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)

A 34-year-old man presented with classic glucagonoma syndrome manifested by weight loss, dermatitis, stomatitis, anemia, and mild diabetes mellitus. The diagnosis of glucagonoma was made by light and electron microscopic demonstration of a metastatic alpha cell carcinoma in a liver biopsy specimen. Plasma glucagon concentration was abnormally high. The patient also had symptoms and signs of involvement of the central nervous system. Radionuclide and CAT scans of the brain, negative CSF cytology and myelography excluded the possibility of metastases or other space-occupying lesions. Glucagon was demonstrated in the CSF. We postulate that the neurologic symptoms were due to direct or indirect effect of this hormone on the brain. Following therapy with streptozotocin and 5-fluorouracil, the patient had a subjective and objective clinical and hormonal remission of his disease including amelioration of his neurological impairment.
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PMID:Neurologic involvement in glucagonoma syndrome: response to combination chemotherapy with 5-fluorouracil and streptozotocin. 22 32

The dialysis encephalopathy syndrome has a geographical distribution related to the aluminium content of the dialysis water supply. There is a close relationship between concentrations of water aluminium and serum aluminium, and patients with dialysis encephalopathy have serum aluminium concentrations greater than 400 microgram/litre. High serum aluminium is also associated with osteomalacic bone disease, and worsening anaemia. In dialysis encephalopathy, elevated concentrations of aluminium are found in CSF and in grey matter, and an aluminium burden of 2-8 g is calculated from whole body in vivo analysis. There is sufficient evidence for an aluminium toxicity syndrome to warrant specific removal of aluminium by water purification systems.
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PMID:Aluminium studies in dialysis encephalopathy. 74 Jun 62

The restless legs syndrome could represent a folate responsive disorder in both patients with acquired-folate deficiency and those with familial symptomatology. Patients with acquired folate-deficiency could be divided into two subgroups. (i) those with minor neurological signs (restless legs syndrome, vibration sense impairment and tactile hypoesthesia in both legs with diminished ankle jerks and a prolonged or assymetrical Achilles-reflex time) and (ii) those with major neurological signs (subacute combined degeneration with or without neuropathies). In some of these patients the classical triad of the malabsorption syndrome is replaced by another triad, constipation, abnormal jejunal biopsy and abnormal d-xylose absorption. A low folic serum acid level could induce minor neuropsychiatric symptoms while an additional low CSF folate could induce major neurological symptoms in spite of the presence of a normal erythrocyte folate level and in the absence of frank anemia. Possible further studies are described.
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PMID:Folate deficiency and neurological disorders in adults. 95 35

Hematopoietic growth factors were found as factors stimulating hematopoietic colony formation in in vitro culture system using bone marrow cells as a source of hematopoietic progenitor cells. Erythropoietin, a growth factor stimulating erythroid lineage has now been clinically used as an therapeutic agent for anemia of chronic renal failure. Macrophage colony-stimulating factor (M-CSF), a growth factor stimulating the production of leukocytes including monocytes and neutrophils has been clinically used as an agent for leukopenic patients after anti-cancer therapy. M-CSF improves a survival rate after bone marrow transplantation (BMT) through the reduction of mortality rate associated with BMT such as bleeding, engraftment failure and GVHD. M-CSF accelerated platelet production when injected to thrombopenic patients with solid tumor after anticancer therapy. Granulocyte CSF (G-CSF) is a most powerful agent for various kinds of neutropenia such as neutropenia after anti cancer therapy, neutropenia after BMT, aplastic anemia, chronic neutropenia of children and myelodysplastic syndrome. However, since G-CSF stimulates growth of leukemic cells in vitro, careful observations should be required when clinically used on leukemic patients. Clinical studies of granulocyte-macrophage CSF (GM-CSF) and interleukin 3 (IL-3) are now in progress, in which a promoting activity of leukocyte production of these factors is evaluated.
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PMID:[Clinical application of hematopoietic growth factor (IL-3, G-CSF, GM-CSF, and EPO)]. 127 40

Sera of 25 healthy controls and 75 patients suffering from myelodysplastic syndromes (MDS) were investigated for serum concentration of interleukin-1 alpha (IL-1 alpha), IL-3, IL-6, granulocyte-colony-stimulating factor (G-CSF), granulocyte-macrophage-CSF (GM-CSF), erythropoietin (Epo), and tumor necrosis factor-alpha (TNF-alpha). According to French-American-British (FAB) classification, 21 refractory anemia (RA), seven refractory anemia with ring sideroblasts (RARS), 15 chronic myelomonocytic leukemia (CMML), 12 refractory anemia with excess of blasts (RAEB), and 20 RAEB in transformation (RAEBt) were examined. TNF-alpha levels were inversely correlated with lower levels of hemoglobin concentration (r = -0.31, p = 0.005), irrespective of the requirements for transfusion in anemic MDS patients. Significant differences in TNF-alpha levels between CMML (26.2 +/- 5.9 pg/ml) and the FAB subgroups (16.1 +/- 1.6 pg/ml) were detected. There was an overall inverse relationship between the level of erythropoietin and the degree of anemia, but a wide range of Epo response between patients with similar hemoglobin concentrations. Serum levels of IL-1 alpha and GM-CSF were undetected in most of the patients. In 57% of the samples there were detectable levels of G-CSF, without a correlation of the serum levels with blood cell counts, nor with any of the FAB subcategories. Overall, 29% and 25% of the patient sera exhibited elevated IL-3 and IL-6 levels, respectively. There was no correlation of the serum levels with any of the blood counts, other cytokines, nor FAB subcategories. In conclusion, simple negative feedback mechanism between a specific cytokine and the production of blood cells seems not to be the case in MDS, except for red cell production and erythropoietin concentration. Our data may suggest the involvement of TNF-alpha in the pathogenesis of anemia in MDS.
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PMID:Measurement of serum cytokine levels in patients with myelodysplastic syndromes. 128 Jul 51

A case of B cell lymphoma with clinical and histological features of malignant histiocytosis was described. A 57-year-old male was admitted to Shinshu University Hospital because of transverse myelopathy. Five months before admission, he noticed urinary disturbance, which progressed to urinary obstruction. The following month, bilateral muscular weakness appeared in his legs. A few days later he could not stand up, and was admitted to a local hospital. Neurological examination revealed sensory disturbances below the level of Th12 in all modalities, and marked weakness and hyperreflexia in the lower limbs. A spinal tumor was suspected. However, myelography showed no abnormality. The patient's condition worsened and he became bed-ridden in February 1990. He was transferred to Shinshu University Hospital for further evaluation. On admission he was poorly nourished with fever, anemia, hepatomegaly, and bilateral pretibial pitting edema. No lymphadenopathy was observed. Neurological examination showed total sensory loss below the level of Th12, spastic paraplegia, hyperreflexia in the legs, and urinary obstruction. Laboratory findings revealed an elevated erythrocyte sedimentation rate, increased CRP, pancytopenia, and hypoalbuminemia. Serum level of IgG, IgA, IgM, LDH, ALP, GPT and total bilirubin were increased. CSF and MRI imaging of the spinal cord were normal. Proliferation of atypical histiocytes with marked erythrophagocytosis, which is a characteristic pathological feature of malignant histiocytosis, was observed in peripheral blood and aspirated bone marrow. Immunoenzyme staining of bone marrow using monoclonal antibody L-26, which is a B-cell marker, revealed B-cell lymphoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of B-cell lymphoma with clinical and histological features of malignant histiocytosis]. 130 24

The usual first-line treatment for Trypanosoma brucei gambiense sleeping sickness is melarsoprol, but when that fails the outlook has hitherto been grim. The polyamine synthesis inhibitor eflornithine (difluoromethylornithine, DFMO) has emerged as an alternative therapy. 207 patients with late-stage T b gambiense sleeping sickness were treated in rural Zaire with three different regimens of DFMO in an open-trial design. During treatment, trypanosomes disappeared from the CSF of all 87 patients in whom parasites had been seen before DFMO administration, and there was a sharp fall in CSF white cell count from a mean of 186/microliters to 21/microliters. 152 patients have been followed for at least a year after DFMO treatment, and only 13 (9%) have relapsed. Treatment failures were more common in children less than 12 years, among patients treated with oral DFMO only, and among patients who received DFMO as the initial treatment of their recently diagnosed trypanosomiasis. Toxicity was acceptable. Only 4 patients died during or shortly after treatment. Bone marrow suppression resulting in anaemia (43%) or leucopenia (53%) was common but bore little consequence. This open trial shows that DFMO is as active as and possibly less toxic than melarsoprol. For economic and logistic reasons DFMO may not be the first-choice therapy in rural Africa but for the vast majority of patients who relapse after melarsoprol DFMO will be curative.
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PMID:Efficacy and toxicity of eflornithine for treatment of Trypanosoma brucei gambiense sleeping sickness. 135 19

A systemic necrotizing vasculitis of unknown etiopathogenesis may be termed juvenile polyarteritis syndrome (JPS). The syndrome has been recognized primarily in young Beagles used for toxicologic studies. We studied 9 young Beagles with JPS. Affected dogs had fever (40 to 41.5 C), anorexia, and signs of pain in the cervical area. They had a characteristic hunched stance, and were unwilling to move. Laboratory abnormalities in all dogs included nonregenerative anemia, hypoalbuminemia, and leukocytosis characterized by a mature neutrophilia. Analysis of CSF revealed a moderate to severe neutrophilic pleocytosis and a mildly high protein concentration in most dogs. Signs of disease resolved rapidly with high doses (2.2 mg/kg of body weight, PO) of prednisone. If untreated, clinical signs and laboratory abnormalities had a remitting and relapsing course in most dogs. Findings at necropsy included necrotizing arteritis with fibrinoid necrosis, periarteritis, thrombosis, and intimal proliferation that most frequently affected small- to medium-sized vessels in the cervical spinal cord, mediastinum, and heart. An immune-mediated pathogenesis for this disease is suspected.
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PMID:Systemic necrotizing vasculitis in nine young beagles. 136 39

This investigation is retrospective and comprises 20 patients with bone-marrow insufficiency. During the period 1.4.1988-1.3.1991, these patients were treated with erythropoietin (Epo), the granulocyte-macrophage-colony-stimulating factor (GM-CSF) or the granulocyte-colony-stimulating factor (G-CSF). Thirteen patients had primary bone-marrow insufficiency: six had the myelodysplastic syndrome, three had primary myelofibrosis, two aplastic anemia and two myelomatosis. On account of dominating symptoms of anemia, five patients received Epo while eight received GM-CSF as part of an extensive clinical trial of this preparation. Seven patients with relapse of the haematological malignant disease had bone-marrow insufficiency and pancytopenia secondary to intensive chemotherapy/irradiation: four of these patients received GM-CSF and two received G-CSF with the object of increasing bone-marrow regeneration and to render further chemotherapy possible. One patient received GM-CSF with the object of improving bone-marrow function after autologous bone-marrow transplantation. Treatment with Epo for ten months combined with treatment with interferon for six months resulted in normalization of the haemoglobin concentration in one patient with bone-marrow insufficiency on account of primary myelofibrosis. Treatment with Epo for briefer periods in lower doses was without effect in four other patients with primary bone-marrow insufficiency. Treatment with GM-CSF and G-CSF resulted in neutrophil leukocytosis in 12 out of 15 patients (80%) and, in six out of 14 patients (43%), increased marrow cellularity was demonstrated by means of histological examination of the bone-marrow. One patient showed normal haemoglobin levels during treatment with GM-CSF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hematopoietic growth factors in primary and therapy-related bone marrow insufficiency]. 137 68

Anemia and neutropenia are common complications of HIV infection. Antiretroviral therapy with zidovudine exacerbates bone marrow suppression by inhibiting proliferation of blood cell progenitor cells. In addition, treatment for opportunistic infections or malignancies can involve the use of myelosuppressive drugs. As a consequence, severe anemia and neutropenia can result, thereby limiting the utilization of antiretroviral drugs. Since antiretroviral therapy can increase survival, drugs that ameliorate myelosuppression are important adjuncts in the treatment of HIV-infected patients. Three hematopoietic growth factors are effective in the treatment of anemia or neutropenia. In four placebo-controlled trials, erythropoietin (EPO) at doses up to 600 U/kg/wk decreased mean transfusion requirements by 37%, increased mean hematocrit by 4.5% and corrected anemia in the majority of patients receiving zidovudine over a 12-week period. In a separate study, granulocyte colony-stimulating factor (G-CSF) corrected leukopenia and isolated neutrophil defects in 22 patients with AIDS without altering HIV expression. When erythropoietin was added to the regimen, combined G-CSF and EPO corrected both anemia and leukopenia and lessened subsequent zidovudine toxicity. Similarly, granulocyte macrophage-colony-stimulating factor (GM-CSF) corrected leukopenia and pre-existing neutrophil defects in patients with HIV infection. In controlled and uncontrolled trials, GM-CSF also appears to reduce toxicity from zidovudine, ganciclovir, and antineoplastic therapy. New combinations of hematopoietic stimulants are being used to decrease the toxicity from combination antiretroviral therapy with alpha interferon and cytotoxic chemotherapy in the treatment of AIDS-related malignancies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hematopoietic growth factors as adjuncts to antiretroviral therapy. 138 Feb 56


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