Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Equine and canine Cushing's syndrome, both of which are the result of elevated cortisol levels, show some different pathogenetical and clinical features and require different therapeutical approaches. In older horses the equine Cushing's syndrome (ECS) is not uncommon. Nearly all cases result from excessive hormone production in cells of the pars intermedia of the pituitary. Besides elevated levels of adrenocorticotrope hormone (ACTH), high peripheral levels of pro-opiomelanocortin, beta-endorphines and alpha-melanocyte-stimulating hormone can be measured. In middle-aged and geriatric dogs, Cushing's syndrome is the most frequently diagnosed endocrinologic abnormality. 80-85% of cases are pituitary-dependent and 15-20% are caused by cortisol producing tumors of the adrenals. 90% of pituitary lesions can be identified as adenomas, which are localised in most cases in the pars distalis of the gland, but may occur rarely in the pars intermedia, too. Clinical symptoms in both species are characterised by wasting despite good appetite or polyphagia, reduction of muscle mass with altered fat deposition and lethargy. Whereas polydipsia/polyuria is a very common feature in dogs with Cushing's syndrome, in horses it is almost invariably a sign of concurrent secondary diabetes mellitus. A typical symptom in ECS is a continuously growing haircoat (hirsutism), whereas in canine Cushing's syndrome generalised alopecia may bring the owner to consult a veterinarian. The symptoms and diagnostic procedures in a 33-year-old mare are described. Useful diagnostic tests are reviewed with special attention to species differences in reacting to them. The therapeutic approach with dopamine-agonists such as bromocriptine and pergolide as well as cyproheptadine to ECS is reviewed.
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PMID:[Equine Cushing syndrome (ECS). Case report, review of its diagnosis and therapy and substantial differences from Cushing syndrome in dogs]. 962 47

The cardinal clinical manifestations of major depression with melancholic features include sustained anxiety and dread for the future as well as evidence of physiological hyperarousal (e.g., sustained hyperactivity of the two principal effectors of the stress response, the corticotropin-releasing-hormone, or CRH, system, and the locus ceruleus-norepinephrine, or LC-NE, system). Sustained stress system activation in melancholic depression is thought to confer both behavioral arousal as well as the hypercortisolism, sympathetic nervous system activation, and inhibition of programs for growth and reproduction that consistently occur in this disorder. Data also suggest that activation of the CRH and LC systems in melancholia are involved in the long-term medical consequences of depression such as premature coronary artery disease and osteoporosis, the two-three-fold preponderance of females in the incidence of major depression, and the mechanism of action of antidepressant drugs. In addition, recent data reveal important bidirectional interactions between stress-system hormonal factors in depression and neural substrates implicated in many discrete behavioral alterations in depression (e.g., the medial prefrontal cortex, important in shifting affect based on internal and external cues, the mesolimbic dopaminergic reward system, and the amygdala fear system). We have also advanced data indicating that the hypersomnia, hyperphagia, lethargy, fatigue, and relative apathy of the syndrome of atypical depression are associated with concomitant hypofunctioning of the CRH and LC-NE systems. These data indicate the need for an entirely different therapeutic strategy than that used in melancholia for the treatment of atypical depression, and they suggest that this subtype of major depression will be associated with its own unique repertoire of long-term medical consequences.
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PMID:The endocrinology of melancholic and atypical depression: relation to neurocircuitry and somatic consequences. 989 54

An 11-month-old, neutered female miniature schnauzer presented with a severe head injury. The dog was treated for the acute effects of craniocerebral trauma and was hospitalized for just over a week. Several weeks later, she became weak and lethargic. A diagnosis of hypoadrenocorticism was confirmed with an adrenocorticotropin hormone (ACTH) stimulation test. An endogenous ACTH assay confirmed secondary hypoadrenocorticism. The dog was tested for hypopituitarism with canine thyroid-stimulating hormone and thyroxine serum assays and an insulin-like growth factor assay. These tests could not confirm panhypopituitarism in this dog. The hypoadrenocorticism was treated with prednisone, and the dog remains controlled adequately three years later.
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PMID:Secondary hypoadrenocorticism associated with craniocerebral trauma in a dog. 1010 79

Twenty-eight dogs with iatrogenic hyperadrenocorticism were studied. The most common clinical signs were cutaneous lesions (27/28), polydipsia (21/28), polyuria (19/28), and lethargy (16/28). The most predominant findings on biochemical profile were elevated alkaline phosphatase (ALP, 15/28) and alanine transferase (ALT, 14/28); hypercholesterolemia (14/28); elevated aspartate transferase (AST, 12/28); and elevated triglycerides (12/18). Baseline cortisol levels of all 28 dogs were at the lower end of the reference range and exhibited suppressed or no response to adrenocorticotropic hormone (ACTH) stimulation. The mean time for each dog to show initial improvement of clinical signs after corticosteroid withdrawal was six weeks, with another mean time of 12 weeks to demonstrate complete remission.
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PMID:Iatrogenic hyperadrenocorticism in 28 dogs. 1033 57

Primary hypoadrenocorticism was diagnosed in an eight-year-old neutered male cat. The predominant presenting complaint was dysphagia. Other historical signs included lethargy, weight loss, polydipsia, polyuria, muscle weakness and occasional vomiting. The signs had waxed and waned over the two months before presentation and had improved when the cat was treated with enrofloxacin and prednisolone by the referring veterinarian. On referral, dehydration, depression and poor bodily condition were found on physical examination. Results of initial laboratory tests revealed mild anaemia, hyperkalaemia, hyponatraemia, hypochloraemia and elevations in serum creatinine and creatine kinase. The diagnosis of primary adrenocortical insufficiency was established on the basis of results of an adrenocorticotropic hormone (ACTH) stimulation test and endogenous plasma ACTH determination. Initial therapy for hypoadrenocorticism included intravenous administration of 0.9 per cent saline and dexamethasone, and oral fludrocortisone acetate. Within one week the cat was clinically normal and two years later was still alive and well on fludrocortisone acetate treatment only.
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PMID:Hypoadrenocorticism in a cat. 1132 66

A 34-year-old woman was hospitalised with hypotension, lethargy and ventricular tachycardia, five months after an uneventful pregnancy and delivery. Laboratory values were compatible with anterior (abnormal concentrations of adrenocorticotropin hormone, thyroid stimulating hormone, prolactin) and posterior (diabetes insipidus) pituitary gland insufficiency. An MRI scan revealed that there was no pituitary enlargement and that the pituitary stalk was normal. The prompt recognition of hypophysitis as a potentially fatal condition is important, as a life-saving treatment is available.
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PMID:[Clinical thinking and decision making in practice. A patient with postpartum malaise, anorexia, and ventricular tachycardia]. 1177 Feb 65

A 74-year-old man presented in a near terminal state with progressive generalized muscular weakness, gastrointestinal disturbances, and lethargy. Investigations revealed hypotension, hyponatremia, hypoglycemia, and low plasma cortisol concentration accompanied by undetectable plasma adrenocorticotropic hormone (ACTH) level. The patient died shortly after admission to hospital, with adrenocortical failure being the provisional cause of death. Autopsy disclosed profound bilateral atrophy of adrenal cortices with evidence of a mild focal inflammatory reaction. The pituitary gland appeared normal on both gross and histologic examinations. There was no histologic evidence of inflammation, fibrosis, or adenohypophysial cell hyperplasia. By immunocytochemistry, no ACTH and B-endorphin immunoreactive cells were identified in the adenohypophysis. In situ hybridization (ISH) for pro-opiomelanocortin (POMC) mRNA yielded conclusively negative results. The case presented here was regarded as isolated ACTH deficiency. Although the remaining pituitary functions were not assessed, clinical and morphologic findings strongly support the supposition that aside from ACTH deficiency, secretory function of other pituitary hormones was preserved. This is the first case in which the pituitary was studied by immunocytochemistry and ISH. The possible pathogenetic mechanisms accounting for the isolated ACTH deficiency are discussed.
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PMID:The Pituitary in Isolated ACTH Deficiency: A Histologic, Immunocytochemical, and In Situ Hybridization Study. 1211 37

A 13-year-old, crossbreed dog presented with a history of recent onset polydipsia, progressive lethargy, weakness and reduced appetite. Blood tests showed raised concentrations of alkaline phosphatase and alanine aminotransferase with marginally low serum potassium. There was a leucocytosis with a mature neutrophilia and no eosinophils. Endocrine tests showed a normal aldosterone concentration and an exaggerated adrenocorticotropic hormone (ACTH) stimulation test, consistent with a diagnosis of hyperadrenocorticism (HAC). A diagnosis of adrenal-dependent HAC was made, based on the presence of a calcified mass involving the left adrenal gland, and hepatomegaly, on radiography and ultrasonography. The owners declined surgical adrenalectomy. Medical management with trilostane rapidly improved the clinical signs and normalised the serum chemistry. ACTH stimulation tests showed an improvement in post-ACTH cortisol concentrations and were used to make dose adjustments where necessary. At the time of writing, no adverse side effects had been seen and the dog remained well after 80 weeks of treatment.
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PMID:Trilostane treatment of a dog with functional adrenocortical neoplasia. 1265 28

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

Here we report an infant who had herpes simplex virus (HSV) encephalitis and sustained severe bilateral damage to the posterior frontal lobes, postcentral gyri, and the thalami despite intravenous acyclovir treatment. At 7 months of age, the patient developed infantile spasms and was treated with corticotropin injections. After 10 days of corticotropin treatment, she developed lethargy, fever, and opisthotonic posturing. Her cerebrospinal fluid again was positive for HSV DNA, indicating recurrent HSV encephalitis, and repeat MRI revealed new lesions of the right frontal, parietal, temporal, and occipital lobes. Immunosuppression by corticotropin may have led to the reactivation of the HSV encephalitis. Corticotropin should be relatively contraindicated for use when a patient has a history of HSV infection, or intravenous acyclovir should be administered concurrently.
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PMID:Herpes simplex virus central nervous system relapse during treatment of infantile spasms with corticotropin. 1660 80


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