Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of peripheral T-cell lymphoma classified, according to the updated Kiel classification, as a large pleomorphic T-cell lymphoma with a high content of reactive histiocytes and blood hypereosinophilia is reported. Light microscopic examination revealed a diffuse effacement of the lymph node structure by large pleomorphic lymphoma cells mixed with eosinophils and many histiocytes, some of them presenting discrete features of hemophagocytosis. The neoplastic cells were CD3, CD5, CD8 and HLA-DR positive but failed to show CD30 antigen. DNA molecular analysis displayed simultaneous rearrangements of the genes coding for the delta chain of the T-cell receptor and for the Ig heavy chain. Increased serum levels of angiotensin converting enzyme and ferritin were found and probably induced by the reactive histiocytes. Immunoassays (ELISA) with antibodies directed against some cytokines and against the Tac peptide (sIL-2R) were performed. They demonstrated high serum levels of sIL-2R and a slight increase in GM-CSF, but neither IL-5 nor IL-3. The association of blood hypereosinophilia and histiocytic hyperplasia with a peripheral T-cell lymphoma is discussed.
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PMID:A case of pleomorphic T-cell lymphoma with a high content of reactive histiocytes presented with hypereosinophilia. 747 65

A number of cytokines have been implicated in the suppression of myeloid stem and progenitor cell proliferation. It has been suggested that some of these act directly on the stem/progenitors themselves, based on the effects of these cells, plated in culture at low seeding densities, on highly enriched populations. These studies, however, do not definitively rule out effects on accessory cells. To more rigorously evaluate direct-acting suppressive effects of cytokines, such cytokines were assessed for their effects on colony formation initiated by single bone marrow (BM) or umbilical cord blood (CB) CD34 cells sorted into single wells in the presence of a combination of growth-stimulating cytokines (erythropoietin [Epo], steel factor [SLF], granulocyte-macrophage colony-stimulating factor [GM-CSF], and interleukin-3 [IL-3]) and in the presence or absence of serum. Under these conditions, it was demonstrated that H-ferritin, transforming growth factor-beta 1 (TGF-beta 1), and members of the chemokine family (macrophage inflammatory protein-1 alpha [MIP-1 alpha], MIP-2 beta, platelet factor 4 [PF4], IL-8, and macrophage chemotactic and activating factor [MCAF]) had direct significant suppressive activities on single stem/progenitor cells from adult human BM in the presence or absence of serum. Single sorted CB cells were much less sensitive to inhibition by these cytokines. The reasons for this differential sensitivity are not known. Of possible relevance to this for cytokines, such as H-ferritin and the chemokines that have actions during S-phase of the cell cycle, CB progenitors were in slower cycle at initiation of culture than were BM progenitors.
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PMID:Comparative effects of suppressive cytokines on isolated single CD34(3+) stem/progenitor cells from human bone marrow and umbilical cord blood plated with and without serum. 769 34

Iron is believed to play a role in the pathogenesis of both Parkinson's disease (PD) and Alzheimer's disease (AD). We measured ferritin, which is considered to be the iron storage protein, in CSF of patients with PD, AD, and multiple system atrophy (MSA) as well as control subjects. We found a significant increase in CSF ferritin in AD compared with both PD and age-matched controls. No significant differences were found between PD patients with dementia (PDD) and non-demented PD patients. For non-demented PD patients a positive correlation between CSF ferritin and age was found. Our results may indicate that iron has a role in the pathophysiology of AD.
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PMID:Cerebrospinal fluid ferritin levels of patients with Parkinson's disease, Alzheimer's disease, and multiple system atrophy. 771 Jun 63

Superficial hemosiderosis (SH) of the CNS is a rare disease caused by repeated subarachnoid hemorrhage, with progressive superficial siderosis of the CNS. We report a patient with SH whose clinical picture was marked by progressive gait ataxia, hearing loss, dysarthria, and recurrent episodes of hemifacial spasm. Iron and ferritin levels in the CSF were significantly higher than in a control group of patients. Six month's treatment with the iron-chelating agent trientine dihydrochloride led to clinical improvement, with a concomitant reduction of CSF iron level. We suggest that, in addition to magnetic resonance imaging findings, CSF levels of iron and ferritin should be used as diagnostic criteria for SH, as well as to estimate the efficacy of iron chelation treatment.
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PMID:Superficial hemosiderosis of the central nervous system. 855 30

The purpose of this study was to improve erythropoiesis in patients with anemia due to myelodysplastic syndromes (MDS). We treated 13 patients first with recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) for 6 weeks, then with recombinant human erythropoietin (rhEpo) and rhGM-CSF for the next 12 weeks. Five patients had refractory anemia (RA), 3 refractory anemia with ringed sideroblasts (RAS), and 5 refractory anemia with excess of blasts (RAEB). Ten patients were transfusion-dependent at the time of inclusion. Eleven patients completed this phase II study. Five responded with an increase in hemoglobin level (3 patients) or a reduction in transfusion requirement (2 patients). We registered no response in the remaining 6 patients during treatment. Patients responding to combined treatment had relatively low concentrations of plasma Epo and plasma ferritin before treatment with rhEpo and a normal karyotype throughout the study. Long-term bone marrow cultures did not predict the response. Still, responders seemed to have a higher number of colony-forming progenitors than nonresponders. In conclusion, combined therapy with rhGM-CSF and rhEpo may stimulate hematopoiesis and correct or improve anemia in some patients with MDS.
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PMID:Recombinant human granulocyte-macrophage colony-stimulating factor plus recombinant human erythropoietin may improve anemia in selected patients with myelodysplastic syndromes. 823 92

Peptide-specific IgG from a rabbit immunized with an alanine-lysine-proline-arginine ((ALA1)-tuftsin) containing 14-mer "ferritin" peptide neutralized rat liver ferritin inhibition of in vitro CSF-1-dependent monocytopoiesis. Antiferritin IgG similarly neutralized the inhibitory effect of ferritin but did not neutralize peptide inhibition of the in vitro myelopoietic response. No cross-reactivity between the respective antibodies and Ag was detected either by Western immunoblot or by competitive ELISA. Depletion of adherent cells before marrow cell culture significantly reduced the inhibitory effect of ferritin but did not influence peptide inhibition of CSF-1-stimulated colony formation. Adherent marrow cells and P388D1 cells treated with both CSF-1 and ferritin, but not either alone, produced inhibitory supernatant culture media that were neutralized by antipeptide but not antiferritin IgG. High resolution molecular sieve chromatography of the inhibitory adherent marrow cell and P388D1 supernatants resolved two peaks of 50 to 60 kDa and approximately 30 kDa in each. The inhibitory activity in all four peaks was neutralized by antipeptide but not antiferritin IgG. The ferritin/CSF inhibitors were not further characterized although identity with IL-6, IL-8, TNF-alpha, transforming growth factor-beta, and IFN-alpha/beta could be eliminated. The results indicate that ferritin inhibition of CSF-1-dependent monocytopoiesis is mediated by an endogenously produced inhibitor, or inhibitors, that shares antigenic similarity with the (ALA1)-tuftsin-containing 14-mer peptide and that adherent marrow cells, most likely monocytes or macrophages, produce the endogenous inhibitors in response to both CSF-1 and ferritin.
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PMID:Cytokine mediation of the suppressive effect of ferritin on colony-stimulating factor-1-dependent monocytopoiesis. 849 5

The aim of this randomized, comparative, double-blind study was to determine the efficacy of zidovudine (ZVD) either alone or in combination with recombinant granulocyte-colony stimulating factors (rG-CSF) and erythropoietin (Epo) in asymptomatic HIV-infected subjects with a CD4+ cell count < 500/mm3, classified as CDC II stage. We recruited 20 HIV Ab+ asymptomatic patients who were randomized into two groups: A and B. Group A was treated with ZVD at the dosage of 500 mg daily in combination with rG-CSF (10 micrograms/Kg/biweekly) and Epo (50 IU/Kg/biweekly). Group B was treated with ZVD (500 mg/day) alone. The primary end-point was progression to an AIDS-defining event and the secondary end-point included changes in the CD4+ cell count, p24 Ag status, beta-2-microglobulin, and ferritin levels. The patients of Group A showed no significant changes in transaminase, ferritin and beta-2-microglobulin levels while CD4 cells, Hb and neutrophil levels increased significantly compared to Group B (p < 0.001) and baseline values (p < 0.05). Conversely, 5 patients in Group B showed a significant decrease in CD4 cells (p < 0.01), Hb and neutrophil levels (p < 0.01) compared to baseline values, while beta-2-microglobulin increased (p < 0.05) compared to initial values. Our preliminary study may indicate that the combination of zidovudine with these hematopoietic growth factors could reduce the possibility of virus-related hematologic toxicity and could be more efficacious than zidovudine alone in prolonged therapy.
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PMID:Combined therapy with zidovudine, recombinant granulocyte colony stimulating factors and erythropoietin in asymptomatic HIV patients. 883 12

The plasma concentrations of erythropoietin (Ep), soluble transferrin receptors (sTfRs), iron, total iron binding capacity (TIBC) and ferritin were monitored in five leukaemia patients undergoing autologous bone marrow stem cell transplantation (BMSCT) and in 10 lymphoma and 21 ovarian cancer patients undergoing autologous peripheral blood SCT (PBSCT); 9/21 ovarian cancer patients received recombinant human G-CSF and Ep and six recombinant human GM-CSF and Ep following SCT. All parameters were evaluated in relation to the kinetics of erythroid reconstitution as evaluated by haemoglobin (Hb) and reticulocyte levels [including the fraction of immature reticulocytes, also called highly fluorescent reticulocytes (HFR)]. Leukaemia patients undergoing BMSCT showed only a delayed (occurring at days 35-50 after SCT) and partial RBC, neutrophil and platelet recovery, whereas all patients undergoing PBSCT exhibited a rapid (occurring at days 10-15 after SCT) and sustained haemopoietic recovery. The various levels of erythroid rescue observed among these patients markedly influenced the kinetics of the different parameters investigated: (i) in leukaemia BMSCT patients sTfRs declined following SCT and remained at low levels thereafter, whereas Ep, iron. TIBC and ferritin showed a progressive and significant increase; (ii) in the different groups of patients undergoing PBSCT: (a) sTfR levels first declined following SCT and then returned to pre-therapy values at days 12-16, this response preceded erythropoietic recovery; (b) Ep, total iron, TIBC and ferritin showed an initial increase in the first days following SCT and then returned to pre-therapy values. Altogether, these observations indicate that: (i) both sTfR levels and reticulocyte counts are predictive parameters of erythropoietic recovery; (ii) coordinated changes of biochemical parameters underlying iron metabolism (iron, TIBC and ferritin) accompany erythroid rescue following SCT.
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PMID:Autologous stem cell transplantation: evaluation of erythropoietic reconstitution by highly fluorescent reticulocyte counts, erythropoietin, soluble transferrin receptors, ferritin, TIBC and iron dosages. 907 20

A 58-year-old woman developed slowly progressive hearing loss, anosmia, and unsteady gait. She had neither repeated episode of headache nor a past history of neurosurgical operation or head injury. Neurological examination revealed anosmia, moderate degree of sensorineural hearing loss. She showed loss of caloric response bilaterally. No nystagmus was found. Romberg sign was present. No cerebellar ataxia was noted in the finger-to-nose or the heel-to-knee test. No adiadochokinesis was noted. Deep tendon reflexes were increased in both upper and lower extremities. Sensation was intact. She showed disturbance of the righting reflex in the tilt-table examination. CSF were under normal pressure, xanthochromic with siderophages. CSF total protein and ferritin level were elevated. T2-weighted image (TE4000/TR100) of high field strength magnetic resonance imaging (MRI) showed marginal hypointensity of the brain stem, the Sylvian fissures, the tips of temporal lobes, anterior cerebellar surfaces and the entire spinal cord. Angiography of the cerebral vessels and spinal arteries failed to identify the source of bleeding. It seemed likely that she had lost bilateral vestibular and auditory functions caused by hemosidelin deposition to her eighth nerves which are often affected by this disorder. Her disturbance of gait and station was apparently similar to cerebellar ataxic gait, however, she did not have limb ataxia. The electronystagmogram revealed marked degree of vestibular dysfunction (VOR) and relative sparing of cerebellar function (OKN). Her disturbance of the righting reflex in the tilt-table examination and the characteristic feature of her Romberg sign with directional preponderance also indicate that the bilateral loss of vestibular functions, i.e., vestibular ataxia caused her dysequilibrium syndrome. It is our impression that vestibular ataxia might precede cerebellar ataxia commonly reported so far.
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PMID:[A case of superficial siderosis of the central nervous system with bilateral vestibular dysfunction]. 936 92

CSF and serum were obtained from 16 patients with idiopathic restless legs syndrome (RLS) and 8 age-matched healthy control subjects. Patients with RLS had lower CSF ferritin levels (1. 11 +/- 0.25 ng/mL versus 3.50 +/- 0.55 ng/mL; p = 0.0002) and higher CSF transferrin levels (26.4 +/- 5.1 mg/L versus 6.71 +/- 1.6 mg/L; p = 0.018) compared with control subjects. There was no difference in serum ferritin and transferrin levels between groups. The presence of reduced ferritin and elevated transferrin levels in CSF is indicative of low brain iron in patients with idiopathic RLS.
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PMID:Abnormalities in CSF concentrations of ferritin and transferrin in restless legs syndrome. 1076 22


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