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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemoglobin and ferritin are important biomarkers of iron status but are both altered by inflammation. We used the inflammation biomarkers C-reactive protein (CRP) and alpha1-acid glycoprotein (AGP) to adjust hemoglobin and ferritin concentrations to clarify interpretation of iron status. Apparently healthy adults who tested positive twice for HIV but who had not reached stage IV or clinical AIDS were randomly allocated to receive a food supplement (n = 17 and 21) or the food plus a micronutrient capsule (MN; 10 men and 34 women, respectively) containing 30 mg iron/d. Hemoglobin, ferritin, CRP, and AGP concentrations were measured at baseline and 3 mo and subjects were divided into 4 groups (reference, no inflammation; incubating, raised CRP; early convalescence, raised AGP and CRP; and late convalescence, raised AGP). Correction factors (the ratios of the median for the reference group over each inflammatory group) improved the consistency of the ferritin but not the hemoglobin results. After correction, ferritin (but not hemoglobin) increased in both men (48 microg/L; P = 0.02) and women (12 microg/L; P = 0.04) who received MN but not in the food-only group. However, hemoglobin did improve in subjects who showed no inflammation both at baseline and mo 3 (P = 0.019), but ferritin did not increase in this group. In conclusion, ferritin concentrations were more closely linked to current inflammation than hemoglobin; hence, correction by inflammation biomarkers improved data consistency. However, low hemoglobin concentrations were the consequence of long-term chronic inflammation and improvements in response to MN supplements were only detected in subjects with no inflammation.
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PMID:The influence and benefits of controlling for inflammation on plasma ferritin and hemoglobin responses following a multi-micronutrient supplement in apparently healthy, HIV+ Kenyan adults. 1828 75

This study investigates how the extent of pre-treatment radiological disease and early anti-tuberculous treatment response affect levels of selected circulating host immune markers. Twenty HIV-uninfected tuberculosis patients with BACTEC culture positivity for Mycobacterium tuberculosis at diagnosis and treated with directly observed short course anti-tuberculosis chemotherapy and 13 healthy community controls were enrolled. Serum samples were collected throughout treatment. After the intensive phase of treatment, 12 patients remained sputum culture-positive (slow responders) and eight patients were culture negative (fast responders). C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), soluble urokinase plasminogen activator receptor (suPAR), soluble lymphocyte activation gene-3 (sLAG-3), granzyme B, soluble tumour necrosis factor receptor one and two (sTNFR I and sTNFR II) and soluble death receptor 5 (sDR5) concentrations were measured. High levels of CRP at diagnosis were found to be associated (p</=0.05) with the presence of multiple cavities on chest x-rays and high levels of suPAR and sICAM-1 at diagnosis were associated (p</=0.05) with the extent of alveolar disease. Also significant were the associations between the level of granzyme B (p</=0.01) and LAG-3 (p</=0.05) at diagnosis, and the size of the cavities. The combination of diagnosis and week one measurements of selected serological markers in mathematical models was able to identify the fast responders with up to 87.5% accuracy and the slow responders with up to 83.3% accuracy These preliminary results suggest that predictive models for differential early treatment responses using combinations of host markers hold promise.
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PMID:Immune parameters as markers of tuberculosis extent of disease and early prediction of anti-tuberculosis chemotherapy response. 1835 89

The objective of this study is to systematically review the epidemiology and the clinical and virologic aspects of multicentric Castleman's disease in HIV-positive patients and to evaluate treatment strategies and outcome, especially in relation to HAART administration. The authors have conducted a systematic review of the English literature for all cases of newly diagnosed multicentric Castleman's disease in HIV-positive patients. The 25 studies which met the selection criteria included 84 HIV-positive patients with multicentric Castleman's disease (20 pre-HAART and 64 post-HAART era). Of them, the majority (90%) were men with 33 months median time from detection of HIV-positivity to multicentric Castleman's disease diagnosis in the HAART era. Fever and lymphadenopathy were the most common presenting symptoms and cytopenias, hypoalbuminemia, polyclonal hypergammaglobulinemia and raised C-reactive protein the most frequently revealed laboratory findings. Kaposi's sarcoma was present in 72% of the patients and respiratory system involvement in 34%. Although the majority of cases reported were positive for human herpesvirus-8, none of the reviewed patients was found to suffer from polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS) syndrome. Of the 48 patients on HAART, 64% were already on HAART at multicentric Castleman's disease diagnosis, having a better immunologic profile and a lower incidence of Kaposi's sarcoma than the 35% of patients who initiated HAART after multicentric Castleman's disease diagnosis. Nevertheless, the two groups did not have significantly different mortality rates (30 vs. 38%). At multicentric Castleman's disease diagnosis, a wide range of CD4 counts was recorded, suggesting that disease presentation could occur at any CD4 count. With regard to treatment, the study confirmed the high rates of response with rituximab (anti-CD20 monoclonal). Monochemotherapy seems to give short-lived responses, which require maintenance to be sustained. Polychemotherapy with CHOP has given long-term remission in a subset of patients. Other regimens used in the treatment of HIV-related multicentric Castleman's disease were antiviral agents, immunomodulatory agents, and thalidomide. The fatality rate among HIV-related multicentric Castleman's disease cases reviewed was 44%, significantly lower than that of HIV-negative individuals (65%), while median survival of the latter was 29 months longer than that of HIV-infected individuals. The fatality rate among pre-HAART patients was 75 vs. 29% among HAART patients. Infection, multiorgan failure, Kaposi's sarcoma, non-Hodgkin lymphoma and progressive multicentric Castleman's disease were the most often reported causes of death. In conclusion, multicentric Castleman's disease is a lymphoproliferative disorder with an increasing prevalence in HIV-infected individuals. Even though life expectancy in multicentric Castleman's disease seems to have significantly improved in the HAART era, it remains a disease with a poor prognosis and an increased incidence of non-Hodgkin lymphoma in the HIV-context.
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PMID:Multicentric Castleman's disease in HIV infection: a systematic review of the literature. 1838 78

The lung is a site for repeated or chronic inflammatory insults. Epidemiologic research has provided evidence to support the hypothesis that tissue damage caused by inflammation can initiate or promote the development of lung cancer, possibly in conjunction with tobacco use. For example, some studies suggest an increased risk of lung cancer among persons with lung infections, such as tuberculosis, bacterial pneumonia, or inflammatory lung diseases. Elevated serum levels of C-reactive protein, an inflammation marker, are associated with heightened lung cancer risk. Recent studies also demonstrate increased lung cancer risk among immunosuppressed individuals infected with HIV. Other research indicates an association between genetic polymorphisms in the inflammation pathway, which might modulate the inflammatory response and lung cancer risk.
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PMID:Inflammation in the development of lung cancer: epidemiological evidence. 1840 27

Blood lipids and high-sensitivity C-reactive protein (hsCRP) are used to assess cardiovascular disease (CVD) risk. We evaluated in a cross-sectional design the relationship of hsCRP to markers of liver function (aspartate and alanine transaminases [AST and ALT, respectively]), CVD risk factors and HIV-disease progression markers in 226 HIV-1 sero-positive drug users. hsCRP showed a significant inverse relationship with ALT and high-density lipoprotein, independent of age, gender, viral load, CD4 cell-count and antiretroviral (ARV) use, and was not significantly associated with HIV-disease progression markers. Serum markers of liver damage, AST and ALT, were associated with lower hsCRP, total cholesterol, low-density lipoproteins and triglycerides. Elevated liver enzymes (> or =40 IU/L) were predictive of hsCRP levels that are considered a low risk for CVD. In conclusion, hsCRP may not be a reliable marker of CVD risk in populations with HIV at-risk for elevated liver enzymes due to high hepatitis B virus/hepatitis C virus prevalence and ARV use.
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PMID:C-reactive protein: a poor marker of cardiovascular disease risk in HIV+ populations with a high prevalence of elevated serum transaminases. 1859 80

Castleman disease (CD) was recently classified as a unicentric hyaline vascular variant, unicentric plasma cell variant, and multicentric plasma cell variant. It is rare that unicentric CD is presented as multiple retroperitoneal lymphadenopathy. The clinical manifestations and prognosis depends on histologic type. We report an unusual case of CD with multiple retroperitoneal lymphadenopathy, which had unicentric hyaline vascular variant histologically but was clinically multicentric. The patient experienced anemia, weight loss, elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes syndrome), and plasmacytosis in bone marrow without human herpesvirus-8 or HIV. After exploratory laparotomy and lymphadenectomy under presumptive diagnosis of CD, the patient's symptoms recovered, and CRP and ESR decreased. Therefore, we suggest that unicentric CD is not clearly distinguished from multicentric, the type in this report, focusing on the useful role of CRP, ESR, and positron emission tomography/computed tomography in the disease activity of CD.
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PMID:Unicentric castleman disease is not clearly distinguished from multicentric type: a case report. 1876 16

Treated HIV infection and HIV-lipoatrophy increases risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). Circulating inflammatory molecules may, in part, explain this increased risk. This study examined circulating inflammatory molecules in treated HIV infection in relation to insulin sensitivity, lipids total body, and intramyocellular fat, compared to insulin-resistant obesity (an index group at high risk of diabetes). Detailed metabolic phenotypes were measured in 20 treated HIV-infected men (with and without subcutaneous lipoatrophy) vs. 26 insulin-resistant obese men (IR-O, n = 26), including inflammatory molecules, insulin sensitivity, total body fat (TBF), visceral fat (visceral adipose tissue (VAT)), and intramyocellular lipid (IMCL). C-reactive protein (CRP) levels in treated HIV were similar to those in IR-O, despite lower TBF and greater insulin sensitivity in treated HIV. In HIV-lipoatrophy, CRP was higher than that found in IR-O. Adiponectin was similar between treated HIV and IR-O, but significantly lower in those with HIV-lipoatrophy. In treated HIV, subjects with higher CRP had significantly higher total cholesterol, VAT, and IMCL. In treated HIV, subjects with lower adiponectin had significantly lower HDL and higher triglycerides, glucose, VAT, and IMCL. In conclusion, a proinflammatory milieu equivalent to that of insulin-resistant obesity characterizes lean men with treated HIV infection, worse in those with subcutaneous lipoatrophy. These factors may contribute to the accelerated diabetogenesis and cardiac risk observed in treated HIV infection.
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PMID:Proinflammatory markers, insulin sensitivity, and cardiometabolic risk factors in treated HIV infection. 1900 69

Although the list of clinical complications associated with HIV therapy continues to grow, the underlying mechanisms remain incompletely understood. Metabolic abnormalities, such as dyslipidaemia, insulin resistance and cardiovascular disease continue to top the list, but there is an increasing appreciation of the effect of HIV and antiretroviral therapy on body composition, bone metabolism, muscle function and autonomic nervous system control of lipid and glucose metabolism. The 10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV brought together physicians and researchers in the area of HIV management with world experts involved in adipose tissue metabolism and lipid regulation, bone and muscle metabolism and renin-angiotensin and blood pressure control to review and discuss recent findings in these areas. The data presented at the meeting highlight that studies of adipose tissue remain a major focus of attempts to unravel the pathophysiology that accompany lipodystrophy associated with HIV infection and/ or its therapy. There is also a growing appreciation and understanding of the direct role of HIV in the development of various comorbidities, including bone disease, cardiac dysfunction and neuropathologies, including peripheral neuropathy. Two key emerging themes were those of mitochondrial dysfunction and a heightened basal inflammatory state, exemplified by increased levels of proinflammatory cytokines, chemokines and markers such as C-reactive protein. These might prove to be the common denominators that link HIV-associated pathologies with diverse organ systems.
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PMID:Key data from the 10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV, 6-8 November 2008, London, UK. 1919 38

IgG4-related disease sometimes involves regional and/or systemic lymph nodes, and often clinically and/or histologically mimics multicentric Castleman's disease or malignant lymphoma. In this study, we examined clinical and pathologic findings of nine patients with systemic IgG4-related lymphadenopathy. None of these cases were associated with human herpes virus-8 or human immunodeficiency virus infection, and there was no T-cell receptor or immunoglobulin gene rearrangement. Histologically, systemic IgG4-related lymphadenopathy was classified into two types by the infiltration pattern of IgG4-positive cells: interfollicular plasmacytosis type and intra-germinal center plasmacytosis type. The interfollicular plasmacytosis type showed either Castleman's disease-like features or atypical lymphoplasmacytic and immunoblastic proliferation-like features. By contrast, the intra-germinal center plasmacytosis type showed marked follicular hyperplasia, and infiltration of IgG4-positive cells mainly into the germinal centers, and some cases exhibited features of progressively transformed germinal centers. Interestingly, eight of our nine (89%) cases showed eosinophil infiltration in the affected lymph nodes, and examined patients showed high elevation of serum IgE. Laboratory examinations revealed elevation of serum IgG4 and soluble interleukin-2 receptors. However, the levels of interleukin-6, C-reactive protein, and lactate dehydrogenase were within normal limits or only slightly elevated in almost all patients. One patient showed a high interleukin-6 level whereas C-reactive protein was within the normal limit. Autoantibodies were examined in five patients and detected in four. Compared with the previously reported cases of multicentric Castleman's disease, our patients with systemic IgG4-related lymphadenopathy were significantly older and had significantly lower C-reactive protein and interleukin-6 levels. In conclusion, in our systemic IgG4-related lymphadenopathy showed pathologic features only partially overlapping those of multicentric Castleman's disease, and serum data (especially C-reactive protein and interleukin-6) are useful for differentiating the two. Our findings of eosinophil infiltration in the affected tissue and elevation of serum IgE may suggest an allergic mechanism in the pathogenesis of systemic IgG4-related lymphadenopathy.
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PMID:Systemic IgG4-related lymphadenopathy: a clinical and pathologic comparison to multicentric Castleman's disease. 1927 Jun 42

Interleukin (IL)-18 levels have been identified as important predictors of cardiovascular mortality and are often elevated in human immunodeficiency virus (HIV)-infected individuals. To investigate a possible function for IL-18 in atherogenesis in the context of early HIV infection, we used the simian immunodeficiency model of HIV infection. Acutely simian immunodeficiency virus-infected and uninfected rhesus monkeys (Macaca mulatta) on an atherogenic diet were evaluated prospectively for atherosclerotic lesion development relative to a panel of plasma markers including IL-18, IL-8, IL-1beta, IL-6, C-reactive protein, soluble vascular cell adhesion molecule-1, soluble E-selectin, and soluble intercellular adhesion molecule-1. Although no significant differences in lesion development were identified between groups after 35 days of infection, levels of plasma IL-18 measured 1 month before virus inoculation correlated significantly with atherosclerotic plaque cross-sectional area at the carotid bifurcation (P<0.001, R=0.946), common iliac bifurcation (P<0.01, R=0.789), and cranial abdominal aorta (P<0.01, R=0.747), as well as with extent of CD3+ and CD68+ cellular infiltration in vascular lesions (both P<0.001, R>or=0.835) in both groups. Atherosclerotic plaque area at the carotid and common iliac bifurcations also showed a weaker inverse correlation with baseline IL-8 levels, as did CD68+ signal area. Results implicate a strong role for IL-18 in early atherosclerosis progression and raise the possibility that the chronically elevated IL-18 levels seen in later stages of HIV infection may contribute significantly to accelerated atherogenesis in this population.
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PMID:Interleukin-18 predicts atherosclerosis progression in SIV-infected and uninfected rhesus monkeys (Macaca mulatta) on a high-fat/high-cholesterol diet. 1938 Nov 33


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