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)

The nutritional status of a tumor patient can be negatively influenced by the local and systemic effects of the malignant tumor (tumor cachexia, anorexia, difficult oral food intake), by the effects of the various antitumoral therapy modalities (surgery, radiotherapy, chemotherapy), and by the complications associated with such modalities (anorexia, nausea, vomiting, mucositis, xerostomia, alterations of the smell and taste sensations, odynophagia, dysphagia, maldigestion, malabsorption, diarrhea, steatorrhea, conditioned aversions, radiogenic late effects), as well as by the psychological reactions of the patient to the real or feared existence of his tumor. The radiation-induced nutritional disorders depend on the tumor localization, the region irradiated, the dose and length of radiotherapy, the fractionation, the volume irradiated, and the combination with other therapeutic modalities ("combined modality therapy"). The acute radiation-induced reactions are usually of limited duration and for this reason tend to interfere with the nutritional status to a lesser extent than the permanent chronic consequences of irradiation. Weight loss and malnutrition tend to develop particularly in patients in whom segments of the gastrointestinal tract are subjected to irradiation. The incidence and severity of deficient nutrition depend not only on the region irradiated (head-neck region, thorax, abdomen, pelvis) but also, and most particularly, on the volume of the digestive tract irradiated. Chemotherapy and radiotherapy combined act very strongly on rapidly proliferating cell populations (skin, mucosa, epithelium of the gastrointestinal tract). In this context, actinomycin D and adriamycin act like real sensitizers, whereas the majority of the other drugs are likely to produce only an additive effect. The first named cytostatics give rise to the so-called recall phenomenon, i.e., the reactivation of latent radiation effects in response to the subsequent administration of the drug. Malnutrition impairs organ function and ultimately results in increased morbidity and mortality. For this reason it has proven mandatory and reasonable that the organism of all tumor patients suffering from malnutrition is provided with the missing essential nutrients (especially amino acids for protein synthesis). This tends to clearly improve the Karnofsky performance status, with a positive effect on response rates, toxicity, and survival rates in retrospective studies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Malnutrition and the role of nutritional support for radiation therapy patients. 314 Mar 23

The medical records of 32 cats with small intestinal adenocarcinoma were reviewed. Common clinical signs included vomiting, dehydration, weight loss, cachexia, anorexia, and lethargy. In 50% of the cats, an abdominal mass was palpated, and in 38%, a mass was seen on radiographs. Biopsy of the tumor without resection was performed in 9 cats; 8 cats were euthanatized at the time of surgery, 7 because of metastases, and 1 cat died 1 day after surgery. In 23 cats, resection was performed. Eleven of these died within 2 weeks after surgery (mean survival time, 2.6 days); 8 had lymph node metastasis. Twelve cats survived greater than 2 weeks after surgery. The mean survival of 11 of these cats was 15 months. Six cats were euthanatized because of recurrent signs; 5 of the 6 had a recurrent abdominal mass. One cat was alive 2 years after surgery. Results of this study indicated that cats with adenocarcinoma, even those cats with advanced disease, can have long-term survival after surgery.
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PMID:Small intestinal adenocarcinoma in cats: 32 cases (1978-1985). 335 Jul 52

A number of problems seen in veal calves are associated with insufficient adaptation to the changes in husbandry connected with the fattening system. These problems include chronic tympanitis, chronic vomiting, cachexia, unthriftiness, abomasal erosions and ulcers. Some of these problems are associated with failure of the reticular groove reflex, and result in ruminal drinking. Persistent ruminal drinking causes a syndrome characterised by a variety of symptoms such as unthriftiness, severe growth retardation, inappetence, recurrent tympany, abdominal distension, a long dry haircoat and clay-like faeces. Clinical studies performed to investigate the pathogenesis of the syndrome are described. It was found that the milk was stored in the rumen and was partly broken down. The presence of milk in the rumen induced typical changes in the ruminal mucosa (hyper/parakeratosis) and also inhibited casein clot formation in the abdomasum. The small intestinal mucosa showed villous atrophy. After training, the reticular groove reflex was re-established in a number of patients but the growth rate of these calves did not return to normal.
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PMID:Consequences of failure of the reticular groove reflex in veal calves fed milk replacer. 341 70

Following abdominal radiation, a 16-year-old male developed persistent vomiting, metabolic alkalosis, and cachexia secondary to gastric stasis, atony, and dilatation in the absence of mechanical obstruction. Fluoroscopically and manometrically, antral motility was found to be severely impaired. Antral motor activity was not influenced by metoclopramide, but stimulated by carbachol. During oral maintenance carbachol therapy, gastric emptying of food was restored and sufficient oral nutrition could be resumed. The improvement persisted even after termination of therapy four months later. Systematic investigations on the effects of abdominal radiation on gastrointestinal motility appear to be necessary.
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PMID:Gastroparesis after radiation. Successful treatment with carbachol. 380 38

A 10-year-old girl with undifferentiated (embryonal) sarcoma of the liver reported here had abdominal pain, nausea, vomiting and weakness when she was 8 years old. Chemical analyses of the blood and urine were normal. Serum alpha-fetoprotein was within normal limits. She died of cachexia 1 year and 8 months after the onset of symptoms. Autopsy showed a huge tumor mass in the liver and a few metastatic nodules in the lungs, which were consistent histologically with undifferenitated sarcoma of the liver. To our knowledge, this is the second case report of hepatic undifferentiated sarcoma of children in Japan, the feature being compatible with the description of Stocker and Ishaka.
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PMID:Undifferentiated (embryonal) sarcoma of the liver. 739 19

Chronic adriamycin (ADR) intoxication with cardiomyopathy developed in young Beagle dogs given weekly IV injections (1 mg/kg of body weight) for 20 weeks (cumulative dose 400 mg/m2). Eighteen dogs were allotted equally to three groups: group A received ADR only, group B was given ADR and simultaneous weekly doses of vitamin E (17 mg/kg of body weight as alpha-tocopherol acetate), and group C received ADR, weekly doses of vitamin E as in group B, and selenium (0.06 mg/kg of body weight as selenite). The dogs reacted with cutaneous hyperemia, head shaking, and vomiting immediately after ADR injection. After 4 to 6 weekly injections, all the dogs developed alopecia that was present initially over the head and subsequently extended to the ventral portions of the neck, thorax, and abdomen and the proximal inner areas of the limbs. Other skin lesions present in alopecic areas were secondary ulcerative dermatitis and melanosis. Testicular atrophy and cachexia developed in the dogs, but damage was not present in bone marrow, alimentary tract, kidney, and bone with the dosage schedule utilized. Hematologic studies showed no significant alterations. Supplementation with vitamin E alone or with selenium failed to alter the incidence and severity of extracardiac ADR-induced lesions. This study shows that the dog is a good model for studies of chronic ADR-induced cardiotoxicity, as cardiac damage was consistently produced and ADR-associated extracardiac lesions were of minimal severity.
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PMID:Clinical observations, cutaneous lesions, and hematologic alterations in chronic adriamycin intoxication in dogs with and without vitamin E and selenium supplementation. 740 87

In 1956 we evaluated a patient who had a debilitating disease of a 2 yr duration, characterized by recurrent vomiting, diarrhea, cachexia, massive edema, hypoproteinemia, and dilated intestinal lymphatics. During our initial evaluation of this patient, we observed that 42% of her circulating protein pool was lost into her gastrointestinal tract daily, whereas normal gastrointesinal loss of protein does not exceed 1.6%. Her disease appeared to represent a classic example of intestinal lymphangiectasia. She was treated symptomatically for 13 yr with essentially no change. In 1969 the patient developed a stage IV diffuse, undifferentiated (non-Burkitt's) malignant lymphoma. Using immunoperoxidase staining, the neoplastic cells were found to contain cytoplasmic IgMKappa, suggesting that the lymphoma had a monoclonal B-cell origin. She was successfully treated with cyclophosphamide, vincristine, and prednisone. Shortly after the initiation of this systemic combination chemotherapy, her serum protein concentration returned to normal, her edema resolved, and she was cured of gastrointestinal symptoms. Moreover, repeat studies revealed that her protein loss had fallen to only 2%. The simultaneous cure of both the intestinal lymphangiectasia and lymphoma with combination chemotherapy suggests new relationships between these conditions as well as new possibilities for the treatment of acquired forms of intestinal lymphangiectasis associated with overwhelming gastrointestinal protein loss.
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PMID:Resolution of longstanding protein-losing enteropathy in a patient with intestinal lymphangiectasia after treatment for malignant lymphoma. 745 Apr 3

There have been reports of chemical attacks in which sulfur mustard might have been used (a) on Iranian soldiers and civilians during the Gulf War in 1984 and 1985 and (b) in an Iraqi chemical attack on the Iranian-occupied village of Halbja in 1988, resulting in many civilian casualties. Heavy use of chemical warfare in Afghanistan by the Soviet military is a recent innovation in military tactics that has been highly successful and may ensure further use of chemical agents in future military conflicts and terrorist attacks as a profitable adjunct to conventional military arms. Mustard is a poisonous chemical agent that exerts a local action on the eyes, skin, and respiratory tissue, with subsequent systemic action on the nervous, cardiac, and digestive systems in humans and laboratory animals, causing lacrimation, malaise, anorexia, salivation, respiratory distress, vomiting, hyperexcitability, and cardiac distress. Under extreme circumstances, dependent upon the dose and length of exposure to the agent, necrosis of the skin and mucous membranes of the respiratory system, bronchitis, bronchopneumonia, intestinal lesions, hemoconcentration, leucopenia, convulsions with systemic distress, and death occur. Severe mustard poisoning in humans is associated with systemic injury, which is manifested as headache, epigastric distresses, anorexia, diarrhea, and cachexia and is usually observed at mustard doses of 1000 mg/min/m3 with damage to hematopoietic tissues and progressive leucopenia. Sulfur mustard is a cell poison that causes disruption and impairment of a variety of cellular activities that are dependent upon a very specific integral relationship. These cytotoxic effects are manifested in widespread metabolic disturbances whose variable characteristics are observed in enzymatic deficiencies, vesicant action, abnormal mitotic activity and cell division, bone marrow disruption, disturbances in hematopoietic activity, and systemic poisoning. Indeed, mustard gas readily combines with various components of the cell such as amino acids, amines, and proteins. Although evidence of an association between lung cancer and mustard gas encountered on the battlefields of World War I is at best suggestive if not problematical (Case and Lea, 1955; Beebe, 1960; Norman, 1975), the epidemiological data accumulated from the poison gas factories in Japan (Yamada et al., 1953; Wada et al., 1968; Inada et al., 1978; Shigenobu, 1980; Nishimoto et al., 1983; Hirono et al., 1984; Takuoka et al., 1986), in Germany (Weiss, 1958; Hellmann, 1970a; Weiss and Weiss, 1975; Klehr, 1984) and in England (Manning et al., 1981; Easton et al., 1988) are substantial (International Agency for Research on Cancer, 1975). Unfortunately, attempts to seek confirmatory and substantial evidence in laboratory animals such as mice (Boyland and Horning, 1949; Heston, 1950; Heston, 1953a; McNamara et al., 1975) and rats (Griffin et al., 1951; McNamara et al., 1975; Sasser et al., 1996) have not been consistent. Sulfur mustard has been shown to be mutagenic in a variety of different species using many different laboratory techniques from fruit flies, microorganisms and mammalian cell cultures (Fox and Scott, 1980). Evidence is slowly accumulating from human data (Hellmann, 1970a; Lohs, 1975; Wulf et al., 1985). Evidence for the teratogenicity of mustard has been negative in assessment of fetotoxicity and adverse effects of mustard on the reproductive potential of both human and animal studies. Indeed, investigations of women adversely affected by mustard are minimal because most of the studies have been performed on former men employees of poison gas factories and have been negative or questionable. We have recently emphasized the need to assess the affect of a suspected teratogen on maternal toxicity in laboratory animals before any conclusions can be made.(ABSTRACT TRUNCATED)
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PMID:Toxicology and pharmacology of the chemical warfare agent sulfur mustard. 880 7

Overt diabetic gastroparesis is a rare long-term complication of diabetes, probably resulting from autonomic neuropathy of vagus nerve. It is now clear that neural damage plays a pivotal role in the pathogenesis of the disease. Some studies showed high basal gastrin levels in patients with diabetic gastroparesis, but the clinical meaning of this observation is still unclear. We report the case of a young woman with Insulin Dependent Diabetes Mellitus (IDDM) who was referred to evaluate nausea and vomiting associated to ketoacidosis. Our hypothesis of autonomic neuropathy with gastroparesis was confirmed. We observed a progressive increase in fasting gastrin concentration (20-fold normal values) in the absence of any clinical and laboratory signs of Zollinger-Ellison (ZE) syndrome. The increasing vomiting induced a severe state of cachexia, which required total parenteral nutrition for a long period. All therapeutic approaches were unsuccessful, and the patient rapidly died, suggesting a possible link between the severity of the clinical picture and the gastrin plasma levels.
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PMID:Extreme but asymptomatic hypergastrinemia with gastroparesis in a young woman with insulin dependent diabetes mellitus. 964 55

Two siblings (one man, one woman), presenting with diarrhea, severe weight loss peripheral neuropathy, ophthalmoparesis, asymptomatic leukoencephalopathy were diagnosed as a new cases of Mitochondrial Neuro Gastro Intestinal Encephalomyopathy syndrome (MNGIE). Hirano (1994) defined four criteria for the diagnostic: peripheral neuropathy, ophthalmoparesis, gastro intestinal dysmotility, muscle biopsy with histologic features of mitochondrial myopathy (ragged-red fibers, muscle fibers with increased succinate deshydrogenase stain or ultra structurally abnormal mitochondria). In a review of the literature, we found 31 cases with MNGIE. With our two cases, we study this group of 33 patients. First symptoms begin about 13.5 years with a median of 10 years and extremes for 1 to 32 years. The first signs are gastro intestinal symptoms (recurrent nausea, vomiting or diarrhea with intestinal dysmotility) in 22 cases, an ophthalmoparesia in 4 cases, intestinal and ocular signs in 1 case, gait ataxia or peripheral neuropathy in 3 cases, hearing loss in 1 case, gait ataxia or peripheral neuropathy in 3 cases, hearing loss in 1 case. During the evolution, besides the cardinal signs, the following features have been observed with a variable frequency: hearing loss, short stature, facial palsy, dysphonia, dysarthria, sweating, orthostatic hypotension, bladder dysfunction, hepatomegalia, The laboratory features are: abnormal Nerve Condition Studies/EMG compatible with a sensory motor neuropathy, lactic acidosis, mitochondrial respiratory chain defect (essentially complex IV deficiency, complex I deficiency or multiple complex defect), MRI leukodystrophy, elevated CSF protein, heart block, ragged-red fibers or increased SDH stain. The prognosis is poor, due to a severe weight loss bordering on cachexia 13 patients died with a mean age of 28.5 years (median 24 years, extreme 3 years to 51 years). The prognosis seems to be worsened by a young age of onset. The 33 patients belong to 19 families with 7 cases of consanguinity. 25 patients had a brother, a sister or a cousin affected. The study of these families is compatible with an autosomic recessive transmission, suggesting a pathology of the nuclear genomi, probably impliying the control of the mitochondrial DNA replication. In fact, in 13 cases, a study of the mt DNA was realized: multiple deletions were founded in 6 cases, multiples mutations in one case, unique mutation in 1 case. In 5 cases ther was no evidence of abnormality. These precise etiology and pathophysiologic significance of the mt DNA deletions, and the heterogeneity of the modifications of the mt DNA remain unknown. However, the possibility of various phenotypes for a same genotype or inversely is known in mitochondriopathies.
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PMID:[MNGIE syndrome in 2 siblings]. 968 18


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