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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic fatty infiltration complicating jejunoileal bypass can be massive and may require restoration of gastrointestinal continuity. This fatty infiltration appears to be caused by protein depletion associated with adequate or high carbohydrate intake. The present study has shown that calorie-free amino acid alimentation can reverse these changes. In three of thirteen patients who underwent 12 inch to 6 inch jejunoileal bypass procedures, symptomatic hepatomegaly developed with near total replacement of hepatocytes by massive fatty infiltration. After undergoing liver scan, liver biopsy, and liver function tests, the patients were started on a peripheral infusion of 2L per day of a 4.25 per cent crystalline amino acid solution, allowing for fat mobilization while preserving body protein stores. All oral intake was withheld except for water. At the end of a fourteen to twenty-one day infusion period, serum albumin levels increased by 1 gm in all patients. Decreases in liver volume of 83, 45, and 40 per cent occurred. During the infusion period ketonuria was 4 plus in all patients indicating active lipolysis. Weight loss was impressive (17, 19, and 40 pounds). All patients showed marked symptomatic improvement, and postinfusion liver biopsy specimens showed a return to near normal architecture. Maintenance of normal liver size by a high-protein, low-carbohydrate diet was observed in a five to seven month follow-up period. In contrast to previous studies using standard hyperalimentation solutions, the use of calorie-free amino acid solutions reverses the hepatic fatty infiltration seen after intestinal bypass by mobilization of fat. This fat mobilization does not occur as readily in the presence of large amounts of glucose.
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PMID:Reversal of severe fatty hepatic infiltration after intestinal bypass for morbid obesity by calorie-free amino acid infusion. 80 74

Thirteen cats with diabetes mellitus were evaluated. Clinical signs included polydipsia, polyuria, polyphagia, lethargy, and weight loss. Results of physical examination included obesity, hepatomegaly, mild seborrhea sicca, muscle wasting, and dehydration. One cat walked plantigrade and was suspected of having a diabetic neuropathy. Persistent hyperglycemia, glucosuria, high liver enzyme activities, hypercholesterolemia, hyperproteinemia, and low electrolyte concentrations were the common laboratory findings. In 3 cats diabetes mellitus developed after megestrol acetate therapy; 2 of these cats required only temporary insulin treatment. In a 3rd cat, which had no history of receiving diabetogenic drug therapy, remission of diabetes mellitus also was observed. Serum insulin and plasma glucose concentrations were determined in 6 cats after administration of an intermediate-acting insulin (isophane insulin) and in 3 cats after administration of a long-acting insulin (protamine zinc insulin). The insulin concentration peaked 2 to 6 hours after the injection of intermediate-acting insulin and 6 to 12 hours after the injection of long-acting insulin. The lowest glucose concentration was recorded 4 to 8 hours after injection of intermediate-acting insulin, and 6 to 12 hours after injection of long-acting insulin. It was concluded that, although insulin therapy must be adjusted to the individual, the diabetic cat usually requires twice-daily administration of isophane insulin; however, the protamine zinc insulin can be given once daily for satisfactory control.
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PMID:Insulin therapy in cats with diabetes mellitus. 629 64

Intravenous (i.v.) infusion of excessive energy has been associated with hepatic steatosis. The time course of liver lipid accumulation was examined during 6 days of i.v. hyperalimentation with fat-free infusate. Adult male rats with indwelling superior vena cava cannulas received a dextrose-amino acid infusate for 0, 1/2, 1, 2, 4 or 6 days to provide 146% of nonprotein energy requirement [congruent to 350 non-protein kcal/(kg . day)] and 335% of nitrogen requirement [congruent to 2.7 g amino nitrogen/(kg . day)]. Significant hepatomegaly was apparent by day 1/2. Initially, glycogen deposition accounted for the liver enlargement, but after day 2, liver glycogen was declining and liver lipid was increasing. By day 4, liver lipid had increased fourfold and was the major contributor to hepatomegaly. Concurrent with fatty liver metamorphosis, hepatic essential fatty acid deficiency (EFAD) developed by day 4; liver linoleic acid levels had dropped from 20 to 1% of total fatty acids, and liver triene:tetraene ratio was 0.68. Similar changes in hepatic phospholipid fatty acids were observed. Enhanced lipogenesis and impaired lipid transport is known to accompany EFAD and may underlie the observed steatosis. A doubling of plasma cholesterol levels was also associated with steatosis. The mechanism leading to this increase in plasma cholesterol warrants further investigation.
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PMID:Development of hepatic steatosis and essential fatty acid deficiency in rats with hypercaloric, fat-free parenteral nutrition. 643 8

Concurrent diabetes mellitus and hyperadrenocorticism were diagnosed in 30 dogs over a 2-year period. Clinical signs included polyuria, hepatomegaly, polyphagia, abdominal distension, truncal alopecia, anorexia, and vomiting. Because of the similar clinical and laboratory findings for hyperadrenocorticism and diabetes mellitus, hyperadrenocorticism was initially overlooked in some dogs. Insulin resistance, characterized by high daily insulin requirements, developed in the diabetic dogs with untreated hyperadrenocorticism. Therapy with o,p'-DDD resulted in precipitous declines in insulin requirements. By lowering the dosage of o,p'-DDD and supplementing with glucocorticoids during the o,p'-DDD loading period, serious hypoglycemia was avoided. Control of coexisting hyperadrenocorticism lessened the severity of the diabetes mellitus, but insulin therapy remained a necessity in all dogs.
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PMID:Diagnosis and management of concurrent diabetes mellitus and hyperadrenocorticism in thirty dogs. 700 30

Recent attempts to reduce weight by patients with anorexia nervosa have sometimes led to life-threatening hematologic complications. This report describes an instance in which a patient with anorexia nervosa and pancytopenia drastically improved with treatment that included administration of granulocyte colony-stimulating factor. The patient had lost 27 kg of body weight within 8 months. Even after admission, the blood cell count continued to decrease rapidly as follows: platelet, from 244 x 10(3)/microliters to 44 x 10(3)/microliters; erythrocyte, from 4.04 x 10(6)/microliters to 2.58 x 10(6)/microliters; and leukocyte, from 4.8 x 10(3)/microliters to 1.6 x 10(3)/microliters (granulocyte, 0.8 x 10(3)/microliters). Complications included pneumomediastinum, pneumothorax, purpura, petechiae, hepatomegaly, fever, gangrenous stomatitis, and somnolence. Bone marrow aspiration disclosed absence of fat cells, marrow hypoplasia, and infiltration of the mature lymphocytes. Intravenous hyperalimentation, blood transfusion, gamma-globulin, and antibiotics were administered, but leukopenia and fever remained. However, administration of recombinant human granulocyte colony-stimulating factor dramatically reversed the leukopenia and fever. With careful nutrition therapy, the patient's blood cell count and bone marrow normalized by the time of discharge. It was concluded that severe hematologic disorders may occur in patients with anorexia nervosa, and advanced treatment may be required to save the patient's life.
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PMID:Case report: reversal of severe leukopenia by granulocyte colony-stimulating factor in anorexia nervosa. 768 51

The study population in this report by Lin et al. was ob/ob mice that have an inherited genetic deficiency of the appetite-suppressing hormone leptin. These mice develop hyperinsulinemia, insulin resistance, and fatty livers. Compared with their lean littermates and wild-type C57BL-6 mice, ob/ob mice have hepatomegaly. In this study, the authors compared three different groups of adult mice (aged 8-10 wk), including male ob/ob C57BL-6 mice, their lean littermates, and wild-type C57BL-6 mice of the same age and sex. The primary purpose of this study was to test the efficacy of metformin for treatment of fatty liver disease in obese, ob/ob mice that develop hyperinsulinemia or insulin resistance and fatty livers. Metformin therapy was found to eliminate fatty liver disease in this model. The potential mechanisms of the action of metformin were the inhibition of hepatic tumor necrosis factor (TNF)alpha and several TNF-inducible responses, which are likely to promote hepatic steatosis and necrosis. In these experiments, ob/ob mice were divided into three treatment groups. Group 1 consisted of eight mice that were treated with metformin and permitted to consume a nutritiously replete liquid mouse diet ad libitum. Mice in group 2 (n = 8) did not receive metformin but were pair-fed the same volume of liquid diet that the mice in the metformin-treated group had consumed on the previous day. Obese ob/ob mice in group 3 (n = 4) and lean mice received no metformin, as with the mice in group 2, but were permitted to consume the liquid diet ad libitum. Liquid diet was given to facilitate accurate daily comparison of food intake among the various treatment groups. All mice were weighed at the beginning of the study and weekly thereafter until killed and then sera, fat, and liver tissues were collected. Tissues were either fixed in buffered formalin and processed from the deceased mice for histology or snap frozen in liquid nitrogen and stored until RNA and proteins were isolated. The feeding protocol was repeated with a second group of 18 ob/ob mice. After 4 wk, hepatocytes were obtained by in situ liver perfusion with collagenase and assayed for cellular adenosine triphosphate (ATP) content. In each experiment, hepatocytes isolated from 3 mice from each treatment group were suspended in a medium and pooled for subsequent analysis to evaluate cell viability, determine the number of obtained cells, and to assay cellular ATP content. These experiments were repeated using another 3 mice from each treatment group, so that analysis of hepatocytes took place from six ob/ob mice in each feeding group.Hepatic steatosis was decreased significantly only in the metformin-treated group. The authors found that metformin's beneficial effect on the fatty liver disease of mice was not due to its ability to constrain hyperphagia, nor due to decreased caloric ingestion, because the daily caloric intakes of the metformin-treated mice and the pair-fed control mice were virtually identical. These caloric intakes were consistently approximately 20% less than that of another obese control group that was permitted to consume diet ad libitum. The authors also observed no significant effect of metformin on serum glucose concentration from fed, ob/ob mice. Metformin is known to reduce hyperinsulinemia by about 40% in both of these obese hyperinsulinemic and insulin-resistant rodent strains. In conclusion, Lin et al. documented that metformin improves fatty liver disease and reverses hepatomegaly, steatosis, and aminotransferase abnormalities in mice. In addition, the authors suggest that metformin might inhibit dieting-induced redistribution of lipid from the liver to adipose tissue depots. In summary, this study identifies a potential treatment for fatty liver disease in humans.
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PMID:Current biochemical studies of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis suggest a new therapeutic approach. 1449 93

Hyperadrenocorticism is a common endocrinopathy which results from the excessive production of cortisol by the adrenal cortex. In the majority of cases, this increased secretion of cortisol results from stimulation of the adrenal cortex by adrenocorticotrophic hormone secreted from the pituitary gland. In a smaller number of cases adrenal tumours are present. Clinical signs are variable but commonly include polydipsia and polyuria, polyphagia, obesity, a pendulous abdomen, hepatomegaly, alopecia, lethargy, weakness and anoestrus. Haematology, serum chemistry analysis and urinalysis should be performed on a dog with suspected hyperadrenocorticism. Finding a significant number of changes that are consistent with hyperadrenocorticism often allows a presumptive diagnosis to be made. Other tests can then be used to confirm the diagnosis and to help localise the cause, including liver biopsy, radiology, ultrasonography, gamma camera imaging, computed tomography, and measurement of blood and urine hormone levels. The ACTH stimulation test, low dose dexamethasone suppression test and measurement of the urine cortisol:creatinine ratio are used to assess whether hyperadrenocorticism is present. The high dose dexamethasone suppression test, measurement of plasma ACTH, corticotropin-releasing hormone stimulation test, and a modification of the urinary cortisol:creatinine ratio test are then implemented to determine the aetiology. The treatment of choice for adrenal neoplasia is surgical removal of the affected adrenal. On the other hand, pituitary hyperplasia or neoplasia may be treated either surgically, by bilateral adrenalectomy or hypophysectomy, or medically. The drug which is chosen most commonly for medical management is 1,1-dichloro-2(O-chlorophenyl)-2-(P-chlorophenyl) ethane (op'-DDD), which can be used to suppress adrenal function or to completely destroy the adrenal cortex. The antifungal agent ketoconazole also suppresses adrenal steroid synthesis and provides an alternative form of medical treatment for hyperadrenocorticoid dogs.
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PMID:Canine hyperadrenocorticism. 1603 96

Nonalcoholic steatohepatitis (NASH) is one of the leading causes of chronic liver disease worldwide. However, details of pathogenetic mechanisms remain unknown. Deletion of both p62/Sqstm1 and Nrf2 genes spontaneously led to the development of NASH in mice fed a normal chow and was associated with liver tumorigenesis. The pathogenetic mechanism (s) underlying the NASH development was investigated in p62:Nrf2 double-knockout (DKO) mice. DKO mice showed massive hepatomegaly and steatohepatitis with fat accumulation and had hyperphagia-induced obesity coupled with insulin resistance and adipokine imbalance. They also showed dysbiosis associated with an increased proportion of gram-negative bacteria species and an increased lipopolysaccharide (LPS) level in feces. Intestinal permeability was elevated in association with both epithelial damage and decreased expression levels of tight junction protein zona occludens-1, and thereby LPS levels were increased in serum. For Kupffer cells, the foreign body phagocytic capacity was decreased in magnetic resonance imaging, and the proportion of M1 cells was increased in DKO mice. In vitro experiments showed that the inflammatory response was accelerated in the p62:Nrf2 double-deficient Kupffer cells when challenged with a low dose of LPS. Diet restriction improved the hepatic conditions of NASH in association with improved dysbiosis and decreased LPS levels. The results suggest that in DKO mice, activation of innate immunity by excessive LPS flux from the intestines, occurring both within and outside the liver, is central to the development of hepatic damage in the form of NASH.
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PMID:Deletion of both p62 and Nrf2 spontaneously results in the development of nonalcoholic steatohepatitis. 2927 15