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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic neuropathic cachexia is characterized by neuropathic pain and severe weight loss of unknown aetiology. We describe four patients with diabetic neuropathic cachexia who were found to have malabsorption. Four diabetic patients presented with neuropathic pain, anorexia, depression and weight loss of 16 (range 10-21) kg. None complained of diarrhoea. There were three males and one female, median age 54 (46-67) years. A butterfat test showed a serum turbidity difference of 9 (6-10) light scattering units (normal greater than 60 units). The median serum xylose was low and there was delayed urinary xylose excretion. Urinary indicans, small bowel histology, liver function tests, and thyroid and renal function were normal. Ultrasound scans of liver, gall bladder and pancreas, and endoscopic retrograde cholangiopancreatogram were normal. The patients were treated with pancreatic supplements and a high calorie diet. Three have completely recovered and the other patient is improving. Thus these cases of diabetic neuropathic cachexia appeared to be associated with malabsorption which may be due to pancreatic dysfunction. It is suggested that the management of diabetic neuropathic cachexia should include the investigation and treatment of malabsorption.
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PMID:Diabetic neuropathic cachexia associated with malabsorption. 156 56

In a prospective open study, 61 consecutive patients with advanced cancer admitted to a Palliative Care Unit underwent survival estimation by two independent physicians after a complete medical exam performed during the first day of admission. An independent research nurse also assessed each patient during the first day of admission. The assessment included activity, pain, nausea, depression, anxiety, anorexia, dry mouth, dyspnea, dysphagia, weight loss, and cognitive status. After the assessment was completed, patients were followed until discharge or death. In 47 evaluable patients, logistic regression showed a significant correlation between survival and dysphagia, cognitive failure, and weight loss. Accordingly, an "indicator of poor prognosis" was considered to exist in any patient who demonstrated weight loss of 10 kg or more plus cognitive failure (Mini-Mental State Questionnaire less than 24) plus dysphagia to solids or liquids. This indicator had a similar level of sensitivity, specificity, and overall accuracy, and a higher level of significance as compared with the assessment by physician #1 and physician #2, respectively. Our data suggest that three simple determinations, which may be performed by a nurse, can predict survival more or less than 4 wk as well as the assessments of two skilled physicians. These results need to be confirmed in other trials with large numbers of patients. Perhaps confirmation of these results and identification of other prognostic factors will result in staging systems for survival estimation of terminally ill cancer patients.
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PMID:Estimate of survival of patients admitted to a palliative care unit: a prospective study. 157 89

Lumpy skin disease caused by a capripoxvirus was observed in a captive-bred female Arabian oryx (Oryx leucoryx) at the National Wildlife Research Center, Taif, Saudi Arabia. Clinical signs included severe general depression with fever, anorexia, greater than 1,000 nodular cutaneous lesions and gradual recovery over 2 mo. The virus was found by electron microscopy and paired sera showed an increasing virus neutralization antibody titer against capripoxvirus. A serologic survey of the herd of 90 oryx showed a low prevalence (2%) of this infection. This report describes the first case of lumpy skin disease in an Arabian oryx.
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PMID:Capripoxvirus disease in an Arabian oryx (Oryx leucoryx) from Saudi Arabia. 160 85

Epidemiological, clinical, necropsy and histopathological data were accumulated during the study of 15 outbreaks of Senecio spp poisoning in cattle occurring during the last 3 y in the State of Rio Grande do Sul, Brazil. Morbidity averaged 17% and mortality was virtually 100%. The peak mortality occurred during spring and early summer. The most constant clinical signs included anorexia, depression, tenesmus often followed by rectal prolapse, and rough hair coat. Affected animals remained apart from the rest of the herd, lost weight, presented ascites, and had signs of digestive and neurological disturbances. Icterus, photodermatitis, polydipsia, and dependent subcutaneous edema were occasionally noticed. Two main clinical courses could be distinguished. In the protracted form, progressive weight loss terminated with death within many weeks or months. Alternatively, an acute or subacute course led to death in a few days. In both forms, necropsy and histopathological findings included diffuse fibrosis of the liver, hepatomegalocytosis, and biliary hyperplasia. Extrahepatic lesions included gastrointestinal and mesenteric edema, distension, edema and adenomatoid hyperplasia of the gallbladder, and spongy degeneration of the cerebral white matter. S brasiliensis and S oxyphyllus were the species involved in the field outbreaks.
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PMID:Senecio spp poisoning in cattle in southern Brazil. 160 98

Monensin, lasalocid, salinomycin, narasin and maduramicin are carboxylic ionophores intended for use as anticoccidial drugs for poultry and as growth promotants for ruminants. Generally, ionophores have been found safe and effective in the target animals receiving recommended dosage levels. However, toxic syndromes can result from overdosage and misuse situations. More information and reports of adverse reactions are available for monensin than the other ionophores because of monensin's longstanding and widespread use in the poultry and livestock industries. Care must be exercised in the diagnosis of ionophore toxicoses since clinical signs and lesions are not pathognomic. However, a feed-related problem characterized clinically by anorexia, diarrhea, dyspnea, ataxia, depression, recumbency and death, and pathologically by focal degenerative cardiomyopathy, skeletal muscle necrosis, and congestive heart failure may warrant a presumptive diagnosis of ionophore toxicity. Confirmatory diagnosis will require considerations of differential diagnoses and laboratory assays to determine the specific ionophore involved. Presently, there is no antidote or treatment for toxicoses induced by the ionophores. Judicious use, avoidance of overdosing, and adherence to species recommendation will help prevent the occurrence of adverse effects associated with this class of compounds.
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PMID:The veterinary importance of the toxic syndrome induced by ionophores. 162 67

Since its first recognition, a number of researchers have endeavored to link anorexia nervosa to underlying pathology. For example, in the past, attempts were made to associate anorexia with such psychiatric disturbances as schizophrenia, anxiety disorders, and obsessive-compulsive and antisocial personality disorders. Most recent efforts have focused on the possible link between anorexia nervosa and affective disorders. This article reviews the literature concerned with investigating psychiatric disturbances and genetic variables hypothesized as predisposing factors in the etiology of anorexia nervosa. Particular emphasis is given to research which discusses the association between anorexia nervosa and depression. Psychopharmacological evidence and family genetics studies are reviewed. Suggestions for future research are also made.
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PMID:Predisposition factors in anorexia nervosa. 162 68

Cholangiohepatitis was diagnosed in a dog with a 4-day history of anorexia, vomiting, fever, and icterus. Additional findings included signs of depression, dehydration, hepatosplenomegaly, and abdominal discomfort. Exploratory laparotomy was performed, and specimens of liver, spleen, and bile were obtained. Histologic evaluation of liver and spleen revealed acute, suppurative cholangio-hepatitis and splenitis, respectively. Cultures of liver and bile yielded Klebsiella sp. The dog responded to rehydration and intravenous administration of chloramphenicol. Although uncommon, cholangiohepatitis should be suspected in dogs with anorexia, fever, vomiting, icterus, and signs of abdominal discomfort. Definitive diagnosis requires bacterial cultures of liver and bile. Administration of an appropriate antibiotic should resolve clinical signs.
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PMID:Cholangiohepatitis in a dog. 162 52

Two adult Hampshire rams, unrelated and from separate farms, were examined for the cause of intermittent bloat and, or anorexia which lasted for three to six weeks and caused depression and cachexia. The rumen of each ram was hypermotile and ballottement of the ventral abdomen of each animal revealed an enlarged doughy viscus. Mild prerenal azotaemia, hypokalaemia with metabolic alkalosis, and high rumen chloride concentrations were evident. One ram died during the induction of anaesthesia for an abomasotomy and the other was euthanased after unsuccessful medical therapy. The abomasum of each ram was four to six times larger than that of a normal adult ram and filled with coarse, semi-moist, impacted ingesta. This abnormality was clinically identical to the abomasal emptying syndrome which has been described only in the Suffolk breed.
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PMID:Abomasal dilatation and impaction in two Hampshire rams. 162 57

Severe anemia was found in a 4-month-old heifer, which was admitted with a 1-day history of anorexia, signs of depression, and recumbency. A diagnosis of immune-mediated hemolytic anemia (IHA) was made on the basis of a Coomb's titer of 1:128 and decreased resistance to osmotic stress, as determined by an RBC fragility test. Anaplasmosis and leptospirosis were ruled out as possible causes of the IHA. Other causes of hemolytic anemia, including intoxication by copper, water, Brassica spp, or drugs were ruled out. Therefore the IHA was considered idiopathic. Treatment consisted of supportive therapy, oxytetracycline, and dexamethasone. After 60 days of treatment, CBC, Coomb's test result, and RBC fragility were within normal limits.
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PMID:Idiopathic immune-mediated hemolytic anemia in a calf. 164 56

A diagnosis of cholecalciferol toxicity in a young dog was made on the basis of adequate history and the finding of extremely elevated serum calcium levels. The traditional treatment of fluid therapy, diuresis and corticosteroids resulted in lowering the serum calcium levels over a 5-d period. The dog displayed clinical signs of severe depression, anorexia and intermittent vomiting during this time interval. Serum calcium levels rose on day 6 and remained elevated up until the dog was euthanized on day 9. Gross and histopathological examinations revealed diffuse metastatic mineralization throughout the body, particularly involving the lung, kidney, atria and stomach. The amount of cholecalciferol ingested was determined well below the lethal dose reported in dogs. This report indicates that young dogs may be much more susceptible to the lethal effects of this compound than initially believed.
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PMID:Accidental ingestion of a cholecalciferol-containing rodent bait in a dog. 165 54


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