Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ferritin is an acute phase protein which is often elevated in acute and chronic inflammation, as well as in neoplastic disease. In adults with human immunodeficiency virus (HIV) infection, elevated serum ferritin levels indicate advanced or progressive disease. In the present study, ferritin levels were evaluated in 88 HIV-infected children. Ferritin levels greater than 100 ng/ml were found in 93% of patients with advanced disease. Increasing levels always accompanied or closely preceded rapid disease progression. Serum ferritin levels may prove to be a useful marker to monitor disease progression and therapeutic efficacy in HIV-infected children.
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PMID:Ferritin levels in pediatric HIV-1 infection. 784 98

To investigate nutritional status and heterosexual human immunodeficiency virus (HIV) transmission, we performed a nested case-control study of sexually active, adult women in Kigali, Rwanda. Forty-five women who seroconverted during the 24-month study period were compared to 74 women who remained seronegative throughout the study. Seroconvertors and nonseroconvertors did not differ in preseroconversion serum levels of vitamin A, carotenoids, vitamin E, selenium, albumin, ferritin, or cholesterol. Weight loss, however, was a significant predictor of eventual HIV seroconversion. Subsequent seroconvertors lost an average of 1.5 kg during the first 6 months of the study compared with a 1.0-kg gain (p = 0.001) for nonconvertors. Nine of 27 (33%) seroconvertors, compared with one of 44 (2%) controls, lost at least 5 kg in the 6-month period beginning 1 year before their seroconversion (odds ratio, 21.5, 95% confidence interval 4.1-112). The association between weight loss and seroconversion was independent of other potential risk factors such as socioeconomic status, pregnancy, and genital ulcer disease. In addition to these findings for measured weight loss during follow-up, reported weight loss before enrollment was also a risk factor for subsequent seroconversion. Additional studies of heterosexual HIV transmission are needed to determine whether or not weight loss is causally related to susceptibility for HIV infection.
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PMID:Role of nutritional status and weight loss in HIV seroconversion among Rwandan women. 849 90

Highly specialized, state-of-the-art diagnostic tests are available for identifying congenital and acquired immune defects. These methods should only be resorted to when less complicated means have created suspicion of an immune defect. The case history, including the family history, represents the core of the diagnostic procedure. Initially, only simple clinical investigations are indicated. These should enable the physician to exclude or delimit a defect in the immune system which then can be defined more closely by specific tests. Screening includes clinical chemistry (erythrocyte sedimentation rate, total serum protein, serum electrophoresis, C-reactive protein, blood count including differential blood count, ferritin, urine analysis, and a quantitative assay of the immunoglobulins A, G and M), bacteriological, serological, and radiological investigations, and finally skin tests with recall antigens. Thereby, it is usually possible to reliably detect primary B cell defects with humoral antibody deficiency syndromes. Lymphocyte subset counts, immunoelectrophoresis, and bone marrow biopsy are necessary for the differential diagnosis, or for the confirmation, of malignant lymphatic proliferation, especially in adults. IgG subclass defects as well as granulocyte dysfunction and complement defects must be excluded in patients who are susceptible to bacterial infection despite normal immunoglobulin concentrations. In suspected cases of primary or secondary (HIV, cytomegalovirus, Epstein-Barr virus) T cell defects, lymphocyte subset counts and, where applicable, T cell function tests are indicated. The majority of secondary immunodeficiency syndromes, in which the primary disease is known, do not currently require specialized diagnosis. Nevertheless, monitoring of the lymphocyte subsets in HIV-positive patients has already become standard practice in health care (for evaluating the prognosis and deciding on the therapy).
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PMID:[Laboratory diagnosis of immune deficiency]. 849 52

The cause of cerebral atrophy in patients with acquired immunodeficiency syndrome (AIDS) is obscure because human immunodeficiency virus type 1 (HIV-1)-related histopathological changes hardly correlate with cerebral atrophy. In this study, brain ventricular expansion was compared to the frontal lobe density of mononuclear and astroglial cells at autopsy. Twenty-eight male patients with AIDS displaying varying degrees of atrophy were compared to 17 age-matched male control subjects without AIDS or atrophy. An index of ventricular expansion was measured in uniformly sliced, formalin-fixed brain specimens, and immunochemically marked cells in coronal sections of the left superior frontal gyrus (Brodmann area 8) were quantified by field counting and planimetry. In the cortex, diffuse ferritin-stained microglia and glial fibrillary acidic protein-positive astrocytes were about twice as numerous in the patients with AIDS. Sixty-five percent (18/28) of the patients with AIDS had a microglial cell density greater than 2 standard deviations above the control mean. Microglial cell density was correlated positively with the severity of ventricular expansion (r = 0.71, p < 0.0001), while hypertrophied astroglial cells were very weakly related. In white matter, Ham-56-positive macrophages and glial fibrillary acidic protein-positive astrocytes were not meaningfully correlated with the index of ventricular expansion. Brain ventricular expansion and diffuse cortical microgliosis are highly prevalent anomalies in patients with AIDS, and their interrelationship may be more important than previously recognized.
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PMID:Diffuse microgliosis associated with cerebral atrophy in the acquired immunodeficiency syndrome. 851 82

A 13-year-old girl with a history of 4 months of perianal skin lesions is described. Physical examination revealed three 0.5 I 1-cm red, swollen, fleshy, skin tags extending from the perianal area to the perineum (Fig. 1). The patient reported intermittent fever, diarrhea, and abdominal pain, and her body weight was below the third percentile for her age. Laboratory studies showed an erythrocyte sedimentation rate of 101 mm/h; hematocrit of 26%; white blood cell count of 9800/mm3; serum iron of 15 mg/L (normal value (NV), 60-160 mg/L); ferritin of 43.4 microg/L (NV, 12-150 microg/L); transferrin of 203 mg/100 mL (NV, 200-400 mg/100 mL); transferrin saturation of 6% (NV, 20-50%); hypoalbuminemia; negative purified protein derivative (PPD), cytomegalovirus (CMV), human immunodeficiency virus (HIV), venereal disease research laboratory (VDRL), and antinuclear antibody tests; and Toxoplasma titers of 1/16, Van de Kamer 1.67 g/day. A barium examination revealed marked irregularity of the descending colon, and a colonoscopy showed uneven areas of mucosal edema and pseudopolyps in the transverse and descending colon, associated with irregular thickening and stenosis. Histopathologically, large intestine and skin lesions consisted of noncaseating epithelioid and giant cell granulomas (Fig. 2). Cultures for acid-fast bacilli and fungi were negative, and under polarized light no foreign bodies were seen. Treatment with metronidazole (250 mg three times a day), prednisone (0.5 mg/kg/day), and acetylsalicylic acid (75 mg/kg/day) was moderately effective. Vitamin, folic acid, and iron supplements were also added.
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PMID:Perianal Crohn's disease. 1097 32

The relationships among hemoglobin, ferritin, and transferrin receptor levels and 2 markers of human immunodeficiency virus (HIV) disease severity--HIV load and CD4(+) lymphocyte count--were characterized among 483 pregnant women in Malawi, Africa. The only significant correlation was an inverse correlation between hemoglobin level and plasma HIV load (r=-.104; P<.03). The prevalence of iron deficiency anemia was not significantly different across quartiles of HIV load or CD4(+) lymphocyte count. In contrast to previous studies, these data suggest that iron status is not related to markers of HIV disease severity in pregnant women in Africa.
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PMID:Iron status and indicators of human immunodeficiency virus disease severity among pregnant women in Malawi. 1171 3

Chronic granulomatous disease (CGD) is an inherited primary immunodeficiency characterized by phagocytes devoid of a functioning nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. The failure of CGD phagocytes to produce reactive oxygen species (ROS) results in a marked increase in the susceptibility of affected patients to life-threatening bacterial and fungal infections. This study investigated whether loading of CGD phagocytes with glucose oxidase (GO)-containing liposomes (GOLs) could restore cellular production of bactericidal ROS (eg, H2O2 and HOCl) in vitro. Results indicate that GO encapsulated in liposomes enabled NADPH oxidase-deficient phagocytes to use H2O2 for the production of highly bactericidal HOCl. The intracellular colocalization of bacteria and liposomes (or liposome-derived ferritin) was demonstrated by confocal laser microscopy and electron microscopy. After uptake of GOLs (approximately 0.2 U/mL at 1 mM total lipid concentration, size approximately 180 nm), CGD granulocytes produced HOCl levels comparable to those of normal phagocytes. Remarkably, after treatment with GOLs, CGD phagocytes killed Staphylococcus aureus as efficiently as normal granulocytes. Moreover, treated cells retained sufficient motility toward chemotactic stimuli as measured by chemotaxis assay. Side effects were evaluated by measuring the H2O2 concentrations and the production of methemoglobin in whole blood. These studies revealed that H2O2 produced by GOLs was degraded immediately by the antioxidative capacity of whole blood. Elevated methemoglobin levels were observed only after application of extremely high amounts of GOLs (2 U/mL). In summary, the application of negatively charged GOLs might provide a novel effective approach in the treatment of patients with CGD at high risk for life-threatening infections.
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PMID:Reconstitution of bactericidal activity in chronic granulomatous disease cells by glucose-oxidase-containing liposomes. 1169 96

Although anemia is a common finding among human immunodeficiency (HIV)-infected infants in sub-Saharan Africa, the factors contributing to the pathogenesis of anemia have not been well characterized. We sought to characterize the relative contribution of iron deficiency and chronic disease to the anemia among infants. Hemoglobin, ferritin, erythropoietin, tumor necrosis factor-alpha (TNF-alpha), neopterin, CD4(+) lymphocyte count and plasma HIV load were measured in 165 HIV-infected and 39 uninfected 9-mo-old infants seen in an outpatient pediatric clinic in Kampala, Uganda. Among HIV-infected and uninfected infants, the prevalence of anemia (hemoglobin < 110 g/L) was 90.9 and 76.9%, respectively (P = 0.015), and the prevalence of iron deficiency anemia (hemoglobin < 110 g/L and ferritin < 12 microg/L) was 44.3 and 45.4%, respectively (P = 0.92). The relatively higher prevalence of anemia among HIV-infected infants was attributed to the anemia of chronic disease. Among infants with and without iron deficiency, the fitted regression line was log(10) plasma erythropoietin = 2.86 - 0.016.hemoglobin, and log(10) plasma erythropoietin = 4.11 - 0.028.hemoglobin, respectively, with a difference in the slope of the regression lines between log(10) erythropoietin and hemoglobin among infants with and without iron deficiency (P = 0.049). Infants in Uganda have an extremely high prevalence of anemia, and nearly half of the anemia is due to iron deficiency. The erythropoietin response to anemia appears to be upregulated among infants with iron deficiency.
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PMID:Iron deficiency anemia is highly prevalent among human immunodeficiency virus-infected and uninfected infants in Uganda. 1188 May 66

Anemia of chronic disease (ACD) is frequent in patients with human immunodeficiency virus (HIV) and its etiology is multifactorial. In a group of 111 patients with HIV, 19 were diagnosed with ACD. Parameters related to iron metabolism, such as serum iron (SI), serum ferritin (SF), and soluble transferrin receptor (sTfR) were correlated to levels of interferon-gamma (IFN-gamma) and results compared to a group of 42 nonanemic patients with HIV. Measurements of erythropoietin (EPO), CD4/CD8 T-cell ratio, and reticulocyte count (RTC) were determined to verify aspects related to severity of disease and bone marrow response. The results showed higher SF concentrations in ACD patients and normal or slightly increased sTfR measurements in both groups. There was no correlation between IFN-gamma and SF and between IFN-gamma and sTfR determinations. Lower CD4/CD8 values were obtained in ACD, and an inverse correlation was observed between IFN-gamma and CD4/CD8 in groups with and without anemia. RTC counts and EPO concentrations were similar in both groups: immature RTC were increased in patients with anemia, indicating an apparent attempt of marrow response to compensate the increased demand. Our data showed no correlation between IFN-gamma levels and iron disturbances in ACD, but results reinforced the observation of enhanced immunologic system deterioration in patients with HIV and ACD.
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PMID:Human immunodeficiency virus-related anemia of chronic disease: relationship to hematologic, immune, and iron metabolism parameters, and lack of association with serum interferon-gamma levels. 1222 86

Eight hemochromatosis probands with HFE C282Y homozygosity had frequent, severe, or unusual infections and common variable immunodeficiency (CVID) or immunoglobulin (Ig) G subclass deficiency (IgGSD). Thus, we performed serum Ig isotyping and other characterization of 43 additional unselected probands, 5 human leukocyte antigen (HLA)-identical siblings, and 240 consecutive CVID or IgGSD index patients. C282Y allele frequencies were estimated in 58 CVID or IgGSD index patients without hemochromatosis phenotypes and in 341 controls. HLA-A and -B haplotypes and frequencies were determined in all 51 probands, 186 CVID or IgGSD index patients without hemochromatosis phenotypes, and 751 controls. Thirteen unselected probands (30%) had CVID or IgGSD. Among all 21 hemochromatosis probands with CVID (n = 4) or IgGSD (n = 17), Ig subclass deficiency patterns were IgG(1) (n = 5), IgG(1) and IgG(3) (n = 6), IgG(3) (n = 9), and IgG(1), IgG(3), and IgG(4) (n = 1). IgG(2) or IgA deficiency was not detected; one proband had IgM deficiency. Mean values of total IgG, IgG(1), and IgG(3) were significantly lower in probands with CVID or IgGSD. Mean values of age, transferrin saturation, and ferritin at diagnosis and phlebotomy units required to induce iron depletion were similar in probands with or without CVID or IgGSD; phlebotomy had no apparent effect on IgG levels. C282Y frequencies were similar in CVID or IgGSD index cases without hemochromatosis phenotypes and in controls. There was concordance of Ig and hemochromatosis phenotypes in probands and respective HLA-identical siblings. Eight of 240 CVID or IgGSD index patients had hemochromatosis phenotypes and C282Y homozygosity (3 vs 0.7% and 0.2% controls; P < 0.0001, respectively). The frequency of A*03-B*07 was greater in CVID and IgGSD index cases without hemochromatosis phenotypes than in controls (0.0968 vs 0.0546, respectively; P = 0.0032). HLA-A*03-B*07 was the predominant haplotype in probands grouped by presence or absence of CVID or IgGSD. Some probands in each group were A*03-B*07 homozygotes; group A*03-B*07 frequencies were similar. We conclude that serum IgG abnormalities characteristic of CVID or IgGSD are common in hemochromatosis probands, and that the prevalence of hemochromatosis is increased in CVID and IgGSD index cases. These observations could be explained by the increased frequencies of HLA-A*03-B*07 in C282Y homozygotes and in CVID and IgGSD, and by the common occurrence of putative CVID or IgGSD allele(s) on haplotypes bearing C282Y.
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PMID:Common variable immunodeficiency and IgG subclass deficiency in central Alabama hemochromatosis probands homozygous for HFE C282Y. 1285 Apr 93


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