Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Clinical and necropsy observations in lepromatous leprosy associated with severe emaciation and accompanying hypoproteinemia suggest that protein deprivation may be of pathogenic significance in the ulcerative phenomenon that is designated "Lazarine leprosy". 2. An experimental utilizing Wiersung rats infected with Mycobacterium lepraemurium and maintained on a protein-free diet was developed for the purpose of studying the effect of protein starvation on the course of chronic mycobacterial disease similar to lepromatous leprosy with respect to pathogen and host inflammatory response. 3. It was possible to maintain the experimental animals on a protein-free diet for up to 18 weeks of concomitant M. lepraemurium infection. This was long enough for the infection to disseminate to a degree that was evident in control animals only several weeks later. 4. The protein-deprived animals showed decreased inflammatory response to the pathogen, presented more rapid dissemination of the infection and harbored more bacilli per macrophage than did animals similarly infected but maintained on a protein adequate diet. This indicates impairment of native cellular immunity by protein deprivation through decrease in ability of macrophages to inhibit bacillary multiplication. 5. There was no evidence of impairment of macrophage ability to phagocytose the pathogens. 6. Morphologically the increased dissemination of pathogens and decrease in inflammatory response was similar to the increase in number and extent of visceral lesions seen in Lazarine leprosy. Decreased ability to dispose of the infecting bacilli was similar in the two models, human and animal. The animal model does not, as does lepromatous leprosy, involve the skin in the infection. Hence comparable ulcerative phenomena were not replicated in the animals. 7. It is suggested that Lazarine leprosy may result from enhanced lepromatous leprous infection occurring as a result of protein malnutrition. The pathogenic mechanism appears to be impairment of cellular immunity probably enhanced by concomitant impairment of humoral antibody immunity resulting also in decreased resistance to pyogenic and other secondary pathogens. The tissue edema attendant on decreased serum osmotic pressure due to lowering of the serum protein fractions enhances the probability of ulceration.
 ...
PMID:The role of protein malnutrition in the pathogenesis of ulcerative "Lazarine" leprosy. 82 11

Prenatal starvation in the guinea pig causes reduced pulmonary diffusing capacity and retarded alveolarization among neonates. To study the impact of such starvation on biochemical and mechanical properties of the neonatal lung, pregnant guinea pigs were fed ad libitum throughout gestation or starved with 50% rations during their last trimester. Neonatal body weight was 35% less due to starvation, and dry lung weight, DNA, and protein contents were decreased 26, 36, and 31%, respectively (P less than 0.001 for all). Hematological data indicated no anemia, hypoproteinemia, or altered glucocorticoid levels due to starvation. Total surfactant phospholipids in these neonates were reduced 61% in lavage and 35% in the neonatal lung tissue, although surfactant compositions were similar to controls. Specific lung compliance in the air-filled lungs was not altered, but the saline-filled lungs were more distensible over deflation pressures of 9-18 cmH2O (transpulmonary). Although starvation retarded both lung cellularity and surfactant, only that portion of lung elastic recoil attributable to tissue forces was affected.
 ...
PMID:Lung mechanics, cellularity, and surfactant after prenatal starvation in guinea pigs. 375 59

Famine edema was produced experimentally in 34 normal men who lost a quarter of their body weight while subsisting for 6 months on a European type of semi-starvation diet. The ratio of extracellular water to cellular tissue was roughly doubled. Their clinical state closely resembled that seen in Europe in 1945. There were no signs of renal or cardiac failure. The plasma protein concentration fell only slightly and the A/G ratio remained within normal limits. The venous pressure was roughly 50 per cent below normal. Data from the field lend support to these indications that famine edema is not simply a result of hypoproteinemia or of renal or cardiac failure. It is concluded that there is a dynamic nonequilibrium state of the capillary wall and, accordingly, calculations from equilibrium equations are inadmissible.
 ...
PMID:Famine Edema and the Mechanism of Its Formation. 1775 25