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PubMed1983

Hepatic pathology in porphyria cutanea tarda.

We examined clinical and laboratory data and the liver pathology of 48 patients in whom porphyria cutanea tarda was related to alcohol ingestion, estrogen use and pregnancy, or was idiopathic. Biochemical test results, when abnormal, tended to be mild in most cases, with less than two-fold elevations of serum aminotransferases and alkaline phosphatase and mild hyperbilirubinemia. Fatty change, liver cell and Kupffer cell hemosiderosis and glycogenation of hepatocyte nuclei were frequent histologic findings in the 58 liver specimens studied. Alcoholic hepatitis, chronic hepatitis and cirrhosis were uncommon. Granuloma-like lobular aggregates consisting of iron- and ceroid-laden Kupffer cells, chronic inflammatory cells and fat droplets ("lobular lesions of porphyria cutanea tarda") were found in nearly two-thirds of specimens and appeared to be the most characteristic form of parenchymal damage in this form of porphyria. These lesions may be associated with pericentral fibrosis in alcoholic as well as estrogen-treated patients and may remit following therapeutic phlebotomy.

Adult↗
PubMed1976

Immunoglobulin levels in children with homozygous beta-thalassemia.

Patients with hereditary hemolytic anaemias have been known to have immunoglobulin alterations related to an increased susceptibility to infection. In the present series, immunoglobulins, G, A and M have been estimated in 50 thalassemic children aged 10 months to 13 years. No significant difference was found in any of the immunoglobulins between patients and age-matched controls. No correlation could be shown between immunoglobulin levels and (a) the severity of anaemia, (b) the degree of hemosiderosis, and (c) the frequency of febrile infections per year. Against clinical impressions patients did not shown any increased susceptibility to infections.

Adolescent↗
PubMed1980

Pathophysiology of thalassemia.

The clinical manifestations in homozygous thalassemia may be attributed to the defect in hemoglobin synthesis (Figure 16). It is best typified by beta thalassemia, where excess alpha chains accumulate to form intracytoplasmic erythrocytic inclusions. This leads to anemia, bone marrow hyperplasia, osteoporosis, hemosiderosis, and organ failure.

Bone Marrow↗
PubMed2003

MR quantification of hepatic iron concentration.

PURPOSE: To evaluate the accuracy of magnetic resonance (MR) imaging in the quantification of hepatic iron concentration. MATERIALS AND METHODS: Between April 1999 and June 2001, 112 patients were recruited prospectively. All had undergone liver biopsy and hepatic iron concentration quantification with spectrophotometry, followed by MR imaging. MR imaging involved use of four gradient-echo sequences and one spin-echo sequence. Signal intensity (SI) was measured on images obtained with each sequence by means of regions of interest placed in the liver and paraspinal muscle to obtain the liver-to-muscle SI ratio. The relationship between hepatic iron concentration and SI ratio for each sequence was analyzed with multiple linear regression. Receiver operating characteristic analysis was performed to find the diagnostic thresholds. RESULTS: Sixty-eight patients had normal hepatic iron levels (<36 micromol/g), 23 had hemosiderosis (36-80 micromol/g), and 21 had hemochromatosis (>80 micromol/g). With all sequences, an inverse linear relationship between iron concentration and SI ratio was apparent. The authors generated a mathematic model to estimate the iron concentrations from MR imaging data (r = 0.937). For estimated concentrations of more than 85 micromol/g, the positive predictive value for hemochromatosis was 100%; for those less than 40 micromol/g, the negative predictive value for hemochromatosis was 100%. For estimated concentrations of more than 58 micromol/g, the positive predictive value for iron overload was 100%; for those less than 20 micromol/g, the negative predictive value for iron overload was 100%. CONCLUSION: MR imaging is a useful and noninvasive diagnostic tool for quantification of hepatic iron concentration.

Adult↗
PubMed1990

Correction of serious iron overload in a chronic hemodialysis patient by recombinant human erythropoietin and removal of red blood cells: confirmation by follow-up liver biopsy.

A chronic hemodialysis case, a 46-year-old woman with secondary hemosiderosis induced by parenteral iron and blood transfusion due to a refractory anemia, was effectively treated with recombinant human erythropoietin and the removal of red blood cells. The cumulative dose of the iron removed was 5,712 mg. Plasma ferritin decreased from 8,290 to 2,203 micrograms/l during 18 months. Concomitantly, liver histology performed before and after the therapy revealed a prominent regression of the deposited iron.

Anemia, Refractory↗
PubMed1996

Estimation of statistical moments for desferrioxamine and its iron and aluminum chelates: contribution to optimisation of therapy in uremic patients.

We investigated the best time of administration of desferrioxamine (DFO) with respect to the dialysis session, using the approach of the stochastic dynamic system, integrated with the classical pharmacokinetic models. In the 6 patients studied, the mean arrival times of DFO, aluminoxamine (AlO) and ferrioxamine (FO) were, respectively, 193, 1,350 and 126 min, the mean residence times were 1,048, infinite, 1,190 min, respectively. AlO serum levels reach steady state in a mean time of 7 h and 22 min and remain stable in the interdialytic period. FO achieves a peak at the end of DFO infusion and declines during the interdialytic period. DFO, AlO and FO persist a very long time in the body of the uremic patient, thus the dialysis session should be administered when AlO and FO reach steady state. With a dose of 5-10 mg/kg b.w. of DFO, we propose to start the dialysis 8-12 h after the infusion if the main purpose is to treat Al overload or 2-3 h after the infusion if the main purpose is the treatment of hemosiderosis.

Aluminum↗
PubMed1981

Chronic tubulointerstitial nephritis and wasting disease in marmosets (Callithrix jacchus).

Six marmosets (Callithrix jacchus), 20 months to 16 years old, died from a disease characterized by weakness and paralysis of the hind legs, weight lose, anemia and transient diarrhea. The lesions most prominent at necropsy were subacute to chronic tubulointerstitial nephritis, subacute to chronic pancreatitis, and generalized hemosiderosis. Chronic protein deficiency is believed to be the underlying pathogenic mechanism, since the diet contained no more than 15% animal protein during the last two years, and increasing the amount of protein was accompanied by disappearance of the syndrome.

Animals↗
PubMed1991

Veno-occlusive disease in snow leopards (Panthera uncia) from zoological parks.

Livers from 54 snow leopards, 4 days to 23 years old, that had died in 23 US zoos, were evaluated histopathologically to determine if the hepatic fibrosis, which has been noted to be prevalent in this species, was due to chronic active hepatitis from hepadnaviral infection, Ito cell proliferation, or hemosiderosis. Forty-two of 54 snow leopards had subintimal vascular fibrosis with partial or total occlusion of central and sublobular veins (veno-occlusive disease) of unknown origin. All 21 leopards older than 5 years were affected. Four leopards had chronic active hepatitis, and 12 leopards had cholangiohepatitis; but these lesions were not connected anatomically to central and sublobular venous fibrosis. Hepatocellular and Kupffer cell siderosis and Ito cell proliferation were prevalent and often coexisted with perisinusoidal, central, and sublobular venous fibrosis; but fibrosis was present in leopards without siderosis or Ito cell proliferation. The pattern and prevalence of veno-occlusive disease in these leopards was similar to that reported in captive cheetah (Acinonyx jubatus), suggesting that a common extrinsic factor may cause the majority of hepatic disease in these large felid animals in captivity.

Animals↗
PubMedDate not supplied

Reproductive toxicity screen of 1,3,5-trinitrobenzene administered in the diet of Sprague-Dawley rats.

Several Army installations targeted for restoration have measurable quantities of 1,3,5-trinitrobenzene (TNB) in the soil and groundwater. As part of the process of developing environmental and health effects criteria for restoration, a modified Screening Information Data Set (SIDS) reproductive study was performed. Male and female Sprague-Dawley rats received a diet containing approximately 30, 150, or 300 mg TNB/kg diet. Mating occurred following 14 days of treatment. All dams, one-half the males, and representative pups were maintained for a total of 90 days of treatment. No mortality occurred during the study; however, a decrease in mean body weights was noted in both sexes of high-dose rats. A dose-related effect was noted in measurements of sperm function/activity. Sperm depletion and degeneration of the seminiferous tubules were noted histopathologically. Methemoglobinemia and splenic hemosiderosis were common findings in the high- and mid-dose levels of both sexes at necropsy. No adverse effects were noted in mating or fertility indices. No significant treatment-related differences were found in length of gestation, sex ratio, gestation index, or mean number of pups per litter.

Animals↗
PubMed2000

Anthracycline cardiotoxicity in a black rhinoceros (Diceros bicornis): evidence for impaired antioxidant capacity compounded by iron overload.

Two weeks before dying of congestive heart failure, a juvenile black rhinoceros (Diceros bicornis minor) received a single low dose of doxorubicin as part of combination chemotherapy for acute lymphoblastic leukemia. Diffuse hemosiderosis was present at necropsy in a pattern indicative of dietary iron overload, but unique iron-positive degenerative lesions were found in isolated myocardiocytes. Serum analyses revealed hyperferremia, 87% transferrin saturation, and 5- to 10-fold elevations in ferritin concentration, reflecting markedly increased tissue iron stores. Since both toxic and therapeutic effects of anthracyclines are mediated by formation of reactive free radicals via iron-catalyzed reactions, these observations suggest that iron overload may have enhanced myocardial susceptibility to cardiotoxic effects of doxorubicin. Impairments in other myocardial antioxidant defenses, such as deficiencies in catalase and glutathione S-transferase that are known to exist in rhinoceros erythrocytes, may have been underlying factors contributing to an inherent sensitivity of rhinoceros tissues to oxidant-induced injury.

Animals↗
PubMed1982

Idiopathic pulmonary hemorrhage. Ultrastructural and mineralogic study.

A nine-year-old girl was hospitalized because of hypoxemia and anemia. Antibasement-membrane antibodies were present in the serum, but there was no renal involvement suggestive of Goodpasture's glomerulonephritis. Biopsy of the lung showed pulmonary hemosiderosis. In ultrastructural analysis, no lesion of the alveolar basement membrane or capillary endothelial cells was found; however, ferritin-looking deposits were present on alveolar basement membranes and the elastic lamina of arterioles and venules. Mineralogic studies showed these deposits to be made of iron and calcium (this latter element was probably precipitated on altered basement membranes or elastic lamina). Hemosiderin inclusions in the macrophages contained iron but no detectable calcium.

Basement Membrane↗
PubMed1986

Reversible pulmonary changes in rats dosed intravenously with imidazoles.

Pulmonary changes were studied in Sprague-Dawley-rats dosed intravenously with various dosages around the LD 50 in acute studies, and with 0 (control), 0.001, 0.01 and 0.1 mg/kg b. wt./day St 91-Cl or with 0, 1, 5 and 25 mg/kg b. wt./day St 600-Cl for 4 weeks in subacute studies. Doses of 0.01 mg/kg St 91-Cl and 1 mg/kg St 600-Cl were well tolerated. At higher doses, both compounds caused acute pulmonary congestion, edema and bleeding. The acute changes obviously occurred after each single i.v. injection, and were followed by an intensive hemosiderosis of alveolar macrophages. All findings were reversible. No pulmonary changes were observed in oral subacute studies with both compounds.

Animals↗
PubMed1994

[Toxicity studies of paclitaxel. (III)--Six-month intermittent intravenous toxicity in rats].

Paclitaxel, an antineoplastic agent, was intravenously given to Crj:CD (SD) rats of both sexes at 0 (saline), 0 (vehicle), 0.3 (low dose), 1.0 (intermediate dose) and 3.3 (high dose) mg/kg at seven-day interval over a six-month period (total of 27 doses) to investigate its repeated dose toxicity. The results obtained are summarized as follows: 1. No deaths occurred in this study. Vehicle-related salivation was seen for some high dose and vehicle control rats. Soiling of the perigenital region was observed for some high dose females. 2. Red blood cell count, hemoglobin, hematocrit and white blood cell count were decreased for high dose rats. Reticulocyte count was increased and relative neutrophil count was decreased for high dose males. 3. Relative erythroid and myeloid cell count were decreased for high dose rats in bone marrow smear examinations. 4. Bone marrow hypoplasia and splenic hemosiderosis were observed for high dose rats, and thymic atrophy and lymphoid depletion were seen for some high dose males. Based on the these results, the no-toxic effect dose of paclitaxel was estimated to be 1.0 mg/kg in rats under this study condition.

Animals↗
PubMed1991

Value of dual-energy CT in differentiating focal fatty infiltration of the liver from low-density masses.

Focal (irregular, partial) fatty infiltration of the liver may simulate neoplastic or other hypodense masses on CT. On the basis of previous observations of the phenomenon that differences in X-ray attenuation diminish with increasing energy of X-rays used, we performed a preliminary study to determine if dual-energy CT could be used to discriminate between fatty infiltration and hypodense liver masses. Dual-energy CT at 140 and 80 kVp was performed in 14 patients undergoing liver biopsy and in seven control subjects with presumedly normal liver. Attenuation measurements were taken, and the changes in attenuation between 140 and 80 kVp were calculated. The mean changes in attenuation were 3.5 H for normal liver (n = 7), 2.5 H for hypodense liver masses (n = 6), 13 H for fatty liver (n = 5), 0.3 H for fatty liver combined with hemochromatosis or hemosiderosis (n = 3), and 2 H for the spleen (n = 18). The change in attenuation increased as the fat content in the liver increased. Analysis of variance showed a statistically significant difference (p less than .001) between fatty liver and the other groups. A difference greater than 10 H was unique to fatty infiltration. These results suggest that dual-energy CT may help to differentiate focal fatty infiltration of the liver from low-density neoplastic or other lesions, but only if the iron content of the liver is not increased.

Adult↗
PubMed1986

Hepatic iron overload in renal transplant recipients: ultrastructural observations.

This study describes the ultrastructural features of hemosiderosis occurring in five transplant recipients. Iron deposits in the form of homogeneous and heterogeneous siderosomes (iron-laden lysosomes) were found within the hepatocytes and macrophages in areas of fibrosis, and to a lesser degree within Kupffer cells and bile duct epithelium. Disruption of siderosomal membranes with extrusion of ferritin particles into the cytosol was demonstrated in these specimens and may be significant in the pathogenesis of hepatocellular injury.

Adult↗
PubMed1983

Iron overload disorders: natural history, pathogenesis, diagnosis, and therapy.

Hemochromatosis is a syndrome which, when fully expressed, is manifested by melanoderma , diabetes mellitus, and liver cirrhosis, with iron overload involving parenchymal and reticuloendothelial cells in many organ systems. This clinical presentation may arise as a consequence of either hereditary or acquired abnormalities of iron overload, although the mechanisms are quite different. In hereditary hemochromatosis (also known as primary, or idiopathic, hemochromatosis), increased intestinal iron absorption leads to excessive accumulations of iron, throughout the body, particularly in parenchymal cells. In secondary forms of iron overload including transfusional hemosiderosis, alcoholic cirrhosis, thalassemia, sideroblastic anemia, and porphyria cutanea tarda, iron accumulates in the reticuloendothelial system initially, but with increasing amounts of total body iron, excessive iron deposits eventually accumulate in parenchymal cells throughout the body producing a picture indistinguishable from hereditary hemochromatosis. In this article, the course, prognosis, and therapy of iron overload will be reviewed in detail. Clinical and experimental data concerning the pathogenesis of the different forms of iron overload will be examined critically. In particular, information relating to possible abnormalities of reticuloendothelial function, intestinal mucosal iron transport, and alterations in serum and tissue isoferritin patterns in hereditary hemochromatosis will be analyzed, and possible directions for future research will be suggested. The mode of inheritance and linkage with the major histocompatibility (HLA) complex will be discussed. Theories on the pathogenesis of tissue damage by excess iron will be evaluated. Methods for measuring the extent of iron overload in clinical practice will be described, including measurements of serum iron, serum ferritin, iron absorption, cobalt excretion, desferrioxamine excretion, liver biopsy and tissue iron determinations, and HLA typing. Finally, unresolved problems in the understanding of the disease process, diagnosis, and therapy will be delineated.

Anemia, Hypochromic↗
PubMed2005

[Factors associated with the severity of liver damage in chronic hepatitis C].

BACKGROUND: Twenty percent of patients with chronic hepatitis C evolve to cirrhosis in 10 to 20 years. The degree of steatosis and hepatic iron stores in liver biopsy increase the risk. Age, high body mass index, diabetes mellitus and alcohol consumption are factors associated to the severity of liver damage. AIM: To study the association of steatosis and increased iron stores in the liver biopsy and age, overweight, alcohol consumption and diabetes with the severity of liver damage in patients with hepatitis C virus infection. PATIENTS AND METHODS: Retrospective study of 84 liver biopsies of patients with chronic infection with hepatitis C virus were studied. The pathological appearance was classified as stage I when chronic hepatitis with mild activity without fibrosis was observed; as stage II when moderate chronic hepatitis with mild fibrosis was observed and as stage III when there was a moderate chronic hepatitis with fibrosis or cirrhosis. The amount of steatosis and iron deposition in the biopsy were also assessed. RESULTS: Forty one percent of patients were in stage I, 32% in stage II and 27% in stage III. Patients in stage I were younger than those in stages II and III (40.7 and 52.2 years respectively, p <0,001). No association between the severity of liver damage and the degree of steatosis, hemosiderosis, body mass index or alcohol intake, was observed. The frequency of diabetes mellitus increased along with pathological staging (3, 15 and 30% in stages I, II and III, respectively, p <0,05). CONCLUSIONS: This study confirms that severity of chronic hepatitis C is associated with age and the presence of diabetes mellitus.

Adult↗
PubMed1978

Goodpasture's syndrome: diagnosis by transbronchial lung biopsy.

A 28-year-old man developed recurrent hemoptyses, breathlessness, anemia, and bilateral pulmonary infiltrates after mild smoke inhalation. He had no laboratory evidence of kidney involvement. Transbronchial lung biopsy showed erythrocytes, iron-containing macrophages within alveolar spaces, normal basement membranes, and strongly positive linear staining of alveolar septa for immunoglobulin G (IgG). Serum antiglomerular basement-membrane antibody was strongly positive by radioimmunoassay. Kidney biopsy showed normal findings by light and electron microscopy but strongly positive linear staining of glomerular capillaries for IgG. Follow-up 9 months later while the patient was taking prednisone revealed no clinical evidence of pulmonary or renal disease. This case shows that immunopathologic study of transbronchial lung biopsies is helpful in differentiating between Goodpasture's syndrome and idiopathic pulmonary hemosiderosis, while the absence of clinical and microscopic evidence of kidney disease does not exclude Goodpasture's syndrome.

Adult↗