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

A 78-year old male with ureteral carcinoma manifesting hypercalcemia is reported. He was diagnosed as having ureteral carcinoma of the left side 2 years previously and was treated by nephrectomy with ureterovesicostomy. In October 1991, he was admitted for anorexia. A clinical examination revealed recurrence of the ureteral carcinoma with metastasis to the rectum and liver. His serum calcium level was elevated (13.9 mg/dl). In addition to rehydration and furosemide, treatment with eel-calcitonin and prednisolone failed to decrease his serum calcium level. Finally, he was administered mithramycin but he died 13 days later. He had no evidence of bone metastasis or hyperparathyroidism. Nephrogenic cAMP and urinary parathyroid hormone-related protein (PTHrP) were markedly elevated. Immunohistochemical study demonstrated expression of PTHrP in the tumor cells. Thus, the hypercalcemia was thought to be mediated by PTHrP secreted from the neoplastic tumor. Although there have been several reports of ureteral carcinoma associated with humoral hypercalcemia of malignancy, this is considered to be the first case associated with elevation of PTHrP.
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PMID:Humoral hypercalcemia of malignancy associated with parathyroid hormone-related protein producing transitional cell carcinoma of the ureter. 801 40

Hypercalcemia is an extremely rare complication of prostatic carcinoma. It occurs mainly in patients with disseminated osseous metastases and may be corrected by bilateral orchiectomy or hormonal manipulation. Humoral factors may be involved in its pathogenesis. Its occurrence is an ominous prognostic sign. We report a case of hypercalcemia that developed in a man suffering from adenocarcinoma of the prostate and who had undergone bilateral orchiectomy. Mental confusion, anorexia, and abdominal pains were the presenting symptoms. The hypercalcemia was refractory to treatment with fluids, furosemide, steroids, and calcitonin, and responded only to mithramycin. Cessation of this medication resulted in a prompt recurrence of the hypercalcemia.
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PMID:Hypercalcemia in prostatic carcinoma. Case report and review of the literature. 832 11

Interleukin-1 beta (IL-1 beta) is a cytokine released by activated macrophages and monocytes, which mediates many of the local and systemic responses to inflammation. Interleukin-1 beta induces anorexia in rats when administered peripherally or centrally. An endogenous antagonist for the IL-1 type I receptor has been characterized and cloned (IL-1ra). We have used this protein to ascertain the site of action for the anorexic effects of IL-1 beta. Male rats were food restricted and trained on an operant schedule for food reinforcement. Administration of recombinant human IL-1 beta (4 micrograms i.p. or 40 ng i.c.v.) induced profound decreases in operant responding, with maximal effects 1-4 h post-injection. Interleukin-1ra pretreatment (2.4 mg i.p. or 24 micrograms i.c.v.) completely blocked these effects when administered by the same route. In contrast, i.c.v. Il-1ra only partially blocked the effects of i.p. IL-1 beta, and i.p. IL-1ra was unable to block the effects of i.c.v. IL-1 beta. Interleukin-1ra did not affect responding by itself. These results suggest that IL-1 beta acts as both peripheral and central IL-1 receptors to reduce food motivated behavior. To determine the central site of action of IL-1 beta, small quantities of IL-1 beta (5 and 30 ng) were infused into the ventromedial hypothalamus of male rats. Both doses produced profound decreases in responding; the magnitude and time course of these effects were nearly identical to those observed after i.c.v. administration. These results suggest that the VMH may serve as a central site of action for the depressive effects of IL-1 beta on food intake. There is much controversy over the pathways of communication from the immune system to the brain. To test the hypothesis that the peripheral immune stimulus is transmitted to the brain via a neutral communication pathway, mice were injected with lipopolysaccharide at a behaviorally active dose (10 micrograms i.p.). This treatment increased the concentrations of substance P, neurokinin A, and calcitonin gene-related peptide in mouse spinal cord in a prostaglandin-dependent manner. Maximal increases in neuropeptide content were observed 1 h post-injection. Finally, subdiaphragmatic vagotomy was found to attenuate the reduction in food-motivated behavior induced by both IL-1 beta and lipopolysaccharide in mice.
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PMID:Mechanisms of sickness-induced decreases in food-motivated behavior. 862 24

Initial sensory nerve reactions to dental injuries include terminal sprouting and intensified immunoreactivity for calcitonin gene-related peptide (CGRP) and substance P (SP); those reactions are reduced at 4 days after injury when rats are treated daily with dexamethasone (DEX) [17]. Here we have analyzed long-term effects of DEX (daily, 0.2 mg/kg) on wound healing, sensory nerve sprouting, and CGRP/SP intensity at 7-14 days after cavity preparation. All DEX treated rats had loss of appetite and stopped growing during the postoperative periods while controls had normal postoperative growth. After 7-14 days, CGRP immunoreactivity (IR) was decreased to one-third of normal (P < 0.05) compared to vehicle in both the intact and injured molar pulp, and SP also decreased, but the neuropeptide intensity in adjacent periodontal innervation was not changed. Pulpal injury and inflammation were reduced by DEX treatment, but reparative dentin was formed just as well in the DEX rats as in the vehicle group. When the injured teeth formed fibrous dentin, there was sprouting of nerves towards that matrix, and DEX did not inhibit that reaction. The sprouts could contain intense neuropeptide immunoreactivity in DEX rats even though the CGRP/SP intensity in uninjured pulp was reduced. We conclude that (1) chronic DEX treatment causes a generalized decrease in CGRP and SP neuropeptides in pulpal nerves but not in periodontal ligament; (2) it reduces abscess formation in injured teeth; (3) it does not block reparative dentin formation; and (4) it does not block sprouting of pulpal nerves towards fibrous dentin. The selective loss of pulpal neuropeptides CGRP and SP during dexamethasone treatment may be caused by reduced dental function since there was substantial loss of appetite and chronic weight loss during the 1-2 week treatment periods.
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PMID:Chronic dexamethasone treatment and its effects on sensory neuropeptides, pulpal injury reactions and reparative dentin. 881 89

Using dual-labeling in situ hybridization histochemistry, the neurotransmitter expression of immune-responsive neurons in the pontine parabrachial nucleus, a major relay for interoceptive information, was investigated. Intravenous injection of bacterial wall lipopolysaccharide resulted in dense c-fos mRNA expression in the external lateral parabrachial nucleus, and a majority of the c-fos expressing cells also expressed calcitonin gene-related peptide (CGRP) mRNA. In contrast CGRP-positive cells in the adjoining external medial subnucleus were c-fos negative. Taken together with previous hodological and behavioral studies, these data suggest that CGRPergic parabrachial neurons may mediate lipopolysaccharide-induced anorexia by means of their projection to central nucleus of the amygdala.
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PMID:Feeding-related immune responsive brain stem neurons: association with CGRP. 1149 18

An intestinal carcinoid with multiple metastases was identified in a 5-year-old male Shih Tzu with a clinical history of anemia, fatigue, anorexia, vomiting, intermittent diarrhea, intestinal bleeding, and progressive emaciation. There was a yellowish-white mass 15 mm in diameter in the anterior jejunum and white nodules consistent with metastases in many organs. Histopathologically, the mass consisted of neoplastic cells arranged in lobules, trabeculae, or closely interdigitating islands of cells. Neoplastic cells were generally polygonal with round hyperchromatic nuclei, modest amounts of eosinophilic cytoplasm, and eosinophilic cytoplasmic granules. Mitoses were common. Rosette formations of tumor cells were apparent in metastatic tumors. Immunohistochemically, tumor cells stained positive for cytokeratin 13, synaptophysin, protein gene product 9.5, neuron-specific enolase, chromogranin A, calcitonin gene-related peptide, serotonin (5-HT), and Leu-7. Serum 5-HT concentrations for this dog were increased 10-fold compared with those of normal dogs. All findings were consistent with a diagnosis of a malignant intestinal carcinoid.
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PMID:Immunohistochemical evaluation of a malignant intestinal carcinoid in a dog. 1263 63

A 93 year-old woman was admitted due to anorexia and unconsciousness. Biochemical examination of serum showed hypercalcemia (corrected Ca; 16.6 mg/dl). The level of intact parathyroid hormone (i-PTH) was suppressed, whereas parathyroid hormone-related peptide (PTHrp) was to 5.0 pM (normal range: below 0.6 pM). IL-6 and renal cAMP were also elevated. We started to ameliorate hypercalcemia by saline infusion, furosemide and calcitonin. However, hypercalcemia was not improved and the patient died of DIC and renal failure. Autopsy revealed primary lesion of NHL (diffuse large B cell type) to be in the stomach with infiltration of lymphoma into the liver, pancreas, spleen, adrenal glands, jejunum, and lumbar vertebrae. The results of immunohistochemical examination demonstrated the expression of PTHrP in lymphoma cells. PTHrP was also found in lymphoma cells of the spleen by the RT-PCR technique. These findings indicated that hypercalcemia was caused by overexpression of PTHrP from lymphoma cells.
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PMID:[An elderly case of non-Hodgkin's lymphoma (NHL) with hypercalcemia]. 1270 52

Hypercalcemia associated with subcutaneous fat necrosis (SCN) is a well known but rare event in the newborn. A newborn infant with a history of SCN was admitted because of anorexia, adynamia, polyuria and polydipsia at 6 weeks of age. Serum calcium was markedly increased on admission, while it was normal on the first day of life. Evolution was favourable after treatment including isotonic saline solution, furosemide, corticosteroids, calcitonin and a low calcium and vitamin D diet. Hypercalcemia was severe enough to potentially induces fatal complications in this case. Neonates who develop skin lesions consistent with SCN should be followed-up for possible onset of hypercalcemia and treated in due time. The treatment of hypercalcemia in SCN is reviewed.
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PMID:[Subcutaneous fat necrosis in the newborn: a risk for severe hypercalcemia]. 1292 5

Migraine is one of the leading causes of disability. Topiramate has multiple mechanisms and may reduce neurotransmission through the trigeminocervical complex to prevent migraine. In clinical trials for the prevention of migraine, the mean monthly migraine frequency decreased from 5.6 to 4.5 in the placebo group and larger decreases were observed with topiramate (100 mg/day, 5.8 to 3.5; 200 mg/day, 5.1 to 3.0). However, topiramate use is associated with a high incidence of adverse events (paraesthesia, fatigue, anorexia, diarrhoea), which may limit the willingness of patients to use topiramate for the prevention of migraine. BIBN 4096 BS is a non-peptide calcitonin gene-related peptide-receptor antagonist that has recently been trialled in migraine attacks. The primary efficacy end point was the reduction of severe or moderate headache prior to treatment to mild or no headache at 2 h. This endpoint was achieved in 21 of 32 (66%) patients with BIBN 4096 BS 2.5 mg, compared to 27% of patients given placebo. Although BIBN 4096 BS is a non-peptide, it is still administered intravenously, which will probably limit its use to medical centres.
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PMID:New drugs for the prevention and treatment of migraine: topiramate and BIBN 4096 BS. 1501 83

The herbal medicine Ninjin-to has been used for the treatment of gastroenteritis, esogastritis, gastric atony, gastrectasis, vomiting, and anorexia. One of the mechanisms of the empirical effects is assumed to be due to local changes in neuropeptide levels. Sensory afferent neurons in the gastrointestinal mucosa regulate neuropeptides [calcitonin gene-related peptide (CGRP), substance P, etc.], which play various physiologic roles. To determine whether the pharmacologic effects of Ninjin-to on the gastrointestine are due to changes in gastrointestinal mucosa regulatory peptide levels, we examined the effects of Ninjin-to on the levels of CGRP-like immunoreactive substances (IS) and substance P-IS in plasma taken from five healthy subjects. A single oral administration of 6.0 g of Ninjin-to caused significant increases in plasma CGRP-IS at 40 min and 60 min, and in substance P-IS levels at 90 min, compared with a placebo group. These results may indicate that the pharmacologic actions of Ninjin-to are closely related to changes in CGRP-IS and substance P-IS levels.
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PMID:Effects of Ninjin-to on levels of calcitonin gene-related peptide and substance P in human plasma. 1557 27


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