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At least 775 records · Page 43Linked to original sources
PubMed1996

[Giant cell hepatitis and autoimmune hemolytic anemia: efficacy of splenectomy on hemolysis].

BACKGROUND: The previously reported cases of giant cell hepatitis with autoimmune hemolytic anemia were improved by prednisone plus azathioprine. CASE REPORT: A 14-month-old boy suffered from giant cell hepatitis with auto-immune hemolytic anemia and positive direct Coombs test. Prednisone and azathioprine administration improved the liver disease but failed to control hemolysis so that repeated blood transfusions were necessary. Persistance of severe degree of hemolysis required splenectomy that was promptly and definitively effective. Azathioprine and prednisone were pursued for a total duration of five years. Twelve years after the onset of the disease, the child is well without any treatment. CONCLUSION: This is the first reported case of such an association in which poorly controlled auto-immune hemolytic anemia benefited from splenectomy.

Anemia, Hemolytic, Autoimmune↗
PubMed1995

[Transient erythroblastopenia in early childhood].

BACKGROUND: Transient erythroblastopenia is rare in young children although its frequency is increasing. POPULATION AND RESULTS: Six infants (four boys, two girls), aged 29-41 months (mean: 33) were admitted for polar and asthenia. Only one displayed infectious episode two months earlier. Hemoglobin ranged from 40 to 67 g/l and reticulocyte number from 1 to 10 G/l. Mean corpuscular volume was normal as was Coombs' test. There was a profound erythroblastopenia in the bone marrow in five of the six patients. Parvovirus B19 infection was excluded in all. The white cell and platelet counts were normal. All patients were given an unique blood transfusion. Reticulocytosis spontaneously appeared within a few weeks in three patients. Another patient had normal number of erythroid precursors in the bone marrow 1 month after admission. CONCLUSION: Diagnosis of transient erythroblastopenia can only be made after exclusion of known causes such as drugs, virus, immune deficiency, leukemia and of Blackfan-Diamond disease. Its persistence must lead to search for another cause.

Age Factors↗
PubMed2005

In vitro nonspecific mitogenic response of T-cell subsets in acute and chronic brucellosis.

The aim of the present study was to determine the cellular immune response on the course of brucellosis by investigating the proliferation response of T-cell subsets to phytohemagglutinin (PHA), that is, nonspecific mitogen in the patients with acute and chronic brucellosis. The study was performed in 19 patients with untreated brucellosis (acute, n = 11; chronic, n = 8) and 19 healthy controls. Standard tube agglutination and Coombs tests for brucellosis were performed. CD4+ and CD8+ T cell were investigated by the flow cytometry and sorting methods in all of cases. After these cells were cultured and stimulated with PHA, [H3]-thymidine uptake and stimulation indices (SIs) were established. In all of the patients with brucellosis, CD4+ SIs and CD8+ SIs were found to be 1.40 +/- 0.63 and 1.45 +/- 0.42, respectively, and in the controls CD4+ SIs and CD8+ SIs were 1.59 +/- 0.36 and 1.64 +/- 0.37, respectively. In acute cases, CD4+ SIs were 1.71 +/- 0.64 and CD8+ SIs were 1.54 +/- 0.45. CD4+ SIs were 0.97 +/- 0.25 and CD8+ SIs were 1.32 +/- 0.37 in chronic cases. Although in acute cases CD4+ SIs and CD8+ SIs were not different from those in the control group, CD4+ SIs of chronic brucellosis cases were found to be significantly low as compared with those of acute brucellosis cases and the controls (P < 0.01). CD8+ SIs of acute and chronic brucellosis cases were not found to be different from those in the controls. Brucella agglutination titers of the patients with acute and chronic brucellosis were not found related with CD4 SIs and CD8 SIs. The findings of significantly low results of CD4+ T-cell proliferative responses of chronic brucellosis to PHA as compared with control and acute brucellosis cases remind that the development of chronic infection might be a result of T-helper proliferation defect.

Adolescent↗
PubMed2005

Benzo(a)pyrene-induced anemia and splenomegaly in NZB/WF1 mice.

Benzo(a)pyrene (BaP), a polycyclic aromatic hydrocarbon, is a known immunomodulator. At high doses, BaP is immunosuppressive but at low doses it can enhance the immune response. Studies were conducted to determine if BaP would exacerbate the development of autoimmune disease in genetically prone NZB/WF1 mice. Five week old female NZBW/F1 mice were exposed dermally to 5, 20 and 40 mg/kg BaP for 30 days. Vehicle mice were exposed to an acetone:olive oil mixture for 30 days. BaP did not increase total IgG, anti-DNP-HSA or anti-dsDNA antibody levels. However, hematological evaluation revealed a decrease in erythrocyte number, hemoglobin and hematocrit and an increase in mean corpuscular volume and red cell distribution width in the 20 and 40 mg/kg dose groups. Liver and spleen weights were increased in the high dose groups; however, an increase in spleen cell number was not observed. Histopathological evaluation revealed splenic red pulp expansion in a mouse treated with 40 mg/kg BaP. An increase in splenic CFU-e production was observed in mice treated with 20 and 40 mg/kg BaP. A decrease in splenic total B cells, total T cells, CD4(+) and CD8(+) T cells was observed in mice treated with 20 and 40 mg/kg BaP. An increase in splenic null cells (non-T, non-B cells) was also observed in the high dose groups, consistent with extramedullary hematopoiesis. Coombs' tests, flow cytometry and an immune-mediated hemolysis assay indicated that the anemia was not autoimmune-mediated. Although no change was observed in the percentage of reticulocytes in these animals, further bone marrow analysis is needed to determine if the anemia is due to bone marrow suppression, possibly caused by BaP exposure, or chemical-induced hemolysis, perhaps contributed to by erythrocyte fragility inherited from a parent strain, NZB, which spontaneously develops autoimmune hemolytic anemia and subsequent splenomegaly.

Anemia↗
PubMed2006

Etiology of anemia in patients with advanced heart failure.

OBJECTIVES: We prospectively investigated the causes of anemia in patients with advanced congestive heart failure (CHF). BACKGROUND: Anemia is common in patients with advanced CHF, and its etiology is generally considered to be multifactorial. However, despite its importance, precise information is lacking regarding the prevalence of putative etiologic factors. METHODS: Patients who were hospitalized for decompensated advanced CHF and who were stabilized after their initial treatment underwent evaluation of "clinically significant" anemia, defined as a hemoglobin content <12 g/dl for men and <11.5 g/dl for women. Patients with a serum creatinine concentration >3 mg/dl or patients with concurrent diseases that are known to cause anemia were not included. The initial evaluation included measurements of vitamin B(12), folic acid, thyroid-stimulating hormone, erythropoietin, lactate dehydrogenase, Coombs test, multiple fecal occult tests, and bone marrow aspiration. Patients without diagnosis by these methods underwent red cell mass measurement with (51)Cr assay. RESULTS: The mean age of the 37 patients was 57.9 +/- 10.9 years and mean left ventricular ejection fraction 22.5 +/- 5.9%. Iron deficiency anemia was confirmed by bone marrow aspiration in 27 patients (73%), 2 patients (5.4%) had dilutional anemia, and 1 patient (2.7%) had drug-induced anemia. No specific cause was identified in 7 patients (18.9%) who were considered to have "anemia of chronic disease." Serum ferritin for the iron-deficient patients was not a reliable marker of iron deficiency in this population. CONCLUSIONS: In this group of patients, iron deficiency was the most common cause of anemia. The iron status of patients with end-stage chronic CHF should be thoroughly evaluated and corrected before considering other therapeutic interventions.

Aged↗
PubMed2004

Transient antiphospholipid syndrome in an infant with segmental small bowel infarction.

The clinical picture of venous or arterial thrombosis in the presence of circulating antiphospholipid antibodies is referred to as the antiphospholipid syndrome. A 5-month-old baby girl who was quite healthy so far was referred to our clinic with irritability, vomiting, and abdominal distension for 30 hours. Surgical exploration exposed a gangrenous ileal segment about 15 cm long. The postoperative period was unremarkable. Investigation to identify the risk factors for mesenteric thrombosis found anticardiolipin antibodies (isotype Ig G) and decreased protein C level. Protein S and antithrombin III were within normal levels. Hb electrophoresis results showed no HbS, and neither Factor V Leiden nor prothrombin 20210 mutations were detected. Eight months postoperatively, anticardiolipin antibodies were found within normal levels. Lupus anticoagulant, ds DNA, and ss DNA were negative. Direct coombs test and protein C, C3, and C4 were also within normal levels. She had no thrombotic episode in the 24 months postoperatively, although no anticoagulant medication was administered. To the authors' knowledge this case is the first report of segmental intestinal infarction in transient antiphospholipid syndrome in the pediatric population.

Antibodies, Anticardiolipin↗
PubMed1996

Safety of cefepime: a new extended-spectrum parenteral cephalosporin.

The purpose of this study was to compare the safety profile of cefepime, a new extended-spectrum, fourth-generation cephalosporin used to treat mild-to-severe bacterial infections, with that of ceftazidime. A total of 2,032 patients enrolled in North American and European cefepime trials were analyzed. The study population spanned adolescence to the elderly (15-100 years); the median age was 62 years. Cefepime was compared with ceftazidime (1,456 patients), a third-generation cephalosporin. Cefepime dosing was 1-4 g/day (0.5-2.0 g twice daily) for adults; ceftazidime dosing was 1-6 g/day (0.5 g every 12 hours to 2.0 g every 8 hours). A limited number of cefepime-treated patients received 2 g every 8 hours. The median length of dosing for both cefepime and ceftazidime was 7 days. In randomized trials in which cefepime (2,032 patients) was compared with ceftazidime (1,456 patients), analysis of comparative data indicated that adverse events of probable or unknown relation to study drugs were observed in 13.8% of cefepime patients and 15.6% of ceftazidime patients. The most commonly observed adverse event for cefepime was headache (2.4%), followed by nausea (1.8%), rash (1.8%), and diarrhea (1.7%). For ceftazidime, the most commonly observed adverse event was diarrhea (3.2%), followed by headache (2.5%), nausea (2.1%), rash (1.9%), and constipation (1.5%). The incidence of positive Coombs' test was higher in high-dose cefepime recipients than in ceftazidime recipients (14.5% vs 8.7%; p = 0.043), although there was no evidence of hemolysis in either treatment group. Coadministration of analgesics, diuretics, and anticoagulants did not increase incidence of adverse events associated with study-drug therapy. Adverse renal and hematologic events, as well as anaphylaxis and death, were rare in both groups. In the comparative trials with cefepime, anaphylaxis was reported in no patients receiving cefepime and in one patient receiving ceftazidime. None of the three seizures reported in patients receiving cefepime and one of six seizures in patients receiving ceftazidime were of probable or possible relationship to the study drugs. None of the 12 cases of gastrointestinal hemorrhage reported in cefepime patients or five cases reported in ceftazidime patients were judged to be related to treatment drug. Tolerance for intravenous administration in both treatment groups was similar. Cefepime did not effect any significant or unusual allergic, hematologic, gastrointestinal, neurologic, or renal toxicity when administered to patients with mild-to-severe infections, including those receiving concomitant medications. The safety profile of cefepime is excellent and comparable to that of ceftazidime and those reported for other cephalosporins.

Adolescent↗
PubMed1996

Synthesis and application of alpha-D-mannosyl clusters as photoaffinity ligands for mannose-binding proteins: concanavalin A as a model receptor.

Mono-, di-, and tri-antennary alpha-D-mannopyranosyl derivatives were synthesized as oligosaccharide mimics. The compounds vary in the length of the acyclic aglyconic spacers linking, in the case of the di- and tri-antennary derivatives, the glycosyl endgroups. By haemagglutination assay (Coombs test) the affinity of the alpha-D-mannopyranosyl ligands against Con A was determined in comparison with methyl alpha-D-mannopyranoside. Affinity enhancement and strong cross-linking capacity were found with the di- and tri-antennary compounds where alpha-D-mannopyranosyl endgroups are separated by spacers of 5-37 atoms in length. The optimal ligand had Ki of 5.1 microM in comparison with 3.12 microM for methyl alpha-D-mannopyranoside. The monoantennary compound and, to certain extents, one di- and short tri-antennary ligands with short spacer lengths did not differ significantly in affinity from methyl alpha-D-mannopyranoside. A triantennary, radiolabelled ligand equipped with a photolabile diazirino group was used to covalently modify Con A by photoaffinity labelling. A significant degree of covalent cross-linking of Con A monomers was observed.

Affinity Labels↗
PubMed1981

Severe giant cell hepatitis with autoimmune hemolytic anemia in early childhood.

Four children, aged 6 1/2 months to 2 years, presented with liver disease and autoimmune hemolytic anemia. Clinical signs included fever, jaundice, firm or hard hepatomegaly, and splenomegaly. Direct Coombs test results were of the mixed (IgG + C) type. Liver function tests showed high direct bilirubin transaminase, and serum gamma globulin values, and a prolonged prothrombin time. The liver histology was characterized by marked lobular fibrosis and giant cell transformation. The course of the disease was severe, resulting in the death of three patients from liver failure. However, the liver disease seemed responsive to corticosteroid treatment, which in one patient was clearly beneficial.

Anemia, Hemolytic, Autoimmune↗
PubMed1980

Immune Hemolytic anemia.

Immune hemolytic anemia is an acquired anemia resulting from the premature destruction of red cells caused by the presence of antibody and/or complement on the red cell surface. The Coombs test, modified and improved, remains the mainstay of diagnosis.

Adrenal Cortex Hormones↗
PubMed1991

Immunology and clinical importance of antiphospholipid antibodies.

Having reviewed the literature on the association of aPL antibodies with clinical manifestations, it is clear that this group of autoantibodies are of considerable importance. The presence of aPL antibodies in some but not all individuals confers a risk of a clinical syndrome characterized by recurrent arterial or venous thrombosis, thrombocytopenia, hemolytic anemia, or positive Coombs' test, and in females, recurrent idiopathic fetal loss. In SLE, the risk is approximately 40%, compared with a risk of 15% in the absence of aPL antibodies. However, only one half of persons possessing these antibodies have SLE, and overall the risk is around 30%. In some circumstances, such as in chlorpromazine or infection-associated aPL antibodies, there appears to be no increased risk. At the other end of the spectrum are seen patients whose only clinical manifestations comprise features of this clinical syndrome, and this entity has been designated the primary antiphospholipid syndrome (PAPS). aPL antibodies are also important because they are not uncommon. They have been found frequently in women with idiopathic recurrent fetal loss (30%), in non-autoimmune patients with ischemic heart disease (20%), or venous thrombosis (up to 30%), or stroke (4-47%), and in chronic immune thrombocytopenia (30%). These autoantibodies can be detected using sensitive solid-phase immunoassays employing the CL antigen, or in appropriate coagulation tests to detect LA activity. These assays are simple to perform but require care in selection of the best test and in interpretation of results. Current tests do not distinguish between those persons at risk of the clinical events and those not at risk. Detection of specific isotypes (especially IgG) and antibody level may aid in such a designation. Treatment of aPL antibody-associated syndromes remains a controversial subject. Since thromboses are associated with significant morbidity and potential mortality, there is a good argument for long-term preventive antithrombotic therapy, at least for as long as the antibodies are detectable, in those patients in whom clinical complications have previously occurred. It is not generally recommended that this treatment be offered to individuals in whom aPL antibodies are detected but who have not suffered previous thromboses, since the risk of such events does not appear to be equal within a group of aPL antibody-positive persons. This particularly applies to pregnant women, since live births and uncomplicated pregnancies are observed regularly in the presence of aPL antibodies without specific treatment. A previous history of at least one unexplained, late fetal loss is considered a prerequisite before intervention in subsequent pregnancies.(ABSTRACT TRUNCATED AT 400 WORDS)

Anemia, Hemolytic↗
PubMed1978

Immunologic methods for the detection of humoral and cellular immunity.

A variety of immunologic techniques have been introduced during the past few years. Many of these techniques are being applied to clinical specimens in an attempt to help the practicing veterinarian make a diagnosis. The introduction of new techniques requires extensive testing with clinically normal and diseased patients. It is essential for the practicing veterinarian to understand that the techniques available for the detection of immunologic disorders in the dog and cat are not routine diagnostic procedures and that adequate information has not been developed for any of the techniques described to assure the clinical significance of either positive or negative results (Table 3). This should not discourage the practitioner from submitting samples, but should encourage him or her to question the significance of those results and to attempt to correlate them with history and clinical signs before arriving at a final diagnosis.

Agglutination Tests↗
PubMed1984

The serological responses of calves to live Salmonella dublin vaccine--a comparison of different serological tests.

The serological responses to live Salmonella dublin vaccine was assessed in three groups of calves; three-day-old colostrum-deprived (3DO C-), three-day-old colostrum-fed (3DO C+) and three-month-old (3MO), by the following tests; serum agglutination test (SAT), indirect haemagglutination test (IHA), complement-fixation test (CFT) and antiglobulin test (AGT). Serological activity was detected by all the tests in the 3MO calves. In the 3DO C+ calves no serological activity was detected by either the somatic SAT or IHA but low levels of CF and somatic AGT antibodies were produced. In 3DO C- calves serological activity, often at low levels, was detected by all the tests except the somatic SAT. High levels of flagellar agglutinins were detected in both groups of 3DO calves. It was concluded that with the exception of the flagellar SAT the tests were affected by the age of the calf and in 3DO calves also by the presence of colostral antibodies. However, the use of the SAT in 3MO calves would provide an indication as to the potency of salmonella vaccines.

Agglutination Tests↗