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

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.
 ...
PMID:[Neurologic disorders in Whipple's disease]. 910 28

Of 96 Parkinson's disease patients surveyed at the University of Florida Movement Disorders Center, one (1%) met diagnostic criteria for binge-eating disorder. Eight (8.3%) exhibited subthreshold binge eating. Psychometric criteria classified problem gambling in 17.8%, hoarding in 8.3%, compulsive buying in 11.5%, hypersexuality in 1.0%, and mania in 1.0% of patients. More overeaters met psychometric criteria for at least one additional impulse-control disorder (67% versus 29%). No more overeaters than non-overeaters were taking a dopamine agonist (44% versus 41%). More overeaters had a history of subthalamic deep brain stimulation (DBS; 44% versus 14%). History of DBS was the only independent predictor of overeating.
 ...
PMID:Binge eating in Parkinson's disease: prevalence, correlates and the contribution of deep brain stimulation. 2130 39

Nighttime eating is categorized as either night eating syndrome (NES) or the sleep-related eating disorder (SRED). Both diseases are often connected with an increase of the body mass, obesity, and with psychiatric disturbances. NES is characterized by evening hyperphagia, abnormally increased food intake after the evening meal, nocturnal awakings with ingestions, morning anorexia, and insomnia. Patients suffering from NES are aware of their nocturnal ingestions. It is suggested that NES is an abnormality in the circadian rhythm of meal timing that occurs in people with normal circadian rhythm of sleep. Other factors underlying NES include genetic predispositions, hormonal and neurochemical disturbances, and mood disorders. SRED is characterized by recurrent episodes of eating or drinking after arousal from nighttime sleep, unaware in tight the most cases, with adverse consequences. The distinctive features of SRED are amnesia of night eating episodes and consumption of non-typical food or dangerous articles. SRED is frequently associated with other sleep disorders, e.g., restless leg syndrome, periodic limb movement disorder, obstructive sleep apnea, and somnambulism. It can be also induced by medicines applied by a patient (e.g. zolpidem). It is hypothesized that the syndrome represents a variation of somnambulism. In the treatment of NES both non-pharmacological methods (psychotherapy, phototherapy) as well as the pharmacotherapy (aimed to increase serotoninergic neurotransmission in the brain, predominantly by sertraline, a selective serotonin re-uptake inhibitor) are used. SRED can be treated by controlling comorbid sleep disorders and eliminating provocative sedative hypnotics.
 ...
PMID:[Nighttime eating disorders--clinical symptoms and treatment]. 2138 71