Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fresh frozen plasma (FFP) contains higher levels of intact coagulation factors and coagulation and fibrinolysis inhibitors than solvent/detergent-treated plasma (SD plasma), and also greater residual cell contamination. SD plasma is a particle-free plasma of uniform quality. SD treatment, however, has the specific result of reducing the activities of some inhibitors. Both plasma types carry a minimal residual risk of transmitting human immunodeficiency virus (HIV)-1/2, hepatitis virus B (HBV), and hepatitis virus C (HCV), but SDP is, in addition, also safe with respect to other lipid-enveloped viruses and perhaps with respect to hepatitis virus A (HAV), also due to its antibody (Ab) content. Future revisions of therapeutic plasma safety and quality standards should consider the following points:For FFP:reduce residual cell count in all FFP units to values below 5 x 10(6) leukocytes/l;screen donors for Parvovirus B19 genome and antibodies in order to establish a sufficiently large collection of genome-negative and antibody-positive donors whose FFP can be used for selected patients;For SDP:introduce pool testing for Parvovirus B19 genome; fix an upper limit for genome and a lower limit for antibody content;in addition to the standard quality control methods for therapeutic plasma, focus on assays to test for functionally intact proteinase inhibitors such as alpha(2)antiplasmin (alpha(2)AP) and alpha(1)proteinase inhibitor (alpha(1)PI) that are important for plasma indications. Commercially available kits may not be sufficient to show changes in inhibition kinetics. For both types:introduce an activation marker such as thrombin-antithrombin complex (TAT) as a random test to monitor activation processes during withdrawal, separation, manufacturing, and storage;abolish inappropriate parameters like Antithrombin III (AT III) and coagulation factor XI that are not relevant for changes in plasma quality;finally, support every effort towards establishing an efficient documentation and reporting system on efficacy and side effects of plasma transfusions. Effective reporting alone might help to reveal deficiencies of specific plasma quality and to overcome them through modifications to manufacturing processes and testing, or by defining its indications more precisely.
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PMID:Quality of therapeutic plasma-requirements for marketing authorization. 1237 93

Viral infections can be the causative agent in many glomerular diseases, and diagnostic criteria include clinical and laboratory data and tissue molecular analysis. Hepatitis B virus (HBV) is a well known cause of membranous glomerulonephritis (MGN), membranoproliferative GN (MPGN) and IgA nephropathy (IgAN), frequently in Asian populations. Hepatitis C virus (HCV), besides cryoglobulinemia-mediated glomerulonephritis (GN), is reported to cause other forms of GN. Human immunodeficiency virus (HIV) infection is closely related to a collapsing focal segmental glomerulosclerosis (FSGS), a distinct disease that affects mainly Africans and African-Americans. In the course of HIV infection other immune complex (IC) GN can occur, most frequently in whites. Nephrotic syndrome and progression to renal insufficiency are the main clinical manifestations. HIV-HCV co-infection is related to an IC glomerular disease, sometimes with immunotactoid deposits. Recent reports emphasize the role of parvovirus B19 (PV B19) for "idiopathic" collapsing FSGS and ICGN, and of Coxsackie B virus for IgAN. Renal biopsy is useful for defining virus-related glomerular lesions and a guide for prognostic and therapeutic evaluation.
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PMID:Virus-related glomerular diseases: histological and clinical aspects. 1245 12

To improve the quality of diagnostics and treatment of patients with immunodeficient states, two groups of patients were examined for the presence of cytomegalovirus (CMV) infection, among them 1,348--with clinical manifestations of CMV infection (group 1) and 335 hematological patients (group 2); in addition, 36 patients with secondary immunodeficiency and 31 patients with aplastic and hemolytic anemia, or with anemia of unclear origin were examined for the presence of parvovirusinfection (B19). The results of enzyme immunoassay, polymerase chain reaction and immunofluorescence tests active CMV infection, confirmed by determination of IgM, low avidity IgG, antigen and DNAemia, was registered in group 2 more often than in group 1. Examinations on the presence of parvovirus infection revealed that in anemia patients with the low level of IgG or its absence IgM was also detected more often than in group 1. In mixed infection caused by CMV and parvovirus B19 the disease took a more severe course than in monoinfection, which was probably due to the parallel action exerted by parvovirus on erythrocyte production in hematopoiesis and by CMV on the monocytic and macrophagal row of cell.
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PMID:[Laboratory diagnostics of infections caused by cytomegalovirus and parvovirus B19 in patients with secondary immunodeficiency]. 1252 2

Research was carried out in 335 blood specimens of patients in the age of 3-35 y.o. in order to optimize diagnosis and treatment of such patients with aplastic anemia and hemoblastosis who got hemotransfunction to eliminate cytomegaloviral infection (CMVI). IgM were found out in 37.9% cases (2.8 times higher than in donors), low-avide IgG--in 44.8%. "early" proteins CMV--29.9% and DNA--in 36.8% cases. Concerning the DNA presence, preference was given to research of leucocytic suspension compared with blood serum. Of 28 children of 3-13 y.o. with anemia being seropositive in CMV, IgG antibodies were detected in 13 children while IgM antibodies to Parvovirus B19 were found in 10 children. 7 children with a grave form of disease showed combined infection of Parvovirus B19 and CMV with activation signs. It is not excluded that parallel influence of Parvovirus B19 on erythrocytic hemopoiesis growth and that of CMV on lymphocytic-monocytis cells aggravates immunodeficiency and promotes development of infection complications.
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PMID:[Laboratory diagnosis of cytomegaloviral infection in patients with anemia and hemoblastosis in the Omsk region]. 1258 56

Collapsing glomerulopathy is a morphologic variant of focal segmental glomerulosclerosis (FSGS) characterized by segmental and global collapse of the glomerular capillaries, marked hypertrophy and hyperplasia of podocytes, and severe tubulointerstitial disease. The cause of this disorder is unknown, but nearly identical pathologic findings are present in idiopathic collapsing glomerulopathy and human immunodeficiency virus (HIV)-associated nephropathy, and collapsing glomerulopathy has been associated with parvovirus B19 infection and treatment with pamidronate. The pathogenesis of collapsing glomerulopathy involves visceral epithelial cell injury leading to cell cycle dysregulation and a proliferative phenotype. Clinically, collapsing glomerulopathy is characterized by black racial predominance, a high incidence of nephrotic syndrome, and rapidly progressive renal failure. Collapsing glomerulopathy also may recur after renal transplantation or present de novo, often leading to loss of the allograft. The optimal treatment for collapsing glomerulopathy is unknown. Treatments may include steroids or cyclosporine in addition to aggressive blood pressure control, angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, and lipid lowering agents. The role of other immunosuppressive agents such as mycophenolate mofetil in the treatment of collapsing FSGS remains to be defined. Prospective clinical trials are needed to define optimal therapy of this aggressive form of FSGS.
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PMID:Collapsing glomerulopathy. 1270 81

Association of drug-induced hypersensitivity syndrome with viral infection is debated. Human herpesvirus 6 (HHV-6) reactivation has been the most frequently reported infection associated with this syndrome. However, a case of cytomegalovirus (CMV) infection was recently described associated with anticonvulsant-induced hypersensitivity syndrome. We report a case of severe allopurinol-induced hypersensitivity syndrome with pancreatitis associated with Epstein-Barr virus (EBV) infection. Active EBV infection was demonstrated in two consecutive serum samples by the presence of anti-EBV early antigen (EA) IgM antibodies and an increase in anti-EBV EA IgG antibodies, whereas no anti-EBV nuclear antigen IgG antibodies were detected. EBV DNA was detected by polymerase chain reaction (PCR) in peripheral blood mononuclear cells. Reactivation of HHV-6 was suggested only by the presence of anti-HHV-6 IgM antibodies, but HHV-6 DNA was not detected by PCR in the serum. Other viral investigations showed previous infection (CMV, rubella, measles, parvovirus B19), immunization after vaccination (hepatitis B virus), or absence of previous infection (hepatitis C virus, human immunodeficiency virus). We suggest that EBV infection may participate in some cases, as do the other herpesviruses HHV-6 or CMV, in the development of drug-induced hypersensitivity syndrome.
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PMID:Drug-induced hypersensitivity syndrome associated with Epstein-Barr virus infection. 1278 38

The method of immune-enzyme assay was used to examine 113 patients with secondary immunodeficiency, including 16 HIV-infected drug-addicts (group 1), 36 patients with cytomegalovirus infection (CMVI) and with immunoregating index CD4/CD8 below 1.0 (group 2), 30 patients with CMVI and with CD4/CD8 below 1.2 (group 3) and 31 patients with aplastic anemia and with anemia of unclear genesis (group 4), for parvovirus infection caused by parvovirus B19. As for groups 1 and 4, the antibodies were detected in 50 and 48.4% of cases; it is noteworthy that an active parvovirus infection was registered in the above groups more often than in groups 2 and 3. There were patients with the antibodies in group 2 by 1.8 times more than in group 3. It is suggested that the simultaneous impact of HIV, CMV and parvoviruses significantly aggravates the immunodeficiency and contributes to a more severe clinical course.
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PMID:[Diagnosis of parvovirus B19 infection in patients with secondary immunodeficiency diseases]. 1282 4

Intravenous immunoglobulins (IVIg) are therapeutic preparations of normal human IgG that have been used for more than 20 years for substitutive therapy in patients with primary antibody deficiencies. Recent studies pointed out the need to obtain normal residual levels of IgG (i.e. 8 g/L) in order to reduce the number and severity of bacterial infections in these patients. The IVIg are also prescribed for the substitutive therapy of secondary immunodeficiencies such as chronic lymphoid leukemia and multiple myeloma with hypogammaglobulinemia and severe and/or recurrent infections, and human immunodeficiency virus (HIV)-infected children with recurrent bacterial infections before the era of highly active antiretroviral agents. However, in the latter situation, no recent study has evaluated IVIg therapy in acquired immunodeficiency syndrome (AIDS) children receiving highly active antiretroviral agents (HAART), and the use of IVIg must probably be restricted to the currently rare clinical situation in Western Europe of children with AIDS who develop recurrent infections despite the administration of HAART and prophylactic cotrimoxazole. IVIg have also been reported to prevent infections, interstitial pneumonia and graft-vs. host disease during the first 90 days post-transplant in allogeneic bone-marrow transplant recipients. However, this result was not confirmed by two recent studies and IVIg therapy should probably only be proposed for a subgroup of bone-marrow allografted patients such as those with hypogammaglobulinemia and sepsis. With the exception of erythrovirus B19 infection with erythroblastopenia, no clear benefit of IVIg therapy has been reported for the curative management of other infectious diseases.
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PMID:Intravenous immunoglobulins in infectious diseases: where do we stand? 1284 45

A Committee of the Health Council of The Netherlands has expressed its opinion on introducing testing of blood products for parvovirus B19 (B19). Although infections with B19 generally run their course without any serious health problems, for some groups, such as pregnant women, patients with underlying haematological problems and patients with immunodeficiency, infections with B19 can result in serious complications. For cellular blood products, which are derived either from a single donor or a limited number of donors and are administered either to a single patient or to a limited number of patients, the Committee recommends that a risk-group approach be adopted and that 'Big-virus safe' blood products be administered to the risk groups mentioned above. The Committee defines as 'Big-virus safe' cellular blood products from a donor in which IgG antibodies against B19 have been detected in two separate blood samples, one taken at least six months after the other. Patients other than those in the risk groups should continue to receive cellular blood products that have been produced in accordance with current safety criteria. For plasma products, which are prepared from plasma pools and are administered to large numbers of patients, the measures must be aimed at cutting down the levels of B19 infectivity in such pools. For plasma pools, the Committee proposes a maximum permissible limit of 104 genome copies of Bl9 per ml.
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PMID:Blood products and parvovirus B19. 1291 40

We evaluated the prevalence of persistent parvovirus B19 (B19) infection and associated anemia in human immunodeficiency virus (HIV)-infected and HIV-uninfected children. B19 persistence was defined as B19 DNA detected in specimens collected >16 weeks apart. Of 182 children, 3 HIV-infected children and two HIV-uninfected children had evidence of persistent B19 infection. Of the 5 children, none had evidence of B19-associated anemia. Our data suggest that B19 infections can persist in children without the development of symptomatic anemia.
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PMID:Persistent parvovirus B19 infection without the development of chronic anemia in HIV-infected and -uninfected children: the Women and Infants Transmission Study. 1497 2


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