non-HIV Infection Research Articles

Spectre étiologique des hyperferritinémies

Serum ferritin levels may be increased in many conditions: renal diseases, liver diseases, human immunodeficiency virus infection. The purpose of this study was to assess the aetiological spectrum of high serum ferritin levels in a 1200-bed university hospital, to compare our results with the data already published and to assess a potential association between aetiology and ferritin levels.Patients with a serum ferritin level higher than 600 microg/l were retrospectively included between 15 November 2003 and 15 January 2004, and their medical records were reviewed.Ninety-eight patients (38 women and 60 men; median age: 59,5 years [19-92]) were recruited in departments of hepatology and gastroenterology (22%), haematology (14%) and internal medicine (18%). Diagnosis performed were: non-HIV systemic infections (23,8%), haematological diseases (16,1%), alcoholism (11,2%) and malignancies (9,8%). Dialysed chronic renal failure, liver diseases, haemochromatosis and systemic inflammatory diseases counted for 4.2 to 5.2% of cases. Serum ferritin level lied between 600 and 1000 microg/l for 50 patients, between 1000 and 1500 microg/l for 24, and over 1500 microg/l for 24. There was no significant difference between the three groups as regards the etiological distribution.In our study, chronic renal failure was not a major cause of high ferritin level: this is probably due to the current use of erythropoietin, which has decreased the use of blood transfusions. The two major aetiology of hyperferritinemia were non-HIV infections and malignancies.

Significado clínico de los valores elevados de ferritina sérica

We aimed to determine the diagnostic alternatives indicated by serum ferritin levels (2000 ng/ml, and to establish the clinical processes associated with very high levels (5000-10 000 ng/ml). We retrospectively analyzed cases with serum levels of ferritin serum equal to or greater than 2000 ng/ml between March 2000 and November 2001. Data were obtained from the laboratory's computerized database. Patients' medical records were reviewed by means of a protocol which established the clinical conditions associated with these serum ferritin values. The study involved 135 patients with ferritin levels equal to or greater than 2000 ng/ml. Clinical syndromes included hematological diseases (45.9%), liver diseases (23%), chronic renal failure (17.78%), neoplastic diseases (10.4%), systemic inflammatory diseases (7.4%), chronic transfusions (7.4%), and non-HIV systemic infections (5.9%). Syndromes which are not usually associated with extreme serum ferritin levels were identified in 3.7% of the patients. The highest concentrations were seen in the systemic inflammatory disease group: 5856 (2492) ng/ml. Within this group, four patients with adult onset Still's disease (AOSD) displayed the highest mean ferritin levels: 11 322 (5474) ng/ml. Elevated serum ferritin levels act as a non-specific marker for a large number of disorders. In certain inflammatory diseases such as adult onset Still's disease (AOSD), this finding may be an important tool.

From HIV infection to AIDS: a dynamically induced percolation transition?

The origin of the unusual incubation period distribution in the development of AIDS is largely unresolved. A key factor in understanding the observed distribution of latency periods, as well as the occurrence of infected individuals not developing AIDS at all, is the dynamics of the long-lasting struggle between HIV and the immune system. Using a computer simulation, we study the diversification of viral genomes under mutation and the selective pressure of the immune system. In non-HIV infections, vast spreading of viral genomes in genome space usually does not take place. In the case of an HIV infection, this may occur, as the virus successively weakens the immune system by the depletion of CD4+ cells. In a sequence space framework, this leads to a dynamically induced percolation transition, corresponding to the onset of AIDS. As a result, we obtain a prolonged shape of the incubation period distribution, as well as a finite fraction of non-progressors that do not develop AIDS, comparing well with results from recent clinical research.

Cytoplasmic Abnormalities in Monocytes from Patients with AIDS

This report describes cytoplasmic abnormalities in monocytes from patients with AIDS. Visualized on Wright-stained peripheral blood smears, these abnormalities were not found in normal monocytes, monocytes from patients receiving chemotherapy, monocytes from patients with monocytosis related to non-HIV viral or bacterial infection, or monocytes from patients with monocytic leukemia (French-American-British [FAB] classification M4 or M5). The cytoplasmic abnormalities were detected on panoptically stained blood smears using an ordinary light microscope. As such, a medical technologist and pathologist can detect them as a part of reviewing peripheral blood specimens that are flagged by modern hematology analyzers. Materials and Methods As enumerated in [T1], from a total of 275 samples of peripheral venous blood samples anticoagulated with EDTA (no more than 2 hours old), peripheral blood smears were made in an automated slidemaker-stainer (Sysmex M) and stained with a modified Wright stain. In the study, 82 of the 275 samples were obtained from patients who were HIV positive by Western blot. Other samples used as controls for the study were not subjected to Western blot analysis. At the time that blood smears obtained from these samples underwent microscopic review, this author was aware that they were HIV positive. From all 82 patients, simultaneous samples were obtained for flow cytometry. At the time that the blood smears were being reviewed microscopically, the author was not aware of the CD4 values of the blood samples from which the slides were made. Of the 82 HIV-positive patients, 34 had CD4 counts less than 200/μL (0.2 × 109/L) and fit the current definition for AIDS.1 In 48 patients with abnormal lymphocyte subsets, CD4 counts were greater than 200/μL (0.2 × 109/L). For controls, blood smears were obtained from 66 hematologically normal persons and from 43 patients whose peripheral blood specimens were flagged by the analyzer for monocytosis (monocytes 2,000/μL [0.2 × 109/L] or greater). For HIV testing [cytology | hematology | immunology | virology] Cytoplasmic Abnormalities in Monocytes From Patients With AIDS

Cerebral infarction in adult AIDS patients: observations from the Edinburgh HIV Autopsy Cohort.

Autopsy series of patients with AIDS have found a 4% to 29% prevalence of cerebral infarction. Little is known of the prevalence of cerebral infarction when not associated with non-HIV central nervous system (CNS) infection, lymphoma, or cardioembolic sources. Clinical correlation has seldom been available. We describe the pathological and clinical features of patients from the Edinburgh HIV Cohort Study found to have had cerebral infarcts without evidence of non-HIV CNS infection, CNS lymphoma, or cardioembolic sources at autopsy. From 183 autopsy cases, 26 without evidence of opportunistic cerebral infection or lymphoma were selected. These 26 cases went through a second selection process in which the presence of cerebral infarction, in the absence of the conditions mentioned, was verified. Histology and clinical records for the remaining patients were reviewed. Ten (5.5%) cases fulfilled the inclusion criteria and demonstrated similar hypoxic-ischemic lesions. Small-vessel thickening was seen in all cases, and perivascular space dilatation, rarefaction, and pigment deposition, with vessel wall mineralization and perivascular inflammatory cell infiltrates, were seen in some cases. Vasculitis was not found. One patient had had a transient ischemic attack, and no patient had had a stroke. Cerebral infarcts in HIV-infected patients are not common in the absence of cerebral non-HIV infection, lymphoma, or embolic sources. We found an HIV-associated vasculopathy with similar features in all risk groups. In AIDS patients presenting with stroke or transient ischemic attack, potentially treatable causes, such as cerebral coinfection or tumor, should be sought.

Extremely elevated serum ferritin levels in a university hospital: Associated diseases and clinical significance

To establish the frequency with which serum ferritin levels > or = 1,000 ng/mL occur in a general hospital population, and to determine the clinical significance of this finding. All serum ferritin determinations performed between June 1992 and July 1993 at the University of Cincinnati Medical Center were reviewed and patients with serum ferritin levels > or = 1,000 ng/mL identified. The medical records of these patients were then reviewed. Of 1,826 serum ferritin determinations performed during the study period, 122 (6.7%) were > or = 1,000 ng/mL. Associated clinical syndromes found in the 95 patients with serum ferritin > or = 1,000 ng/mL included liver disease (20.0%), renal disease (17.9%), malignant disease (17.9%), human immunodeficiency virus (HIV) infection (16.8%), non-HIV systemic infections (15.8%), chronic transfusions (10.5%), and sickle cell syndromes (10.5%). No syndrome usually associated with extreme serum ferritin elevations was identified in 8.4% of patients, and 16.8% of the patients fell into more than one category. The highest mean serum ferritin levels occurred in the chronically transfused and sickle cell groups. Concomitant serum transferrin saturation values were determined with 82 (86.3%) of the elevated serum ferritin levels and did not correlate well with them. The highest mean transferrin saturation levels occurred in the liver disease group. Transferrin saturation > or = 50%, suggestive of iron overload, was significantly more frequent in the liver disease group (P = 0.002); and saturation < or = 15%, suggestive of iron-deficient erythropoiesis, was significantly more frequent in the HIV group (P = 0.001). Outside the setting of clinical syndromes associated with iron overload (liver disease, transfusions, sickle cell syndromes), serum ferritin levels > or = 1,000 ng/mL serve as a nonspecific marker for a variety of significant disorders, including infectious and neoplastic diseases. Further study of the regulation of ferritin production may provide insight into the pathogenesis of disorders associated with extreme serum ferritin elevations.

Prophylaxis of HIV Infection following Occupational Exposure

To review the risk of HIV infection following occupational exposure, the theoretical basis for chemoprophylaxis, investigative experience with chemoprophylaxis in animals and humans, and the economic aspects of postexposure chemoprophylaxis. English-language articles and conference proceedings pertaining to the risk of occupational HIV infection and to postexposure chemoprophylaxis. Studies evaluating chemoprophylaxis of HIV infection following occupational exposure were selected for review. Abstracts reporting ongoing clinical trials were also included. In vitro studies are discussed to provide the immunologic rationale for chemoprophylaxis. Animal studies examining the efficacy of chemoprophylaxis in preventing non-HIV retroviral infection are reviewed, and their applicability to human HIV infection is critically evaluated. Human studies and case reports describing attempts at chemoprophylaxis of HIV infection following occupational exposure are discussed. Chemoprophylaxis of HIV infection following occupational exposure has focused on the use of zidovudine (ZDV) because it was previously the only antiretroviral agent approved for treating HIV infection. Animal models of retroviral infection provide conflicting data regarding the efficacy of ZDV chemoprophylaxis, and there are important questions about the applicability of animal data to human HIV infection because of differences in natural histories of non-HIV retroviral infections, inoculum size, dosing of ZDV, and routes of infection. Human surveillance studies are thus far inadequate to determine the efficacy of ZDV prophylaxis because of the very low HIV seroconversion rates following occupational exposure. ZDV is well tolerated during short-term administration in people without HIV infection, but long-term safety is unknown. In addition, the true cost-benefit ratio of ZDV chemoprophylaxis is uncertain. Current data from in vitro, animal, and human studies are inadequate to define the appropriate role of ZDV in preventing HIV infection following occupational exposure. Limited toxicity data and the high cost of treatment must be weighed against the theoretical benefits of ZDV use in this setting. The decision to employ ZDV for postexposure prophylaxis must ultimately be based on existing institutional policies, the attitude of the responsible physician regarding such practice, and/or the desires of the exposed healthcare worker after being properly informed of potential risks and benefits.

Pathology of the Kidney in Childhood Immunodeficiency: Aids-Related Nephropathy is Not Unique

Clinical and nephropathologic findings in autopsy material from 7 children with acquired immune deficiency syndrome (AIDS), 13 with severe combined immune deficiency (SCID), and 6 with a variety of other congenital immune deficiencies were reviewed in an effort to understand better the pathophysiology of the AIDS-related nephropathy. Non-HIV viral infection seemed to be associated with the development of the pathologic changes considered to be components of the AIDS-related nephropathy, and these changes, including focal segmental glomerulosclerosis (FSGS) and tubular epithelial cell injury and ectasia, were not limited to the kidneys of children with AIDS but were present in many of the congenital immune deficiencies. Of the 5 children with congenital AIDS, only the 3 who survived longer than a year developed AIDS-related nephropathy, whereas the two children with transfusion-acquired AIDS did not develop renal disease despite surviving for several years after initial infection.