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)

Lysinuric protein intolerance (LPI), an autosomal recessive defect of diamino acid transport, is characterized chemically by renal hyperdiaminoaciduria, especially lysinuria, and by impaired formation of urea with hyperammonemia after protein ingestion. Our 20 patients thrived during breast-feeding, but ingestion of cow's milk caused diarrhea and vomiting. When able to select their diet, they rejected all protein-rich foods. They were short staturated and had weak atrophic muscles, osteoporosis, hepatomegaly and often splenomegaly. Four patients were mentally retarded. Fifteen patients had leukocyte counts below 4,000/mm3, and 17 patients had platelet counts below 150,000/mm3. Serum lactate dehydrogenase activity was constantly increased, and transaminase and aldolase activities were often increased. In the infants' livers, changes were only revealed by electron microscopy: increased and vesicular smooth endoplasmic reticulum, and abundance of glycogen particles in the hepatocytes. In the older patients, light microscopy demonstrated clearly limited areas where hepatocytes had large pale cytoplasm and small pyknotic nuclei. The diamino acids lysine, arginine and ornithine had plasma concentrations only one-third to one-half the normal mean; the renal clearances were clearly increased. Oral diamino acid loading tests suggested impaired intestinal absorption. Urea is built in the liver through transformation of ornithine to arginine, and cleavage of arginine to ornithine and urea. The addition of ornithine to an intravenous I-alanine loading prevented the hyperammonemia and normalized the urea production. Therefore, the diet has been supplemented with arginine, and more protein has been added. This therapy has lead to a remarkable catch-up growth in some patients. The pathophysiology of LPI is explained. Because of defective intestinal absorption and incrased renal loss, the diamino acids have a low plasma concentration. Their transport from plasma to hepatocytes is also impaired, and the liver becomes deficient in ornithine. This retards the urea cycle, and leads to postprandial hyperammonemia and protein aversion. The presence of the transport defect in the hepatocytes distinguishes LPI from other hyperdibasicaminoacidurias.
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PMID:Lysinuric protein intolerance. 115 80

Anorexia nervosa and bulimia nervosa are prevalent illnesses affecting between 1% and 10% of adolescent and college age women. Developmental, family dynamic, and biologic factors are all important in the cause of this disorder. Anorexia nervosa is diagnosed when a person refuses to maintain his or her body weight over a minimal normal weight for age and height, such as 15% below that expected, has an intense fear of gaining weight, has a disturbed body image, and, in women, has primary or secondary amenorrhea. A diagnosis of bulimia nervosa is made when a person has recurrent episodes of binge eating, a feeling of lack of control over behavior during binges, regular use of self-induced vomiting, laxatives, diuretics, strict dieting, or vigorous exercise to prevent weight gain, a minimum of 2 binge episodes a week for at least 3 months, and persistent overconcern with body shape and weight. Patients with eating disorders are usually secretive and often come to the attention of physicians only at the insistence of others. Practitioners also should be alert for medical complications including hypothermia, edema, hypotension, bradycardia, infertility, and osteoporosis in patients with anorexia nervosa and fluid or electrolyte imbalance, hyperamylasemia, gastritis, esophagitis, gastric dilation, edema, dental erosion, swollen parotid glands, and gingivitis in patients with bulimia nervosa. Treatment involves combining individual, behavioral, group, and family therapy with, possibly, psychopharmaceuticals. Primary care professionals are frequently the first to evaluate these patients, and their encouragement and support may help patients accept treatment. The treatment proceeds most smoothly if the primary care physician and psychiatrist work collaboratively with clear and frequent communication.
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PMID:Eating disorders. A review and update. 147 50

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

Synthetic human calcitonin was used in the treatment of 26 patients over a period of 1-14 months. 17 patients had Paget's disease of the bone, 6 postmenopausal osteoporosis and 3 Sudeck's syndrome. Subjective improvement (reduction of pain, improvement of mobility) was found in 15 patients with Paget's disease, in 4 females with postmenopausal osteoporosis and in all 3 patients with Sudeck's syndrome. Radiographic improvement of bone changes developed only very slowly. These results were confirmed by diminution of the exchangeable calcium pool indicating reduction of rates of osseous degradation. Calcitonin tolerance was acceptable. Transitory nausea and occasional vomiting occurred in 3 patients.
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PMID:[Synthetic human calcitonin in Paget's disease of bone and osteoporosis (author's transl)]. 616 31

Lysinuric protein intolerance is an autosomal recessive disease, due to a defect in intestinal, renal and hepatic dibasic amino acid transport. Two new cases in the same family are reported. The disease appears progressively during the first months of life with failure to thrive, anorexia, vomiting, diarrhea, hepatosplenomegaly, muscular weakness, osteoporosis, anemia, leukothrombocytopenia, hyperammonemia and orotic aciduria after a high-protein intake. Hyperdibasicamino-aciduria was associated with subnormal plasma concentrations of the same aminoacids. Oral l-arginine, l-ornithine, l-lysine, and lysyl-glycine loads confirmed the diagnosis. The supplementation of the diet with l-citrulline resulted in normal levels of blood ammonia. However, hepatosplenomegaly, muscular weakness, osteoporosis remained unchanged and growth was not improved. These may be due to lysine deficiency.
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PMID:[Lysinuric protein intolerance: a severe hyperammonemia secondary to l-arginine deficiency (author's transl)]]. 680 Mar 34

Thirty-six patients with primary osteoporosis were treated for up to six years with sodium fluoride, calcium supplements, and, in 24 patients, vitamin D. Major adverse reactions (synovitis, painful plantar fascial syndrome, recurrent vomiting, or anemia) occurred in 15 patients (42%). New vertebral fractures occurred at a rate of 329 fractures per 1,000 years of observation. Almost half of them occurred during the first year of therapy, and they were only one sixth as frequent in 12 patients who had fluoride-induced increased trabeculation on vertebral roentogenograms. Nevertheless, until long-term safety and antifracture efficacy are better established, this regimen should continue to be restricted to investigational use.
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PMID:Treatment of primary osteoporosis with fluoride and calcium. Clinical tolerance and fracture occurrence. 735 65

Cimadronate (YM175) is a novel bisphosphonate with potent inhibitory activity on bone resorption under development for the treatment of tumor-induced hypercalcemia, metastatic bone disease and osteoporosis. We conducted intravenous single and repeated dose toxicity studies of cimadronate in beagle dogs. In the single dose study, animals received a single dose of 0.3, 1, 3 or 10 mg/kg of cimadronate and the animals were observed for at least 14 days. At 10 mg/kg, both the male and female dog showed toxic signs such as vomiting, decreased locomotor activities and hypothermia and were killed in extremis within a week after dosing. In the 30-day study, animals received cimadronate at a dosage of 0 (vehicle), 0.03, 0.1, 0.3 or 1 mg/kg/day. At 0.03 mg/kg/day or more, histological findings indicated an increased amount of primary spongiosa in the rib and ilium. At 1 mg/kg/day, degenerative nephropathy, aggregation of spermatozoa and glandular hypoplasia of the prostate gland were observed. On day 16 of dosing one male animal died of acute renal failure. In the 26-week study, animals received cimadronate once weekly at a dosage of 0 (vehicle), 0.31, 0.62, or 1.25 mg/kg. Histopathological examination showed an increased amount of primary spongiosa in the rib at all dosage levels. In addition, similar findings were observed in the lumbar vertebrae at 1.25 mg/kg/week. Histopathological changes in the kidney and male reproductive organs were not observed.
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PMID:Intravenous single and repeated dose toxicity studies of cimadronate (YM175), a novel bisphosphonate, in beagle dogs. 749 Jul 87

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin I2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.
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PMID:Magnesium deficiency in alcoholism: possible contribution to osteoporosis and cardiovascular disease in alcoholics. 784 87

Milk-alkali syndrome is characterized by progressive hypercalcemia, systemic alkalosis, and renal insufficiency. After calcium carbonate is ingested with diary products, hypercalcemia and alkalosis may develop in susceptible persons, particularly those with underlying renal insufficiency. We describe a young woman who neither drank milk nor had peptic ulcer disease, yet who ingested enough calcium carbonate to require admission to an intensive care unit for acute renal failure. Chronically bulimic, she was taking Rolaids (Warner-Lambert Co, Morris Plains, NJ), which contained calcium carbonate, and was eating yogurt daily to prevent osteoporosis. We discuss the characteristics and complex metabolic interactions of the milk-alkali syndrome, a critical but generally reversible electrolyte disorder. Early recognition of coincident hypercalcemia and alkalosis and prompt cessation of calcium carbonate ingestion are essential for successful recovery. Finally, we suggest that nephrologists should discourage patients with renal insufficiency and chronic vomiting from consuming calcium-containing antacids and excessive dietary calcium.
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PMID:Rolaids-yogurt syndrome: a 1990s version of milk-alkali syndrome. 865 5

The aim of the study was to compare the tolerance of synthetic salmon calcitonin applied in two different ways, intramuscularly or intranasally, in 50 patients with postmenopausal osteoporosis with bone fractures. Thirty patients were treated with calcitonin in intramuscular or subcutaneous injections, whereas in 20 cases calcitonin was applied in nasal spray. In the first group several side effects were observed, like nausea, vomiting, abdominal pains, skin rush, headaches, dropping blood pressure, symptoms of bronchial spasm. Finally in 13 cases it was necessary to stop calcitonin therapy. On the other hand the patients receiving calcitonin in nasal spray did not manifest any severe side effects.
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PMID:[Comparison of calcitonin tolerance after intramuscular or intranasal administration in treatment for postmenopausal osteoporosis]. 871 Nov 77


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