Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myopathy resembling nutritional muscular dystrophy occurred in a colony of 150 guinea pigs. Of 54 animals affected, 27 died. Major clinical signs were depression, conjunctivitis, and reluctance to move. Lesions were widespread throughout skeletal and cardiac musculature. Clinical signs and deaths ceased when the diet was changed to a different commercial ration. A single intramuscular injection of sodium selenite and alphatocopherol brought prompt remission of clinical signs in one group of 20 so treated.
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PMID:Myopathy in guinea pigs. 92 53

From 1971 to 1975, inclusive, 594 pronghorns (Antilocapra americana) were drive trapped in Alberta; subsequently, 74 of these animals were transported to enclosures. Deaths attributable to capture myopathy (CM) occurred in 20 of the trapped pronghorns and in 17 of the pronghorns that were trapped and subsequently transported. Two neonatal pronghorns that had been pursued died with signs and lesions similar to those seen in adult pronghorns affected with CM. The diagnosis of CM was based on history, clinical signs, clinico-pathologic findings, and gross and histologic lesions. Clinical signs of CM included depression, stiffness, weakness, incoordination, recumbency, and paralysis; myoglobinuria was observed in 1 neonatal animal. Of the pronghorns that died, fewer than one-half died acutely during processing, whereas the remainder died from 1 to 13 days following their release. Gross and histologic lesions were observed in the large muscles of the hindlimbs of most affected pronghorns. Values for serum enzymes, potassium, glucose, and creatinine, were higher for drive-trapped pronghorns than for tame, hand-reared pronghorns. These findings indicated extensive damage to muscle and to other organs as a result of the capture procedures.
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PMID:Capture myopathy in pronghorns in Alberta, Canada. 92 65

Fatal myopathy similar to "capture myopathy" described for African game was diagnosed in a wild white-tailed deer. Clinical signs included depression, inability to rise or stand, and myoglobinuria. Values for serum creatine phosphokinase, glutamic oxaloacetic transaminase, and blood urea nitrogen were high. The deer died 42 hours after capture. At necropsy the muscles of the limbs had a waxy, "cooked" appearance and the kidneys were brown. Microscopic findings included severe degeneration and fragmentation of skeletal muscle fibers, nephrosis, centrilobular hepatic necrosis, myocardial degeneration, and anoxic neuronal degeneration.
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PMID:Myopathy and myoglobinuria in a wild white-tailed deer. 97 70

Eight 5-to 8-week-old Beagle pups were allotted to 4 groups of 2 dogs each. For 55 to 70 days, they were fed either a semisynthetic basal diet (BD) deficient in vitamin E and selenium (Se) (group 1) or the BD supplemented with either 30 IU alpha-tocopherol/kg (group 2), 0.5 ppm Se as selenite (group 3), or 1.0 ppm Se as selenite (group 4). In the dogs fed the BD, clinical signs of vitamin E-Se deficiency developed after 40 to 60 days. These signs were accompanied by increased plasma activity of creatine phosphokinase (CPK) and glutamic oxalacetic transaminase (GOT). The dogs were euthanatized after 10 to 15 days of progressive clinical signs, including muscular weakness, subcutaneous edema, anorexia, depression, dyspnea, and eventual coma. Gross lesions seen at necropsy included ventral subcutaneous edema, generalized skeletal muscular pallor and edema with scattered white longitudinal streaking, prominent brownish yellow discoloration of the intestinal musculature, and a layer of white chalky material at the renal corticomedullary junction. Microscopically, there was evidence of extensive skeletal muscular degeneration and regeneration, focal subendocardial necrosis in the ventricular myocardium, intestinal lipofuscinosis, and renal mineralization. Mean hepatic Se content in the dogs fed the BD was 0.10 ppm (wet weight basis) at necropsy. In the dogs fed the 3 supplemented diets, clinical signs of deficiency did not develop. At necropsy, mild skeletal myopathy was evident histologically in the dogs fed BD and 0.5 ppm Se (group 3) but not in the dogs fed the other supplemented diets. Intestinal lipofuscinosis was found in the dogs fed the 3 supplemented diets but was less severe in the dogs fed the diet supplemented with vitamin E than in those fed diets supplemented with Se.
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PMID:Experimentally induced vitamin E-selenium deficiency in the growing dog. 112 Jul 35

Thyroid disease in the elderly can be easily overlooked. Symptoms too often are explained away as normal processes of aging. Development of unstable illness, especially cardiac disease, is a frequent mode of presentation. One symptom or one clinical feature of thyroid disease in the elderly may be overwhelming in its presentation, as in apathetic hyperthyroidism, thyroid myopathy, depression and dementia. Physical examination of the thyroid gland can be helpful but in a high percentage of older patients the gland is normal to palpation. The treatment of hypothyroidism is straightforward. Only myxedema coma requires large doses of levothyroxine parenterally; all other forms of hypothyroidism are treated with oral levothyroxine. The dose is started very low and increased gradually over months. The euthyroid state is achieved gradually and safely. Hyperthyroidism can be treated by several modalities. In the unstable elderly patient, antithyroid medication can quickly produce a euthyroid state. When the patient is stable, further decisions can be made regarding definitive therapy. Radioactive iodine therapy is well-tolerated and effective. On occasion, a second course of therapy is needed to suppress hyperthyroidism. Close follow-up of all patients ever having received this therapy is needed to identify the development of hypothyroidism. Surgical thyroid ablation may be necessary in patients who fail to respond to radioactive iodine therapy. Abnormalities associated with unresolved thyromegaly, dysphagia, or tracheal compression may require surgical intervention. If suspicion exists that the gland is cancerous, surgical intervention is warranted.
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PMID:Hypothyroidism and hyperthyroidism in the elderly. 158 94

Multiple deletions of mitochondrial DNA (mtDNA) have recently been reported in familial progressive external ophthalmoplegia (PEO), in a case of progressive encephalomyopathy, and in inherited recurrent myoglobinuria. The inheritance of familial PEO has been autosomal dominant, which indicates that a mutation in an unknown nuclear gene results in several mtDNA deletions of different sizes in these patients. We report a patient with autosomal dominant PEO, whose major clinical symptom, however, was severe retarded depression. The morphological analyses of the tissue samples derived from autopsy showed various abnormalities in the mitochondria in all the tissues studied. The activities of the respiratory chain enzymes encoded by mtDNA were remarkably reduced in the skeletal muscle. The mtDNA analyses confirmed that besides myopathy, this patient had a multisystem disorder with widespread distribution of multiple deletions of mtDNA. The highest percentage of mutated mtDNA was found in the brain, skeletal muscle and the heart, the relative quantity of mutated mtDNA correlating to the severity of the clinical symptoms.
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PMID:Multiple deletions of mitochondrial DNA in several tissues of a patient with severe retarded depression and familial progressive external ophthalmoplegia. 163 20

Corticosteroid-induced osteoporosis, the principal cause of "secondary" osteoporosis, is usually observed in patients under prolonged systemic corticosteroid therapy and results from the multiple effects exerted by these drugs on bone cell metabolism. Corticosteroids reduce the intestinal absorption of calcium and its tubular reabsorption, thereby negativating the calcium balance and inducing a parathyroid reaction. This reaction is responsible for an increase in bone cell remodelling, but the main manifestation of the direct effect of corticosteroids on bone is osteoblast depression, so that there is disparity between bone resorption and formation, which in turn is responsible for bone tissue deficit. Sex hormone deficiency (due to menopause or treatment) and lack of physical activities (due to the causal disease or to iatrogenic myopathy) amplify bone rarefaction. By quantifying the bone loss, modern densitometry methods provide an early risk evaluation. Osteoporosis of varying intensity exposes some 20% of patients to fractures, vertebral collapse and rib fractures. Preventive measures are always recommended, including minimal effective dose corticosteroid therapy, sodium-free diet, calcium and vitamin D supplement, sex hormone replacement and pursuance of physical activities. Once the stage of fractures by osteoporosis has been reached, the "curative" treatment aims at reducing the incidence of new fractures, either by slowing down osteoclast resorption, or by restoring the bone tissue reserve through stimulation of the osteoblasts. The usefulness of these therapeutic measures in the preventive treatment of corticosteroid-induced osteoporosis remains controverted.
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PMID:[Cortisone-induced osteoporosis: from physiopathology to treatment]. 179 40

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

Any patient who has a Bell's palsy (unilateral or bilateral), aseptic meningitis, chronic fatigue syndrome, atypical radiculoneuropathy, presenile dementia, atypical myopathy, or symptoms of atypical rheumatoid arthritis should be asked specifically about the following: visits to highly endemic areas, any known tick bites, any skin lesion suggestive of erythema migrans, any history of palpitations or of prior Bell's palsy, aching in joints (especially the knees), paresthesias, chronic fatigue and depression, forgetfulness, and eye problems. Any patient showing a chronic iritis with posterior synechiae, vitritis in one or both eyes, an atypical pars planitis-like syndrome, big blind spot syndrome, and swollen or hyperemic optic discs should be asked the same questions. The physician should send one red-top tube of blood containing 2 to 3 ml serum to Microbiology Reference Laboratory, 10703 Progress Way, Cypress, CA 90630-4714, requesting a Lyme/treponemal panel. For $90 the patient will receive an RPR test with titer, serum FTA-ABS test, serum Lyme IFA IgG and IgM, and a serum Lyme ELISA test. If these tests are within normal limits and the physician is still suspicious, a Western blot can be ordered on serum. A green top tube with fresh white blood cells sent out by overnight express on a Monday or Tuesday will produce a Lyme PCR and a lymphocyte stimulation test. Finally, R.K. Porschen, director of MRL Laboratory, will provide information on the urine antigen test on an investigational basis. A careful history with emphasis on the specific questions noted above, a complete neuro-ophthalmological and physical examination ruling out other causative problems, and the laboratory studies here discussed will usually provide sufficient data to choose therapy. Much further active research into Lyme borreliosis is an important priority in medicine.
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PMID:Neuro-ocular Lyme borreliosis. 201 Nov 11

The chronic fatigue syndrome (CFS) was formally defined in 1988 to describe disabling fatigue of at least 6 months' duration of uncertain etiology. Reports of CFS have emerged from the United States, Canada, the United Kingdom, Australia, New Zealand, Israel, Spain, and France. The disease primarily affects individuals between 20 and 50 years of age, and there is a preponderance of females. Although a triggering infectious illness is reported by most patients with CFS, there is no convincing evidence causally linking any currently recognized infectious agent to CFS. Multiple minor immunologic aberrations are frequent but inconsistent and of uncertain significance. There is no consistent evidence for myopathy or physical deconditioning. Depression is found in approximately 50% of CFS patients, with depression preceding the physical symptoms in half of the cases. No therapy has been proved effective in controlled clinical trials with prolonged follow-up, although antidepressants have not been formally evaluated. The long-term prognosis of patients with CFS has not been well studied, but CFS appears to be a disease of prolonged duration with considerable morbidity but no mortality. Further research into the pathogenesis and treatment of CFS is necessary.
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PMID:The chronic fatigue syndrome. 204 89


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