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 purpose of this investigation was to evaluate the significance of enzymatic and biochemical analyses in the classification of chronic inflammatory liver disease and to evaluate the prognosis of these diseases. Chronic hepatitis and cirrhosis were diagnosed by histopathological examination in 79 dogs. Decreased appetite and lethargy were the most common owner complaints (46/79). Vomiting and, or, diarrhoea were reported in 27/79 dogs. Ascites was the most common clinical sign (43/79), whereas icterus was a more unusual finding demonstrated in 16/79 dogs. Liver cirrhosis was diagnosed most frequently, in 33/79 dogs, followed by chronic progressive hepatitis (22/79), chronic cholangiohepatitis (13/79), and chronic non-specific hepatitis (11/79). Hypoalbuminaemia was the most consistent biochemical aberration in liver cirrhosis (25/26) and in chronic progressive hepatitis (13/18). These diseases also showed normal to mildly increased concentrations of serum alanine aminotransferase (ALT) and serum gamma-glutamyl transferase (GGT) and a moderate to marked increase of serum alkaline phosphatase (ALP) and fasting serum bile acid (SBA) concentrations. As expected, icterus and markedly elevated ALT, ALP, GGT and SBA levels were demonstrated in chronic cholangiohepatitis. In this disease hypoalbuminaemia was shown in 6/12 dogs, whereas in dogs with chronic non-specific hepatitis, mean SBA and albumin concentrations were normal. In liver cirrhosis the prognosis was poor, with 94 per cent of the dogs dead within one week of established diagnosis. For dogs with the other types of chronic hepatitis the prognosis was more favourable with the mean survival time ranging from 21.1 to 36.4 months.
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PMID:Diagnosis and prognosis of chronic hepatitis and cirrhosis in dogs. 892 20

Author points to principles upon which not only the control of pain but also of all other symptoms depends: an appreciation of symptoms as a psychosomatic phenomenon, an accurate diagnosis of the cause of the symptom and in reference to pain application of the World Health Organisation's Analgesic Ladder for Cancer Pain. He takes these principles for granted and elaborates on the use of drugs and to lesser extent, other techniques which are used in hospice practise. Morphine is metabolised into M6G i M3G, the first being significantly more potent an analgesic as morphine. Its late and prolonged presence is probably basic for continuous morphine application instead of "as required" way. Author is giving very precise recommendations for per os and parenteral dose titration, discussing the side-effects and data about the related drugs, the analgesia in neuropathic pain and the special techniques like radiation, nerve blocks and epidural analgesia. Speaking about the palliative home care problems the author explains the most important factors enabling a family to continue their care at home. The author keeps discussing the poor appetite, vomiting, dysphagia, constipation. Respiratory problems are elaborated with more details especially those in "death rattle", with the optimal drug option recommendation, and many technical details.
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PMID:[The hospice approach to pain and problems in home palliative care]. 949 Mar 73

We report a hypertrophic pyloric stenosis case with an unusual initial presentation of seizures and Bartter's syndrome like symptoms. This case suffered from vomiting, diarrhea and poor appetite for several days, and seizures developed after these symptoms. From laboratory tests, hypochloremic and hypokalemic metabolic alkalosis associated with hyperreninemia, hyperaldosteronism and normal blood pressure were noted. Pseudo-Bartter's syndrome was diagnosed through these clinical and laboratory tests. Although the first abdominal echo was negative, we still speculated about the peculiar symptoms of vomiting and it's relationship to pseudo-Bartter's syndrome. After all, we found the hypertrophic pyloric stenosis through an upper gastrointestinal series. From these experiences, we postulated that it's very important to put the hypertrophic pyloric stenosis into the differential diagnosis of pseudo-Batter's syndrome.
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PMID:Infantile hypertrophic pyloric stenosis presenting as pseudo-Bartter's syndrome and seizures: report of one case. 968 26

The current mainstay of treatment in glycogen storage disease type I (GSD I) is dietary management that includes providing a frequent source of glucose to prevent hypoglycaemia. To ensure compliance, routine follow-up by a health care team, including a dietitian, experienced in the treatment of GSD is necessary. We describe an adolescent patient with GSD Ib in good metabolic control who was admitted with a 3-month history of weakness, depression, vomiting, decreased appetite and a 11.4-kg weight loss. He had a recent onset of unsteady gait, inability to write, and sore mouth. After an extensive work-up, the patient was found to have vitamin B12, folate, iron and other nutritional deficiencies, which explained his symptoms. The patient improved within 72 h of initiation of total parenteral nutrition and therapeutic doses of deficient micronutrients, with a complete recovery in 2 months. Dietary restrictions, dependence on non-food products (e.g. cornstarch in GSD I), and social and developmental issues place individuals with metabolic disorders at a high risk for developing an array of nutritional deficiencies. This case highlights the importance of both close follow-up of the metabolic control and close monitoring of growth and nutritional intake in individuals with inborn errors of metabolism. This case also illustrates the importance of daily supplementation with appropriate multivitamins, calcium and other minerals needed to meet the Recommended Dietary Allowances (RDAs) in these patients.
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PMID:Nutritional deficiencies in a patient with glycogen storage disease type Ib. 1051 79

The inclusion of a query concerning the presence of snoring in a questionnaires used by the Allergy Service of Childrens Hospital Los Angeles (CHLA) uncovered a significant number of patients who were experiencing prolonged and discomforting symptoms owing to previously undiagnosed obstructive sleep apnea (OSA) caused by adenotonsillar hypertrophy. Of 352 patients who were discharged with a diagnosis of OSA and tonsillectomy and/or adenoidectomy at CHLA in 1996-1997, a retrospective study of the first 45 randomly selected patients who agreed to participate in a telephone interview was performed. Analysis revealed that all patients experienced severe and discomforting symptoms with all describing severe or moderate snoring. Other symptoms included chronic mouth breathing (84%), frequent otitis media (64%), sinusitis (56%), sore throat (51%), choking (47%), and daytime drowsiness (42%). Other symptoms included poor school performance, enuresis, poor appetite and/or weight gain, dysphagia, and vomiting. Symptoms began at a mean age of approximately 2 years ("birth"-9 years), and the mean period of time between the development of significant symptoms and OSA was 3.3 years (6 months-13 years). Delay between onset of significant symptoms and surgery was > 1 year in 82% of the patients, > 2 years in 51% of the patients, > 4 years in 31% of the patients, and > 6 years in 13% of the patients. Forty percent of patients were self-referred to an otolaryngologist for treatment despite their primary care physician being aware of the symptoms. These results indicate that patient with OSA experienced prolonged morbidity and delays in treatment, which is probably widespread. Physician, parent, and third-party factors were found to have contributed to the delays in treatment.
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PMID:Prolonged morbidity due to delays in the diagnosis and treatment of obstructive sleep apnea in children. 1069 47

Activity at the 5-HT2A receptor versus that of the 5-HT2C receptor was studied in three behavioural paradigms. In pigeons trained to discriminate 0.32 mg/kg of 1-(2,5-diemethoxy-4-iodophenyl)-2-aminopropane (DOI) (a mixed 5-HT2A/C receptor agonist) from vehicle, quipazine (0.1-1 mg/kg) and m-chlorophenylpiperazine (mCPP) (1-3 mg/kg) substituted for DOI in a dose-related manner, and this generalization was blocked by MDL100907 (0.0001-0.01 mg/kg), a selective 5-HT2A receptor antagonist. RO60-0175 (a relatively selective 5-HT2C agonist) induced partial substitution at 3 mg/kg that was antagonized by both MDL100907 and by 3 mg/kg of SB242084, a relatively selective 5-HT2C antagonist. MK212 (a mixed 5-HT2C/A agonist) induced partial substitution that was antagonized by SB242084, but not by MDL100907. On a progressive ratio 5 operant schedule (PR5) for food reinforcement, DOI, quipazine, mCPP, MK212 and R060-0175 decreased the break point; mCPP, DOI, MK212 and quipazine also induced vomiting. Although MDL100907 antagonized both the reductions of break point and vomiting, SB242084 only partially attenuated the decrease in break point observed with MK212 and DOI, and was unable to eliminate vomiting. Thus pharmacological activity at the 5-HT2A receptor can be behaviourally distinguished from pharmacological activity at the 5-HT2C receptor in the pigeon. Furthermore, the decrease in the break point of a PR5 schedule induced by 5-HT2C receptor agonists may be related to decreased appetite, whereas that induced by 5-HT2A receptor agonists may be due to unrelated factors, such as emesis.
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PMID:A comparison of the behavioural effects of 5-HT2A and 5-HT2C receptor agonists in the pigeon. 1110 87

Epidemiological studies have demonstrated a marked negative relationship between diarrhoea and physical growth and development of a child. Each day of illness due to diarrhoea produces a weight deficit of 20-40 gms. Poor nutrition is associated with more serious prolonged diarrhoea. 'Catch-up growth' often does not occur in malnourished children. Malnutrition, particularly wasting, is a strong predictor of diarrhoeal duration and the prolonged illness could exacerbate nutritional faltering, thereby increasing the subsequent risk of death. Poor appetite, vomiting, deliberate withholding of food resulting in poor intake; malabsorption of macro and micronutrients; hastening of intestinal transit time; disturbance of metabolic and endocrine functions; and direct loss of protein and other nutrients in gastrointestinal tract are some of the known mechanisms which have an impact on the nutrition during an episode of diarrhea. In addition diarrhoea of infectious origin causes cytokine induced malnutrition which results from the actions of proinflammatory cytokines like tumour necrosis factor and interleukin 1, 6 and 8. Preexisting malnutrition is associated with decreased turnover of epithelial cells resulting in delayed recovery which may prolong an episode of infectious diarrhoea by itself as well as by promoting tissue invasion by other enteropathogens. Malnutrition may also alter protective host factors and thereby favour intestinal colonization by the pathogenic microbes. Mucosal damage varying from moderately severe changes to flat lesions indistinguishable from those of celiac disease may occur in kwashiorkar. Diarrhoea malnutrition interaction represents a dangerous web which can be distangled by prevention of disease transmission by promoting exclusive breast feeding, hygienic weaning practices, safe drinking water and handwashing, improved host defences by breast feeding, improved nutrition, measles vaccine and other vaccines against enteropathogens in the offing; and promotion of standard case management with special emphasis on nutritional support and rehabilitation.
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PMID:Diarrhoea and malnutrition interaction. 1113 59

A 56-year-old, obese woman who had been sexually inactive for 10 years presented at the hospital with high fevers, decreased appetite, nausea, vomiting, and weight loss. Following many diagnostic tests that revealed little, it was found that her estranged husband was being treated for Pneumocystis carinii pneumonia (PCP). The woman was tested for HIV and found to be positive. This is an example of the Centers for Disease Control and Prevention's (CDC) indication that 10 percent of reported AIDS cases occur in people over age 50, that diagnosis is often delayed in older age groups, and that anyone suffering from fever of an unknown origin should be tested for HIV. In such situations it is suggested that general practice include seeking behavioral information and offering HIV testing and counseling.
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PMID:FUO in a 56-year-old woman. 1136 55

To determine the magnitude of the problem posed by primary dengue infection in children and the distinctive clinical clues that may differ from those with secondary infection, 996 children serologically diagnosed with dengue infection and admitted to the Department of Pediatrics, Chulalongkorn Hospital, Bangkok, Thailand between 1988 and 1995 were retrospectively reviewed. One hundred and thirty-nine cases (14.0%) were serologically proved to be primary dengue infection. Of these, 72 were males and 67 were females, with a mean age of 4.8 years. Common manifestations by order of frequency included fever (97.8%), hepatomegaly (71.9%), vomiting (59.0%), decreased appetite (55.4%), coryza (52.5%), drowsiness (39.6%), diarrhea (34.5%), rash (33.8%), abdominal pain (23.0%) and seizure (15.8%). The mean duration of fever before admission was 4.6 days. Common sites of bleeding were skin (41.7%), mucous membrane (14.4%) and the gastrointestinal tract (12.2%). Clinical diagnosis was categorized into dengue fever (22.3%), dengue hemorrhagic fever (60.4%) and dengue shock syndrome (17.3%). Three patients (2.2%) died. Compared with the children with secondary dengue infection (n=139), children with primary dengue infections tended to be younger, presented more commonly with coryza, diarrhea, rash and seizure; and less commonly with vomiting, headache and abdominal pain (p < 0.05). The maximal hematocrit level, the mean difference between maximal and minimal hematocrit values and the maximal percentage of neutrophils were significantly lower in the study group, whereas the maximal percentage of lymphocytes was significantly higher. Dengue fever was more common and dengue shock syndrome was less common in the study group (p < 0.05). This study has emphasized that primary dengue infection is not uncommon and is less severe than secondary infection. Clinical presentations and laboratory findings are somewhat different between the two conditions.
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PMID:Primary dengue infection: what are the clinical distinctions from secondary infection? 1194 2

Vincristine (VCR) and L-asparaginase (L-ASP) are commonly used to treat canine lymphoma. As single agents, these drugs are not myelosuppressive. However, in combination, VCR and L-ASP cause severe neutropenia in some dogs. It has been recommended that L-ASP be administered 12-24 hours after VCR to minimize toxicity. The purpose of this retrospective study was to determine the prevalence of neutropenia after VCR/L-ASP induction therapy for canine lymphoma and to evaluate risk factors for myelosuppression, especially the interval between VCR and L-ASP administration. Medical records of 147 dogs were reviewed. L-ASP was given 0 (n = 50), 6 (n = 23), 18 (n = 20), or 24 (n = 54) hours after VCR. Forty percent of the dogs were neutropenic 7 days after VCR/L-ASP, and 18% had neutrophil counts of <1,000 cells/microL. The median neutrophil count was 3,712 cells/microL (range 0-30,968 cells/microL). No correlation was found between administration interval and day 7 neutrophil count (P = .84) or development of gastrointestinal signs, including vomiting (P = .80), diarrhea (P = .52), and decreased appetite (P = .30). No significant predictors of neutropenia were identified. Higher clinical stage and substage b were associated with decreased appetite after treatment (P = .04 and .01, respectively). Sixteen percent of the dogs were hospitalized. This study demonstrates that VCR/L-ASP induction for canine lymphoma may result in neutropenia but that separation of VCR and L-ASP administration may not be necessary to avoid toxicity.
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PMID:Neutropenia associated with vincristine and L-asparaginase induction chemotherapy for canine lymphoma. 1232 8


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