Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this informal initial study, four female patients with intractable chronic abdominal pain, daily nausea, intermittent vomiting, and altered stool habits due to "functional" disease were investigated. A gonadotropin-releasing hormone (GnRH) analog agonist, leuprolide acetate (Lupron) [D-leu6, Desgly-NH2(10), Proethylamide9], was administered once daily (0.5 mg subcutaneously) for three months. At the end of the three-month period, three subjects were symptom-free and the fourth experienced only mild and intermittent pain. The leuprolide regimen was continued for an additional three months, and estrogen (0.625 mg orally) and calcium (1000 mg orally) were given daily to prevent osteoporosis. The patients remained symptom-free. A challenge with progesterone then induced recurrence of mild symptoms in each subject. Withdrawing leuprolide induced the baseline symptoms in all patients within three to five days. This regimen has now been continued for up to 15 months, and all four patients have remained generally symptom-free. Progesterone has also been given every three months to induce menses. A fifth patient, with Roux-en-Y syndrome, has also been treated with leuprolide. She is symptom-free after six months and has gained weight. In this initial observation period in patients with severe functional (neuromuscular) bowel disease, the GnRH analog agonist leuprolide controlled pain, nausea, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Debilitating "functional" bowel disease controlled by leuprolide acetate, gonadotropin-releasing hormone (GnRH) analog. 249 61

Hyperammonemia is a common side effect of valproic acid (VPA) therapy. This study was designed to investigate a potential nutritional influence on serum ammonia levels during VPA therapy. In 10 VPA-treated young patients (5 receiving monotherapy, 5 receiving VPA-primidone polytherapy), venous serum ammonia, triglycerides, and cholesterol were measured on 3 consecutive days as follows: (a) after a 13-h overnight fast; (b) 2 h after an oral fat load with butter (1.2 g fat/kg body weight); and (c) 2 h after an oral protein load with fresh cheese (1 g protein/kg body weight). Ten young adults served as controls. After protein load VPA patients had significantly higher serum ammonia levels than controls (mean: 194 vs. 75 micrograms/dl in controls; p less than 0.006). Ammonia values were higher after protein load than after fat load or after fasting (p less than 0.0001). Patients receiving polytherapy had higher ammonia levels than patients receiving monotherapy (not significant). There was no correlation to the height of serum VPA levels. Clinical symptoms attributable to hyperammonemia (vomiting, apathy) were found in only one patient, and her serum ammonia was as high as 426 micrograms/dl. Triglycerides and cholesterol did not show any VPA-induced differences. We assume that VPA alters the short-term regulation of ureasynthesis. We recommend the avoidance of high protein intake in patients receiving VPA therapy, especially in young patients receiving polytherapy or comedication, or in risk situations like serious infections.
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PMID:Nutritional influence on serum ammonia in young patients receiving sodium valproate. 308 37

Between May 1983-March 1984, the International Centre for Diarrhoeal Disease Research, Bangladesh conducted a metabolic balance study involving 47 children with acute cholera between 1-5 years old. Researchers randomly assigned 22 children to the intravenous (IV) solution treatment group. The children received it continuously until the diarrhea stopped. The remaining 25 were treated with oral rehydration solution (ORS) and IV fluid as needed. Health staff attempted to maintain hydration in the ORS/IV group with ORS alone, but IV therapy was reinstated if a child vomited excessively or the child exhibited signs of severe dehydration. Within 6-8 hours after admission and initial rehydration, the children took a nonabsorbable charcoal marker before taking in any food. The appearance of the 1st marker in the stool was called 0 hour and all stools, urine and vomitus between the 0-72 hours were collected. At 72 hours, the children ingested a 2nd marker. The ORS/IV group consumed 40% of the fluid orally. Vomiting within this group was significantly higher than the IV group (p.001). Intake of protein on day 2 and intake of both fat and protein on day 3 were significantly higher in the IV group (p.05, p.01). Daily intake and absorption of energy or carbohydrates in both of the groups, however, were similar. No significant differences in the total consumption of nutrients after recovery existed. Nitrogen absorption was significantly higher in the IV group than the ORS/IV group (p.05). This study demonstrates that an adequate amount of food is consumed and utilized by patients with acute diarrhea while receiving ORS and therefore there is no justification for withholding food during the acute stage of diarrhea.
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PMID:Does oral rehydration therapy alter food consumption and absorption of nutrients in children with cholera? 377 23

The effects of intravenous Nitrogen Mustard (NM), given with a total cumulative dose of 0.8 mg/kg BW, were studied in 60 children with idiopathic nephrotic syndrome (INS). Thirty patients were frequent relapser with corticosteroid dependence. In this group the actuarial remission rate was 43, 30 and 15% after 1, 2 and 3 years respectively. The relapse rate per year was decreased from 2.76 +/- 1.56 to 0.88 +/- 0.79 after NM. Ten of the 17 patients showing a partial response to steroids went into complete remission after NM but 6 of them relapsed. Of the 13 patients who did not respond to steroids only 3 went into remission for a short time. Vomiting and leukopenia were noted in one third of cases. The data indicate that NM may improve the course of corticosteroid dependent INS, being less effective in partial responders and probably without effect in non responders.
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PMID:Nitrogen mustard therapy in idiopathic nephrotic syndrome of childhood. 399 69

Recurrent vomiting without apparent cause should alert the physician to the possibility of a disorder of ammonia metabolism. Crystalluria in a three-month-old male infant with a history of intermittent vomiting since birth and incipient coma led to the discovery of orotic aciduria. A diagnosis of ornithine carbamyl transferase (OCT) deficiency was derived from study of the liver after the infant had died; residual activity was about 5% of normal. Ammonia intoxication was the presumed cause of death. Overproduction of orotic acid and other pyrimidines reflects the deficiency of OCT. The possibility of genetic heterogeneity for the hereditary trait under observation must be considered because it may influence prognosis and counselling.
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PMID:Partial ornithine carbamyl transferase deficiency: an inborn error of the urea cycle presenting as orotic aciduria in a male infant. 507 51

There studies examined the effect of dietary arginine deficiency in the mature dog. Deletion of arginine from the diet resulted in a slight but significant loss of body weight. Severe episodes of emesis were observed in all experiments. Muscle tremors and frothing around the mouth were also observed in the experiments where the arginine-free diet was force fed. Increasing the amount of diet force-fed to mature dogs accentuated the symptoms of emesis, muscle tremors and frothing. Elevated plasma ammonia and orotate were detected in dogs fed an arginine-deficient diet. Urinary citric and orotic acid was also increased in mature dogs fed a diet devoid of arginine. Nitrogen balance was not significantly altered by deletion of arginine from the diet. Based on the occurrence of emesis, loss of body weight and alterations in intermediary metabolism, we concluded that the mature dog does require a dietary source of arginine. Dietary inclusions of 0.28% arginine prevented the symptoms of arginine deficiency.
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PMID:Arginine: an indispensable amino acid for mature dogs. 724 Dec 23

Cholecystokinin octapeptide (CCK-8) and the peptide analog ARL 14294, formerly FPL 14294, [Hpa(SO3H)-Met-Gly-Trp-Met-Asp-N(Me)Phe-NH2], have been reported to induce satiety by interaction with the CCK-A receptor subtype. ARL 15849 [Hpa(SO3H)-Nle-Gly-Trp-Nle-N(Me)-Asp-Phe-NH2] is an improved ARL 14294 analog with enhanced CCK-A receptor selectivity, greater stability, and a longer duration of action. The affinity of ARL 15849 for the CCK-A receptor (Ki = 0.034 nM) is 6,600 fold greater than for the CCK-B receptor (Ki = 224 nM), whereas CCK-8 and ARL 14294 are nonselective. Although comparable in potency to contract isolated gallbladder and induce pancreatic phosphatidylinositol hydrolysis, ARL 15849 is 3- and 100-fold more potent than ARL 14294 and CCK-8, respectively, to inhibit 3-h feeding in rats. The duration of feeding inhibition was significantly longer for ARL 15849 (>5 h), compared to equipotent doses of ARL 14294 (3 h), and CCK-8 (1 h). Intranasal administration of ARL 15849 inhibits feeding in beagle dogs with a greater separation between doses that induce emesis and those that inhibit feeding. Therefore, ARL 15849 is a potent, selective, intranasally active anorectic agent which may be useful in the treatment of eating disorders.
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PMID:ARL 15849: a selective CCK-A agonist with anorectic activity in the rat and dog. 947 93

After its discovery in 1931, substance P (SP) remained the only mammalian member of the family of tachykinin peptides for several decades. Tachykinins thus refer to peptides sharing the common C-terminal amino acid sequence Phe-X-Gly-Leu-Met x NH2. In recent years the family of mammalian tachykinins has grown with the isolation of two novel peptides from bovine and porcine central nervous system (CNS), neurokinin A and neurokinin B. In parallel with the identification of multiple endogenous tachykinins several classes of tachykinin receptors were discovered. The receptors described so far are named tachykinin NK1 receptor, tachykinin NK2 receptor and tachykinin NK1 receptor, respectively. The present review focuses on the pharmacology and putative function of tachykinin NK1 receptors in brain. The natural ligand with the highest affinity for the tachykinin NK1 receptor is SP itself. The C-terminal sequence is essential for activity, the minimum length of a fragment with reasonable affinity for the tachykinin NK1 receptor is the C-terminal hexapeptide. A rapid advance of knowledge was caused by development of non-peptidic tachykinin NK1 receptor antagonists. This area is under rapid development and a variety of different chemical classes of compounds are involved. Species-dependent affinities of tachykinin NK1 receptor antagonists reveal two clusters of compounds, targeting the tachykinin NK1 receptor subtype found in guinea pig, human or ferret or the one in rat or mouse, respectively. The most recently developed compounds are highly selective, enter the brain and are orally bioavailable. Distinct behavioural effects in experimental animals suggest the involvement of tachykinin NK1 receptors in nociceptive transmission, basal ganglia function or anxiety and depression. Recent clinical trials in man showed that tachykinin NK1 receptor antagonists are effective in treating depression and chemotherapy-induced emesis. Therefore, it is well possible that tachykinin NK1 receptor antagonists will be clinically used for treatment of specific CNS disorders within a short period of time.
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PMID:The tachykinin NK1 receptor in the brain: pharmacology and putative functions. 1044 64

Ammonia, normally produced from catabolism of amino acids, is a deadly neurotoxin. As such, the concentration of free ammonia in the blood is very tightly regulated and is exceeded by two orders of magnitude by its physiologic derivative, urea. The normal capacity for urea production far exceeds the rate of free ammonia production by protein catabolism under normal circumstances, such that any increase in free blood ammonia concentration is a reflection of either biochemical or pharmacologic impairment of urea cycle function or fairly extensive hepatic damage. Clinical signs of hyperammonemia occur at concentrations > 60 micromol/L and include anorexia, irritability, lethargy, vomiting, somnolence, disorientation, asterixis, cerebral edema, coma, and death; appearance of these findings is generally proportional to free ammonia concentration, is progressive, and is independent of the primary etiology. Causes of hyperammonemia include genetic defects in the urea cycle ("primary") or organic acidemias ("secondary"), as well as genetic or acquired disorders resulting in significant hepatic dysfunction. Thus, because of the neurotoxic implications of hyperammonemia and the typical absence of other specific laboratory abnormalities, appearance of the clinical signs should trigger an emergent search for elevated blood ammonia concentration.
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PMID:Hyperammonemia, bane of the brain. 1549 74

We have reported previously the efficacy of antiprotozoal drugs against canine giardiasis (In press, Journal of Veterinary Clinic, the Korean Society of Veterinary Clinics). Fenbendazole was found to be the most efficacious for the treatment of canine giardiasis. There were no significant differences between the efficacy of albendazole and fenbendazole against canine giardiasis. On the other hand, the efficacy of metronidazole for the treatment of canine giardiasis, the efficacy was lower when compared to that of albendazole and fenbendazole. On the basis of these results, to evaluate clinical effect of silymarin, we evaluated the therapeutic efficacy of metronidazole alone, or combined with silymarin for 2 weeks for canine giardiasis. In addition, to observe effects on nutrition, we investigated the changes of body weight, the serum biochemical indicators for liver inflammation (GOT, GPT, NH3), the liver cell regeneration indicators (total protein, albumin) and the hematological changes during treatment (WBC, RBC, MCV, MCH and MCHC). The dogs were allocated to four groups; one group was treated with silymarin (3.5 mg/kg once a day, oral), another with metronidazole (50 mg/kg once a day, oral), and the other group with silymarin (3.5 mg/kg once a day, oral) plus metronidazole (50 mg/kg once a day, oral), while control group remained nontreated. The fecal samples from all the dogs were examined, using the ZSCT and giardia antigen test kit (SNAP(*) Giardia, IDEXX Laboratories), from each dog of each group for three times a week for 2 weeks. Dogs were considered to have giardiasis when one or more of the fecal samples had positive results for Giardia cysts. Seven days after treatment, the efficacy of silymarin plus metronidazole was found 79%, whereas that of metronidazole was 72%. Ten days post-treatment the efficacy of metronidazole plus silymarin (91%) was significantly different in comparison with that of metronidazole (75%). Two weeks post-treatment no cysts were detected in the fecal samples in the dogs of metronidazole or silymarin plus metronidazole-treated groups. Whereas, the fecal samples of all the dogs of the control and only silymarin-treated groups were giardia positive. Signs of side effects were not observed in silymarin plus metronidazole-treated dogs. But poor appetite and intermittent vomiting signs were observed in two dogs of the metronidazole-treated group that resolved when metronidazole administration was discontinued. The body weight of those treated with metronidazole was significantly decreased in comparison with those treated with silymarin and metronidazole plus silymarin. There were significant differences of body weight between the dogs treated with silymarin and metronidazole. Two weeks after metronidazole treatment, serum concentration of GOT, GPT and NH3 were significantly increased in comparison with those treated with silymarin. On the other hand, the serum concentration of GOT, GPT and NH3 were not significantly increased when treated with silymarin plus metronidazole compared to those treated with metronidazole. Serum total protein and albumin concentrations were decreased after metronidazole treatment as compared to those treated with silymarin and silymarin plus metronidazole. The concentrations of serum total protein and albumin decreased significantly in metronidazole-treated group as compared to that of treated with silymarin. The numbers of WBC and RBC did show significant differences in the dogs treated with metronidazole, while MCV, MCH were significant by different between silymarin and metronidazole-treated dogs. On the other hand, there were no significant differences in MCHC in any groups. These data suggest that silymarin, in supplement with antiprotozoal drugs, can influence the therapy of canine giardiasis.
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PMID:Evaluation of silymarin in the treatment on asymptomatic Giardia infections in dogs. 1615 41


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