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At least 1,333 records · Page 74Linked to original sources
PubMed1996

Laparoscopic liver biopsy to evaluate hepatic dysfunction in patients with hematologic malignancies: a useful tool to effect changes in management.

Hepatic dysfunction is common in patients who receive intensive chemotherapy and it is important to determine the etiology in order to institute appropriate therapy. The role of laparoscopic liver biopsy in patients with neutropenia, thrombocytopenia, or both was evaluated as a mean of making treatment decisions and as a determinant of clinical outcome. Laparoscopic liver biopsy was performed in 29 subjects who were receiving intensive cytotoxic therapy with or without bone marrow transplantation. One to three direct-vision laparoscopic liver biopsies were performed in each patient using a Tru-cut needle during general anesthesia. Platelet concentrate transfusions were usually given before, during, and immediately after biopsy. Bleeding was controlled with spatula electrocautery. Thirty-two biopsies were obtained in 29 patients. At the time of liver biopsy, white blood cell and platelet counts ranged from 0 to 14,300/microliters (median: 2500/microliters), and 1000 to 47,000/microliters (median: 20,000/microliters), respectively. Bleeding at the liver biopsy site was readily controlled during the procedure without clinical evidence of significant bleeding; no procedure-related complications were noted and no patients required re-exploration. All biopsies were informative and the lesions observed in 32 biopsies revealed graft-versus-host disease (n = 5), hepatic candidiasis (n =1), hepatic veno-occlusive disease (n = 3), cholestasis (n = 19), hemosiderosis (n = 26), toxic injury (n = 8), hepatic steatosis (n = 4), granuloma (n = 1), viral infection (n =1), and malignancy (n = 1). Laparoscopic liver biopsy has been proven to be an effective means of assessing the cause of liver dysfunction in patients who were thrombocytopenic and immunosuppressed. The diagnosis obtained at laparoscopic liver biopsy altered therapy in nine of 29 (31%) patients.

Adult↗
PubMed1996

Induction of renal cell carcinoma in male Wistar rats treated with cupric nitrilotriacetate.

Systemic administration of copper, an essential trace metal in the human body, has never been reported to be carcinogenic in animals. We investigated the induction of tumors by the cupric complex of nitrilotriacetic acid (Cu-NTA) in male Wistar rats. Thirty-two animals received ip injections of Cu-NTA, 3 to 5 mg of copper/kg body weight 5 days a week for 12 weeks, and were kept under close observation. For comparison, 31 animals received ip injections of ferric nitrilotriacetate (Fe-NTA), 5 to 10 mg of iron/kg body weight, and 16 animals received nitrilotriacetic acid (NTA) alone at the molar dose equivalent to Cu-NTA for the same period of time. Sixteen animals were left untreated as controls. Fourteen animals in the Cu-NTA group died of hepatic failure during the treatment period, and renal cell carcinoma (RCC) was induced in eight animals (25%). Of these, four animals died of either pulmonary metastasis or intraperitoneal hemorrhage. A total of 12 RCC were obtained, of which six tumors were > or = 5 mm. The Cu-NTA group yielded fewer RCC and required a longer latent period for their incubation than the Fe-NTA group. Furthermore, the Cu-NTA group showed one hepatocellular carcinoma and one high-grade sarcoma of hepatic origin. No renal or hepatic tumor was observed in the NTA or control groups. The nontumorous part of the kidney treated with Cu-NTA presented hemosiderosis caused by copper-induced hemolytic anemia. This is the first report that systemic administration of copper compounds can induce malignant tumors in animals. Not only copper but also iron may play a role in the Cu-NTA-induced renal carcinogenesis model.

Animals↗
PubMed1996

[Treatment of porphyria cutanea tarda with chloroquine and its effect on associated liver disease: retrospective analysis].

BACKGROUND: Chloroquine may improve cutaneous symptoms and liver disease manifestations in patients with porphyria cutanea tarda. AIM: To retrospectively analyze the effects of choloroquine in patients with porphyria cutanea tarda. PATIENTS AND METHODS: Five patients (one female), aged 45 to 65 years old, were studied. The duration of the disease ranged from 2 to 15 years. One patient was alcoholic and other was a hepatitis C virus carrier. All patients received chloroquine 125 mg twice weekly. Before, during and after treatment, cutaneous signs, serum bilirubin, hepatic enzymes and urine copro and uroporphyrin were assessed. Four patients were subjected to a liver biopsy before starting chloroquine. RESULTS: All patients had increased levels of urine porphyrins, four had abnormal serum liver enzymes. All liver biopsies showed variable hemosiderosis, two patients had a chronic active hepatitis (one with cirrhosis), one a chronic persistent hepatitis and one had mild rague alterations. During chloroquine treatment, cutaneous symptoms improved in all patients, transaminases and gamma glutamyl transferase decreased. In three, urine uroporphyrin increased initially and normalized afterwards. Choloroquine was well tolerated. CONCLUSIONS: Chloroquine improved cutaneous symptoms, urine uroporphyrin and serum liver enzyme levels in treated patients.

Aged↗
PubMedDate not supplied

Proliferative responses of lymphocytes to food antigens are useful for detection of allergens in nonimmediate types of food allergy.

Food allergy is clinically classified into two types, immediate and nonimmediate. Radioallergosorbent test (RAST) is a sensitive procedure for the diagnosis of IgE-mediated hypersensitivity but not for other types of hypersensitivity. There is not yet a sensitive blood examination for detection of allergens in nonimmediate types of food allergy. Of the total number of subjects in our study, twenty-two children had nonimmediate types of food allergy (hen's egg, cow's milk, soybean, or buckwheat flour), atopic dermatitis, allergic tension fatigue syndrome or pulmonary hemosiderosis. For these children, manifestations of the allergy did not appear earlier than 2 hours after ingestion of the offending food. Eighteen children in the study developed acute urticaria, angioedema, or bronchial asthma appearing within 2 hours of the challenge. Fifteen nonatopic healthy children were selected as controls. Proliferative responses of peripheral blood mononuclear cells (PBMCs) to food antigens were measured in nonimmediate types of food allergy. The proliferative responses of PBMCs to each offending food antigen in patients with nonimmediate types of food allergy were significantly higher than those of healthy controls and patients with immediate types of food allergy, respectively. Moreover, in each case with nonimmediate type, the proliferative responses to food antigens other than the offending food were not detected. When PBMCs were twice stimulated with the offending food antigen, the same results were obtained. These results indicate that the proliferative response of PBMCs to food antigens is specific to each offending food antigen in nonimmediate types of food allergy. Taken together, proliferative responses of PBMCs to each food antigen are useful for detection of allergens in nonimmediate types of food allergy.

Adolescent↗
PubMed1997

Lifetime treatment of mice with azidothymidine (AZT) produces myelodysplasia.

AZT has induced a macrocytic anemia in AIDS patients on long term AZT therapy. It is generally assumed that DNA elongation is stopped by the insertion of AZT into the chain in place of thymidine thus preventing the phosphate hydroxyl linkages and therefore suppresses hemopoietic progenitor cell proliferation in an early stage of differentiation. CBA/Ca male mice started on AZT 0.75 mg/ml H2O at 84 days of age and kept on it for 687 days when dosage reduced to 0.5 mg/ml H2O for a group, another group removed from AZT to see recovery, and third group remained on 0.75 mg. At 687 days mice that had been on 0.75 mg had average platelet counts of 2.5 x 10(6). Histological examination on 9 of 10 mice with such thrombocytopenia showed changes compatible with myelodysplastic syndrome (MDS). A variety of histological patterns was observed. There were two cases of hypocellular myelodysplasia, two cases of hypersegmented myelodysplastic granulocytosis, two cases of hypercellular marrow with abnormal megakaryocytes with bizarre nuclei, one case of megakaryocytic myelosis associated with a hyperplastic marrow, dysmyelopoiesis and a hypocellular marrow and two cases of myelodysplasia with dyserythropoiesis, hemosiderosis and a hypocellular marrow. Above mentioned AZT incorporation may have induced an ineffective hemopoiesis in the primitive hemopoietic progenitor cells, which is known to be seen commonly in the myelodysplastic syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Thrombosis and secondary hemochromatosis play major roles in the pathogenesis of jaundiced and spherocytic mice, murine models for hereditary spherocytosis.

Jaundiced mice, ja/ja, suffer from a severe hemolytic anemia caused by a complete deficiency of erythroid beta-spectrin. We used these mice as a model to investigate the pathophysiological consequences of the deficiency, including the effects in the nonerythroid tissues where this protein is expressed. Because the ja/ja mice rarely survive beyond the fourth postnatal day, methods were assessed for extending lifespan into adulthood. Neonatal transfusion increased lifespan to a mean of 3.7 months, allowing a more complete characterization of the pathophysiology. Blood parameters and histopathology of the jaundiced mouse were compared with that from spherocytic mice, which have a hemolytic anemia caused by deficiency of erythroid alpha-spectrin, yet can survive the postnatal period transfusion free. The adult jaundiced and spherocytic mice present with greatly decreased hematocrit and red blood cell counts, reticulocytosis, and bilirubinemia, leading secondarily to hepatosplenomegaly and cardiomegaly. Jaundiced and spherocytic mice were analyzed histopathologically between 1.0 and 9.5 months of age. Interestingly, the complete absence of erythroid beta-spectrin in jaundiced mice leads to no detectable structural defects in brain, cardiac, or skeletal muscles. However, fibrotic lesions and lymphocytic infiltration were observed in cardiac tissue from 4 of 13 jaundiced mice and 15 of 15 spherocytic mice, and thrombi were detected at either the atrioventricular valves or within the atria of 2 of 13 jaundiced mice and 15 of 15 spherocytic mice. In addition, all affected mice had a progressive renal hemosiderosis concurrent with hydronephrosis and glomerulonephritis. The severity of the renal disease and its presence in all moribund mice suggests kidney failure rather than the fibrotic heart lesions as the major cause of death in these mice.

Alternative Splicing↗
PubMed1996

Hematological modifications induced by estrogens in cirrhotic animals.

Estrogens are known to have mitogenic activities and to influence hematic crasis. A wide literature on this subject allows us to re-evaluate the results of research performed in 1950. Estrogens injected into the peritoneum (estradiol propionate 2.5-5 mg, twice weekly) or into tibial bone marrow (estradiol propionate 1.5 mg weekly) of guinea pigs, after carbon tetrachloride induced cirrhosis (CCI4 inhalation for 7-15 min twice weekly), caused hyperchromic anemia, with erythroblastosis and leucocytosis; hyperplasia of reticulo-hystiocitary cells of bone marrow and lymphoid organs; splenic hemosiderosis; hyperplasia of immature bone marrow cells, with maturative inhibition; and terminal bone marrow hypoplasia. Our results agree with recent literature data concerning the role played by natural estrogens and environmental xenoestrogens that are capable of stimulating bone marrow progenitor cell proliferation and delaying their maturation, by the secretion of growth factors, especially from hyperplastic stromal cells, in solid and hematological tumors.

Animals↗
PubMed1997

[Enzootic spinal ataxia in fallow and wild red deer in Upper Bavaria].

Since 1993 several cases of spinal ataxia occurred in adult red and/or fallow deer in four farms in Southern Bavaria. The disease based on a secondary copper deficiency due to a high level of molybden and a low level of copper content in the feed. Some of the animals suffer from a severe disturbance of motion. In most cases the animals are shot at the beginning of illness. Histologically the most important lesions are in the spinal cord consisting mainly in a bilateral symmetric degeneration of dorsolateral and ventral areas of the white matter. Degeneration is caused by lamellar disintegration of the myelin connected with deposition of fine-granulated substances detectable by electronmicroscopical investigation. In the liver and other organs we always found a hemosiderosis which is also believed to be caused by copper deficiency.

Animals↗
PubMed1998

Copper toxicosis in sheep: a case report.

Two ewes died after being fed rabbit ration and mineral salts designated for cows. This food is known to contain copper levels above that indicated for sheep. Blood counts revealed anemia, and serological tests showed high blood urea nitrogen, glutamic pyruvic transaminase and glutamic oxalacetic transaminase values. At necropsy, the animals had hepatopathy and nephropathy. Hepatic copper levels were 414 ppm. Histological examination revealed chronic active hepatitis with bile casts and tubular nephrosis. The liver, spleen and kidneys had hemosiderosis. This was attributed to the massive hemolysis caused by the copper. The liver failure and hemolytic anemia caused death in these sheep.

Alanine Transaminase↗
PubMedDate not supplied

[Long term evolution in Blackfan-Diamond hypoplastic anemia (author's transl)].

Six cases of Blackfan-Diamond hypoplastic anemia are reported. Five were initiated within six months of life. All cases showed intense anemia, severe reticulopenia and hypersideremia. Two of them had associated malformations. Treatment was established with Dexametasone at high doses, followed by a maintenance treatment at lower doses. A partial response was obtained in all cases. Treatment with deforroxiamine was used in order to paliate hemosiderosis. Two cases developped microangiopathic hemolitic anemia; relations with primary disease could not be determined.

Abnormalities, Multiple↗
PubMedDate not supplied

[Calcium phosphate metabolism in thalassemia].

The AA. performed a screening test on 113 patients affected by beta thalassemia major ranging between 2 and 40 years of age, randomized among those who come to the Microcitemic Center of our Institute, and on a control group. In all of them serum levels of calcium, phosphate, parathyroid hormone (PTH), calcitonin and 25-OH vitamin D were measured. Average serum levels of PTH were significantly (P < 0.001) lower in our patients than in control group and 12.4% of the former were clearly under normal range, especially in the group over 16 years of age. Also serum levels of 25-OH vitamin D were lower in thalassemic patients than in controls, because of the presence of 32 patients with average values under normal limit. Our results are in agreement with current literature and underline the increasing incidence of endocrine complications in thalassemic patients who undergo high transfusion regimens, because of to the increase of hemosiderosis due to the low compliance to iron chelation therapy. Controversial is the pathogenesis of the absence of hypocalcemia in many patients with hypoparathyroidism and the cause of the deficit of vitamin D.

Adolescent↗
PubMedDate not supplied

Distribution, persistency, toxicity, and lack of replication of an E1A-deficient adenoviral vector after intracardiac delivery in the cotton rat.

Adenoviral vectors were inoculated via intracardiac injection into 5- to 1O-week-old cotton rats (Sigmodon hispidus) to evaluate the effects of systemic delivery. Cotton rats were chosen as a model because they are semipermissive to the replication of human adenoviruses. The vector used was AdV.RSV-tk, a replication-deficient adenovirus with a herpes simplex virus thymidine kinase gene inserted in the E1 region. Vector doses were 3 x 10(8), 3 x 10(9), and 3 x 10(10) viral particles per animal with and without ganciclovir at 10 mg/kg twice a day. Animals were sacrificed and necropsied at 24 hours, 7 days, and 14 days postinoculation. Gross and microscopic pathologic observations in dosed groups were compared with an unmanipulated control group. From each animal, 10 different organ systems were analyzed for histopathology and vector distribution. The only significant microscopic lesions observed were epicardial inflammation and splenic hemosiderosis. Vector sequences persisted throughout the 14-day assay with preponderance in the heart, lung, and lymphoid organs. Infectious virions were detected for 24 hours, and these virions were only detected at the site of injection of two animals in the highest dose group. No viral replication was detected. Therefore, systemic delivery of up to 3 x 10(11) viral particles/kg was well tolerated in this semipermissive host model and did not result in any significant pathology.

Adenovirus E1A Proteins↗
PubMed1998

[Pathogenetic aspects of hemolysis and changes of blood rheology in hereditary hemochromatosis].

AIM: To establish changes of and correlations between erythrodieresis and blood rheology in hereditary hemochromatosis (HHC). MATERIALS AND METHODS: Hemorheologic indices (asymptomatic blood and plasma viscosity, that of blood at low shift speed, red cell deformity and aggregation) were studied in 42 HHC patients and 23 healthy donors. The patients were divided into groups by homozygous (groups 1 and 2) or heterozygous (groups 3 and 4) allel genes and sex (females-groups 2 and 4, males-groups 1 and 3). RESULTS: All the patients had increased resistance of red cells in high percentage of their high-resistance populations (correlation index 0.8-0.9) due to destruction and elimination from the circulation. These changes were more pronounced in males, similar in homo- and heterozygotes. The presence in the peripheral blood of red cells with high resistance is associated with a 25-30% decrease in the red cell rigidity, in groups 1 and 3 this decrease reached 30-40%. To a certain degree high deformity and aggregation of red cells is explained by high plasma viscosity (correlation index 0.4). Plasma viscosity was high in all the patients of all groups. CONCLUSION: HHC runs with rejuvenascence of erythroid cells. Changed activity of erythrodieresis and damage to red cells at the level of microcirculation may be involved in iron metabolism disturbance and development of tissue hemosiderosis.

Adolescent↗
PubMedDate not supplied

[Magnetic resonance Imaging in the diagnosis of hemophilic lesions of joints].

A complex clinical, X-ray, and magnetic resonance tomographic study of 327 joints was made in 114 patients with different forms of hemophilic arthropathy. The diagnostic potentialities of MRI were defined and the MRI symptoms of hemophilic arthropathy, including degeneration of the articular cartilage, meniscus, ligaments, proliferation of the synovial membrane, fibrosis, blood accumulation, and hemosiderosis were revealed. Comparative analysis of the X-ray and MRI imaging findings of the joints at different stages of hemophilic arthropathy has shown that MRI has advantages in diagnosing acute and chronic hemarthrosis, moderate hemophilic osteoarthrosis as it can reveal abnormal processes in the X-ray negative structures of joints.

Adolescent↗