Severe Hepatopathy Research Articles

Morphologic lesions and acute toxicity in rainbow trout(Salmo Gairdneri)treated with 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin

To determine effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on growth, mortality, and morphologic lesions in rainbow trout, juvenile Shasta or Wytheville strain fish, obtained from 4 hatcheries, were administered graded single doses of TCDD, 0.1-125 micrograms/kg, ip. TCDD doses of 25 and 125 micrograms/kg caused 85% lethality 2-4 wk after treatment. At these high doses, death occurred before body weight loss could be detected. A lower dose of 5 micrograms/kg caused decreased growth and cumulative mortality of 20% after 11 wk. Stress associated with netting and weighing the fish at weekly intervals significantly shortened the delay period prior to TCDD-induced lethality. Gross and microscopic lesions were evident in rainbow trout treated with 10 micrograms TCDD/kg, but not in fish treated with 1 or 0.1 microgram/kg. Morphologic lesions occurred consistently in epithelial and lymphomyeloid tissues of TCDD-treated fish. Lymphomyeloid lesions included thymic involution, splenic lymphoid depletion, and hypocellularity of hematopoietic tissues in the head kidney and trunk kidney. In association with decreased hematopoiesis, peripheral leukopenia and thrombocytopenia occurred in Shasta strain yearling trout treated with 1 microgram/kg or more TCDD. Regarding epithelial lesions, all 4 hatchery strains treated with 10 micrograms/kg or more TCDD showed multifocal necrosis of gastric cardiac glandular mucosa, 3 of 4 hatchery strains showed vacuolar inclusions in exocrine pancreatic cells, and 2 of 4 hatchery strains showed fin necrosis. The severity and character of lesions in the liver and gastric mucosa varied markedly between hatchery strains of trout. One hatchery strain showed no hepatic lesions, two showed mild hepatocyte lesions, and one exhibited severe diffuse hepatopathy. In this severely affected hatchery strain, hyaline intracytoplasmic inclusions occurred in hepatocytes at 14 and 34 d after TCDD exposure, and bile-duct hyperplasia occurred at 34 d following TCDD exposure. One of 4 hatchery strains showed atrophy of serous gastric glands and 1 of 4 hatchery strains showed hyperplasia of these same glands at 25 and 34 d, respectively, following TCDD treatment. Thus, lymphomyeloid and epithelial tissues are the primary targets for TCDD-induced pathologic lesions in rainbow trout, and the incidence and severity of these lesions is influenced by the strain of trout used and the hatchery from which the trout were obtained.

Pathophysiology of Antithrombin III Deficiency

This article focuses on the pathophysiology of thrombosis in patients with acquired antithrombin III deficiency. Antithrombin III is an important natural inhibitor of the hemostatic mechanism, and a hypercoagulable state is often induced in diseases causing antithrombin III deficiency. Laboratory determination of antithrombin III activity is particularly useful in the clinical evaluation and therapeutic management of patients with disseminated intravascular coagulation, nephrotic syndrome, and severe hepatopathy.

Specific treatment of advanced schistosomiasis liver disease in man: favourable results.

One hundred eighty-four patients with hepatosplenic schistosomiasis mansoni from the northeast of Brazil were studied. All were treated with a single dose of Oxamniquine or Praziquantel, and were observed over 6 to 12 months. Special attention was given to the evolution of severe hepatopathy. Favourable results were obtained, particularly with the compensated hepatosplenic form. Hepatic function showed great improvement. Hepatomegaly and splenomegaly were significantly reduced in size, to a greater or lesser extent, in the great majority of patients. The implications of the results obtained are considered below.

Identification of Ferrous Sulfate Toxicity in a Commercial Broiler Flock

A 2.5% mortality rate was observed in a flock of 19,000 commercial one-day-old broiler chicks that had been placed 24 hours previously on litter treated with ferrous sulfate heptahydrate. Ulcerative ventriculitis and severe hepatopathy were the primary lesions observed grossly and microscopically. Pooled digesta contained 6854 ppm iron. Lesions identical to those found in the field case were reproduced experimentally.

Glomerular lesions induced in Pekin ducks by dietary administration of dimethylnitrosamine

Histochemical and electron microscopic studies were completed on the kidneys of Pekin ducks receiving a dietary supplement of dimethylnitrosamine at a concentration of 0.005%. Ducks were given the diets when 36 hours of age; test and control ducks (fed only mash) were killed by decapitation at weekly intervals for 8 weeks for necropsy and collection of tissue for histopathology. Tissues for electron microscopic examination were obtained after 5 and 6 weeks, fixed in Palade's solution, and embedded in Epon. Necropsy findings included subcutaneous edema, ascites, hydropericardium, splenomegaly, hepatic necrosis, and swelling of the kidneys. Obvious alterations in the glomeruli were present after 3 weeks of feeding and consisted of a reduced cellularity of the glomerular tufts with diffuse thickening of the capillary loops; but, early, the basal stalk region was spared. In severely affected glomeruli, the normal architecture was replaced by a solid amorphous, hyaline, eosinophilic material. The deposits stained variably with Gomori's trichrome. The material in the glomeruli was negative for amyloid by Congo red staining, took the silver component of the Humason and Lushbaugh stain, was inconsistently stained by Weigert's method for fibrin, and was PAS positive. Since the PAS staining response was not removed by diastase or hyaluronidase digestion and was not metachromatic with toluidine blue, the material is apparently not a simple mucopolysaccharide. Ultrastructural alterations included thickening of the basement membrane of the glomerular capillaries by “deposits” of an electron dense material. The amorphous material was distributed through the various divisions of the basement membranes throughout the glomerulus. In severely affected glomeruli the ultrastructural features were obliterated by the deposited material. There were no recognizable signs of collagen, fibrin, or amyloid in the thickened basement membranes. The glomerular lesions resemble the glomerulosclerosis described in experimental diabetes and in experimental toxicoses characterized by severe hepatopathy.