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)

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in haemodialyzed patients. Two groups of haemodialyzed patients, each of which comprised 17 subjects, were examined. The first one treated by EPO (EPO group) while the second one did not receive this hormone (NO-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9 and 12 months of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex and age-matched healthy subjects. After EPO therapy an increase of the haematocrit value from 21.8 +/- 0.9% to 32.6 +/- 0.9% was observed which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the NO-EPO group a significant although less marked rise of the haematocrit value (21.4 +/- 0.4% to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose and alkaline phosphatase plasma levels as well as plasma concentrations of calcium related hormones (PTH, calcitonin, 1.25(OH)2D3) and vasopressin (AVP). EPO treatment induced a significant decline of somatotropin (HGH), prolactin (PRO), follitropin (FSH), lutropin (LH), ACTH, cortisol, plasma renin activity, aldosterone, insulin (IRI), glucagon (IR-G), pancreatic polypeptide (PP) and gastrin plasma levels and an increase of plasma estradiol, testosterone and atrial natriuretic peptide (ANP). These EPO induced endocrine alterations were restricted mostly to the first 6 months of EPO administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of long-term erythropoietin therapy on endocrine abnormalities in haemodialyzed patients. 145 6

Tiratricol has been used to suppress pituitary TSH secretion, with reported attenuation of extrapituitary thyromimetic effects. A randomized, double-blind trial was performed to define precisely the tissue-specific thyromimetic actions of tiratricol. Ten athyreotic patients, treated for thyroid carcinoma, were randomly assigned to receive L-T4 sodium 0.7 micrograms/kg daily and either tiratricol 10 micrograms/kg or placebo twice daily. The daily dose of L-T4 was increased by 25-50 micrograms increments until the TRH-stimulated TSH level was less than 0.1 mU/L. After measurement of biochemical and physiological parameters of thyroid hormone actions, patients crossed treatment groups. Patients required 46% less L-T4 to achieve equivalent TSH suppression when taking tiratricol. Hepatic effects were enhanced by tiratricol administration, with significant increases in sex hormone binding globulin and ferritin concentrations, 14% and 37%, respectively. Levels of serum cholesterol, LDL cholesterol, and apolipoprotein B were reduced by 7%, 10%, and 13%, respectively, during tiratricol therapy. Triglyceride levels also declined, but there were no changes of high density lipoprotein cholesterol or apolipoproteins AI and AII. Resting metabolic rate, body weight, urea nitrogen excretion, and symptoms did not differ between the two treatment regimens. Cardiovascular function, as reflected by mean arterial pressure and pulse wave arrival time, was not different during tiratricol therapy. Skeletal metabolic activity was affected by tiratricol, with marked elevation of osteocalcin without significant change in serum calcium, PTH, and urinary calcium and hydroxyproline excretion. Tiratricol has increased hepatic and skeletal actions of potential therapeutic value, but does not have enhanced thyromimetic activity specific to the pituitary gland.
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PMID:Organ-specific effects of tiratricol: a thyroid hormone analog with hepatic, not pituitary, superagonist effects. 151 83

Radioimmunological determinations of the tumour markers CEA, TPA, CA 19-9, ferritin and also osteocalcin were carried out in 250 patients with ablatio mammae for breast cancer over a follow-up period of at least 1 year. Metastases were detected in 49 of the 250 patients. The normal control group comprised 193 healthy persons. CEA proved to be the most valuable tumour marker, but TPA and ferritin were also significantly elevated in metastatic breast cancer. Combined determination of all 3 parameters gave the best results. Additional measurement of CA 19-9 was helpful in only one of the 49 patients with metastases in whom the 3 other parameter were negative throughout. Hence, determination of CA 19-9 appears unnecessary in breast cancer. In progressive disease the markers generally increased and fell again following successful therapy. In a few cases the opposite was found or no changes were observed. Cases with small local recurrence or an additional carcinoma at an early stage did not exhibit increased marker values as compared to patients without metastases. Not infrequently the increase in markers preceded the manifestation of metastases by several months. Very high concentrations of tumour markers signify a poor prognosis. Osteocalcin was elevated in patients with bone metastases, but not soft tissue metastases. In general, however, it paralleled the serum alkaline phosphatase level.
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PMID:[The tumor markers CEA, TPA and CA 19-9 and ferritin and osteocalcin in follow-up studies in breast cancer]. 387 42

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in hemodialyzed patients. Two groups of hemodialyzed patients, each of which comprised 17 subjects, were examined. The first group was treated by EPO (EPO group) while the second one did not receive this hormone (No-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9, and 12 month points of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex- and age-matched healthy subjects. After EPO therapy, an increase of the hematocrit value from 21.8 +/- 0.9 to 32.6 +/- 0.9% was observed, which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the No-EPO group, a significant although less marked rise of the hematocrit value (21.4 +/- 0.4 to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change plasma levels of electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose, and alkaline phosphatase as well as plasma concentrations of calcium-related hormones (PTH, calcitonin, 1,25[OH]2D3), vasopressin, and triiodothyronine. EPO treatment induced a significant decrease in somatotropin, prolactin, follitropin, lutropin, ACTH, cortisol, plasma renin activity, aldosterone, noradrenaline, adrenaline, dopamine, glucagon, pancreatic polypeptide, and gastrin plasma levels and an increase in plasma insulin, estradiol, testosterone, atrial natriuretic peptide, thyrotropin, and thyroxine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Function of endocrine organs in hemodialyzed patients of long-term erythropoietin therapy. 762 22

Subjects with thalassemia major frequently have bone disorders of debatable pathogenesis. We attempt here to analyze the relationships between siderosis and thalassemic osteodystrophy by assessing calcium-phosphorus balance, hormone-vitamin homeostasis, osteoblastic-osteoclastic activity parameters, and bone mineral density (BMD) in 30 patients with thalassemia major (16 males, 14 females, age range 17-30 years). We found a significant increase in ferritin (p < 0.001) and significant decreases in serum i-PTH, 25OHD3, 1.25(OH)2D3, osteocalcin, estradiol, testosterone and FT4 (p < 0.001) in both sexes. In all patients a net decrease of bone mineral density was documented (p < 0.001). These results were then submitted to linear regression analysis: positive correlations between BMD and FT3, testosterone, estradiol (p < 0.01), were documented, and an inverse correlation between osteocalcin and ferritin was confirmed. Our findings suggest that thalassemic osteodystrophy is the result of several inhibitory influences on osteoblastic activity and bone apposition (related to hormone deficits and siderosis) which are aggravated further by anemia, chronic hypoxia and red marrow expansion.
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PMID:[Osteodystrophy in thalassemia major]. 816 77

To define which noninvasive investigations are of value in predicting bone histology, we analyzed transiliac bone specimens (66 biopsies, 14 autopsies) from 80 uremic patients on chronic dialysis. Results were compared with values of different measurements of parathyroid hormone (PTH), alkaline phosphatase (APH), osteocalcin, calcitonin, baseline and post-deferroxamine (DFO) aluminium (Al),--beta 2 microglobulin, ferritin and bone mineral density. Among histomorphometric parameters, woven osteoid, active osteoblastic surface and resorption surface showed the best correlations with dynamic and biochemical marks of active bone metabolism. Among biochemical parameters, intact PTH and APH were better related to histomorphometric and dynamic bone parameters than other PTH measurements as well as osteocalcin, while calcitonin was related to no parameters. Stainable Al alone, and not total bone Al content was related to bone histology. Baseline Al was related to lamellar osteoid, while post-DFO Al was related to stainable Al. beta 2 microglobulin was positively related to active osteoid surface and ferritin was inversely related to the mineral apposition rate, while bone mineral density was related only to total bone volume. We conclude that, though definite diagnosis requires the use of histological methods, few simple biochemical parameters may offer insight to the bone metabolic status, useful to the physician in day to day clinical practice.
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PMID:Correlations between bone histopathology and serum biochemistry in uremic patients on chronic hemodialysis. 980 45

One of the classic histologic forms of renal osteodystrophy is osteitis fibrosa, and its distinguishing characteristic is bone marrow (BM) fibrosis, caused by the activation of marrow parenchymal cells. A bone biopsy must be performed in order to establish the diagnosis of renal osteodystrophy. The clinical use of bone biopsy is restricted, however, due to the invasiveness of the procedure. In recent studies, bone scans have provided information useful for the differential diagnosis between osteomalacia and osteitis fibrosa. However, bone scans can not provide information on the bone marrow status. Bone marrow immunoscintigraphy (BMIS) using Tc-99m anti-granulocyte antibody (AGA), a highly sensitive test for the detection of bone marrow abnormalities which is also a noninvasive method, has rarely been reported in chronic renal failure (CRF). BMIS can provide information in patients with myelofibrosis. The purpose of this study was to evaluate the usefulness of BMIS in CRF patients with special regards to biochemical parameters. Nineteen CRF patients (13 men, 6 women; mean age: 48 +/- 11 years) in whom bone scintigraphy using Tc-99m MDP (methylene diphosphonate) showed the so-called superscan pattern were included in the study. Their primary renal diseases were chronic glomerulonephritis (n = 14), diabetes (n = 4), and polycystic kidney disease (n = 1). Modes of therapies were continuous ambulatory peritoneal dialysis (CAPD) (n = 13; mean duration: 9.5 months), HD (n = 5; mean duration: 7.8 months), and conservative treatment (n = 1). BMIS using Tc-99m labeled anti-granulocyte monoclonal mouse antibody BW250/183 was performed, and the results were compared with the biochemical parameters of the patients. According to the presence of BM expansion, which may represent marrow fibrosis, the 19 patients were divided into two groups: Group I (n = 7) with BM expansion and Group II (n = 12) with normal marrow distribution. The biochemical parameters and bone markers of Group I were compared with those of Group II. There was no significant difference in biochemical parameters (blood hemoglobin, serum ferritin, erythropoietin, BUN, creatinine) between the two groups. There were no significants difference in serum calcium, phosphorus, tartate-resistant acid phosphatase (TRAP), and intact parathyroid hormone (iPTH) between the two groups. Serum alkaline phosphatase (ALP) and osteocalcin were significantly (P < 0.05) higher in Group I than in Group II. These results suggest that patients with bone marrow expansion in BMIS have increased levels of ALP and osteocalcin, indicating an increased osteoblastic activity. BMIS may be useful for the detection of bone marrow expansion due to marrow fibrosis in renal osteodystrophy, and for the evaluation of the extent of bone marrow fibrosis.
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PMID:Bone marrow immunoscintigraphy (BMIS): a new and important tool for the assessment of marrow fibrosis in renal osteodystrophy? 1064 20

We investigated the biochemical markers of bone metabolism in children with Helicobacter pylori infection. Biochemical markers of bone metabolism and serum levels of vitamin B12, ferritin and estradiol were measured in 41 H. pylori-positive (+) children (23 girls, 18 boys; aged 11.8+/-3 years). Serum levels of intact parathyroid hormone, ss-collagen I carboxy terminal telopeptide, total alkaline phosphatase (ALP), bone-specific ALP, N-terminal cross-links of human procollagen type I, N-mid-osteocalcin, calcium, phosphate, ferritin, and estradiol did not differ significantly between H. pylori(+) and H. pylori negative (-) children. Vitamin B12 levels were significantly decreased in H. pylori(+) compared to H. pylori(-) children. H. pylori infection was not accompanied by significant changes in markers of bone metabolism in children, although vitamin B12 levels were decreased. Further studies are required to clarify whether H. pylori infection causes time-dependent changes in bone turnover markers during the long course of this inflammatory disease.
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PMID:Biochemical markers of bone metabolism in children with Helicobacter pylori infection. 1731 89

The life expectancy of patients with thalassemia has greatly improved over the last decade as a result of regular transfusions and increased compliance with iron chelation therapy, however, this improvement is often accompanied by a series of serious complications including osteopenia and osteoporosis. The pathogenesis of these skeletal disorders is multifactorial which may be due to hormonal deficiency, compromised nutritional status, bone marrow expansion due to erythroid hyperplasia, increased iron stores or desferrioxamine toxicity. The non invasive assessment of bone turnover has markedly improved with the development of specific and sensitive markers of bone formation. The aim of this work is to assess the value of bone formation markers in patients with beta-thalassemia. To achieve this goal, 36 patients with thalassemia were recruited in this study. There were 20 males (56.6%) and 16 females (44.4%) and their ages ranged from 3 to 18 years. A control group of 20 apparently healthy subjects of matched age and sex was used. The patients were selected from the outpatient clinic and inpatients of the Hematology/Oncology Unit of Mansoura University Children's Hospital (MUCH). The selected subjects were subjected to thorough history taking, clinical examination, radiological evaluation and laboratory investigations in the form of: complete blood count, serum iron, serum ferritin, total iron binding capacity, serum calcium, serum phosphorus and estimation of bone formation markers as alkaline phosphatase and osteocalcin. The results were as follows: serum calcium level was within normal range and showed no statistical significance (p = 0.176) when compared to the control group, while serum phosphorus level was significantly higher in thalassemic patients than the controls (p = 0.002); this may reflect hypoparathyroidism. Analysis of the level of bone formation markers showed serum alkaline phosphatase levels slightly higher in patients than controls but not significant (p = 0.055), and this elevation can be referred to associated liver disease in these patients. On the other hand, osteocalcin level was significantly lower in patients than controls (p = 0.011), and this may be due to osteoblast poisoning by iron overload. In conclusion, thalassemic patients have unbalanced bone turnover between the bone formation and resorption markers and this is evidenced by non significant changes or decreased levels of bone formation markers, while bone resorption is an active process.
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PMID:Unbalanced bone turnover in children with beta-thalassemia. 1732 62

Vascular calcification plays a role in the pathogenesis of atherosclerosis, diabetes, and chronic kidney disease. Human aortic smooth muscle cells (HSMCs) undergo mineralization in response to elevated levels of inorganic phosphate (Pi) in an active and well-regulated process. This process involves increased activity of alkaline phosphatase and increased expression of core binding factor alpha-1, a bone-specific transcription factor, with the subsequent induction of osteocalcin. Mounting evidence suggests an essential role for the heme oxygenase 1 (HO-1)/ferritin system to maintain homeostasis of vascular function. We examined whether induction of HO-1 and ferritin alters mineralization of HSMCs provoked by high Pi. Upregulation of the HO-1/ferritin system inhibited HSMC calcification and osteoblastic differentiation. Of the products of the system, only ferritin and, to a lesser extent, biliverdin were responsible for the inhibition. Ferritin heavy chain and ceruloplasmin, which both possess ferroxidase activity, inhibited calcification; a site-directed mutant of ferritin heavy chain, which lacked ferroxidase activity, failed to inhibit calcification. In addition, osteoblastic transformation of HSMCs provoked by elevated Pi (assessed by upregulation of core binding factor alpha-1, osteocalcin, and alkaline phosphatase activity) was diminished by ferritin/ferroxidase activity. We conclude that induction of the HO-1/ferritin system prevents Pi-mediated calcification and osteoblastic differentiation of human smooth muscle cells mainly via the ferroxidase activity of ferritin.
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PMID:Ferritin prevents calcification and osteoblastic differentiation of vascular smooth muscle cells. 1942 91


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