Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Daily, for 14 days, rabbits of one group were injected with corticotropin, i.e. ACTH-zinc-phosphate (10 units/kg), whereas rabbits of another group were given (in addition) sodium ribonucleate (40 mg/kg) through a tube into the stomach. Formation of lysyl-tRNA, leucyl-tRNA, and alanyl-tRNA in the liver and the skeletal muscles proved to be significantly greater in the animals which received ACTH together with sodium ribonucleate, as compared to that in the animals given the hormone alone. Hyperglycemia, hepatomegaly, and emaciation were less pronounced in the animals given both the preparations.
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PMID:[Effect of enteral administration of sodium ribonucleate on the synthesis of amino acyl t RNA in the liver and skeletal muscles of rabbits in experimental hypercorticism]. 19 79

A 74-year-old housewife was admitted to the hospital with complaints of high fever and general fatigue. The physical examinations on admission showed no particular findings except for mild hepatomegaly, but laboratory findings showed severe liver dysfunction, active inflammation and negative tuberculine test. On the 4th day, she suddenly complained of severe respiratory distress. A chest X-ray film demonstrated surprising changes in comparison with that taken on admission. On suspicion of adult respiratory distress syndrome (ARDS) associated with military tuberculosis (Miliary TB), administration of Methylpredonisolone (1000 mg a day for 3 days) in addition to antituberculous drugs was immediately started. With this therapy she was recovered from such ill condition, but the general exhaustion and slight fever continued. We suspected that her condition might be due to adrenocortical involvement of Miliary TB and hormonal examinations were performed. Unexpectedly, Cushing's syndrome was suspected on the basis of the following; high level of plasma cortisol without normal daily variation, normal ACTH level, an absent response to the Dexamethasone suppression test. Computed tomography revealed left side adrenal mass. During these examinations, renal dysfunction probably due to Miliary TB grew gradually worse and she died of renal failure on the 56th day. Necropsy revealed disseminated tuberculosis involving the lungs and the liver, but the adrenal glands were not examined.
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PMID:[A case of miliary tuberculosis (miliary TB) accompanied with adult respiratory distress syndrome (ARDS) in a patient with Cushing's syndrome]. 140 68

Of cases of hyperadrenocorticism in small animals 80-85% are the result of adrenocortical hyperplasia. Middle-aged or older Poodles, Dachshunds, Boston Terriers and Boxers are most commonly affected, and cats rarely. Clinical signs include polydipsia, polyuria, alopecia, abdominal distension, lethargy, weakness, hepatomegaly, calcinosis cutis, testicular atrophy and anestrus. Hematologic and biochemical changes may include neutrophilia, lymphopenia, monocytosis, eosinopenia, increased blood levels of alkaline phosphatase, SGPT, cholesterol, Na and glucose, and decreased K and T4 levels. The high-dosage dexamethasone suppression test helps differentiate pituitary-dependent hyperadrenocorticism from that caused by adrenal tumors. The low-dosage dexamethasone suppression test, determination of plasma ACTH levels, and ACTH response test are additional diagnostic aids in the diagnosis of Cushing's disease. Medical treatment involves oral use of mitotane (o,p'-DDD) at 50 mg/kg/day for 7 days and prednisone or prednisolone at 0.05 mg/kg/day. Hypophysectomy has been used with only 5% mortality in cases of pituitary-dependent hyperadrenocorticism. Adrenalectomy is indicated in cases of adrenal neoplasia.
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PMID:Diseases of the adrenal cortex of dogs and cats. 633 May 21

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