fibrillation had been diagnosed for which the patient was put on ticlopidine, 250 mg daily, that was taken regularly, without any adverse event. The patient had no history of cholestatic hepatitis or biliary colic. The abdominal ultrasonography was negative for biliary tract diseases and histological features were compatible with drug induced hepatotoxicity. Laboratory tests for viral and bacterial infection were negative. No other medications, apart from 2 doses of nimesulide, had been taken by the patient in the previous days. Ticlopidine was discontinued on admission and both bilirubin and platelet count rapidly normalized. We think that, in our patient, ticlopidine may be responsible of concomitant hematologic and hepatic toxicity and the trigger event might have been the reduced renal excretion of the drug following acute renal failure.
ABSTRACT
A case of simultaneous infection with HIV and HCV characterized by a rapidly progressive clinical course was studied retrospectively over 3.5 years. Molecular analysis indicated interference between HIV and HCV and between HCV subtypes 1a and 1b. An ineffective immune response was suggested by the persistence and sequence conservation of the HCV HVR1 variants isolated during the follow-up.
Subject(s)
AIDS-Related Opportunistic Infections/virology , HIV-1/isolation & purification , Hepacivirus/classification , Hepatitis C/virology , AIDS-Related Opportunistic Infections/drug therapy , Antiviral Agents/therapeutic use , Female , Follow-Up Studies , HIV Core Protein p24/genetics , Hepacivirus/genetics , Hepacivirus/isolation & purification , Hepatitis C/drug therapy , Humans , Interferon-alpha/therapeutic use , Longitudinal Studies , Middle Aged , Retrospective Studies , Viral Envelope Proteins/genetics , Zidovudine/therapeutic useABSTRACT
Plasmodium vivax infections caused by strains with low sensitivity to primaquine are widespread in the Western Pacific and Southeast Asia, and have been recently reported from Central America as well. We report a case of primaquine failure in a P. vivax infection acquired in Guatemala. A 28-year-old Italian woman developed two months after returning from Guatemala a vivax malaria attack that was treated with a standard chloroquine course (1,500 mg over three days) combined with primaquine (15 mg/day for 14 days). Two months later, she had a relapse that was again treated with chloroquine and primaquine at the same doses. After two more months, a second relapse occurred: this time primaquine (30 mg/day for 14 days was administered; the patient remained well during a follow-up period of six months and all parasitologic examination results were negative. Doses of primaquine as high as 6 mg/kg total dose may be indicated in the treatment of vivax malaria cases from Central America.
Subject(s)
Antimalarials/therapeutic use , Malaria, Vivax/drug therapy , Plasmodium vivax/drug effects , Primaquine/therapeutic use , Adult , Animals , Chloroquine/therapeutic use , Drug Resistance, Microbial , Drug Therapy, Combination , Female , Guatemala , Humans , Malaria, Vivax/transmission , RecurrenceABSTRACT
Although the development of antibodies against the hepatitis B virus surface antigen generally leads to the clearance of the infecting virus, anti-HBs reactivity has been reported in patients with chronic hepatitis. In the present study we analyzed the viral genome and the antibody specificity in a series of serum samples collected from a patient who seroconverted to anti-HBs during interferon therapy without clearing HBsAg. The appearance of an anti-HBs response was accompanied by the emergence of a pre-S1 defective viral genome. However, the wild-type adw2 molecular species remained largely dominant during follow up. The patient's antibody response to the surface viral antigens was directed towards the heterologous y subdeterminant and the pre-S1 fragment deleted in the variant hepatitis B virus. These results suggest that the selection of the escape viral mutant does not play a major role in viral persistence.
Subject(s)
Genome, Viral , Hepatitis B Antibodies/biosynthesis , Hepatitis B Surface Antigens/immunology , Hepatitis B virus/genetics , Hepatitis B/immunology , Adult , Amino Acid Sequence , Antibody Specificity , Base Sequence , Chronic Disease , Female , Follow-Up Studies , Hepatitis B Antibodies/blood , Humans , Molecular Sequence DataABSTRACT
Hepatitis C virus RNA, anti-hepatitis C virus immune response and biochemical markers of liver injury were investigated in 17 patients with acute non-A, non-B hepatitis. At the first observation, 1 to 3 wk from the clinical onset, all patients had hepatitis C virus RNA in their serum, and most (15 of 17) were positive for second-generation anti-hepatitis C virus enzyme immunoassay. Follow-up serum samples were available for 10 patients. The rate of recombinant immunoblot assay-confirmed anti-hepatitis C virus enzyme immunoassay reactivities increased from 67% in the first 3 wk to 86% after 21 wk. Elevated ALT levels were associated with hepatitis C virus RNA positivity in most of cases, but the viral nucleic acid was also detected in sera with normal or slightly increased enzyme values. None of the single antibodies tested were related to hepatitis C virus RNA positivity or to the clinical phase of the infection. Therefore hepatitis C virus RNA determination might provide important additional information as compared with anti-hepatitis C virus markers, allowing earlier diagnosis, discrimination of active infection and, possibly, prognostic evaluation.
Subject(s)
Hepacivirus/genetics , Hepatitis Antibodies/analysis , Hepatitis C/genetics , RNA, Viral/analysis , Acute Disease , Base Sequence , Hepacivirus/immunology , Hepatitis C/immunology , Hepatitis C Antibodies , Humans , Immunoblotting , Immunoenzyme Techniques , Molecular Probes/genetics , Molecular Sequence Data , Polymerase Chain Reaction , Sensitivity and SpecificityABSTRACT
The AA. report a case of CNS cryptococcosis with vasculopathic complications in a woman in perfect physical conditions. The patient was admitted to hospital after complaining for 20 days of fever, headache and rachialgia. CSF examination revealed hypoglicorrachia (18 mg %), cells 440 mmc (polymorphonuclear leukocytes 90%), brain CT scan negative. During antimycobacterial treatment right hemiparesis appeared; brain CT: hypodense lesion in the posterior brachium of the left inner capsule; at its base the lesion showed a hypodense streak coherent with thromboembolic damage or deep vasculitis. OKT4 lymphocytes were 6% (absolute number: 70). The antimycotic treatment, following the positive reaction of the CSF culture to Cryptococcus Neoformans, entirely cured the hemiparesis and normalized the CSF while OKT4 lymphocytes rapidly grew.