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)

Four patients having high-level quadriplegia developed elevated serum calcium concentrations (11 to 15.8 mg/100 ml) within three months of injury. All were young males (ages 15 to 19 years) and quadriplegic (C4-C7). Presenting symptoms were nausea, vomiting, polydipsia, polyuria and lethargy. In two patients severe muscle wasting and cachexia with clinical symptoms developed and persisted for several months. Laboratory studies in all patients showed negative calcium balance with hypercalciuria. Reduced renal function was seen in all patients but returned to normal with return of normal serum calcium. Alkaline phosphatase level was normal in three and elevated in one. Serum parathormone levels were normal. Roentgenograms revealed diffuse demineralization. Nephrocalcinosis and soft tissue calcifications developed in one patient. Primary treatment included reduced calcium intake, correction of dehydration, sodium infusion and remobilization. Corticosteroids, oral phosphates, furosemide and mithramycin were used with varying success to control prologned symptoms and severe hypercalcemia.
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PMID:Immobilization hypercalcemia in spinal cord injury. 83 59

Twelve Yankasa rams aged between 2 1/2 and 3 years with good semen characteristics were used in this 15-week study. Six rams were infected with Trypanosoma vivax, while six served as controls. The infected rams developed chronic trypanosomosis accompanied by fluctuating pyrexia, lethargy, anaemia, scrotal oedema and cachexia. There was a drastic and progressive deterioration in semen quality in all infected rams manifested by a decrease in volume or cessation of semen production, oligozoospermia, a sharp decrease in progressively motile sperm, elevated numbers of dead (eosinophilic) sperm and 100% morphological abnormalities of sperm in most animals. The rams were all deemed unfit for breeding by 3 weeks post-infection. Uninfected rams were healthy and had good semen characteristics throughout the investigation. The results show that rams infected with T. vivax may become infertile within a short interval due to rapid deterioration of semen characteristics and this trypanosome species may be an important causative agent of infertility in endemic areas.
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PMID:Effect of Trypanosoma vivax infection on semen characteristics of Yankasa rams. 136 6

The literature contains about 500 cases of equine leucosis, though the reports are deposited in a great number of journals and vary considerably concerning particular topics. During the last years there has been a remarkable increase of publications about this syndrome in the equine. The clinical leucosis key recommended by us has been confirmed in principle considering the latest literature. In about 70 individual symptoms which can be clinically observed in equine with leucosis 11 can be considered as main symptoms because of their frequency; they are again classified in primary (lymph node tumours including splenomegaly--loss of condition, weakness--cachexia, weight loss, periphery oedema), secondary (anorexia, inappetence--fever--paleness of mucous membrane--anaemia--tachycardia) and accessory (incoordination--tachypnoea, dyspnoea--apathy, lethargy) main symptoms. Furthermore in future it will be necessary to take into more consideration the symptoms "recurrent colic" and "hydrothorax" within differential diagnosis. The main symptom "incoordination" (ataxia, asynergy, paresis, paralysis) is used by us more precisely only in case of impairment of nervous system by neoplastic infiltrations and does not signify as possible symptoms of general physical weakness, for example faltering, staggering, tumbling or lameness. The morphological classification follows further on our previous recommendation. There exist generalized forms with tumour infiltrations in abdominal and in thoracic cavity as well as especially in peripheral lymph nodes. On the other hand there are characteristic manifestations in certain regions of the body, which establish distinctly the clinical symptomatology. They are marked as regional multicentric forms with the main localizations "mediastinal", "splenic", "mesenteric" or "intestinal".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical diagnostic keys and special manifestations in equine leukosis]. 195 30

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

We have developed a rabbit model of toxic shock syndrome that uses a subcutaneous infusion pump to administer toxic shock syndrome toxin 1 (TSST-1). A dose of 150 micrograms, infused at a constant rate over a period of 7 days, resulted in a characteristic illness highlighted by fever, conjunctival hyperemia, cachexia, and lethargy. The illness was uniformly fatal, with a mean interval until death of 3.2 +/- 0.4 days. Serial determinations of serum chemistries confirmed the multisystem nature of this illness. Rabbits developed profound hypocalcemia, with levels falling from 15.5 +/- 0.2 to 7.6 +/- 0.4 mg/dl under the influence of TSST-1. Blood urea nitrogen and creatinine rose dramatically, in the setting of oliguria or anuria. Serum glutamicpyruvic transaminase was the most reliable indicator of hepatic dysfunction, with the mean rising from 48 U/liter before administration of TSST-1 to 546 U/liter among rabbits surviving 2 days of the infusion. Creatine phosphokinase also rose dramatically in 10 of 16 rabbits. Rabbits demonstrated relative neutrophilia and lymphopenia as well as an increase in the partial thromboplastin time. Histopathologic examination demonstrated disease of multiple organs, particularly the liver, spleen, and lymph nodes, all of which demonstrated inflammation, thrombosis, hemorrhage, and erythrophagocytosis. The concurrent administration of prednisolone with TSST-1 prevented death in four of four rabbits and greatly lessened the morbidity. Rabbits were not protected from morbidity or mortality by the concurrent administration of polymyxin B. We believe that a constant, subcutaneous infusion of TSST-1 in rabbits provides a reproducible model for studying the pathogenesis of TSS.
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PMID:A rabbit model of toxic shock syndrome that uses a constant, subcutaneous infusion of toxic shock syndrome toxin 1. 357 Apr 55

Megaesophagus was diagnosed in 9 adult ferrets. Clinical history of the ferrets included regurgitation, difficulty in swallowing, partial anorexia, and lethargy. Cachexia, dehydration, weakness, and ptyalism were observed on physical examination. Radiography revealed the esophagus of each ferret to be dilated in the thoracic and cervical regions. Of 4 ferrets that had lymphocytopenia, 2 had concurrent leukopenia. Serum biochemical analysis revealed high activity of alanine transaminase (4 ferrets) and aspartate transaminase (3), and hypoglycemia (4). Treatment included administration of fluid, antibiotics, and agents directed against possible primary causes of megaesophagus. Treatments were ineffective, and all of the ferrets died or were euthanatized. All 6 ferrets that were submitted for necropsy had bronchopneumonia, hepatic lipidosis, mild esophagitis, and gastritis. The etiopathogenesis of megaesophagus in the ferrets was not determined.
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PMID:Megaesophagus in nine ferrets. 796 Oct 71

Nutritional support of patients with HIV or acquired immune deficiency syndrome (AIDS) has many similarities to other disease states in that the same nutritional products and techniques are used. Some patients with HIV, and many with AIDS without secondary infection, experience a metabolic milieu similar to patients with cancer cachexia. In providing dietary counselling to the HIV patient, we encounter many of the obstacles that must be overcome to improve nutrition in cancer: anorexia, gastrointestinal discomfort, lethargy, and poor nutrient utilization, which limit the ability for nutritional repletion. When a secondary infection is superimposed on HIV, patients resemble more highly catabolic trauma patients or patients in the intensive care unit (ICU), where, despite aggressive efforts to feed, there is usually a net nitrogen wasting leading to the more rapid development of cachexia. However, even in this setting, feeding will limit substantially net catabolism when compared to total starvation. Because the nutritional needs of HIV patients vary greatly, individual strategies have to be designed as the patient moves through the stages of disease. Patients are generally able to consume adequate nutrition either as regular food or dietary supplements during the latency period of viral replication. Once secondary infections become prevalent, artificial diets administered by tube or by vein may be required during the period of active secondary infections, with dietary supplements often helpful during more quiescent periods. Patients with HIV are among the most challenging for clinicians providing nutritional support. Knowledge from treatment of patients with other diseases may be useful, but more data must be gathered on the unique aspects of aetiology and treatment of the anorexia, malabsorption, and ultimate wasting associated with AIDS.
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PMID:Nutrition support and the human immunodeficiency virus (HIV). 811 86

Most attempts at developing a model of autoimmune inner ear disease have focused on the immunization of healthy animals with cochlear tissue. We have chosen an alternate route of studying this entity utilizing the MRL-lpr/lpr (Lupus) mouse, an animal known to spontaneously develop multisystemic, organ nonspecific autoimmune disease. We report on the auditory pathology found in animals at early stages of this systemic disease. At the onset of clinical signs of illness (cachexia, weight loss, lethargy) animals were sacrificed and their cochleas and kidney prepared for morphologic analysis. Significant pathology was seen in the MRL/lpr animals involving the basal and middle turns of the cochlea which could not be correlated with the presence or degree of glomerulonephritis. Findings included outer and inner haircell degeneration, strial edema and degeneration, and an acellular infiltrate in the tunnel of Corti. Cochlear pathology was not found in control animals. Thus, at early stages of systemic disease, MRL/lpr mice manifest significant cochlear pathology not seen in control animals. The implications of these results with regard to the pathogenesis of these lesions as well as their clinical relevance are discussed.
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PMID:The MRL-lpr/lpr mouse: a potential model of autoimmune inner ear disease. 847 29

Interleukin-6 (IL-6), among other cytokines, is thought to be involved in the regulation of sickness behavior (e.g., anorexia, cachexia, fever, and lethargy) induced by infections bacterial and viral origin) and sterile tissue necrosis (burns and surgical traumas). Mice deficient in IL-6 (IL-6 KO) were generated by gene targeting. Homozygous IL-6 KO male and female mice and their appropriate controls were implanted with biotelemeters to monitor body temperature (Tb) and motor activity (Act). Normal circadian rhythms in Tb and Act as well as rates of food intake and weight gain did not differ significantly between sex-matched IL-6 KO and control groups at 30 degrees C in a 12:12-h light-dark cycle. Sterile tissue damage was induced in mice by subcutaneous injection of turpentine (0.1 ml, left hindlimb). Influenza pneumonitis was induced by intranasal inoculation of mouse-adapted influenza A virus (17.5 plaque-forming units). Lack of IL-6 completely prevented fever, anorexia, and cachexia because of turpentine abscess in both sexes. It did not prevent lethargy, although IL-6 KO mice recovered to normal Act significantly sooner than wild-type mice. Symptoms of sickness were only slightly modified during influenza virus infection in IL-6 KO mice. Attenuation of sickness behavior was more pronounced in IL-6 KO female than in male mice. We conclude that, although IL-6 is induced during both turpentine abscess and influenza infection, this cytokine appears to be more critical in induction of the symptoms of sickness behavior during sterile tissue abscess than during influenza infection.
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PMID:Sickness behavior in mice deficient in interleukin-6 during turpentine abscess and influenza pneumonitis. 912 87

We tested the hypothesis that increased dietary fish oil levels (via modulation of the production of inflammatory mediators) modulate sickness symptoms (i.e., anorexia, cachexia, fever, lethargy) of systemic and local inflammation. Swiss Webster mice were implanted with biotelemeters to measure body temperature and motor activity and were fed a diet high in n-3 fatty acids (17% wt/wt menhaden oil) or a reference diet (17% wt/wt hydrogenated coconut oil or normal rodent chow) for 6 wk. Local inflammation was induced by subcutaneous injection of turpentine (100 microl/mouse). Systemic inflammation was elicited by intraperitoneal injection of lipopolysaccharide (LPS; 2.5 mg/kg). Fever, lethargy, anorexia, and weight decrease during turpentine abscess were all inhibited (P < 0.05) in mice fed the fish oil diet. Indomethacin, similar to the fish oil diet, attenuated the turpentine-induced symptoms in mice fed a normal diet. Dietary n-3 fatty acids prevented fever and attenuated the decrease in body weight caused by LPS but did not affect the LPS-induced lethargy and anorexia. Within 90 min of LPS injection, the bioactivity of plasma tumor necrosis factor-alpha (TNF-alpha) increased to 98.2 +/- 5.1 ng/ml in mice fed fish oil compared with 32.6 +/- 3.6 ng/ml in those fed the reference diet (P < 0.05). Plasma prostaglandin E2 (PGE2) levels after LPS injection of mice fed the control diet increased within 90 min to 16.4 +/- 5.1 pg/ml. Mice fed the fish oil diet did not show any elevation in plasma PGE2 levels at that time (P < 0.05). We speculate that dietary n-3 fatty acids suppressed PGE2-related responses, including a PGE2-dependent negative feedback on TNF-alpha production, which resulted in differential modulation of sickness behavior depending on the locus of inflammation.
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PMID:Dietary n-3 fatty acids differentially affect sickness behavior in mice during local and systemic inflammation. 914 33


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