Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe renal oxalosis was diagnosed in 4 male and 1 female purebred Beefmaster calves from herds in southeastern and northwestern United States. Clinical signs included weakness, anorexia, lethargy, alopecia, dehydration, and diarrhea. Results of serum biochemical analysis for 2 calves were consistent with end-stage renal disease. Calves died 2 days to 6 weeks after birth. At necropsy, renal calyces were dilated and contained pale yellow granular calculi. Histologically, there was renal interstitial fibrosis, and cortical and medullary tubules were distended with calcium oxalate crystals. Oxalate crystals were also in the tracheal glands of 1 calf. Severe renal oxalosis in young purebred calves, on widely varied diets, with no known exposure to exogenous oxalates is suggestive of an inherited metabolic defect resulting in primary hyperoxaluria.
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PMID:Severe renal oxalosis in five young Beefmaster calves. 148 14

A fatal case of poisoning by a mixture of methanol and ethylene glycol is described. A 72-year-old man was hospitalized when he was found stuporous to semicomatose, and despite massive bicarbonate therapy, died 36 hr after the admission. While the presence of numerous oxalate crystals in urine strongly suggested ethylene glycol intoxication, the GC analysis of the liquid the patient ingested revealed that he presumably drunk about 150 to 200 ml of a mixture of methanol (80%) and ethylene glycol (20%), the amount well over the lowest lethal dose when the additiveness of toxicity was considered. Retrospective evaluation of the signs suggested that while some of them such as oxalate crystalluria, elevated CPK, hypocalcemia, renal failure are attributable to the toxicity of ethylene glycol, others including elevated serum amylase and cyanosis are indicative of methanol poisoning. Disturbed consciousness was considered to be of metabolic origin; the high anion gap observed (38.2 mEq/liter) may be due not only to lactic acidosis but also to acidogenicity of the two chemicals ingested. The importance of gas chromatographic analysis for identification of the causative chemical(s) is stressed.
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PMID:A case of poisoning by a mixture of methanol and ethylene glycol. 667 Jan 3

A 9-year-old castrated male domestic shorthair cat with dysuria, anorexia, vomiting, and lethargy was admitted to the veterinary teaching hospital. A large, firm mass was palpable in the ventral cervical region. Hypercalcemia, azotemia, and nonregenerative anemia were evident on serum biochemical analysis and CBC, and multiple uroliths were detected by abdominal radiography. At necropsy, light microscopy of the ventral cervical mass revealed a parathyroid adenocarcinoma. Light microscopy of sections of the kidneys revealed multifocal, chronic, lymphocytic/plasmacytic, tubulointerstitial nephritis, as well as moderate multifocal acute tubular necrosis. On quantitative analysis, the uroliths were composed of calcium oxalate. Determination of serum calcium concentration is indicated in cats with calcium oxalate urolithiasis to aid in detection of primary hyperparathyroidism.
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PMID:Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. 775 34

Upon ingestion ethylene glycol (EG, monoethylene glycol) is rapidly absorbed from the gastrointestinal tract, and depending on the severity of exposure signs of toxicity may progress through three stages. Neurological effects characterize the first step consisting of central nervous depression (intoxication, lethargy, seizures, and coma). The second stage, usually 12-24 h after ingestion, is characterized by metabolic acidosis due to the accumulation of acidic metabolites of EG, primarily glycolic acid (GA), contributing to the ensuing osmolal and anion gaps. Stage 3, generally 24-72 h after ingestion, is determined mainly by oxalic acid excretion, nephropathy, and eventual renal failure. Because the toxicity of EG is mediated principally through its metabolites, adequate analytical methods are essential to provide the information necessary for diagnosis and therapeutic management. The severe metabolic acidosis and multiple organ failure caused by ingestion of high doses of EG is a medical emergency that usually requires immediate measures to support respiration, correct the electrolyte imbalance, and initiate hemodialysis. Since metabolic acidosis is not specific to EG, whenever EG intoxication is suspected, every effort should be made to determine EG as well as its major metabolite GA in plasma to confirm the diagnosis and to institute special treatment without delay. A number of specific and sensitive analytical methods (GC, GC-MS, or HPLC) are available for this purpose. Due to the rapid metabolism of EG, the plasma concentration of GA may be higher than that of EG already upon admission. As toxicity is largely a consequence of metabolism of EG to GA and oxalic acid, the simultaneous quantification of EG and GA is important. Formation of calcium oxalate monohydrate in the urine may be a useful indicator of developing oxalate nephrosis although urine crystals can result without renal injury. The pathways involved in the metabolism of EG are qualitatively similar in humans and laboratory animals, although quantitative differences have been reported. Comparison between species is difficult, however, because the information on humans is derived mainly from acute poisoning cases whereas the effects of repeated exposures have been investigated in animal experiments. Based on published data the minimum human lethal dose of EG has been estimated at approx. 100 ml for a 70-kg adult or 1.6 g/kg body weight (calculation of dose in ml/kg to mg/kg based in EG density=1.11 g/l). However, human data from case reports are generally insufficient for the determination of a clear dose-response relationship and quantification of threshold doses for systemic toxicity, in particular renal effects, is limited. As toxicity is largely a consequence of metabolism of EG to GA, it is important to note that no signs of renal injury have developed at initial plasma glycolate concentrations of up to 10.1 mM (76.7 mg/dl). Plasma EG levels of 3.2 mM (20 mg/dl) are considered the threshold of toxicity for systemic exposure, if therapeutic strategy is based on the EG concentration alone.
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PMID:Ethylene glycol: an estimate of tolerable levels of exposure based on a review of animal and human data. 1537 38

A 14-month-old intact male Syrian hamster was admitted for lethargy and hematuria. A total body radiographic image and abdominal ultrasonography showed the presence of a vesical calculus. During cystotomy, a sterile urine sample was obtained and sent to the diagnostic laboratory along with the urolith for analysis. Urine culture was found negative for bacterial growth, and the urolith was identified as a calcium-oxalate stone. Diet supplementation with palmitoylethanolamide, glucosamine and hesperidin was adopted the day after discharge. One year follow up revealed no presence of vesical calculi. Although this is the report of a single clinical case, this outcome differs from the results reported in the literature characterized by recurrences after few months. Considering the positive outcome and the beneficial properties of palmitoylethanolamide, glucosamine, and hesperidin, these nutritional elements in Syrian hamsters, are recommended to reduce recurrence after surgical treatment of urolithiasis.
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PMID:Cystolithiasis in a Syrian hamster: a different outcome. 2754 May 15

Feline lower urinary tract diseases are known to be life threatening conditions in cats, especially when they occur as obstructive diseases in males. Early diagnosis and treatment is necessary, otherwise it may lead to death. A 3-year-old male Persian cat was referred to the clinic with a history of anuria, lethargy, loss of appetite and exploratory cystotomy 6 months ago due to urethral obstruction following urolithiasis. Urinary bladder was enlarged and painful on palpation and urine accumulation was observed in ultrasonography. Biochemical and hematological analyses revealed hypocalcemia, hyperphosphatemia and hyperkalemia and increase in blood urea nitrogen, creatinine, white blood cell (WBC), red blood cell (RBC) and hematocrit. Urine analysis showed a turbid appearance, protein 1+, blood 3+, pH reduction, increased WBCs and RBCs and presence of bacteria, calcium oxalate crystals and epithelial cells. Urine culture reveled Staphylococcus saprophyticus. Postoperatively, microscopic examinations of the urinary bladder biopsy showed pathological lesions of bacterial cystitis. Based on these findings, bacterial cystitis and urethral obstruction due to post-operative urinary tract infections were diagnosed. For treatment, electrolyte imbalances were corrected firstly, cystotomy was performed and a catheter was conducted into the urethra; then, urethra was flushed and obstruction was resolved. Ampicillin was effective in reducing the bacterial count in urine. Despite the fact that cystotomy is a common procedure in veterinary medicine, clinicians should be aware of its complications such as post-operative urinary tract infections.
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PMID:Obstructive bacterial cystitis following cystotomy in a Persian cat. 3006 10

Background: We describe for the first time the use of chia seeds (Salvia hispanica L.) as a non-pharmacological solution in managing feline idiopathic hypercalcemia when dietary change alone fails. Case Summary: Over a 2-year period of time, three female spayed, middle-aged, Domestic Shorthair cats were diagnosed with idiopathic hypercalcemia. Reason for consultation were lethargy and dysorexia, with a single episode of vomiting described in one cat and dysuria in another. Thorough diagnostic work-up included complete blood count, serum biochemistry, urinalysis, ionized calcium, calcemic hormones, parathyroid hormone-related protein, and imaging of chest and abdomen. Based on different nutritional reasons, each cat was switched to a different high-moisture pet food as first-step in managing the disorder: a high-fiber diet, a diet formulated for chronic kidney disease management and a diet designed to prevent calcium oxalate urolithiasis. In the three cats, 6 weeks of dietary change alone did not result in normocalcemia. Before resorting to any pharmacological solution, supplementation to the diet of chia seeds (2 g/cat/day) was started. After 4 weeks from the introduction of Salvia hispanica L., all cats achieved normalization of ionized calcium concentration. Conclusion: Chia seeds (Salvia hispanica L.) supplementation could be a useful tool in managing feline idiopathic hypercalcemia.
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PMID:Managing Feline Idiopathic Hypercalcemia With Chia Seeds (Salvia hispanica L.): A Case Series. 3279 47