Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0003123 (anorexia)
 13,794 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
 ...
PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

Intraperitoneal or intracerebral injections of calcitonin in the rat produce several behavioral and hormonal effects which have some analogies with the human depressive syndrome. To determine if calcitonin effects are sensitive to antidepressant drugs, the ability of antidepressants and other psychotropic drugs to interact with calcitonin-induced anorexia was tested. The results show that chronic treatments (21 days) with tricyclic, or with tetracyclic, antidepressants significantly tend to neutralize the anorectic effect of calcitonin. Other antidepressants and other psychotropic drugs had no significant effect. The acute administration (24 h) of clomipramine did not antagonize the effect of calcitonin, and even significantly enhanced it. These results allow the author to propose the effects of calcitonin in the rat as a new animal model of depression, and to raise the hypothesis that a possible mechanism of action of tricyclic antidepressant treatments is to counteract the effects of certain brain peptides.
 ...
PMID:Antagonism of calcitonin-induced anorexia by chronic, but not acute, tricyclic antidepressants in the rat. 149 68

Hypothalamic tissue levels of nine regulatory peptides (bombesin, calcitonin gene-related peptide [CGRP], galanin, neuromedin B, neuropeptide Y [NPY], neurotensin, somatostatin, substance P, and vasoactive intestinal peptide [VIP]) were compared in Aston obese diabetic (ob/ob) and lean (+/?) mice aged 4, 16, and 28 weeks. Neurotensin concentrations were significantly lower in ob/ob mice than in lean mice, with a 20% reduction (P = .03) in the whole hypothalamus at 4 weeks of age, a 24% reduction (P = .009) in the lateral hypothalamus at 16 weeks, and a 50% reduction (P = .0007) in the central hypothalamus at 28 weeks of age. Apart from a 42% increase in vasoactive intestinal peptide concentrations in the central hypothalamus of ob/ob mice at 28 weeks (P = .02), levels of the other eight peptides examined did not differ significantly between obese and lean groups. Neurotensin is known to cause anorexia and increased energy expenditure when injected into the central hypothalamus. Reduced hypothalamic neurotensin concentrations may reflect reduced neurotensinergic activity, which might contribute to hyperphagia and decreased energy expenditure, two major defects that contribute to obesity and diabetes in the ob/ob syndrome.
 ...
PMID:Reduced hypothalamic neurotensin concentrations in the genetically obese diabetic (ob/ob) mouse: possible relationship to obesity. 194 36

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.
 ...
PMID:Management of severe hypercalcemia. 200 13

Hypercalcemia secondary to cholecalciferol rodenticide toxicosis was identified in two dogs. The first dog died shortly after admission. The second dog responded to treatment with sodium chloride solution, prednisolone, furosemide, and calcitonin. Treatment was needed for a longer period than anticipated and the serum calcium concentration did not stabilize for approximately one month. Although not conclusively demonstrated, calcitonin was considered the cause of severe anorexia. This new class of rodenticides has great toxic potential for dogs, and it is recommended that serum calcium concentration be carefully monitored as treatment for hypercalcemia is gradually withdrawn.
 ...
PMID:Hypercalcemia secondary to cholecalciferol rodenticide toxicosis in two dogs. 215 59

This study has been done to evaluate serum calcium, phosphorus (P), magnesium, parathyroid hormone (PTH), calcitonin (CT), and cyclic adenosine monophosphate (cAMP) in recently diagnosed pulmonary tuberculous patient, (n = 61) and the results were compared with the healthy control group (n = 22). Twenty four hours urine was collected for estimation of these electrolytes as well as cAMP. Nephrogenous cAMP (NcAMP) was calculated. Serum Ca and PTH were significantly reduced in TB groups, but CT was elevated. Serum Mg, P and cAMP as well as urinary Ca and Mg in TB groups were similar to that of the control group. Urinary P, cAMP NcAMP were increased in patient groups compared with the control. The reduced serum Ca could be due to impaired intestinal absorption of Ca, or deficient intake as a result of anorexia, decreased plasma albumin, decreased active metabolites of vitamin D or elevated CT. The rise in serum CT in TB might be due to increased CT secreted from the bronchial K-cells. Increased NcAMP might be due to the associated increase in serum antidiuretic hormone (ADH). The elevated urinary P in TB could be attributed to tissue breakdown, decreased serum PTH or increased CT.
 ...
PMID:Calcium homeostasis in untreated pulmonary tuberculosis. I--Basic study. 216 2

A new analog of salmon calcitonin (N alpha-propionyl Di-Ala1,7,des-Leu19 sCT; RG-12851; here termed CTR), which lacks the ring structure of native calcitonin, was tested for biological activity in several in vitro and in vivo assay systems. The analog (CTR) and salmon calcitonin (sCT) stimulated kidney cell adenylate cyclase activity and inhibited bone resorption in organ cultures of fetal rat long bones with similar potencies and efficacies. Furthermore, CTR and sCT, at similar doses, induced comparable hypocalcemic responses in mice following sc injection or infusions. However, unlike sCT, CTR did not induce anorexia and weight loss in rats following sc injection. These data suggest that the ring structure of sCT may be important for the anorexigenic effect but is not required for effect on bone resorption or calcium homeostasis. Clinical studies appear warranted as, potentially, CTR might induce fewer side effects than does sCT.
 ...
PMID:A noncyclical analog of salmon calcitonin (N alpha-propionyl Di-Ala1,7,des-Leu19 sCT) retains full potency without inducing anorexia in rats. 235 Oct 97

Effects of a synthetic derivative of eel calcitonin, [Asu1,7]ECT on feeding behavior, and its direct action on the neuronal activity of lateral hypothalamic area (LHA) were studied in rats. Food intake was significantly reduced in a dose-dependent manner after intra-third ventricular injection of [Asu1,7]ECT (0.2-1.0 U/rat). The neuronal activity of LHA neurons, especially the glucose-sensitive neurons, was inhibited by electrophoretic application of [Asu1,7]ECT. The inhibition was accompanied by a hyperpolarization of the membrane by about 5-7 mV with an increase in the membrane resistance (5.0-8.7%). This effect was also shown to be independent of noradrenergic or serotonergic mechanisms. Phosphodiesterase inhibitors, such as 3-isobutyl-1-methylxanthine and papaverine augmented the inhibitory response, whereas nicotinic acid blocked it. These results suggest that the anorexia caused by [Asu1,7]ECT is mediated through a direct inhibition of chemosensitive neuronal activity in the LHA, caused by an increase in the intracellular level of cyclic 3',5'-adenosine monophosphate.
 ...
PMID:Calcitonin-induced anorexia in rats: evidence for its inhibitory action on lateral hypothalamic chemosensitive neurons. 242 27

A 57-year-old female was admitted to our hospital with general lassitude, loss of appetite, nausea, upper abdominal pain, thirst, polydipsia and polyuria. On admission, she had an asymmetrical pear-shaped tumor in the right supraclavicular region and severe hypercalcemia. Plasma C-PTH was elevated to 22.72ng/ml. Plasma calcitonin was also elevated to 336 pg/ml. She died of respiratory and cardiac failure of two weeks after admission without any positive response to the treatment, including hemodialysis. Pathohistologically, the tumor was a parathyroid adenoma. The concentrations of C-PTH, intact PTH and calcitonin in the tumor tissue were markedly high: 4.56 micrograms/g wet, 13.9 ng/g wet and 50.7 ng/g wet, respectively. Immunohistologically, the tumor cells and the fibrous stroma were stained strongly positive to rabbit anti-human calcitonin antibody and rabbit anti-human N-PTH antibody by indirect immunoperoxidase staining. Calcitonin-producing tumors, except for medullary thyroid carcinoma are rarely reported. To our knowledge, this is the first report of such a calcitonin-producing parathyroid adenoma associated with primary hyperparathyroidism.
 ...
PMID:A case of calcitonin-producing parathyroid adenoma with primary hyperparathyroidism. 258 94

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.
 ...
PMID:Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis. 267 25


1 2 3 4 5 Next >>