Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pharmacokinetics of oral phenobarbitone was studied in 10 clinically healthy adult dogs. The drug was given once daily in tablet form, at a dose of 5 mg kg-1 of body mass. Serial venous blood samples (n = 9) were collected from each dog on Day 1 (the first day of drug dosing), on Day 22, and on Day 24 after continuous dosing. Trough serum concentrations were determined on Day 7, Day 14 and Day 21. The drug was administered to the dogs on an empty stomach, except on Day 24, when it was given with food, in order to assess the influence of food on its absorption. Drug serum concentrations were described by a one-compartmental open model with first order absorption and elimination. An average steady-state trough serum level of phenobarbitone of 52,96 +/- 8.40 mmol l-1 was achieved after 3 weeks of daily dosing. The mean elimination half-lives for Day 1 and Day 22 were 46.3 +/- 11.3 h and 29.3 +/- 4.6 h respectively. The area under the curve for Day 22 was 1,656.17 +/- 186.45 mumol h-1 l-1 and for Day 24 was 1,493.06 +/- 205.4 mumol h-1 l-1. The mean clearance value for Day 22 was 0.0133 +/- 0.0016 l h-1 kg-1. Side effects of polyphagia, polydipsia, sedation and ataxia were commonly observed in the first 2-9 d, but disappeared thereafter. It was concluded that a dose of 5 mg kg-1 would achieve an average serum concentration of 64.59 mumol l-1 in adult dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pharmacokinetics of phenobarbitone in fasting and non-fasting dogs. 228 6

We have described a patient receiving intravenous hyperalimentation in whom hypophosphatemia resulted in a neurologic syndrome characterized by ophthalmoplegia, ataxia, and areflexic paralysis of all extremities, requiring respiratory assistance. We have discussed pertinent literature related to neurologic dysfunction as a result of hypophosphatemia.
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PMID:Peripheral neuropathy with hypophosphatemia in a patient receiving intravenous hyperalimentation. 299 93

An acute limbic-cerebellar syndrome was seen in six industrial workers who inhaled trimethyltin (TMT). Clinical features included hearing loss, disorientation, confabulation, amnesia, aggressiveness, hyperphagia, disturbed sexual behavior, complex partial and tonic-clonic seizures, nystagmus, ataxia, and mild sensory neuropathy. Severity paralleled maximal urinary organotin levels. One patient died and two remained seriously disabled.
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PMID:Acute trimethyltin limbic-cerebellar syndrome. 358 45

Perfusion of 2-deoxy-D-glucose (2-DG) into the IIIrd ventricle (i.c.v.) or intraperitoneal (i.p.) injections produced changes in feeding and other overt behavior, as well as indicative changes in electroencephalograms (EEG). Applications of 2-DG, either i.p. or i.c.v., induced hyperphagia within 4 hr which was then followed by hypophagia for at least 96 hr. EEGs evinced low frequency patterns during the lethargy and ataxia symptoms which were present after i.p. injection. After i.c.v. injections, the low frequency EEG during the lethargy and ataxia were not evident. Present results in connection with prior reports indicate that 2-DG has a long term bimodal effect on feeding which may be mediated through central neurons. Hypophagia after peripheral application of 2-DG appeared to be caused at least as much by concomitant traumatism as by effects on neural control of feeding.
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PMID:Bimodal effect of 2-deoxy-D-glucose on feeding. 689 Nov 21

Wernicke's encephalopathy (WE) is a thiamine deficiency disorder and is characterized clinically by the triad of ocular abnormalities, ataxia and disturbances of consciousness. We report on 3 patients with WE, of whom 2 had insufficient thiamine substitution. In the first patient symptoms disappeared during thiamine substitution. In the second patient acute WE was the terminating event in the sequence of parenteral nutrition, lactic acidosis and cardio-pulmonary decompensation. Possibly due to hereditary deficits WE developed in the third patient despite sufficient thiamine substitution. Attention to thiamine deficiency should be paid in all patients with history of alcoholism, malnutrition, malabsorption, tumors, inflammation, other severe diseases and in parenteral hyperalimentation. In order to prevent WE thiamine should be substituted with at least 100 mg/day i.v. or i.m.
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PMID:Wernicke's encephalopathy--causes to consider. 804 22

On a retrospective basis, the response to adding chronic oral bromide (BR) to phenobarbital (PB) administration in 23 refractory canine idiopathic epileptics between 1986 and 1991 was studied. The mean age for an observed first seizure was 24 months (range 7 to 72) for all dogs. Thirteen (57%) dogs were males with no breed predisposition observed. All dogs were diagnosed as having idiopathic epilepsy based on normal metabolic and neurologic diagnostic evaluations. Dogs were evaluated before BR therapy for a mean time of 22 months (range 5 to 75 months). Seventeen dogs (74%) received multiple antiepileptic drugs (AEDs) before BR therapy. All animals were maintained on PB at least 4 months before the onset of BR therapy, with a mean trough serum concentration of 37.8 mcg/mL and no improvement in seizure severity or recurrence. Twelve dogs presented with generalized isolated seizures and 11 with generalized cluster seizures (two or more seizures within 24 hours) as their first seizure. The effects of BR therapy were evaluated for a mean time of 15 months (range 4 to 33), with 17 dogs (74%) followed for 12 or more months. The mean BR serum concentration for the 0 to 4 months time period was 117 mg/dL compared with 161 mg/dL for the greater than 4 months period. Overall, response to BR therapy was associated with a reduction in the total number of seizures in 83% of the dogs when compared with their respective pre-BR period. For those followed for 1 year after BR, there was a 53% reduction in the number of seizures compared with the previous 12 months. Furthermore, owners reported a decrease in seizure intensity (65% of dogs) and change to a less severe seizure type (22% of dogs) in those dogs that continued to have seizures. Seizure-free status was obtained in 26% of the dogs with protection continuing up to 31 months in one dog. No correlations could be determined between response to BR and either age of onset of the first seizure or interval from the first AED therapy to BR therapy. Adverse effects of concomitant BR and PB therapy were polydipsia (56% of dogs), polyphagia (30% of dogs), excessive sedation (30% of dogs), and generalized ataxia (17% of dogs). As a result of BR treatment, the PB dosage was reduced in eight dogs (35%). In conclusion, concomitant BR and PB was well tolerated in dogs of this study and was effective in treating refractory canine idiopathic epilepsy, regardless of prior interval of seizure activity or previous treatment.
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PMID:Bromide therapy in refractory canine idiopathic epilepsy. 826 51

A 28-year-old woman with inoperable gastric carcinoma was given continuous infusion of 5-fluorouracil (5-FU) and low-dose cisplatin (CDDP) for 4 weeks while receiving intravenous hyperalimentation (IVH). Eleven days after her last treatment, she developed acute diplopia, deafness and gait ataxia, followed by severe confusion. She became markedly acidotic and hypotensive with a systolic blood pressure of 60 mmHg, necessitating intubation, dopamine treatment and hemodialysis for 7 h. She was also given thiamine. Thereafter, her blood pressure stabilized, the acidosis improved, and her deafness, diplopia, and confusion were resolved. This case suggests that FP (5-FU/CDDP) therapy toxicity, manifested as acute metabolic acidosis and Wernicke's encephalopathy, may be associated with IVH and thiamine deficiency.
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PMID:Severe acute metabolic acidosis and Wernicke's encephalopathy following chemotherapy with 5-fluorouracil and cisplatin: case report and review of the literature. 876 81

The disease is named after George H. Whipple who, in 1907, was the first to describe an intestinal "lipodystrophy". Although Whipple's disease is generally recognized as a multisystem chronic granulomatous disease, primarily involving the digestive system, it can also appear as a primary neurological disorder in rare cases. Most often it is manifested with loss of weight, diarrhea, malabsorption, abdominal pain, lymphadenopathy, cardiopathy, hyperpigmentation and hypotension. The presence of periodic acid-Schiff (PAS)-positive macrophages in biopsy specimens (not only jejunal) and demonstration of "Whipple's bacilli" visible by electron microscopy, are diagnostic signs of active Whipple's disease. Whipple's disease confined to the CNS is rare. It is rarely found in the differential diagnosis of patients with progressive neurological deterioration. The most common neurological picture includes progressive dementia, external ophalmoplegia, myoclonus, seizures, ataxia, hypothalamic dysfunction (sleep disorders, hyperphagia, polydipsia) and meningitis. Oculofacial-skeletal myorhythmia as a movement disorder, associated with Whipple's disease, is reported. Fulminant course of cerebral Whipple's disease is unusual and unfavourable. The confusing and nonspecific clinical appearance is typical for primary CNS involvement. It has recently been suggested that CNS involvement occurs in all cases, although only 10-20% of patients may show it. The CNS is the most common site of disease relapse. The CT scans and MRI of the brain are often normal, but may show cortical/subcortical atrophy, hydrocephalus, focal or intracerebral mass lesions. The cerebrospinal fluid can sometimes contain PAS-positive macrophages. Brain biopsy is suggested as a diagnostic method in cases of high suspicion of CNS Whipple's disease. However, the lesions are frequently inaccessible and false negative. Without extended antibiotic therapy, the course of Whipple's disease is lethal. Now, the prognosis is good, although the optimal antimicrobial regimen is not clearly established. Initial parenteral therapy (tetracycline, penicilline, streptomycine, chloramphenicol, ampicilline) and peroral long-term treatment with trimetoprime-sulphametoxasole, are recommended. As CNS relapse of Whipple's disease may occur after several years, long-term treatment should include antibiotics that are able to cross the blood-brain barrier. The CNS relapse, in contrast to the systemic ones, is resistant to the treatment. Appropriate therapy instituted earlier in the course of the disease is associated with a better neurological outcome. Early recognition can be critical in Whipple's disease because of irreversible neurological sequelae seen later in the course of this potentially treatable condition. In cases with high clinical suspicion in which Whipple's disease cannot be diagnosed with procedures such as jejunal biopsy, antibiotic therapy is recommended. Recovery of an established neurological deficit may rarely occur. Longterm follow-up studies would help to identify the optimal antibiotic regimen and duration of treatment.
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PMID:[Neurologic disorders in Whipple's disease]. 910 28

A 13-year-old warmblood mare was presented because of progressive weight loss, general weakness and trembling. On examination the horse stood with its head lowered and the limbs placed under the body. On lifting its head spasms of the neck muscles could be observed. At the same time the horse developed trembling over the lower neck and muscle fasciculations continued over the whole body. Additional signs included frequent recumbency, polyphagia and facial hyperaesthesia. The horse showed no signs of ataxia. Haematology was normal. Blood biochemistry revealed slight increased aspartate aminotransferase (AST: 1060 U/I) and creatine kinase levels (CK: 441 U/I). Based on the clinical findings equine motor neuron disease was diagnosed. The horse was euthanatized due to poor prognosis and the progression of symptoms. The typical neurodegenerative changes found on histological examination of the spinal cord confirmed the diagnosis.
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PMID:[Equine motor neuron disease (EMND). A case report]. 928 83

A four-year-old, male neutered domestic shorthaired cat was presented with a two-week history of nasal and ocular discharge, generalised exfoliative dermatitis, intense pruritus, polydipsia, polyphagia, weight loss, intermittent hindlimb ataxia and lethargy. Cutaneous populations of Malassezia pachydermatis yeast organisms were found to be elevated. The generalised nature of the disease prompted survey radiography which revealed the presence of a cranial mediastinal mass which was subsequently resected and found to be a thymoma. Within six months of surgery, systemic and cutaneous signs had resolved and yeast counts had returned to normal, suggesting a causal relationship between the thymoma and the skin disease.
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PMID:Resolution of exfoliative dermatitis and Malassezia pachydermatis overgrowth in a cat after surgical thymoma resection. 935 5


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