Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vaquez and Aubertin advance three theories in explanation of the adrenal hyperplasia; first, that it may not be the cause of hypertension but "an antitoxic hyperplasia" caused by the retained products of metabolism which may be responsible also for the hypertension; second, that it may be the cause of hypertension but secondary to the renal lesion; third, that it may be the cause of hypertension but may antedate the renal lesion or be entirely independent of it. They, as well as other French writers, insist that this hyperplasia is almost constantly associated with chronic nephritis of the interstitial type and it is seldom found with the parenchymatous type of nephritis, or with other lesions. Hyperplasia of the adrenal, as far as my material enables one to judge, does not occur during the first and second decades. In the third decade it is relatively frequent in the absence of chronic arterial and renal disease but reaches the maximum in association with such disease after the fourth decade. It is an almost constant lesion in arteriosclerosis associated with chronic interstitial nephritis and left-sided heart hypertrophy, but occurs with almost equal frequency in arteriosclerosis with chronic nephritis of the parenchymatous type. It is a relatively frequent lesion of arteriosclerosis without chronic nephritis and of the latter without arteriosclerosis also. As the result of this analysis one is led to the view that while hyperplasia of the adrenal is a very frequent concomitant of chronic renal and arterial disease it is not exclusively a feature of either type of nephritis or yet of chronic vascular disease; but it probably represents the effect of some factor operating in that period of life in which chronic renal and arterial affections are most frequent. Worthy of special emphasis is the observation that the characteristic lesion of an adrenal, the seat of local arteriosclerosis, is of the type of the chronic productive inflammation seen in arteriosclerosis of the pancreas and kidney; that is, thickening of the vessels, increase of connective tissue and round cell infiltration. Associated with these changes is a hyperplasia which is very constant, and which may be, in part, of the nature of a compensatory hyperplasia similar to that seen in the liver of cirrhosis and acute yellow atrophy. A hyperplasia of this type, as has been shown, may occur in destructive lesions of the gland. This, however, does not explain hyperplasia in the absence of local vascular changes which fact is, possibly, as suggested by Landau, evidence, not of a correlation between kidney and adrenal, but of a vicarious hypertrophy depending upon lesions of some other organ of the body than the kidney, possibly some other ductless gland, affected by arteriosclerosis or other disease.
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PMID:THE RELATION OF LESIONS OF THE ADRENAL GLAND TO CHRONIC NEPHRITIS AND TO ARTERIOSCLEROSIS; AN ANATOMICAL STUDY. 1986 60

Heterocyclic indazole derivatives are claimed in patent WO2008138448 as inhibitors of the serum- and glucocorticoid-inducible-kinase 1 (SGK1) and drugs for the pharmacological treatment of SGK1-related diseases, such as diabetes, obesity, metabolic syndrome, systemic and pulmonary hypertension, cardiac fibrosis, hypertrophy and insufficiency, arteriosclerosis, glomerulosclerosis, nephrosclerosis, nephritis, nephropathy, deranged electrolyte excretion, fibrosing and inflammatory disease (e.g., liver cirrhosis, lung fibrosis, rheumatism, arthrosis, Crohn s disease, chronic bronchitis, radiation fibrosis, sclerodermia, cystic fibrosis, scar formation and Alzheimer' disease), tumor growth, peptic ulcers and some disorders hitherto not conclusively shown to involve SGK1. Most of the claims are supported by the literature. SGK1 is ubiquitously expressed and its expression is stimulated by hyperglycemia, cell shrinkage, ischemia, glucocorticoids, mineralocorticoids and several inflammatory mediators including TGF-ss. SGK1 is activated by insulin and growth factors via the phosphatidylinositol-3-kinase pathway. SGK1 regulates ion channels (including ENaC, KCNE1/KCNQ1), carriers (including NCC, NHE3, SGLT1), Na(+)/K(+)-ATPase, enzymes (including glycogen-synthase-kinase-3) and transcription factors (including FOXO3a, ss-catenin, NF-kappaB). A gain-of-function SGK1 gene variant, carried by approximately 3 - 5% of Caucasians and approximately 10% of Africans, is associated with increased blood pressure, obesity and type 2 diabetes. In vitro and in vivo experiments suggested a critical role of SGK1 in renal fluid retention and hypertension, glucose-induced obesity, coagulation and increased matrix protein formation.
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PMID:Heterocyclic indazole derivatives as SGK1 inhibitors, WO2008138448. 2002 Dec 89

Lifestyle diseases characterize those diseases whose occurrence is primarily based on the daily habits of people and are a result of an inappropriate relationship of people with their environment. The main factors contributing to lifestyle diseases include bad food habits, physical inactivity, wrong body posture, and disturbed biological clock. A report, jointly prepared by the World Health Organization (WHO) and the World Economic Forum, says India will incur an accumulated loss of $236.6 billion by 2015 on account of unhealthy lifestyles and faulty diet. According to the report, 60% of all deaths worldwide in 2005 (35 million) resulted from noncommunicable diseases and accounted for 44% of premature deaths. What's worse, around 80% of these deaths will occur in low and middle-income countries like India which are also crippled by an ever increasing burden of infectious diseases, poor maternal and perinatal conditions and nutritional deficiencies. According to a survey conducted by the Associated Chamber of Commerce and Industry (ASSOC-HAM), 68% of working women in the age bracket of 21-52 years were found to be afflicted with lifestyle ailments such as obesity, depression, chronic backache, diabetes and hypertension. The study 'Preventive Healthcare and Corporate Female Workforce' also said that long hours and working under strict deadlines cause up to 75% of working women to suffer from depression or general anxiety disorder, compared to women with lesser levels of psychological demand at work. The study cited scientific evidence that healthy diet and adequate physical activity - at least 30 minutes of moderate activity at least five days a week - helped prevent NCDs. In India, 10% of adults suffer from hypertension while the country is home to 25-30 million diabetics. Three out of every 1,000 people suffer a stroke. The number of deaths due to heart attack is projected to increase from 1.2 million to 2 million in 2010. The diet [or lifestyle] of different populations might partly determine their rates of cancer, and the basis for this hypothesis was strengthened by results of studies showing that people who migrate from one country to another generally acquire the cancer rates of the new host country, suggesting that environmental [or lifestyle factors] rather than genetic factors are the key determinants of the international variation in cancer rates. Some of the common diseases encountered because of occupational lifestyle are Alzheimer's disease, arteriosclerosis, cancer, chronic liver disease/cirrhosis, chronic obstructive pulmonary disease (COPD), diabetes, hypertension, heart disease, nephritis/CRF, and stroke. Occupational lifestyle diseases include those caused by the factors present in the vicinity like heat, sound, dust, fumes, smoke, cold, and other pollutants. These factors are responsible for allergy, respiratory and hearing problems, and heat or cold shock. So, A healthy lifestyle must be adopted to combat these diseases with a proper balanced diet, physical activity and by giving due respect to biological clock. Kids spending too much time slouched in front of the TV or PCs, should be encourage to find a physical sport or activity they enjoy. Fun exercises should be encouraged into family outings. A pizza-and-video evening should be replaced for a hike and picnic. Kids who do participate in sport, especially at a high competitive level, can find the pressure to succeed very stressful. To decrease the ailments caused by occupational postures, one should avoid long sitting hours and should take frequent breaks for stretching or for other works involving physical movements.
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PMID:Occupational lifestyle diseases: An emerging issue. 2044 27

A 6-year retrospective study (2000-2005) of animals slaughtered at the Zango abattoir in Zaria, Kaduna State, Nigeria was carried out to determine disease conditions encountered in slaughtered animals. Records kept at the abattoir were analysed. A total of 69,307 cattle, 3,820 goats and 1,763 sheep were slaughtered for the period under study. Of the 69,307 cattle slaughtered for the period, 22,459 (32.41%) were males and 46,848 (67.59%) were females, while 1,763 sheep were slaughtered comprising of 506 (28.70%) males and 1,257 (71.30%) females, and 3,820 goats made up of 1,212 (31.73%) males and 2,608 (68.27%) were females. The major disease and/or pathological conditions were helminthosis (fascioliasis, haemonchosis and paramphistomosis) 16.20%, Streptothricosis 4.15%, Pericarditis 2.20%, liver cirrhosis 2.08%, abscesses 1.04%, pneumonia 0.14%, nephritis 0.05% and Contagious Bovine Pleuropneumonia, Tuberculosis and Nocardiosis 0.01% each. Out of the 15,075 infected organs, 13,314 (88.38%) were partially salvaged while 1,751 (11.6%) whole organs were condemned. A total of 1,239 pregnant cows, 221 pregnant ewes and 637 pregnant does were slaughtered, representing a foetal wastage of 2.65% for cattle, 17.58% for sheep and 24.43% for goats. The result of this study apart from serving as an indicator of field disease condition also demonstrates cases of serious losses in production due to slaughter of pregnant animals especially for sheep and goats.
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PMID:A 6-year survey of pathological conditions of slaughtered animals at Zango abattoir in Zaria, Kaduna State, Nigeria. 2073 35

The Ras superfamily of guanosine-triphosphate (GTP)-binding proteins regulates a diverse spectrum of intracellular processes involved in inflammation and fibrosis. Farnesythiosalicylic acid (FTS) is a unique and potent Ras inhibitor which decreased inflammation and fibrosis in experimentally induced liver cirrhosis and ameliorated inflammatory processes in systemic lupus erythematosus, neuritis and nephritis animal models. FTS effect on Ras expression and activity, muscle strength and fibrosis was evaluated in the dy(2J)/dy(2J) mouse model of merosin deficient congenital muscular dystrophy. The dy(2J)/dy(2J) mice had significantly increased RAS expression and activity compared with the wild type mice. FTS treatment significantly decreased RAS expression and activity. In addition, phosphorylation of ERK, a Ras downstream protein, was significantly decreased following FTS treatment in the dy(2J)/dy(2J) mice. Clinically, FTS treated mice showed significant improvement in hind limb muscle strength measured by electronic grip strength meter. Significant reduction of fibrosis was demonstrated in the treated group by quantitative Sirius Red staining and lower muscle collagen content. FTS effect was associated with significantly inhibition of both MMP-2 and MMP-9 activities. We conclude that active RAS inhibition by FTS was associated with attenuated fibrosis and improved muscle strength in the dy(2J)/dy(2J) mouse model of congenital muscular dystrophy.
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PMID:The Ras antagonist, farnesylthiosalicylic acid (FTS), decreases fibrosis and improves muscle strength in dy/dy mouse model of muscular dystrophy. 2144 59

The objective is to present results of renal transplantation in patients with end-stage renal disease and chronic virus C/B hepatitis. We retrospectively reviewed outcome of transplantation in patients having received renal allograft from 1985 to 2009 at Zagreb University Hospital Center: graft function, graft and patient survival, hepatic function, and complications of transplantation, i.e. episodes of acute rejection, manifestation of diabetes mellitus, and proteinuria. There were 91 patients, 50 men and 41 women, mean age 40.9. Patients were previously treated with dialysis for 7.8 years, with the mean follow-up after transplantation of 7.3 years. The most frequent diagnoses of end-stage renal disease were chronic glomerulonephritis, reflux nephropathy, tubulointerstitial nephritis, renal hypoplasia/aplasia, and polycystic renal disease. Good graft function (creatinine 200 micromol/L) was recorded in 59.5% of patients. One-year, 5-year and 10-year graft survival was 93%, 64% and 39%, and 1-year, 5-year and 10-year patient survival after transplantation was 98%, 72% and 42%, respectively. Normal values of liver chemistry (AST, ALT) were found in 59.5% and elevated values in 40.5% of patients. Episodes of acute rejection occurred in 56% of patients. Proteinuria was recorded in 27%, diabetes mellitus in 18% and elevated blood pressure in 66% of patients. Patients with chronic C/B virus hepatitis having undergone renal transplantation had worse graft function and worse graft and patient survival than patients without chronic hepatitis. The most common causes of death were cardiovascular diseases, cerebrovascular diseases and cirrhosis hepatitis.
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PMID:[Outcome of renal transplantation in patients with chronic virus hepatitis]. 2235 3

Sodium, the most important extracellular fluid electrolyte, is the focus of several homeostatic mechanisms that regulate fluid and electrolyte balance. Hyponatremia is a common electrolyte abnormality caused by an actual sodium deficiency or extracellular compartment fluid excess. Clinical symptoms are related with acuity and speed with which this abnormality is established. The symptoms are mainly neurological and neuromuscular disorders (headache, confusion, stupor, seizures, coma) due to brain cells edema. Hyponatremia due to sodium deficiency is caused by sodium loss from kidney (nephritis, diuretics, mineralocorticoid deficiency) and / or extrarenal (vomiting, diarrhea, burns). Hyponatremia due to water excess seems to be the most common and it is attributable to cirrhosis, nephrotic syndrome, heart failure, infusion 5% glucose solutions and drugs that stimulate ADH secretion. It was recently highlighted the role of inflammation and IL-6 in the non-osmotic ADH release. Hyponatremia is considered also marker of phlogosis. Acute (<48 h) and severe (<125 mEq/ L) hyponatremia is a medical emergency that requires prompt correction. Patients with chronic hyponatremia have a high risk of osmotic demyelination syndrome if rapid correction of the plasmatic sodium occurs. In combination with conventional therapy, a new class of drugs, vasopressin receptors antagonists (AVP-R antagonists) would be able to increase the excretion of electrolyte-free water and the serum sodium concentration.
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PMID:[Hyponatremic syndrome]. 2236 42

A retrospective study and active abattoir survey were conducted from December 2009 to April 2010 to determine the major causes of organs and carcasses condemnation and to estimate the associated direct financial loss at Luna Export Abattoir, Central Ethiopia. The active abattoir survey was conducted on 674 goats and 451 sheep (n=1125) and three years (2007, 2008 and 2009), retrospective data of 718,395 sheep and goats were also collected. From the retrospective data it was observed that liver was the most frequently condemned organ with condemnation rate of 32.4%, 46.7% and 70.5%, respectively. The major causes of condemnation for liver, lung, heart, kidneys and brain were cirrhosis (12.3%, 17.0% and 12.8%), pneumonia (6.6%, 11.6% and 12.5%), pericarditis (0.6%, 0.8% and 0.4%), nephritis (0.6%, 0.8% and 1.2%) and abscess (0.005%, 0.007% and 0.012%), respectively. Consequently, the overall direct financial loss from organs and carcass condemnation during the three years was estimated to be 22,993,591 Ethiopian birr (ETB) or 1,323,257 United State Dollar (USD). On the other hand, detailed post mortem inspection of liver, heart, kidneys, tongue, brain and carcass during the active abattoir survey revealed that higher losses were caused mainly due to cirrhosis (89.3 kg, 2998 ETB), pericarditis (5.4 kg, 308 ETB), faulty evisceration (8.4 kg, 472 ETB), calcification (8.4 kg, 469 ETB) and Coenurus cerebralis (4.3 kg, 243 ETB) and poor carcass condition (bonny carcass) (1390 kg, 78,500 ETB), respectively. Other causes of condemnation were also recorded and totally, about 110,361 ETB (6351 USD) was lost only from organs and carcasses condemnation during the active abattoir survey. In conclusion, this study identified the major causes of organs and carcass condemnation in Luna Export Abattoir and estimated the associated direct financial losses.
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PMID:Major causes of organs and carcass condemnation in small ruminants slaughtered at Luna Export Abattoir, Oromia Regional State, Ethiopia. 2324 43

This study examined trends in rural-urban disparities in all-cause and cause-specific mortality in the USA between 1969 and 2009. A rural-urban continuum measure was linked to county-level mortality data. Age-adjusted death rates were calculated by sex, race, cause-of-death, area-poverty, and urbanization level for 13 time periods between 1969 and 2009. Cause-of-death decomposition and log-linear and Poisson regression were used to analyze rural-urban differentials. Mortality rates increased with increasing levels of rurality overall and for non-Hispanic whites, blacks, and American Indians/Alaska Natives. Despite the declining mortality trends, mortality risks for both males and females and for blacks and whites have been increasingly higher in non-metropolitan than metropolitan areas, particularly since 1990. In 2005-2009, mortality rates varied from 391.9 per 100,000 population for Asians/Pacific Islanders in rural areas to 1,063.2 for blacks in small-urban towns. Poverty gradients were steeper in rural areas, which maintained higher mortality than urban areas after adjustment for poverty level. Poor blacks in non-metropolitan areas experienced two to three times higher all-cause and premature mortality risks than affluent blacks and whites in metropolitan areas. Disparities widened over time; excess mortality from all causes combined and from several major causes of death in non-metropolitan areas was greater in 2005-2009 than in 1990-1992. Causes of death contributing most to the increasing rural-urban disparity and higher rural mortality include heart disease, unintentional injuries, COPD, lung cancer, stroke, suicide, diabetes, nephritis, pneumonia/influenza, cirrhosis, and Alzheimer's disease. Residents in metropolitan areas experienced larger mortality reductions during the past four decades than non-metropolitan residents, contributing to the widening gap.
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PMID:Widening rural-urban disparities in all-cause mortality and mortality from major causes of death in the USA, 1969-2009. 2436 54


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