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At least 1,297 records · Page 72Linked to original sources
PubMed1985

Iron removal by desferrioxamine in patients on chronic hemodialysis--kinetic study and long-term results.

Serum ferritin levels, cumulative number of administered blood transfusions, number of monthly transfused blood units and total months on hemodialysis (HD) treatment differed significantly in 7 patients on hemodialysis with clinical, biochemical and histological evidence of hemosiderosis, when compared to 37 controls (p less than 0.001 for all parameters). As a new treatment method desferrioxamine (DFO) therapy was introduced for iron detoxification in these hemosiderotic chronically hemodialyzed patients. Hence, to maximize the biological half-time, 30 mg/kg body weight DFO were given after the end of HD in the iron-loaded patients. Iron removal during the subsequent HD and the increase of iron excretion by the stool after DFO was measured by atomic absorption spectroscopy. Iron removal by the artificial kidney was calculated by investigating the function (QDi + QF)CDo over the duration of HD treatment, which equals the total amount of iron removal during HD. Using numerical integration of measured data this removal was found to be 21.8 +/- 6.9 mg whereas cumulative iron loss via the feces was found to be 36.5 +/- 14.6 mg. Therefore, total iron elimination was calculated to be on average 50-60 mg after administration of a single dose of DFO. Furthermore, long-term treatment of 5 patients resulted in a significant decrease of serum ferritin levels from 2,309 +/- 295 to 715 +/- 177 ng WHO/ml (p less than 0.001) after a period of 36 +/- 5 months. We conclude, that DFO in a dosage of 30 mg/kg body weight given at the end of HD is able to remove more than 500 mg iron/month if it is administered following each HD. Long-term results indicate negative iron balance without significant change of transfusion frequency if not more than 2 U of blood (500 mg iron) are administered within 1 month. This treatment schedule might be superior compared to the previously used methods of administration where DFO was given at the beginning or throughout HD.

Adolescent↗
PubMed1986

Iron overload syndromes.

Iron overload is relatively common and is now detected more frequently because of inclusion of serum iron measurement in automated clinical chemistry panels. Secondary hemosiderosis and hemochromatosis result from increased iron absorption associated with increased erythropoiesis compensating for hemolysis, increased dietary iron, inappropriate prolonged oral iron therapy or chronic multiple transfusions. Primary hemochromatosis is a genetic metabolic disorder associated with the HLA locus on chromosome 6 resulting in increased iron absorption, though erythropoiesis and dietary iron are normal, and abnormal diversion of iron from reticuloendothelial (RE) to parenchymal cells. A genetic increase of intracellular iron carrier is a proposed basic mechanism. Only in the cirrhotic stage of primary hemochromatosis do RE iron and serum ferritin increase. Since both serum iron and serum ferritin may remain normal in the precirrhotic stage and may be falsely positive in the absence of iron overload, direct measurement of body iron stores is often useful. Measurement of tissue iron in liver biopsy specimens is widely used. However, quantitation of total mobilizable body iron by measurement of a 6-hour urine collection after intravenous injection of 59Fe-DTPA is noninvasive, sensitive, relatively accurate, and together with other laboratory and clinical data provides a practical means of establishing the correct diagnosis and therapy early enough to minimize organ damage.

Adult↗
PubMed1986

Familial nonspherocytic hemolytic anemia in poodles.

Nonspherocytic hemolytic anemia, characterized by marked reticulocytosis, hepatosplenomegaly, hemosiderosis of reticuloendothelial organs and bone marrow myelofibrosis, and osteosclerosis, was diagnosed in 5 related Poodles. The unremitting anemia was clinically evident by 1 year of age, and was fatal as early as 3 years of age. Despite intense diagnostic endeavors including RBC fragility studies, RBC enzyme assays, and hemoglobin electrophoresis, the cause of this nonspherocytic hemolytic anemia remains to be determined.

Anemia, Hemolytic, Congenital↗
PubMed1985

Experimental babesiosis in coyotes and coydogs.

One splenectomized and 6 intact coyotes (Canis latrans), and 2 coydogs were experimentally inoculated with a recent isolate of Babesia gibsoni. The disease was mild in intact animals, was fatal in the splenectomized coyote, and was characterized by a regenerative hemolytic anemia with the PCV decreasing to 16% in intact animals and to 6% in the splenectomized coyote. Peak parasitemia ranged from 3% to 21% of erythrocytes infected and was inversely correlated to PCV. Serum lactate dehydrogenase, bilirubin, and globulin concentrations were increased in all infected animals. Three weeks after inoculation, specific antibody titers increased to 1:65,536 and remained elevated in the chronically infected animals. The splenectomized coyote had progressive weakness until death, 24 days after inoculation. Intact animals had splenomegaly and anorexia at the height of infection. The splenectomized coyote had generalized edema, omental petechiae, renal and hepatic degeneration, membrano-proliferative glomerulonephritis and congestion, extramedullary hematopoiesis, lymphoid hyperplasia, and severe hemosiderosis in an accessory spleen. The only consistent change in the intact animals was splenomegaly.

Animals↗
PubMed1985

[Recurrent pulmonary hemorrhage with normal kidney function].

A case of Goodpasture's syndrome with normal renal function is described. Clinical, morphological and prognostic features of the diagnosis are compared with the findings in Goodpasture's syndrome with progressive renal failure and with the findings in idiopathic pulmonary hemosiderosis.

Adult↗
PubMed1985

Hepatitis B virus DNA detected in formalin-fixed liver specimens and its relation to serologic markers and histopathologic features in chronic liver disease.

To examine the relationship of hepatitis B virus (HBV) DNA sequences in the liver with histopathologic features and antigenic markers, the authors determined the hepatocytic status of viral DNA by in situ hybridization in formalin-fixed liver sections using a biotinylated probe in 45 patients with various chronic liver diseases. The results were compared retrospectively with the HBV serologic markers and histopathologic features including the presence of ground-glass cells or Shikata staining positivity. The specificity of this in situ detection of HBV DNA has been proven excellent in a double-blind control study in 18 patients in whom liver HBV DNA was also determined by DNA extraction, gel electrophoresis, and the Southern blotting technique. In 41 patients, the findings of HBV DNA and serologic markers were concordant (17 positive and 24 negative). Twelve of the 20 HBV-DNA-positive patients were HBsAg-positive (6 with chronic hepatitis, 3 with cirrhosis, and 3 with hepatocellular carcinoma). Ground-glass cells or Shikata positivity were found in 10 of these 12 patients. HBV DNA sequences were found in the liver of all patients with chronic liver disease and serologic positivity for HBV infection. In liver with normal histologic features, HBV DNA was not demonstrable, despite the positive anti-HBc and anti-HBs. However, a positive HBV DNA was found in 3 serologically negative patients. In another patient the interpretation of findings was impossible because of severe hemosiderosis. From this study, it is concluded that in situ detection of HBV DNA in formalin-fixed liver sections has a clinical value and is suitable for routine use.

Adolescent↗
PubMed1985

Lower limb pain in thalassemia.

A group of 67 homozygous beta thalassemic patients was investigated for disturbances related to their lower limbs. Thirty-six patients presented a variety of complaints. Four distinct types of pain were found. Ischemic crampy muscle pain in 12 patients. Postural pulsating pain after activity or prolonged standing was described by 18 patients. High intraosseous pressure was found in a significant number of these patients. Post transfusion hemosiderosis producing synovitis was diagnosed in 2 patients. Four additional patients presented acute self-limiting episodes of pain. This pain was probably due to microfractures. Some patients presented a combination of various pain patterns.

Adolescent↗
PubMed1977

Lead poisoning in sandhill cranes.

Seven Florida sandhill cranes (Grus canadensis pratensis) and 6 greater sandhill cranes (Grus canadensis tabida) were exposed to lead-base paint containing 27% lead. One bird of each subspecies died enroute to the hospital, with a clinical history of anorexia, weakness, and open-mouth breathing of 36 hours' duration. There were no gross lesions, and microscopic lesions were limited to focal hepatic necrosis and hemosiderosis. Two of each subspecies of cranes developed clinical signs of lead poisoning, which included anorexia, weakness, green diarrhea, regurgitation, and open-mouth breathing. Diagnosis of lead poisoning was confirmed on the basis of blood lead concentrations ranging from 146 microgram/100 ml to 378 microgram/100 ml. These 4 cranes were treated successfully with calcium disodium edetate intramuscularly. Seven of the birds remained clinically normal despite high blood lead levels, especially in the greater sandhill cranes.

Animals↗
PubMed1979

[Hematologic aspects of alcoholism (author's transl)].

Alcohol causes different hematologic alterations on each of the three bone marrow cellular series. Its effect on the red series leads to the appearance of megaloblastic disturbances, erythroblastic vacuolization, iron metabolism abnormalities, and hemolytic syndromes. Megaloblastic disturbances may arise as a consequence of folic acid or vitamin B12 deficiency or of a direct toxic effect of ethanol on the erythroblasts. Iron metabolism alterations include reversible sideroblastic anemia, and hemosiderosis. The three hemolytic syndromes related to the consumption of ethanol are: acanthocytosis, stomatocytosis, and Zieve's syndrome. Alcohol induces leukopenia and functional deffects of the leukocytes; these facts explain the frequent susceptibility of chronic alcoholics to infection. Ethanol may act upon the megakaryocytic series to produce reversible thrombopenia and various alterations in platelet function. Thus alcohol exerts toxic effects on bone marrow, which interfere with the proliferation, maturation, release and survival of the three cellular series, either directly or by means of complex mechanisms related to the metabolism of folic acid, vitamin B12, pyridoxine, or iron. Alcoholism should therefore be considered as a possible cause whenever an obscure hematological condition comes under scrutiny.

Alcoholism↗
PubMed1967

Some medical problems of chronic hemodialysis.

Chronic intermittent hemodialysis may relieve some medical problems of terminal uremia (for example, azotemia, acidosis, hypertension, neuro-muscular disorders, bleeding, pericarditis) to such a degree that many patients are able to resume their normal activity. There remain, however, problems which are not readily changed by hemodialysis (anemia, peripheral neuropathy, pruritus, sexual impotence, renal osteodystrophy). These, together with medical problems possibly caused by hemodialysis (for example, osmotic disequilibrium, errors in dialysate composition, hepatitis, hemosiderosis, isoimmunization from blood transfusions, shunt problems and psychological problems of dependency upon the artificial kidney) represent a limitation of the present type of hemodialysis therapy.

Cardiovascular Diseases↗
PubMed1982

[Iron-deficiency anemia. Hematologist's viewpoint].

Enlarged spleen, fever, increased susceptibility to infections, and thrombocytosis, are manifestations of iron deficiency which are relatively specific of pediatric patients. Iron deficiency anemia is part of everyday pediatrics. Patients are referred to the hematologist in the following situations: 1) Therapy is ineffective for one of the following reasons: the hypochromic anemia is not caused by iron deficiency (hemoglobinopathies); iron is less efficiently used because of transferrin deficiency or infectious, inflammatory or cancerous disease; iron therapy is inadequate either because of insufficient dosage or of suboptimal duration. 2) A relapse occurs in spite of adequate therapy. Before investigating the digestive tract, abnormal hemostasis. Osler-Weber-Rendu syndrome and pulmonary hemosiderosis should be considered. 3) Iron deficiency anemia is less common in adolescents. This condition, known as chlorosis, results mainly from increased needs, unbalanced diet, and onset of menses. In some cases no explanation is found but iron therapy leads to recovery. 4) Difficult problems arise in patients with complex anemias: iron deficiency with folic acid or vitamin B12 deficiency; hyposideremia complicating one of the hemoglobinopathies.

Adolescent↗
PubMed1984

Benign hepatocellular tumors in the young. A clinicopathologic spectrum.

Hepatic tumors unassociated with cirrhosis were encountered in seven patients aged 10 to 19 years. Four patients had received androgens for aplastic anemia. Two patients had transfusional hemosiderosis. One patient had had a renal transplant 2 1/2 years ago. Two patients are alive at 2 3/4 and 2 1/2 years after surgical resections. Nodules were found at autopsy in the others. The tumors were well differentiated and, in the androgen-related cases, differed from the others in the following features: canalicular bile retention, mild nuclear atypia, and acinar formation. No mitoses, vascular invasion, or metastatic tumor were evident. The clinical setting was variable; different factors, including iron overload and androgen therapy, played a role in the development of tumor. Although the androgen-related cases showed mild cellular atypia, biologic evidence of malignancy was lacking as in most previous reports.

Adolescent↗
PubMed1984

Complete recovery of hemopoiesis following bone marrow transplant in a patient with unresponsive congenital hypoplastic anemia (Blackfan-Diamond syndrome).

Allogeneic bone marrow transplantation (BMT) was carried out on a 5-year-old boy with congenital hypoplastic anemia (CHA), who did not respond to corticosteroids and who was displaying signs of progressive hemosiderosis. Pretransplant preparation had to be modified because respiratory failure and cerebral edema supervened. This preparatory regimen consisted of busulfan (2 mg/kg for four days), cyclophosphamide (50 mg/kg for one day), and total body irradiation (750 rad). Hemopoiesis was completely restored and is still maintained 650 days after transplantation. This is the second published report on the use of BMT to treat a patient with CHA, and it is the first time it has resulted in long-term survival. BMT should be considered for patients with CHA who do not respond to corticosteroids.

Anemia, Aplastic↗
PubMed1984

Pulmonary pathology in renal transplant recipients.

Studies of the lungs have revealed multiple functional and histopathological abnormalities in patients with chronic renal failure, but data following renal transplantation are extremely limited. We examined postmortem data from 20 transplant patients and found pulmonary abnormalities in most patients. The number of pulmonary abnormalities noted in patients with poor transplantation, averaged 5.3 per patient. The corresponding number was significantly less (3.4 per patient) in the group with good transplant renal function, surviving more than one year after transplantation. Pulmonary calcification, fibrosis, and hemosiderosis were found in several patients in the former group but in none of the latter group. This observation suggests reversibility of these pulmonary abnormalities with successful renal transplantation.

Adult↗
PubMed1984

[Arthropathy as an early symptom of hemochromatosis. Overview of the literature and 7 case reports].

In seven patients with hemochromatosis, arthropathy was an early symptom, or first clinical symptom, of the hemochromatosis. In all seven patients, serum iron, transferrin saturation, and parameters of storage iron (serum ferritin, Desferal-test) were clearly elevated. In 5 patients hemochromatosis was associated with the HLA loci A3 and B7. Bone scan proved a sensitive detection method for hemochromatosis arthropathy. In one case joint involvement was detected by bone scan prior to clinical symptoms. Parameters of iron metabolism correlated well with other organ manifestations of hemochromatosis. In contrast, joint involvement did not correlate with parameters of iron metabolism or severity of hemosiderosis of other organs, and was not relieved by phlebotomy. These 7 cases confirm that joint symptoms can be an early or leading symptom of hemochromatosis, can lead to early therapy and thereby prevent major organ damage. It remains undecided, however, whether the arthropathy is a consequence of iron storage or an independent disease which is genetically associated with hemochromatosis.

Female↗
PubMed1982

The toxicity of Cassia occidentalis to goats.

The toxic effects of oral administration of Cassia occidentalis to goats was evaluated. The prominent signs of Cassia poisoning were diarrhea, inappetence, dyspnea, staggering, ataxia and recumbency. Lesions consisted of hemorrhages and congestion in the heart, lungs, abomasum and spleen, catarrhal enteritis, hepatic fatty change and necrosis, splenic hemosiderosis, pulmonary emphysema, necrosis and/or degeneration of the epithelial cells of the renal convoluted tubule, and packing of the glomeruli with endothelial and small round cells. These changes were accompanied by increases in GOT activity and in the serum concentrations of ammonia and urea, as well as by decreases in the total protein and calcium in serum. There were decreases in Hb, PCV and RCB, and increased leucocyte counts. Total lipids were higher in the liver, kidneys and heart of the Cassia-poisoned goats.

Animals↗
PubMed1981

[Biochemical, electrocardiographic and pathomorphological studies the monensin poisoning of sheep].

Studies were carried out on the changes in the electrocardiogram, the content of sodium and potassium in the plasma and erythrocytes, and the morphology of the viscera of sheep spontaneously intoxicated with monensin. It was found that in the initial phases of poisoning the plasma level of Na and K strongly rose--410 +/- 12.57 mg% and 36.28 +/- 1.99 mg%, respectively, while after the tenth day it showed a trend of coming back to normal. The electrocardiogram of the poisoned sheep was inevitably deprived of the P deflection, while the QRST complex showed deformations characteristic of ischemia and degeneration of the myocardium. Morphologically, there were catarrhal abomasoenteritis, edomatized and fragile kidneys and liver, enlarged mucous membrane of the gallbladder, showing hyperemia and nodules, hemorrhages in the heart, and hyperemia and edema of the lungs. Histologically, there were dystrophic and necrotic nephrosis and focal glomerulonephritis, granular and fatty dystrophy and necroses of the liver, cholecystitis, granular and hyaline dystrophy of the myocardium, hyperemia, hemorrhages, and edema of the lungs as well as degenerative changes in the ganglion cells of the brain. The cadavers of animals that were ill for seven to ten days and died had multiple hemosiderosis in the kidneys, liver, lungs, and heart.

Animals↗
PubMed1995

[Cardiologic management in patients on a long-term dialysis program].

Cardiovascular complications are the main cause of mortality in patients with chronic renal failure. Hypertension and lipid abnormalities which often lead to left ventricular hypertrophy and accelerated atherosclerosis as well as coronary artery disease are a common cause of death. On the other hand uremia often causes pericarditis and thereby may lead to cardiac tamponade and constrictive pericarditis. Renal failure can also cause secondary hyperparathyroidism, amyloidosis, hemosiderosis and oxalosis which can produce visceral infiltrations and lead to a variety of disturbances of cardiovascular functions. Life-threatening arrhythmias are one of the major cardiovascular complications during maintenance dialysis as their occurrence might result in sudden death. The aim of cardiologic management which includes the complex of preventive and therapeutic measures is to reduce the morbidity and mortality and to improve the quality of life.

Cardiovascular Diseases↗