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 66-year-old male was admitted to our hospital because of persistent fever. Laboratory data revealed leukopenia, thrombocytopenia, marked elevation of serum lactic acid dehydrogenase and ferritin levels, as well as disseminated intravascular coagulophathy (DIC). Bone marrow aspiration showed increased numbers of mature histiocytes with hemophagocytosis and a diagnosis of reactive hemophagocytic syndrome was made. In the broad spectrum of this syndrome, we suspected virus-associated hemophagocytic syndrome (VAHS) but no causative viral infection was detected. Since DIC is known to be a poor prognostic factor, he was given combination chemotherapy containing VP-16 in addition to pulse therapy of methylprednisolone. He completely recovered after the treatment. Chemotherapy is one option in the treatment of adult onset reactive hemophagocytic syndrome.
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PMID:[Reactive hemophagocytic syndrome responded to combination chemotherapy with steroid pulse therapy]. 869 75

We report the cases of six patients with AIDS in whom reactive hemophagocytic syndrome (RHPS) secondary to disseminated histoplasmosis was diagnosed. RHPS was diagnosed by established criteria, including fever (duration of > or = 7 days, with peak temperatures of > 38.5 degrees C), unexplained thrombocytopenia with anemia and/or neutropenia, and bone marrow biopsy findings of hemophagocytic histiocytosis. Disseminated Histoplasma capsulatum infection was diagnosed on the basis of the results of cultures of the bone marrow sample. The serum lactate dehydrogenase (LDH) level was elevated (> 1,000 IU/L) in all patients, and five of six patients had hyperferritinemia (range of ferritin level, 15,848-425,984 ng/mL). Five patients had features resembling severe sepsis with multiorgan dysfunction. Three patients recovered, and the findings of RHPS resolved following therapy with amphotericin B. In patients with AIDS, the combination of fever, cytopenia, elevated serum LDH level (> 1,000 IU/L), and/or hyperferritinemia (ferritin level of > 10,000 ng/mL) is a clue to the diagnosis of RHPS and disseminated histoplasmosis; bone marrow biopsy is valuable in establishing the diagnosis.
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PMID:Reactive hemophagocytic syndrome: a new presentation of disseminated histoplasmosis in patients with AIDS. 874 33

As the clinical manifestations of adult T-cell leukemia (ATL) can be quite diverse, useful indicators for the therapy and prognosis are required for the disease. In this review, the clinical and biological significance of serum tumor markers at diagnosis in ATL patients is described. Serum lactic dehydrogenase (S-LDH), serum thymidine kinase (S-TK) and serum parathyroid hormone-related protein (S-PTHrP) at diagnosis of ATL showed a correlation with among leukocyte count, absolute number of abnormal lymphocytes with polymorphic nuclei, platelet count, serum calcium and the length of survival after the initial diagnosis. Serum beta 2-microglobulin (S-beta 2M) correlated with age, platelet count and survival. A statistical correlation existed between these four serum tumor markers. Other serum tumor markers such as immunosuppressive acidic protein (S-IAP), ferritin (S-Ft) and tissue polypeptide antigen (S-TPA) showed no correlation with clinical and histological data in ATL patients.
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PMID:Clinical and biological significance of serum tumor markers in adult T-cell leukemia. 888 54

The case of a 75-year-old Japanese woman with adult-onset Still's disease who presented with cerebral haemorrhage is described. She had been in clinical remission for 2 years, after induction therapy including non-steroidal anti-inflammatory drugs, prednisolone, cyclophosphamide and mizoribine followed by auranofin, until her cerebral haemorrhage occurred, although her serum level of ferritin had gradually increased. After the onset of cerebral haemorrhage, the patient's serum level of thrombomodulin was elevated although c-reactive protein and lactate dehydrogenase were not increased. Anti-cardiolipin antibody and lupus anti-coagulant were not detected. Patients with adult-onset Still's disease are rarely reported to develop cerebral vascular disease, possibly because the disease is most frequent in young adults. The cerebral haemorrhage may have been caused by the vasculitis due to Still's disease.
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PMID:Cerebral haemorrhage complicating adult-onset Still's disease: a case report. 895 35

Two enriched populations of Leydig cells (hLCI and hLCII) have been characterized in human testes; it is noteworthy, that in the presence of hCG the steroid ouput is higher in hLCII when compared to hLCI; conversely, the basal production of steroids is greater in hLCI than in hLCII. The addition of increasing amounts of seminiferous tubule-conditioned medium to the purified Leydig cells leads to a dose-related enhancement of the steroid production in both Leydig cell fractions under basal and hCG-stimulated conditions. It is therefore obvious that a paracrine factor (or factors) from seminiferous tubular origin influences positively and with a high efficiency the human Leydig cell function. The human Sertoli cell synthesizes lactate, estradiol-17beta and several proteins, namely transferrin, ferritin and inhibin. In the presence of germ cells the Sertoli cell production of estradiol-17beta is decreased whereas the transferrin and inhibin outputs are enhanced. In addition the lactate dehydrogenase, gamma-glutamyl transpepetidase, alkaline phosphatase and creatine phosphokinase activities have been quantitated in various human Sertoli cell preparations. It should be kept in mind that germ cells exert an important influence on the adult Sertoli cell secretory activity through either direct contact and/or via secreted factors; moreover germ cells potentialize the stimulating effect of FSH on the Sertoli cell function and indirectly the Leydig cell output of testosterone via the Sertoli cell secretion of paracrine factor(s).
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PMID:Paracrine control of human Leydig cell and Sertoli cell functions. 896 55

Hemoglobin (Hb) induces heme oxygenase-1 (HO-1), which catalyzes the breakdown of heme to bilirubin, and ferritin. Rats pretreated with Hb have been shown to survive lethal doses of lipopolysaccharide (LPS; see L. Otterbein, S. L. Sylvester, and A. M. Choi. Am. J. Respir. Cell Mol. Biol. 13: 595-601, 1995). The physiological basis of this increased survival and the mechanism(s) involved in the protection against LPS by Hb are unknown. Here we investigated 1) the effects of Hb on the hemodynamic and biochemical parameters of LPS-induced tissue injury and 2) the mechanism(s) by which Hb conferred protection against shock and tissue injury. Hb-treated rats maintained normal mean arterial blood pressure, whereas control rats experienced cardiovascular collapse after a lethal dose of LPS. Hepatic and renal functions, peripheral white blood cells, serum lactate dehydrogenase, and phosphate also remained normal after LPS in Hb-treated rats. Hb also attenuated LPS-induced neutrophil alveolitis and tumor necrosis factor-alpha levels. Pretreatment with both desferoxamine, which, like ferritin, can bind iron, and with exogenous apoferritin failed to protect against LPS. In contrast, treatment with Hb plus desferoxamine, which induced HO-1 but not ferritin, did protect against LPS. Treatment with iron-dextran, which induced ferritin but not HO-1, did not protect against LPS. We conclude that Hb pretreatment reduces the inflammatory and physiological consequences of LPS and that the Hb-induced protection against LPS is dependent on HO-1 and not ferritin induction.
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PMID:Mechanism of hemoglobin-induced protection against endotoxemia in rats: a ferritin-independent pathway. 912 78

We report a 35-year-old man, who had been diagnosed with Weber-Christian disease, presented with acute onset of high fever, malaise, jaundice and hepatosplenomegaly with subcutaneous nodules. Laboratory tests showed elevated serum ferritin and liver enzymes, especially lactate dehydrogenase (LDH), with pancytopenia and coagulation abnormalities. Peripheral blood and bone marrow examinations showed erythro-, leuko- and thrombo-phagocytic histiocytes and macrophages. The patient developed the same clinical features seven years ago. Based on diagnosis of cytophagic histiocytic panniculitis, the patient was treated with steroid pulse therapy and oral cyclosporin A. The combination therapy caused a marked improvement in the clinical condition.
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PMID:A case of cytophagic histiocytic panniculitis: successful treatment of recurrent attacks with steroid pulse therapy and oral cyclosporin A. 925 59

Serum ferritin (SF) and lactate dehydrogenase (LDH) was estimated in 117 patients presenting with a breast lump and in 40 controls. Both pre and post treatment values were determined. Both the values were significantly higher in breast malignancies (p = 0.00) and also corresponded with the clinical stage and bulk of the tumour. The fall in post treatment values was proportional to the response to therapy. Persistent rise in values in the post treatment period was indicative of local recurrence of metastasis.
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PMID:Significance of serum ferritin and lactate dehydrogenase in benign and malignant disease of breast. 935 1

Searching to define diagnostic criteria for malignant and non-malignant pleural effusions, the differential diagnostic value of ferritin (FRT), haptoglobin (Hp), alpha 1-antitrypsin (alpha 1-AT), lactate dehydrogenase (LDH) and complement factors C3 and C4 were investigated prospectively in 100 consecutive patients with pleural effusions of various aetiologies. Pleural effusion FRT, C3 and C4 concentrations were found to be useful in differentiating exudates from transudates, so that transudates practically could be excluded in pleural effusion: serum FRT ratio lower than 0.5 and/or in pleural effusion values for C3 and C4 higher than 300 mg dl-1 and 70 mg dl-1, respectively. A pleural effusion: serum C3 ratio greater than 2 is seen only in malignant effusions. No discriminative pleural: serum ratio could be found in FRT and C4 values capable of differentiating malignant from non-malignant effusions. Pleural effusion alpha 1-AT and LDH values were elevated in exudates, as compared with transudates, and had an excellent sensitivity and predictive value, but low specificity, in differentiating malignant from non-malignant effusions. Finally, the sensitivity, specificity and positive predictive value of pleural effusion Hp concentrations were lower than those of FRT and complement factors C3 and C4, respectively.
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PMID:Diagnostic value of ferritin, haptoglobin, alpha 1-antitrypsin, lactate dehydrogenase and complement factors C3 and C4 in pleural effusion differentiation. 941 51

Astrocytes provide a vital protective function in the brain. These cells are also vulnerable to oxidative stress, thus their loss of function could contribute to neurodegeneration. The goal of this study is to develop a cell culture model to study oxidative stress in astrocytes. Enriched astrocytic cultures were generated from neonatal mice. tertiary-butyl hydroperoxide (t-bOOH) was used as an exogenous peroxide and lactate dehydrogenase (LDH) release as a measure of loss of viability. Exposure to t-bOOH resulted in a linear increase in astrocytic death reaching 91.2% after 4 h exposure. That cell death was due to oxidative injury, was shown by the ability of the antioxidant N,N'-diphenyl-1,4-phenylenediamine (DPPD) to protect the t-bOOH treated cells. The involvement of iron in cell toxicity was demonstrated by the ability of the iron specific chelator desferal (DF) to completely prevent t-bOOH induced LDH release. Cells treated with a lipid soluble iron compound 3,5, 5-trimethyl (hexanoyl) ferrocene (TMH-Ferrocene), were more vulnerable to t-bOOH whereas neither ferrous ammonium sulfate (FAS) nor ferric ammonium citrate (FAC) had an effect. The increased sensitivity of the cells exposed to TMHF was reversible with the iron chelator desferal. Addition of recombinant human heavy chain ferritin or human apo-transferrin (Tf) did not alter LDH release. Electron microscopic analysis indicated astrocytes exposed to t-bOOH exhibited mitochondrial swelling prior to cell death (lactate dehydrogenase release). Additional increases in mitochondrial swelling were seen when the astrocytes were exposed to the lipophilic iron compound TMH-ferrocene and t-bOOH. These studies show that astrocytes are exquisitely sensitive to oxidative stress and that their vulnerability is related to and enhanced by iron. Decreased mitochondrial function in response to oxidative stress may precede cell death.
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PMID:An in vitro model for analysis of oxidative death in primary mouse astrocytes. 955 79


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