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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exercise performance data, circulatory function and respiratory and leg muscle quality, expressed as muscle fiber composition, are reviewed and together with our own data discussed as possible limiting factors for physical performance in chronic obstructive pulmonary disease (COPD). COPD is regarded as synonymous with reduced physical performance, exaggerated breathlessness or dyspnea, muscle hypotrophy and/or wasting and, frequently, malnutrition. Impaired right ventricular circulatory function seems to be essential. The observed preponderance of fast twitch (FT), 'glycogenolytic' and capillary-poor muscle fiber type in the investigated muscles might reflect endowment, a 'hypoxic vasoconstriction'-related downregulation of the other main fiber type: the slow twitch (ST), capillary-rich, fatigue-resistant fiber, and/or selective muscle trauma to ST fibers. Ischemic heart disease (IHD) patients demonstrate a similar fiber type pattern in leg muscles. Both COPD and IHD patients have low leg muscle and plasma deposits of antioxidants such as coenzyme Q10 (CoQ10) and alpha-tocopherol. This could reflect a depressed resistance to radical induced cell trauma and/or malnutrition. The magnitude of the antioxidant reduction is less pronounced in patients rich in FT fibers indicating a ST fiber-related susceptibility to trauma. Treatment of other muscle disorders including heart muscle with, e.g., CoQ10 improves performance due to a causative enhanced antioxidant potential, reduced catabolism and/or an upregulated muscle anabolism, increased mitochondrial volume/function, etc. Such data are lacking in COPD.
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PMID:Exercise-limiting factors in respiratory distress. 151 68

Ovine progressive pneumonia (OPP) is a multi-systemic disease of sheep caused by a nononcogenic exogenous retrovirus belonging to the Lentiviridae subfamily. Characteristics of the disease are chronic lymphocytic pneumonitis, encephalitis, arthritis, mastitis and vasculitis associated with progressive wasting, dyspnea, lameness, indurated udder and, rarely, paralysis. Any one or all of the characteristics may be manifest. Transmission of the virus is predominantly through the colostrum to newborn lambs, however, transmission can occur by contact and in utero. Treatment of the disease is only symptomatic and prevention of infection is only by avoiding the virus.
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PMID:Ovine progressive pneumonia (maedi-visna) in sheep. 305 56

Although pneumonia virus of mice (PVM) is ubiquitous among rodent colonies in the United States, it has not been reported to cause clinically apparent disease in euthymic mice. However, PVM has been reported to cause respiratory disease and death in experimentally infected euthymic and athymic mice. A group of nu/nu mice, housed in quarantine in a Trexler-type isolator, had weight loss and dyspnea. Gross necropsy findings included cachexia and diffuse pulmonary edema or lobar consolidation. Histologically there was diffuse interstitial pneumonia. Electron microscopy revealed filamentous virions budding from plasma membranes, and immunohistochemical staining of lung tissue was positive for PVM antigen. PVM was isolated from affected lung tissue in BHK 21 cells and mouse antibody production tests resulted in seroconversion to PVM. Experimental inoculation of athymic mice with lung homogenate from spontaneously infected mice resulted in clinically apparent respiratory disease and histologic lung changes similar to those in naturally infected mice. Inoculation of athymic mice with infected BHK 21 cell culture fluid resulted in pneumonia which was qualitatively similar to, but less severe than, that observed in mice with spontaneous disease. These findings indicate that naturally occurring PVM infection in athymic mice may cause respiratory disease and wasting.
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PMID:Respiratory disease and wasting in athymic mice infected with pneumonia virus of mice. 337 86

Several cases of wasting disease and dyspnea occurred in outbred Crl: CDI(ICR) nu/nu mice obtained recently from a commercial supplier. Gross necropsy revealed pulmonary consolidation, and histologically there was alveolar-wall thickening and filling of alveoli with macrophages and honey-combed eosinophilic material. Electron microscopic examination of lung tissue confirmed infection with Pneumocystis carinii.
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PMID:Spontaneous wasting disease in nude mice associated with Pneumocystis carinii infection. 348 19

During an 18-year period, 501 cases of thoracic complications of amebic abscess of the liver were studied; 175 had inflammatory reactions of thoracic structures (165 with pleural effusions and pneumonitis, ten with pericarditis) and 326 ruptured through the diaphragm (175 into the airways, 106 into the pleural cavity, 5 into the pericardium, 39 into the airways and pleura, and 1 into the pleura and pericardium). The thoracic complication was preceded by a picture suggesting an acute inflammatory process or a chronic wasting disease. Depending on type, the complication itself was signaled by increase or change in character of right upper abdominal or lower thoracic pain, dyspnea, or overt respiratory insufficiency, hemoptysis, and expectoration of necrotic material, sepsis, tamponade, and shock. Chest roentgenograms showed small to massive pleural effusions, basal pneumonitis, and cardiomegaly; serology, liver scans, and induced pneumoperitoneum were diagnostic. Treatment included metronidazole and emetine, drainage of pleural or pericardial contents or promotion of bronchial drainage, and meticulous care of associated respiratory, circulatory, and systemic derangements. Mortality for cases with rupture was 11.4 percent, due mainly to sepsis, shock, respiratory insufficiency, and tamponade. The rest of the patients were discharged in cured or improved condition.
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PMID:Thoracic complications of amebic abscess of the liver: report of 501 cases. 722 56

This article provides a clinically-oriented overview of palliative care for patients with AIDS. Indicators of decreased survival time are divided into categories of infections/illnesses, clinical signs and symptoms, immunological and serological markers, and psychosocial factors. Primary symptoms in AIDS are discussed according to etiology and treatment. However, treatments of opportunistic infections per se are not directly addressed in this article. Problems discussed include pain, confusion, depression and anxiety, fatigue, fever, dyspnea, nausea and vomiting, diarrhea, wasting, and dehydration. The article also briefly addresses clinical and ethical questions and challenges presented by AIDS to hospice or palliative care providers, and the various stages of HIV infection.
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PMID:Palliative care for patients with acquired immunodeficiency syndrome. 749 35

A case of hereditary motor and sensory neuropathy (HMSN) type 1 (Charcot-Marie-Tooth disease (CMT)) is reported with vocal cords palsy, deafness, diaphragmatic weakness, and cerebellopontine atrophy. A 42-year-old man was admitted to our hospital in April, 1991 with marked respiratory distress. He had been diagnosed as having CMT 14 years previously. On admission to our hospital, he revealed dyspnea with marked stridor during inspiration. Physical examination showed marked use of respiratory accessory muscles with thoracoabdominal paradox in the supine position. Neurologic examination revealed tonic pupils, mild bilateral weakness of facial muscles, deafness, mild bulbar palsy, severe wasting and weakness in both proximal and distal muscles of the arms and legs, areflexia, distal loss of all sensory modalities. Pes cavus and hammer toe were present. Movement of upper extremities was ataxic. No hypertrophic changes were noted in his peripheral nerves. Peripheral nerve conduction study showed undetectable both sensory and motor action potentials. Electromyography showed evidence of denervation, more marked in distal muscles. Auditory brain stem response was undetectable. Chest radiographic film showed a normal-sized heart with marked elevation of both hemidiaphragm. Laryngofiberscopy confirmed the presence of bilateral vocal cord paralysis without tumor formation, inflammation or anomaly. The vocal cords lay near the midline and did not show any movement during respiration. Moderate cerebellopontine atrophy was confirmed on MRI scan. A sural nerve section showed severe decrease of myelinated fibers, and onion bulbs. Diagnosis of HMSN type 1 was made by clinical, electrodiagnostic, and sural nerve sections study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of hereditary motor and sensory neuropathy with vocal cords palsy and diaphragmatic weakness]. 831 89

A case of rigid spine syndrome presenting with respiratory failure was reported. A seven-year-old girl had had dyspnea and orthopnea for one month. Symptoms had aggravated gradually and she was in a state of respiratory failure on arrival at our hospital. There was no evidence of active lung lesions and response to mechanical ventilation was good. Physical examination revealed an extremely thin girl with marked flexion limitation of neck and severe wasting of sternocleidomastoid and intercostal muscles. Serum creatine phosphokinase was moderately elevated (801 IU/L). Muscle biopsy specimen obtained from the right quadriceps femoris revealed increased perimyseal connective tissue and marked Type II fiber atrophy. Electromyography of left paraspinal muscles demonstrated small amplitude, short duration motor unit potentials. She received tracheostomy and a home-care ventilator use during sleep. Ventilatory insufficiency, though rare, should be anticipated in patients with rigid spine syndrome, and timely ventilatory support should be given.
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PMID:Rigid spine syndrome presenting with respiratory failure--report of one case. 836 70

A wasting disease characterized by progressive weight loss and dyspnea has been observed in weaning pigs on a farm in Yamagata Prefecture in 1998. Histopathologic findings in an affected pig were bronchointerstitial pneumonia and intracytoplasmic clusters of basophilic inclusions in macrophages of lymph nodes, which were similar to those in pigs with postweaning multisystemic wasting syndrome (PMWS) recently reported in North America and Europe. Porcine circovirus (PCV)-like particles were observed in bronchial lymph node of the pig by electron microscopy, and PCV antigens were detected in the lesions by immunohistochemical staining. PCV DNA was also detected in the lung and tonsil by PCR, and restriction fragment length polymorphism analysis of the PCR products with HinfI showed the same type of the PCV associated with PMWS (pmws PCV). Homology of nucleotide sequences between the PCR product and corresponding regions of published pmws PCV genomes was very high. These results indicated that virus detected in this study was pmws PCV. To our knowledge, this is the first report on the presence of pmws PCV in Japan.
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PMID:Detection of porcine circovirus from lesions of a pig with wasting disease in Japan. 1056 89

This report describes a case of a 17-year-old girl with Charcot-Marie-Tooth disease (CMT) representing rigid spine and respiratory failure. At age 11, she tended to walk on her toes and had difficulty in getting up from the floor without support. She became aware of flexion limitation of the neck at the age of 12. At 15 years of age, She began to have dyspnea on effort. When she was 17 years old, neurological examination revealed mild weakness of the upper extremities and severe weakness of the distal lower extremities, generalized wasting and areflexia. Superficial sensation was mildly impaired distally, and vibration sensation was severely impaired in the lower extremities. Motor and sensory nerve conduction velocities were mildly reduced, and compound muscle action potential of the tibial and peroneal nerves and sensory nerve action potential on ulnar and sural nerves were absent. Electromyography showed neurogenic changes with denervation potentials. Sural nerve biopsy revealed severe loss of myelinated fibers without any onion-bulb formation. As for family history, her elder sister showed moderate loss of vibration sensation in the lower extremities. On the basis of these findings, she was diagnosed as having CMT type 2, though a mode of inheritance was uncertain. She also had peculiar findings of flexion limitation of the spine (rigid spine), contracture of the hip joint, and fatty degeneration of paraspinal muscles on CT. Percent vital capacity (VC) was 22.5%, and arterial blood gas analysis showed PaO2 of 60.5 mmHg and PaCO2 65.0 mmHg. To our knowledge, this is the first case of CMT accompanied by rigid spine and respiratory failure. Motor and sensory neuropathy combined with rigid spine also have not been reported previously. The relationship between rigid spine syndrome with neurogenic muscular atrophy and CMT type 2C with the clinical characteristics of diaphragm and vocal cord paresis is discussed.
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PMID:[A patient of Charcot-Marie-tooth disease with rigid spine and respiratory failure]. 1100 24


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