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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A three-year-old Border collie was presented with a two-week history of lethargy, stiff gait, polydipsia and polyuria. Biochemical analysis revealed hypercalcaemia. Serum concentrations of 25-hydroxyvitamin D (25[OH]D) and 1,25-dihydroxyvitamin D (1,25[OH]2D) were markedly elevated and parathyroid hormone was undetectable. Subsequent analysis of the dog's diet revealed that the food contained excessive amounts of vitamin D. The hypercalcaemia resolved following treatment with bisphosphonates and dietary change. Hypervitaminosis D was diagnosed in a second unrelated dog, which had been fed the same brand of dog food as case 1. The dog was also hypercalcaemic and had markedly elevated serum concentrations of 25(OH)D and 1,25(OH)2D. Hypervitaminosis D in dogs has been reported to occur secondarily to ingestion of either rodenticides containing cholecalciferol or antipsoriatic ointments that contain vitamin D analogues. Hypervitaminosis D has also been reported following the treatment of hypoparathyroidism. To the authors' knowledge, this is the first report of hypervitaminosis D in dogs following the accidental over supplementation of a commercial diet with vitamin D. While the benefits of adequate dietary vitamin D are well established in dogs, the potential deleterious effects of over supplementation of vitamin D should also be acknowledged.
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PMID:Hypercalcaemia in two dogs caused by excessive dietary supplementation of vitamin D. 1603 50

Iatrogenic hyperadrenocorticism is an extremely rare condition in cats. Twelve cats with a medical history of progressive skin lesions and long-term treatment with corticosteroids were retrospectively studied. Noncutaneous signs in the cats were variable and included anorexia, lethargy, polydipsia, polyuria, and atrophy of the thigh muscles. Laboratory abnormalities included leukocytosis, elevated alanine aminotransferase levels, and hyperglycemia. Transient diabetes mellitus was a secondary complication in four cats, and transient hypothyroidism was suspected in four cats. The mean time for regression of signs was 4.9 months after corticosteroid withdrawal.
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PMID:Iatrogenic hyperadrenocorticism in 12 cats. 1708 87

Psychogenic polydipsia (PPD), a clinical disorder characterized by polyuria and polydipsia, is a common occurrence in inpatients with psychiatric disorders. The underlying pathophysiology of this syndrome is unclear, and multiple factors have been implicated, including a hypothalamic defect and adverse medication effects. Hyponatremia in PPD can progress to water intoxication and is characterized by symptoms of confusion, lethargy, and psychosis, and seizures or death. Evaluation of psychiatric patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria, hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy in psychiatric patients should include fluid restriction and behavioral and pharmacologic modalities.
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PMID:Psychogenic polydipsia review: etiology, differential, and treatment. 1752 21

Sixteen animals affected in 2 outbreaks of pet food-associated renal failure (2 dogs in 2004; 10 cats and 4 dogs in 2007) were evaluated for histopathologic, toxicologic, and clinicopathologic changes. All 16 animals had clinical and laboratory evidence of uremia, including anorexia, vomiting, lethargy, polyuria, azotemia, and hyperphosphatemia. Where measured, serum hepatic enzyme concentrations were normal in animals from both outbreaks. All animals died or were euthanized because of severe uremia. Distal tubular lesions were present in all 16 animals, and unique polarizable crystals with striations were present in distal tubules or collecting ducts in all animals. The proximal tubules were largely unaffected. Crystals and histologic appearance were identical in both outbreaks. A chronic pattern of histologic change, characterized by interstitial fibrosis and inflammation, was observed in some affected animals. Melamine and cyanuric acid were present in renal tissue from both outbreaks. These results indicate that the pet food-associated renal failure outbreaks in 2004 and 2007 share identical clinical, histologic, and toxicologic findings, providing compelling evidence that they share the same causation.
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PMID:Outbreaks of renal failure associated with melamine and cyanuric acid in dogs and cats in 2004 and 2007. 1782 96

A 10-year-old female Dachshund was presented with a history of mammary masses, slight lethargy, polyuria, and polydipsia. Physical examination findings included masses involving the first, second, and fourth mammary glands of the left side. The mandibular, axillary, and right popliteal lymph nodes were mildly enlarged. Serum chemistry results included hypercalcemia (13.9 mg/dL, reference interval 8.0-11.5 mg/dL). Although intact parathyroid hormone (PTH) concentration (1.05 pmol/L) was below the reference interval (2-13 pmol/L), PTH-related protein (PTHrP) concentration was markedly increased (9.40 pmol/L, reference value < 2 pmol/L). The masses were surgically removed, and the histopathologic diagnosis was complex mammary carcinoma. Three weeks after surgery, serum total calcium concentration had decreased to 10.5 mg/dL. Resolution of the hypercalcemia and clinical signs supported a diagnosis of humoral hypercalcemia of malignancy associated with mammary gland carcinoma.
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PMID:Hypercalcemia and high parathyroid hormone-related peptide concentration in a dog with a complex mammary carcinoma. 1804 7

Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes hemorrhagic colitis and acute renal failure. We used a germ-free mouse model to investigate the role of host factors, Shiga toxin 2 (Stx2), and bacterial strain in disease due to EHEC. Germ-free male and female Swiss-Webster mice that were 3 days to 12 weeks old were orally inoculated with 1 of 10 EHEC strains or derivatives of two of these strains with Stx2 deleted. All inoculated mice became infected regardless of the inoculum dose. All bacterial strains colonized the intestines, reaching levels of 10(9) to 10(12) CFU/g of feces by 4 days after inoculation. Seven of the 10 wild-type strains caused disease. However, the two Stx2 deletion mutants, unlike the Stx2(+) parental strains, did not cause disease. The clinical signs of disease in mice included lethargy, dehydration, polyuria, polydypsia, and death. Postmortem examination of affected mice revealed dehydration and luminal cecal fluid accumulation. Histologic examination revealed close adherence of bacteria to the intestinal epithelium in the ileum and cecum but not in the colon. Other lesions included progressive renal tubular necrosis, glomerular fibrin thrombosis, and red blood cell sludging. The severity of disease varied according to the bacterial strain and age, but not sex, of the host. This study demonstrated that EHEC colonizes germ-free mice in large numbers, adheres to the intestinal epithelium, and causes luminal cecal fluid accumulation and progressive renal failure. The disease in mice was Stx2 and bacterial strain dependent. This animal model should be a useful tool for studying the pathogenesis of renal disease secondary to EHEC infection.
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PMID:Pathogenesis of renal disease due to enterohemorrhagic Escherichia coli in germ-free mice. 1844 87

A 3-year-old male nanday conure (Nandayus nenday) was presented with acute lethargy, polyuria, and polydipsia. Marked persistent hyperglycemia, glycosuria, and ketonuria were also noted. The serum insulin concentration (< 3 microU/ml) was lower than reference ranges described for other psittacine birds. Initial treatment included insulin, antibiotics, and supportive care. Insulin therapy was adjusted based on results of serial blood glucose curves. Histopathologic examination of pancreatic biopsy samples revealed normal exocrine pancreatic tissue with rare lymphoplasmocytic infiltrates and absence of pancreatic islets, suggesting atrophy of endocrine pancreatic tissue. Resolution of clinical signs and a normalized blood glucose curve were obtained after administration of long-acting insulin (0.3 IU/kg IM AM and 0.25 IU/kg IM PM). One month after initial presentation, the conure was admitted for severe dyspnea and lethargy and died despite supportive care. Histopathologic examination of the pancreas revealed nearly total depletion of the endocrine pancreas with moderate lymphoplasmocytic pancreatitis. Immunohistochemical evaluation of the remaining pancreatic islets was negative for the presence of insulin and positive for glucagon. Results of polymerase chain reaction tests for Chlamydophila psittaci performed on tissues from the liver, spleen, and lung were negative. Transmission electron microscopy did not demonstrate viruses. Clinical and pathological findings observed in this case are consistent with insulin-dependant type 1 diabetes.
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PMID:Diabetes mellitus in a nanday conure (Nandayus nenday). 1901 99

A 4-year-old male, castrated, mixed-breed dog was presented to the Colorado State University Veterinary Teaching Hospital with a 1-week history of polyuria, polydipsia, lethargy, fever, inappetence, weight loss, and soft mucoid stool. The dog was depressed and had pale, icteric mucous membranes. Results of a CBC included normocytic, normochromic, nonregenerative anemia, neutropenia, and thrombocytopenia, with 43% blast cells (200/microL), many of which contained fine azurophilic granules. Cytologic evaluation of the bone marrow aspirates revealed mild granulocytic hyperplasia that appeared to be left-shifted in an apparent maturation arrest. A large population of blast cells comprised 35% of nucleated cells; the blasts had high nuclear to cytoplasmic ratios, deeply basophilic cytoplasm with vacuoles, and prominent nucleoli. Most cells also contained many fine azurophilic granules clustered in the paranuclear region. At necropsy, neoplastic cells were abundant in the bone marrow. Immunohistochemically the cells expressed CD3epsilon, and an oligoclonal T-cell rearrangement was found. The diagnosis was proliferative disorder of CD3(+) granular lymphocytes, with associated pancytopenia. Because the blast cells were morphologically similar to myeloblasts and immunohistochemistry was required to confirm the diagnosis, T-cell lymphoproliferative disease should be considered in dogs with pancytopenia presenting with similar clinical features.
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PMID:What is your diagnosis? Pancytopenia in a dog. 1905 79

We retrospectively studied seven children (six girls, one boy) aged from 7.5 to 25 months who presented to our institution after taking large doses of vitamin D (900 000-4 000 000 U) prescribed by medical practitioners for wrong indications like failure to thrive, etc. The clinical manifestations were constipation, decreased appetite, lethargy, polyuria, dehydration and failure to thrive. All patients had hypercalcemia (serum calcium ranging from 12 to 16.8 mg/dl), high 25[OH]D levels (ranging from 96 to >150 ng/ml), suppressed intact parathyroid hormone (ranging from <3 to 8.1 pg/ml). Hypercalciuria (urinary calcium/creatinine ranging from 1 to 2.45) was found in all patients, while nephrocalcinosis was present in five patients. All were treated with intravenous fluids, oral prednisolone, restriction of calcium in diet, while four patients received pamidronate infusion for reducing hypercalcemia.
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PMID:Hypercalcemia due to hypervitaminosis D: report of seven patients. 1933 14


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