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PubMed1981

[Iron-overload in patients on maintenance hemodialysis: diagnostic criteria, indications and treatment by desferrioxamine (author's transl)].

33 patients with chronic renal failure were divided into two groups. Group I consisted of 8 non-dialysed patients without any clinical or biochemical sign of liver disturbance nor any iron supplementation. Group II consisted of 25 maintenance hemodialysis (MHD) patients treated from 2 to 13 years. 19 subjects had chronic B hepatitis. Total exogenous iron load parenteral iron and/or blood transfusions) was calculated. Body iron overload (hemosiderosis) was assessed by liver iron concentration (LIC) in needle biopsy specimens according to Barry's method (less than 200 microgram/100 mg dry weight) and serum ferritin levels (less than 360 ng/ml). 4 patients whose serum ferritin was increased with or without hepatic fibrosis and with or without any organ dysfunction due to hemochromatosis received i.v. infusions of desferrioxamine in doses of 2 g at each dialysis. Serum ferritin levels were correlated with LIC (p less than 0.001) and iron load (p less than 0.001). Hemosiderosis was noted in 16 MHD patients (group II) and correlated with iron load. Hemochromatosis was noted in 4 patients (group II). 4 hemodialysed patients with iron overload were treated by desferrioxamine from 6 to 18 months. During this therapy, body iron stores fell and organ dysfunction (heart failure, hepatic cytolysis, anaemia, diabetes mellitus improved. Long-term chelation therapy by desferrioxamine was effective and the chelated iron was readily removed by dialysis. These data show the importance of precise evaluation of iron stores in MHD patients.

Adult↗
PubMed1994

Acute pulmonary hemorrhage/hemosiderosis among infants--Cleveland, January 1993-November 1994.

Hemosiderosis is an uncommon childhood disease characterized by spontaneous pulmonary hemorrhage often associated with iron deficiency anemia. During January 1993-November 1994, eight cases of acute pulmonary hemorrhage/hemosiderosis were diagnosed among infants at a children's referral hospital in Cleveland. In comparison, during 1983-1993, a total of three cases of pulmonary hemosiderosis were diagnosed among infants and children at this hospital. This report summarizes the preliminary results of the ongoing epidemiologic, clinical, and laboratory investigations by pediatric pulmonologists in Cleveland, the Ohio Department of Health, the City of Cleveland Department of Public Health, the Cuyahoga County Board of Health, and CDC.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

[Sideroses of alveolar macrophages. Analysis of a continuous series of 360 bronchoalveolar lavages].

360 consecutive bronchoalveolar lavage fluids (BAL) were studied using semi-quantitative method described by GOLDE (GOLDE score). 44 hemosiderosis were detected (12%). Most of them corresponded to massive alveolar hemorrhage (AH). Depending on pathological contexts, we distinguished three main groups of AH frequency: a group of high frequency (around 40%), an intermediate group (10%) and a low frequency group with less than 5%. Matching cytological results with clinical and radiological data, revealed that AH was often too late diagnosed because inconstancy of typical clinical and radiological signs. Even with a variable prognosis related to different physiopathological mechanisms, AH evolution is unpredictable. The authors suggest thus BAL cytological examination may systematically include a research of hemosiderosis in AH high frequency groups.

Acquired Immunodeficiency Syndrome↗
PubMed1997

[A case of lupus myocarditis and nephritis with transient foramen jugular syndrome].

A 46-year-old man was admitted to our clinic because of acute heart failure. Six years before admission he was pointed out cardiomegary and hematuria. One year later, he was diagnosed as having jugular foramen syndrome. On admission, he had a fever and dyspnea. Pansystolic blowing murmur was audible at the apex. The chest ratio on his chest X-ray was 52.5%. An electrocardiogram showed left ventricular hypertrophy. An echocardiogram showed marked dilatation and severe dysfunction of left ventricle. Radionuclide scanning with technetium 99 m pyrophosphate identified inflammatory change in the apex. Myocardial biopsy showed fibrotic degeneration and IgG deposits in myocardium. Blood examination showed anemia, lymphopenia. positive anti-nuclear antibody (1000 times, shaggy pattern), positive anti ds-DNA antibody and hypocomplementemia. Furthermore, proteinuria was pointed out. Renal biopsy showed focal segmental glomerulonephritis with active necrotizing lesion (type III nephritis). Lupus myocarditis and nephritis was diagnosed. After prednisolone (80 mg/day) was administered. left ventricular function and hypocomplementemia improved. The ACE inhibitor was also used for proteinuria. In spite of a little amount of blood transfusion, he showed hepatic hemosiderosis. We suspect that the cause of hemosiderosis was related chronic inflammation of active lupus. It was treated with Erythropoietin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Comparison of serum iron, total iron binding capacity, ferritin, and percent transferrin saturation in nine species of apparently healthy captive lemurs.

Lemurs kept in captivity have been reported to be highly prone to accumulate excessive amounts of iron in tissues (hemosiderosis). Diagnosis of the condition is most commonly made during a postmortem examination because an antemortem diagnosis requires a liver biopsy, a procedure that may not be well tolerated by all animals. The lack of a noninvasive method to evaluate iron status in captive lemurs limits investigators' ability to effectively screen animals for the presence of hemosiderosis, and to detect the condition early when treatment protocols are most effective. This study was conducted in an effort to provide data regarding iron analyte values in healthy captive lemurs of multiple species. The relationship of various iron-related metabolites was evaluated in 177 clinically normal lemurs of nine different species. Serum iron (sI), total iron binding capacity (TIBC), and ferritin concentration were measured directly and the percent transferrin saturation (TS) was calculated. Significant differences in various iron metabolites were observed among several species, suggesting that normal reference values for iron metabolites in lemurs may need to be developed on a species by species basis.

Age Factors↗
PubMed1988

Functional hemispherectomy for treatment of epilepsy associated with hemiplegia: rationale, indications, results, and comparison with callosotomy.

Hemispherectomy is effective in arresting seizures associated with maximal or near maximal hemiparesis. This procedure, however, carries an unacceptable 33% risk of late complications due to cerebral hemosiderosis. Anatomically partial but functionally complete hemispherectomy was devised to avoid these complications. The frontal or occipital lobes, or both, were left in place with the blood supply intact but with connections to commissures and brainstem divided. The central strip and parietal and temporal lobes were removed. Twenty patients were so treated with a follow-up of 4 to 13 years (average, 7.3 years) in 14. Ten of these are seizure free, 1 had a single nocturnal seizure, 1 had occasional focal twitching, and 2 had a worthwhile but lesser reduction in the seizure tendency. None has developed cerebral hemosiderosis, to date. In appropriately selected patients, functional hemispherectomy is an effective procedure preferable to callosotomy or to partial hemispherectomy. When there is no independent ictal discharge from the opposite hemisphere, arrest of seizures may be expected, leading to improvement in cognitive functioning (mean increase, 10 IQ points), social behavior, and a reduction in or discontinuation of anticonvulsant medication. In these patients, gait and hand use remain unchanged.

Adolescent↗
PubMed2004

Increased duodenal expression of divalent metal transporter 1 and iron-regulated gene 1 in cirrhosis.

Hepatic hemosiderosis and increased iron absorption are common findings in cirrhosis. It has been proposed that a positive relation exists between intestinal iron absorption and the development of hepatic hemosiderosis. The current study investigated the duodenal expression of the iron transport molecules divalent metal transporter 1 (DMT1 [IRE]), iron-regulated gene 1 (Ireg1 [ferroportin]), hephaestin, and duodenal cytochrome b (Dyctb) in 46 patients with cirrhosis and 20 control subjects. Total RNA samples were extracted from duodenal biopsy samples and the expression of the iron transport genes was assessed by ribonuclease protection assays. Expression of DMT1 and Ireg1 was increased 1.5 to 3-fold in subjects with cirrhosis compared with iron-replete control subjects. The presence of cirrhosis per se and serum ferritin (SF) concentration were independent factors that influenced the expression of DMT1. However, only SF concentration was independently associated with Ireg1 expression. In cirrhosis, the expression of DMT1 and Ireg1 was not related to the severity of liver disease or cirrhosis type. There was no correlation between the duodenal expression of DMT1 and Ireg1 and the degree of hepatic siderosis. In conclusion, the presence of cirrhosis is an independent factor associated with increased expression of DMT1 but not Ireg1. The mechanism by which cirrhosis mediates this change in DMT1 expression has yet to be determined. Increased expression of DMT1 may play an important role in the pathogenesis of cirrhosis-associated hepatic iron overload.

Adult↗
PubMed1997

Pathology of chronic hepatitis C in children. Child Liver Study Group of Japan.

Limited information is available regarding the histology of hepatitis C virus infection in children. The aim of this study was to determine the histological pattern of chronic hepatitis C (CHC) in children, and liver biopsy specimens from 109 pediatric patients with CHC were examined. Each biopsy specimen was evaluated based on a numerical scoring system for the stage of fibrosis (1-4), the grade of portal/periportal necroinflammation (0-4), the grade of lobular necroinflammation (0-4), and their sum (final grade). The histological lesions considered to be characteristic of chronic hepatitis were also evaluated. None of the children had liver cirrhosis, and 105 cases (97%) were stage 1 or 2. Only 4 children were stage 3. Two of these 4 cases showed hemosiderosis. A significant correlation was observed between the staging score and the final grade in the pediatric patients (r = .59; P < .0001). The histological characteristics of adult CHC, such as lymphoid aggregate, bile duct injury, and fatty changes, were also observed in the children. In conclusion, the majority of children with CHC presented with mild fibrosis, but a few showed CHC with lobular distortion and hemosiderosis. Frequent blood transfusion may aggravate hepatic lesions in pediatric CHC.

Adolescent↗
PubMed2004

Pulmonary hemorrhage/hemoptysis in children.

Pulmonary hemorrhage and hemoptysis are uncommon in childhood, and the frequency with which they are encountered by the pediatric pulmonologist depends largely on the special interests of the center to which the child is referred. In those centers caring for children with cystic fibrosis or congenital heart disease, these will be by far the most common causes of hemoptysis. Other causes of hemoptysis are far less common, such as bleeding from localized lesions in the upper airway or tracheobronchial tree. Even less common is bleeding into the lungs as part of a systemic disease, usually with renal involvement (pulmonary-renal syndromes), such as systemic lupus erythematosis or Goodpasture's syndrome. Bleeding into the lungs in children with a bleeding diathesis probably only occurs in immunosuppressed children after transplantation. When no other cause is found for pulmonary hemorrhage, the presumed diagnosis is idiopathic pulmonary hemosiderosis. This review discusses the various causes of hemoptysis and pulmonary hemorrhage, and the appropriate investigations to aid in determining the correct diagnosis. The management and prognosis of idiopathic pulmonary hemosiderosis, based on cumulative experience from published reports, are considered in more detail.

Child↗
PubMed1986

Sideroachrestic anemia with iron loading: treatment with desferrioxamine.

A case of nontransfusion-dependent sideroachrestic anemia (SA) with hemosiderosis is described that showed significant improvement of hemosiderosis and fibrosis of the liver following treatment with desferrioxamine. The anemia, although not transfusion dependent, did not allow continued therapy with phlebotomies. Following the removal of about 16 g iron over 4.5 years, normalization of serum ferritin and reversal of fibrosis of the liver were observed. Management problems and the prognostic implications of desferrioxamine therapy are discussed.

Adult↗
PubMed2006

Role of L-type Ca2+ channels in iron transport and iron-overload cardiomyopathy.

Excessive body iron or iron overload occurs under conditions such as primary (hereditary) hemochromatosis and secondary iron overload (hemosiderosis), which are reaching epidemic levels worldwide. Primary hemochromatosis is the most common genetic disorder with an allele frequency greater than 10% in individuals of European ancestry, while hemosiderosis is less common but associated with a much higher morbidity and mortality. Iron overload leads to iron deposition in many tissues especially the liver, brain, heart and endocrine tissues. Elevated cardiac iron leads to diastolic dysfunction, arrhythmias and dilated cardiomyopathy, and is the primary determinant of survival in patients with secondary iron overload as well as a leading cause of morbidity and mortality in primary hemochromatosis patients. In addition, iron-induced cardiac injury plays a role in acute iron toxicosis (iron poisoning), myocardial ischemia-reperfusion injury, Friedreich ataxia and neurodegenerative diseases. Patients with iron overload also routinely suffer from a range of endocrinopathies, including diabetes mellitus and anterior pituitary dysfunction. Despite clear connections between elevated iron and clinical disease, iron transport remains poorly understood. While low-capacity divalent metal and transferrin-bound transporters are critical under normal physiological conditions, L-type Ca2+ channels (LTCC) are high-capacity pathways of ferrous iron (Fe2+) uptake into cardiomyocytes especially under iron overload conditions. Fe2+ uptake through L-type Ca2+ channels may also be crucial in other excitable cells such as pancreatic beta cells, anterior pituitary cells and neurons. Consequently, LTCC blockers represent a potential new therapy to reduce the toxic effects of excess iron.

Biological Transport↗
PubMed2005

LPI-labile plasma iron in iron overload.

Labile plasma iron (LPI) represents a component of non-transferrin-bound iron (NTBI) that is both redox-active and chelatable, capable of permeating into organs and inducing tissue iron overload. It appears in various types of hemosiderosis (transfusional and non-transfusional) and in other iron-overload conditions. Sustained levels of LPI could over time compromise organ (e.g. heart) function and patient survival. With the advent of methods for measuring LPI in the clinical setting, it has become possible to assess the implications of LPI in the management of iron overload based on regimens of iron chelation. As LPI is detected primarily in patients with transfusional iron overload and other forms of hemosiderosis, we review here regimens of iron chelation with deferrioxamine and deferiprone (separately or combined) in terms of their efficacy in minimizing daily exposure to LPI in thalassemia major and thalassemia intermedia patients.

Deferiprone↗
PubMed2001

Reversible renal failure in paroxysmal nocturnal hemoglobinuria.

A Chinese patient with paroxysmal nocturnal hemoglobinuria (PNH) developed acute nonoliguric renal failure with intercurrent urinary tract infection and hemolysis. There was no evidence of renal vein thrombosis. Renal biopsy showed features of acute tubular necrosis (ATN) and hemosiderosis. Magnetic resonance imaging (MRI) showed characteristic features of renal hemosiderosis. The patient was stabilized with temporary hemodialysis and intravenous fluid. The renal function fully recovered 3 weeks later. We review the literature and summarize the clinical features of this disease entity. To our knowledge, this case is the first to report such disorder with thorough investigation including concomitant diagnostic MRI imaging and renal biopsy.

Acute Kidney Injury↗
PubMed2001

Inhalation toxicity of 4-ethoxyaniline (p-phenetidine): critical analysis of results of subacute inhalation exposure studies in rats.

This article addresses results from a single 4-h and repeated 1- and 4-wk inhalation exposure studies in Wistar rats with vapor and/or aerosol atmospheres of 4-ethoxyaniline (p-phenetidine). Groups of 10 rats/sex were exposed nose-only to mean analytical concentrations of 11.1, 86.2, and 882.6 mg p-phenetidine/m(3) using an exposure regimen of 6 h/day, 5 days/wk for 4 wk. Concentrations were selected based on results from a pilot study in which rats were exposed under identical conditions on 5 consecutive days for 6 h/day to mean analytical concentrations of 38.2, 133.0, and 1247.6 mg/m(3). In repeated exposure studies, the focus of endpoints was on hematotoxicity. The LC50 was not determined, but no rats died following a single 4-h exposure to 5085 mg/m(3) as a mixture of vapor and aerosol. No mortality was observed either in the 1- or 4-wk studies. Rats exposed to 882.6 mg/m(3) and above evoked characteristic signs of toxicity that included cyanosis, with no apparent progression of findings during the exposure period. Animals exposed to 86.2 mg/m(3) and above exhibited a concentration-dependent, significant increase in blood methemoglobin and reticulocyte counts as well as a significant decrease in hemoglobin, hematocrit, and red blood cell counts. Spleen weights were significantly increased in groups exposed to 133.0 mg/m(3) and above. Microscopic changes demonstrated an increased hematopoiesis (bone marrow smears) and splenic hemosiderosis at 86.2 and 882.6 mg/m(3) and a hepatic hemosiderosis only at 882.6 mg/m(3). These data suggest that the toxicity of p-phenetidine is similar to that of its structural analog aniline. Based on the erythrocytotoxicity occurring at 86.2 mg/m(3) and above, including the apparent reactive changes in bone marrow (increased erythropoiesis) and spleen (increased erythroclasia), the no-observed-adverse-effect level (NOAEL) of the 4-wk study was 11.1 mg/m(3) air and that of the 1-wk study was 38.2 mg/m(3) air. This difference in NOAELs is considered to be related to the selection of exposure concentrations rather than cumulative toxicity.

Aerosols↗
PubMedDate not supplied

Quantification of liver iron overload by T2 quantitative magnetic resonance imaging in thalassemia: impact of chronic hepatitis C on measurements.

PURPOSE: Measurement of liver T2 values seems to be an accurate and sensitive magnetic resonance imaging (MRI) method for the quantification of liver hemosiderosis in multiple transfused patients with thalassemia. Because many of these patients have coexistent chronic hepatitis C virus (HCV) infection, the effect of inflammatory changes on liver T2 values was assessed. MATERIALS AND METHODS: Liver MRI studies of 35 HCV+ and 17 HCV- patients with beta-thalassemia, 9 HCV+ patients without thalassemia, and 10 healthy controls of the same age range (13 to 32 years) were reviewed. Iron status was assessed by serum ferritin in all patients, and determination of liver iron concentration (LIC) was available in 16 HCV+ patients with thalassemia. Histologic activity index (HAI) and grades of siderosis were evaluated in all HCV+ patients with thalassemia. RESULTS: Patients with thalassemia had significantly lower T2 values (P < 0.0001) than subjects without thalassemia, whereas no difference existed between HCV+ patients without thalassemia and healthy controls. In HCV+ patients, LIC correlated more nearly with T2 values (r = 0.93) than with serum ferritin (r = 0.73). T2 values were not influenced by HAI score or fibrosis. CONCLUSION: Liver T2 values were found to be more accurate than serum ferritin in predicting liver iron overload and were not influenced by the presence of chronic hepatitis C. Therefore, MRI could serve as a noninvasive alternative to liver biopsy for the quantification of hemosiderosis in HCV+ patients with thalassemia.

Adolescent↗
PubMedDate not supplied

Pulmonary parenchymal manifestations of mitral valve disease.

Pulmonary parenchymal manifestations of mitral valve disease are the result of either pulmonary venous hypertension in mitral stenosis or abnormal regurgitant flow into pulmonary veins in mitral insufficiency. Typical radiographic findings in mitral stenosis include pulmonary vascular cephalization; interstitial, perivascular, and occasionally alveolar pulmonary edema; diffuse alveolar hemorrhage; hemosiderosis; and pulmonary ossification. Signs of interstitial pulmonary edema are frequently visible and include septal lines. Radiographic findings in diffuse alveolar hemorrhage consist of diffuse, confluent acinar or ground-glass areas of increased opacity, often sparing the peripheral parenchyma and creating the so-called window frame effect. Hemosiderosis is characterized by small, ill-defined nodules or by coarse reticular areas of increased opacity with a bias for the middle and lower lung regions. Ossification manifests as densely calcified, 1-5-mm nodules, mainly in the middle and lower lungs, with a tendency for confluence and the occasional presence of trabeculae. Imaging findings in mitral regurgitation depend on the acuteness of the disease. The most common parenchymal manifestations of acute mitral regurgitation are symmetric alveolar and interstitial pulmonary edema with indistinct, engorged pulmonary vessels and cephalized blood flow. Familiarity with these manifestations can expedite diagnosis, particularly in rare cases of unsuspected mitral valve disease.

Humans↗
PubMed1988

Serum ferritin and hemochromatosis alleles in chronic hemodialysis patients.

There have been some reports on the risk of developing hemosiderosis in hemodialysis patients when heavily transfused and simultaneously possessing hemochromatosis alleles (HA). We evaluated 99 patients on chronic hemodialysis estimating their serum ferritin (SF) levels, transfusion rate, and prevalence of HLA A3, B7 and B14 alleles, which are considered to be more frequent in idiopathic hemochromatosis. We analyzed the patients as a whole group and also separately as low or high transfusion groups. There was no correlation between the number of HA and the mean SF levels. The presence of HA is not a risk factor for the development of hemosiderosis when excessive transfusions and parenteral iron administration are avoided.

Adult↗