Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medical records of 210 horses that survived ventral midline celiotomy for at least 4 months were examined and owners were queried to determine factors contributing to incisional hernia formation. The incidence rate of incisional hernias within 4 months was 16%. Factors significantly associated with occurrence of incisional hernias were incisional drainage, closure of the linea alba with chromic gut suture material, previous midline celiotomy, excessive incisional edema, castrated male sex, postoperative leukopenia, and postoperative pain (colic). Factors not significantly associated with occurrence of incisional hernias were suture pattern used for linea alba closure, concurrent enterotomy or intestinal resection, postoperative bandage or stent, postoperative fever, hypoproteinemia, diarrhea, respiratory disease (coughing), and peritonitis. Hernias developed in horses within 12 weeks of surgery, with the earliest hernia recognized at week 2. Of 30 horses for which information was available, only one hernia developed in 24 (80%) and two or more hernias developed in 6 (20%) along the incision. Multiple hernias tended to be smaller than single hernias.
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PMID:Incisional hernias in the horse. Incidence and predisposing factors. 253 Jun 84

A 10-year-old Tennessee Walker gelding, with a history of progressive weight loss, intermittent colic and lethargy, had a slight fever, tachycardia, tachypnea, pallor, ascites and marked ventral edema. Blood analyses revealed anemia, leukocytosis, neutrophilia with a left shift, lymphopenia, monocytosis, hypoproteinemia and a slightly increased SDH level. Abdominocentesis produced red-orange fluid with many RBC and an increased fibrinogen content. Rectal palpation revealed a large mass in the left caudal abdominal quadrant. The animal died shortly after resection of the mass. The histopathologic diagnosis was lymphosarcoma, involving the spleen, liver and lung.
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PMID:Splenic lymphosarcoma in a horse. 654 5

In a retrospective study of 269 horses that had been treated with phenylbutazone, horses receiving less than or equal to 8.8 mg/kg of body weight/day for less than or equal to 4 days or 2 to 4 mg/kg of body weight/day for up to 50 days remained clinically normal. Anorexia, depression, colic, hypoproteinemia, diarrhea, melena, weight loss, ventral edema, petechial hemorrhages of mucous membranes, oral and gastrointestinal tract erosions and ulcers, renal papillary necrosis, and death were among the complications seen in horses that had received greater than 8.8 mg/kg of body weight/day. In 2 cases, signs suggestive of gastrointestinal-related shock were also evident.
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PMID:Phenylbutazone toxicosis in the horse: a clinical study. 672 3

Cecocolic intussusception was detected in a 2-year-old male Standardbred horse with a 3-day history of signs of intermittent colic. The entire cecum, which was located within the lumen of the right ventral colon, was edematous and necrotic, and could not be manually reduced. A colotomy was made, and partial typhlectomy was performed. An ileocolostomy also was performed. To prevent eversion of the cecal base, the site of invagination into the colon was oversewn. Several postoperative complications were treated, including peritonitis, thrombophlebitis, anemia, and hypoproteinemia, and 1 year after surgery, the horse was healthy and in training.
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PMID:Partial typhlectomy and ileocolostomy for treatment of nonreducible cecocolic intussusception in a horse. 792 13

The medical records of 19 horses with acute hemoperitoneum were reviewed. The causes for the hemoperitoneum were idiopathic (8 horses), splenic hematoma with capsular tear (7), bleeding from the reproductive tract (3), multicentric hemangiosarcoma (1), and systemic amyloidosis (1). The affected horses were between 4 and 32 years of age (median 11.5 years). The most consistent findings on initial examination were depression, tachycardia, tachypnea, pale mucous membranes, prolonged capillary refill time, colic, and abdominal discomfort. Less common clinical signs included abdominal distention, profuse sweating, ataxia, and broad ligament mass palpated on rectal examination. Clinicopathologic abnormalities commonly detected were anemia, neutrophilia, lymphopenia, thrombocytopenia, hypoproteinemia, hypocalcemia, azotemia, increased creatinine kinase, and sorbitol dehydrogenase activity. Hemoperitoneum was diagnosed on the basis of abdominocentesis, transabdominal ultrasonography, and postmortem examination. Sixteen horses were treated, and 3 horses were euthanized at owners' request because of severe clinical signs. The treatment consisted of the administration of intravenous fluids, plasma or blood transfusion, nonsteroidal drugs, antimicrobial drugs, and antifibrinolytic and procoagulant agents. Rapid clinical deterioration was observed in 2 horses, necessitating euthanasia. The remaining 14 horses survived the abdominal bleeding (survival rate 74%) and were discharged 3-15 days (median 7.0 days) after presentation. Postmortem examination of the 6 nonsurvivors showed massive abdominal hemorrhage from splenic hematoma with capsular tear (2 horses), multicentric hemangiosarcoma with liver rupture (1), systemic amyloidosis with splenic hematoma and capsular tear (1), and bilateral ruptured ovarian hematomas (1). In one horse, no origin of the bleeding could be determined during postmortem examination.
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PMID:Acute hemoperitoneum in horses: a review of 19 cases (1992-2003). 1595 49

The purpose of this study was to compare traditional and quantitative approaches in analysis of the acid-base and electrolyte imbalances in horses with acute gastrointestinal disorders. Venous blood samples were collected from 115 colic horses, and from 45 control animals. Horses with colic were grouped according to the clinical diagnosis into 4 categories: obstructive, ischemic, inflammatory, and diarrheic problems. Plasma electrolytes, total protein, albumin, pH, pCO2, tCO2, HCO3-, base excess, anion gap, measured strong ion difference (SIDm), nonvolatile weak buffers (A(tot)), and strong ion gap were determined in all samples. All colic horses revealed a mild but statistically significant decrease in iCa2+ concentration. Potassium levels were mildly but significantly decreased in horses with colic, except in those within the inflammatory group. Additionally, the diarrheic group revealed a mild but significant decrease in Na+, tCa, tMg, total protein, albumin, SIDm, and A(tot). Although pH was not severely altered in any colic group, 26% of the horses in the obstructive group, 74% in the ischemic group, 87% in the inflammatory group, and 22% in the diarrheic group had a metabolic imbalance. In contrast, when using the quantitative approach, 78% of the diarrheic horses revealed a metabolic imbalance consisting mainly of a strong ion acidosis and nonvolatile buffer ion alkalosis. In conclusion, mild acid-base and electrolyte disturbances were observed in horses with gastrointestinal disorders. However, the quantitative approach should be used in these animals, especially when strong ion imbalances and hypoproteinemia are detected, so that abnormalities in acid-base status are evident.
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PMID:A comparison of traditional and quantitative analysis of acid-base and electrolyte imbalances in horses with gastrointestinal disorders. 1635 83

Equine proliferative enteropathy (EPE) is a disease of foals caused by the obligate intracellular organism Lawsonia intracellularis. This organism is unique in that it causes proliferation of infected enterocytes, resulting in thickening of the intestinal epithelium, most often the small intestine. This disease affects mainly weanling foals and causes fever, lethargy, peripheral edema, diarrhea, colic and weight loss. The diagnosis of EPE may be challenging and relies on the presence of hypoproteinemia, thickening of segments of the small intestinal wall observed on abdominal ultrasonography, positive serology and molecular detection of L. intracellularis in feces. The epidemiology and genetic basis for pathogenesis for this disease is beginning to be elucidated. Phenotypic traits, genomic features, and gene expression profiles during L. intracellularis infection in vitro and in vivo are presented. In addition, this article reviews the epidemiology, pathological and clinicopathological findings, diagnosis, and control of EPE.
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PMID:Lawsonia intracellularis infection and proliferative enteropathy in foals. 2387 78

Lawsonia intracellularis is the etiologic agent for equine proliferative enteropathy (EPE), which typically affects weanling and yearling horses. In North America, EPE cases often occur between August and January, although cases outside of this time frame have been reported. Clinical signs of EPE are usually nonspecific and include lethargy, pyrexia, anorexia, peripheral edema, weight loss, colic, and diarrhea. Diagnosis is based on the presence of hypoproteinemia and hypoalbuminemia along with clinical signs and positive commercial serologic and/or molecular testing. Treatment requires the use of antimicrobials with good intracellular penetration and supportive care to prevent or decrease secondary complications.
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PMID:Lawsonia intracellularis and equine proliferative enteropathy. 2530 Jun 36