Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parvovirus B19 (PVB19) is the causative agent of infectious erythema. In healthy children the virus causes transient erythroid aplasia, whereas in children with chronic hemolytic anemias it can cause severe aplastic crises, and in immunodeficient individuals it can produce chronic red cell aplasia. If contracted during pregnancy, the infection may induce serious damage to the fetus (abortion or hydrops fetalis). Shwachman-Diamond (S-D) syndrome, a rare autosomal recessive condition, consists of exocrine pancreatic insufficiency plus neutropenia; many patients develop either anemia or thrombocytopenia or both. We describe a newborn baby with severe congenital bone marrow failure who was diagnosed with S-D syndrome and persistence of PVB19 virus contracted by the mother in the third trimester of pregnancy.
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PMID:Severe Shwachman-Diamond syndrome and invasive parvovirus B19 infection. 894 Jul 40

We reviewed the literature on relationships between human parvovirus B19 infection and rheumatic diseases. Parvovirus B19 causes erythema infectiosum in childhood, transient anemia in immunocompetent individuals, and potentially severe infections in fetuses; laboratory evidence that the virus is directly responsible for these disorders has been obtained. Acute arthropathy meeting American College of Rheumatology criteria for rheumatoid arthritis and disorders meeting some of the classification criteria for systemic lupus erythematosus are the most striking rheumatic manifestations of parvovirus B19 infection. Purpuric lesions have also been reported. Parvovirus B19 infection may be capable of inducing a number of manifestations that have not yet been described in the literature. Although the relationship between human parvovirus B19 infection and rheumatic diseases has been the focus of many studies, compelling evidence that the virus is directly involved in the pathogenesis of rheumatic diseases has not yet been obtained.
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PMID:Parvovirus B19 infection and rheumatic diseases. 901 Sep 73

Parvovirus B19, the only known human pathogenic parvovirus, is associated with a wide range of disease manifestations. In healthy individuals, the major presentation of B19 infection is erythema infectiosum. In patients with underlying hemolytic disorders, infection is the primary cause of transient aplastic crisis. In immunosuppressed patients, persistent infection may develop that presents as pure red cell aplasia and chronic anemia. In utero infection may result in hydrops fetalis or congenital anemia. Diagnosis is based on examination of bone marrow and virologic studies. Much is known of the pathophysiology of the virus, and studies are in progress to develop a vaccine to prevent this widespread infection.
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PMID:Parvovirus B19 in human disease. 904 45

We describe postpartum onset of systemic lupus erythematosus (SLE) associated with parvovirus B19 infection in a mother presenting with fever, polyarthritis, erythema, and multiorgan involvement. B19 infection was revealed by detection of B19 DNA and IgM antibodies. In addition, our patient showed low CD4+ (384 x 10(6)/l) and CD8+ (213 x 10(6)/l) T cells, high immunoglobulin values (23.77 g/l), hypocomplementemia, thrombocytopenia, leukopenia, and anemia. Her daughter had rash associated with increasingly high B19 IgG levels and transient antinuclear and anti-ds-DNA antibodies, suggesting that both development of SLE and active B19 infection occurred in pregnancy and B19 was transmitted prenatally. A 2 year followup showed persisting polyarthritis in the mother and atopy in the daughter.
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PMID:Postpartum lupus erythematosus associated with parvovirus B19 infection. 915 91

The aim of this study was to evaluate tolerability and efficacy of Leucomax (Sandoz/Schering Plough) used for neutropenia in patients with small cell lung cancer (SCLC) treated with etoposide and cisplatin. The potential influence of granulocyte-macrophage colony stimulating factor (GM-CSF) on chemotherapy relative dose intensity (RDI) was also evaluated. The chemotherapy used was the following, cisplatin 50 mg m-2 i.v. 1 and 7 day, etoposide 170 mg m-2 i.v. 3-5 days, q 3-4 weeks. Patients received a median of six cycles (range 2-8) over 4-36 weeks (median: 20). Thirty-two consecutive patients were treated, six were excluded. Eleven patients received GM-CSF 5 micrograms kg-1 s.c. due to absolute neutrophil count (ANC), 1000/mm3 until recovery (ANC > 2000 mm3) or during 7 days, and thereafter prophylactically 24 hours post subsequent chemotherapy cycles for 7 days. Four patients received single GM-CSF course during the terminal disease phase. In 11 patients, there was no neutropenia requiring GM-CSF during the whole treatment course. Toxicity of chemotherapy was high, including thrombocytopenia, neutropenia, anaemia, mucositis, fever and hypotension. GM-CSF toxicity was the following, first dose reaction-one patient, local erythema-two patients, arthralgia-one patient, hypotension, chills, fever requiring GM-CSF discontinuation one patient RDI of cisplatin/etoposide was 0.77/0.62 in GM-CSF group, and 0.90/ 0.80 in patients who didn't receive Leucomax. Overall objective response rate to chemotherapy and complete response rate were 80% (21/26), 26% (7/26) and median survival of all patients was 10 months. Median disease free survival was 8 months. Four patients are alive, two patients lost during progression, 20 died. Administration of GM-CSF did not appear to improve RDI of chemotherapy, overall response rate (RR) nor survival in this phase I/II clinical study. RDI of chemotherapy was reduced in patients receiving GM-CSF due to thrombocytopenia and/or extrahaematologic toxicity of chemotherapy.
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PMID:Tolerability and efficacy of GM-CSF [Leucomax] in patients with small cell lung cancer treated with intensive chemotherapy. 915 70

Due to the preparative regimen necessary, bone marrow transplantation (BMT) consistently results in severe immunodeficiency, often associated with anaemia, leukopenia and thrombocytopenia. Parvovirus B19 replicates in red blood cell precursors in the bone marrow and causes erythema infectiosum ('fifth disease'), anaemia, arthritis and foetal death. We assessed the significance of B19 infections as a cause of post-BMT complications. Over 900 serial serum samples from 201 allogeneic bone marrow recipients were studied by polymerase chain reaction (PCR) and by modern serodiagnostic methods. During the first 6 months after transplantation all BMT recipients remained B19 PCR-negative. Antibody screening for B19 infections was performed up to 36 months post-transplantation. Three cases of acute B19 infection were diagnosed during the second year post-BMT. To characterize the adoptively transferred immune system we measured subclasses and avidity of anti-VP1 IgG and epitope-type specificity (ETS) of anti-VP2 IgG, which allowed functional differentiation of primary and secondary B-cell responses long after BMT. The profile of the immune response was that of a primary infection in 1 and of reinfection in 2 of the 3 acute cases. Both types were clinically mild. Infection by human parvovirus B19 is not a frequent cause of post-BMT cytopenias. The findings with the new B19 antibody markers support the concept that the donated marrow determines the type of antiviral B-cell responses.
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PMID:Primary and secondary infections by human parvovirus B19 following bone marrow transplantation: characterization by PCR and B-cell molecular immunology. 918 47

Glucagonoma is a neuroendocrine tumor of pancreatic alpha cells manifested by necrolytic migratory erythema, hyperglucagonemia, glucose intolerance, weight loss, anemia and hypopaminoacidemia. We report a case of glucagonoma in a 38 years-old patient diagnosed by the presence of a pancreatic tumor, liver metastasis, weight loss, glucose intolerance, necrolytic migratory erythema, hyperglucagonemia (1400 pg/ml; normal < 200 pg/ml) and histologic demonstration of glucagon and neurospecific enolase by immunocytochemical reaction. Actual therapeutic of glucagonoma includes surgery, chemotherapy, somatostatin or octreotide for control of the symptoms, and more recently alpha-interferon was suggested.
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PMID:[Glucagonoma: case report and literature review]. 920 30

Parvovirus B19 is usually associated with an acute, self-limited disease in children. In patients with a congenital hemolytic anemia, infection with this virus can cause an aplastic crisis. We describe such a crisis in an adult with asymptomatic hereditary spherocytosis. The association between acute red blood cell aplasia and infection with parvovirus B19 is well described in patients with hereditary hemolytic anemia, particularly sickle cell anemia. This association has also been described, although less frequently, in patients with other inherited hemolytic diseases, such as hereditary spherocytosis. In children, human parvovirus B19 causes an acute self-limited illness known as erythema infectiosum (fifth disease). In immunocompromised individuals, chronic infections can occur and cause a severe, persistent anemia. In pregnant women, infection can, but usually does not, lead to fetal infection. An infected fetus can have severe anemia, congestive heart failure, generalized edema (fetal hydrops) and even death. Most cases of aplastic crises associated with parvovirus B19 in patients with hereditary spherocytosis have been reported in children and adolescents. In this paper we describe an aplastic crisis in a 28 year old man with asymptomatic hereditary spherocytosis.
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PMID:Aplastic crisis associated with parvovirus B19 in an adult with hereditary spherocytosis. 930 16

Human parvovirus B19 (HPV-B19) has been known as the etiologic agents of erythema infectiosum in normal childhood, and chronic anemia and thrombocytopenia in immuno-compromised patients. Recently, this virus has been reported as the association with rheumatic manifestation such as rheumatoid arthritis and systemic lupus erythematosus (SLE). We described here a patient whose HPV-B19 infection was mimiking atypical symptoms of SLE at diagnosis, and was persistent because of immuno-suppressive therapy for SLE. A 34-year-old female was admitted to our hospital on 22 June 1995, presenting fever episode and cervical lymph node swelling. Before eighteen months, she was received methyl-predonisolone pulse therapy and plasma exchange by fresh frozen plasma for the treatment of Stevens-Johnson syndrome, and after several weeks these therapy she was suffered from viral infection with lymphadenopathies with a transient appearance of atypical lymphocytes in her peripheral blood smear. On laboratory examination at the present admission, her peripheral blood showed anemia, thrombocytopenia with atypical lymphocytes. Throughout her hospitalization, anti-nuclear antibody (ANA) suspected SLE including anti-DNA and anti-Sm antibody were all negative except of transient week positive ANA screening test. Her physical condition presented poor clinical course with fever elevation, increased ascites and renal dysfunction showing the elevation of CRP and circulating immune-complex (Clq binding method). Her serum was positive for IgM and IgG antibody against VP-1 and VP-2 antigen of HPV-B19 by ELISA in April 1996. And then, HPV-B19 DNA by polymerase chain reaction (PCR) was positive in bone marrow sample in March 1996, and also positive in spleen necropsy at death. We confirmed persistent chronic HPV-B19 infection by measurement of HPV-B19 IgM and IgG antibody by ELISA and HPV-B19 DNA by PCR. The plasmapheresis and administration of intravenous immunoglobulin showed the possible efficacy for her symptom throughout this clinical course. Moreover, bone marrow smear showed the finding of virus-associated hemophagocytic syndrome, and finally, she was died of cervical hemorrhage accompanied with disseminated intravascular coagulation syndrome on July 1996. HPV-B19 infection can present an atypical clinical picture that is highly suggestive of SLE. We suggest that the therapy of steroids and immuno-suppressive agents should be cautious, because these may potentially cause persistent chronic HPV-B19 infection and induced life-threatening clinical course.
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PMID:[Human parvovirus B19 infection mimicking systemic lupus erythematosus: case report]. 931 Dec 85

Nitrates, which have been used for more than a century, are the second oldest drug (after digitalis alkaloids) in the cardiological pharmacological arsenal. However, several facets of their mode of use still remain controversial. Their vasodilator and arteriolodilator action (especially in coronary vessels) and their platelet aggregation inhibitory effect make them useful drugs, particularly in all clinical forms of ischaemic heart disease (unstable or stable angina and acute myocardial infarction), for the prevention or treatment of ischaemic episodes (silent or not) and also in heart failure where nitrates are useful not only as symptomatic treatment (alone or associated with diuretics), but also in view of their positive effect on survival (associated with hydralazine: V-Heft I trial). At the present time, nitrates can be administered via the sublingual, oral, intravenous of transdermal routes in the form of nitroglycerin and isosorbide dinitrate or mononitrate (short-acting and sustained-effect forms). Their rare contraindications concern patients suffering from severe hypotension (< 70 mmHg), severe anaemia, glaucoma or intracranial hypertension. The most serious adverse effects are pulsatile headache (which usually disappear after several days), postural hypotension (possibly causing fainting), facial erythema, vertigo, palpitations or nausea and vomiting. Most of these adverse effects can be controlled by dosage adaptation and it is rarely necessary to stop treatment. However, the major problem raised by the use of nitrates concerns the development of a tolerance. The pathophysiology of this multifactorial phenomenon is still unclear. The protagonist role played by loss of SH groups or activation of humoral feedback mechanisms, with an increase of circulating catecholamine levels, activation of the R-A-A system and increased plasma volume, has been postulated. This complication can be avoided by prescribing intermittent treatment, with a drug-free interval of 10-12 hours per day. A single dose of a sustained-release preparation (60 mg of isosorbide dinitrate or 40 to 60 mg of isosorbide mononitrate), or 2 or 3 doses of a short-acting preparation (20-40 mg of isosorbide mononitrate) can be prescribed via the oral route. When the transdermal route is used, the patch should be left in place for 12 hours. Treatment should be started at low doses, which are then gradually increased. The free period is usually at night, which can be covered, when necessary, by other antiischaemic drugs (for example, beta-blockers and/or calcium channel blockers), already usually used in combination with nitrates. This interruption is not accompanied by a rebound phenomenon. It must be remembered that nitrates potentiate the action of other vasodilators and calcium channel blockers and that, in some patients, intravenous nitroglycerin reduces the anticoagulant effect of heparin, while indomethacin can inhibit their vasodilator effect. Nitrates are therefore in very good health despite their advanced age and, when used correctly, they continue to be very useful in the pharmacological treatment of cardiovascular diseases.
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PMID:[Principles and rules of the use of nitrates]. 945 73


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