Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The angiotensin II (AT II) levels in plasma were measured 68 times by using radio-immunoassay in 30 patients with viral hepatitis B (HB) and in 35 healthy persons as the control group. The results showed that the AT II levels of patients with HB were much higher than those of the control group (P less than 0.001). They were 219.25 +/- 91.31 ng/L and 60.70 +/- 10.73 ng/L, respectively. These indicated that the renin-angiotensin-aldosterone system (RAAS) of the patients was in exciting state. The levels of 8 cases of severe chronic active hepatitis (SCAH) (AT II = 270.40 +/- 106.55 ng/L, 6 cases of subacute fulminant hepatitis (SFH) (AT II = 332.80 +/- 140.12 ng/L), and 4 cases of hepatocirrhosis (HC) (AT II = 218.50 +/- 97.64 pg/ml) were all higher than those of 8 cases of chronic active hepatitis (CAH) (100.50 +/- 83.81 ng/L) and those of 4 cases of acute icteric hepatitis (A1H) (123.33 +/- 64.97 ng/L). These findings showed that the levels of AT II were directly related with the severity of the illness. The AT II levels of 8 cases of HRS (270.50 +/- 66.31 ng/L) were higher that those without HRS (174.50 +/- 78.48 ng/L). After treatment with captopril (CPT), the renal function of the patients returned to normal and the patients got better, while the AT II levels decreased greatly. The results suggested that high AT II levels in plasma may be one of the causes aggressing the HRS. The CPT may inhibit the produce of AT II and there are some therapeutic effects for the HRS.
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PMID:[The relationship between hepatitis B and renin-angiotensin-aldosterone system]. 174 16

The authors studied clinical and biological data occurring in 165 patients observed during 23 years and afflicted with polyarteritis nodosa. Hypertension was present in 52 patients (31.5%) and seven of them suffered from malignant hypertension (4%). Mean age of patients (6 male, 1 female), with malignant hypertension was 38 +/- years old. Mean follow up was 49 +/- 28 months including 26 +/- 21 months after discontinuation of treatment of polyarteritis nodosa. Malignant hypertension occurred during the first year of evolution of polyarteritis nodosa. Renal insufficiency was present in 5 of 7 patients. Proteinuria was greater than 1 gr/d in 4 cases. Renal arteriography was performed in 6 patients and showed in every case renal ischemia and microaneurysms in five. In 4 patients measurements of plasma renin activity and of aldosterone were obtained. A stimulation of those hormones was demonstrated. Some symptoms of polyarteritis nodosa were present with a high incidence in case of malignant hypertension: digestive signs (6/7), orchitis (3/6). HBs antigen was present in 6 cases and hepatitis in 5. Captopril was effective in every case, alone or associated with other treatments. Follow up of hypertension went from 8 months to 4 years. At present time 6 patients are alive and one is lost of follow up. A treatment is necessary in 6 of 7 patients. Creatininemia is greater than 300 micromol/l in 4 patients. A successful kidney transplantation was performed in one case. Our study shows a close relation between malignant hypertension observed in polyarteritis nodosa, vascular nephropathy, digestive and urologic signs. Hepatitis B virus could be responsible of those manifestations.
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PMID:[Malignant arterial hypertension in periarteritis nodosa. Incidence, clinicobiologic parameters and prognosis based on a series of 165 cases]. 287 20

The concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP) and hormones of the renin-angiotensin axis were studied in male rats with carbon tetrachloride-induced hepatitis and the results compared to normal control animals. The rats with hepatitis exhibited lower concentrations of ANP, plasma renin activity (PRA), and angiotensin I (AI) than did the control animals. Plasma concentrations of AVP and aldosterone were not significantly different in the two groups. The results suggest that experimental hepatitis is associated with renal hyperperfusion together with reduction in atrial pressures.
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PMID:Atrial natriuretic peptide, arginine vasopressin, and the renin-angiotensin system in carbon tetrachloride-induced hepatitis in rats. 297 33

We studied the pathogenesis of hypertension in two patients with hepatitis-B surface antigen-positive systemic necrotizing vasculitis. Both presented with hypertension, hypokalemia, and renal potassium wasting. Plasma renin activity and urinary aldosterone levels were markedly elevated. Renal arteriograms showed widespread microaneurysms, and necrotizing vasculitis involving renal arteries was confirmed histologically. Hypertension was refractory to conventional treatment in both patients. In one patient, hypertension was easily controlled with the angiotension-converting enzyme inhibitor captopril. Diffuse renal vasculitis with secondary hyperreninemia and hyperaldosteronism appears to be an important cause of hypertension in patients with systemic necrotizing vasculitis.
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PMID:Hypertension, hyperreninemia, and secondary hyperaldosteronism in systemic necrotizing vasculitis. 610 32

Renal disorders complicating liver disease are a frequent finding. Extrahepatic causes like intoxications and circulatory dysfunction or diseases that simultaneously affect both the liver and the kidney, like multisystem or viral diseases (hepatitis B) have to be differentiated from clinical entities in which, like in liver cirrhosis or in fulminant hepatitis, the manifestation of renal disease has to be understood as a consequence of the hepatic disorders. Functional disturbances like the increases in tubular sodium reabsorption or the hepatorenal syndrome have been thoroughly investigate because of their clinical importance. Substantial research dealing with the consequences of the increased intrahepatic vascular resistance on systemic and renal hemodynamics and with vasoactive substances, either arising from the liver or accumulating due to poor inactivation by the liver, have led - in the last years - to a better understanding of the pathophysiology of renal involvement in liver disease. However, the exact pathophysiologic role of factors like the effective blood volume, the sympathoadrenergic tonus, the activation of the renin-angiotensin-aldosterone system, changes of kinin activity or in prostaglandin release and the accumulation of "false" neurotransmitters and endotoxins still remains to be established.
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PMID:[Kidney involvement in liver diseases. Pathophysiology and clinical course]. 664 4

Plasma renin activity (PRA) and plasma concentrations of angiotensin II (A.II) were measured radioimmunologically in 31 patients suffering from acute virus hepatitis during the course of the disease. Average PRA and A II values did not differ from values of normal persons, neither during the acute phase of the disease nor during the recovery phase though there were deviations from the normal in single cases. PRA and A II were correlated significantly (r = 0,86, p < 0,001), but there was no correlation to the levels of transaminases. There was no indication, that A II plasma levels were lowered because of increased activity of angiotensinases. In some cases PRA and A II were elevated; this however was probably due to increased renin secretion following changes in water and electrolyte balance rather than to decreased hepatic metabolism of renin.
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PMID:[Renin-angiotensin system in acute hepatitis (author's transl)]. 701 96

The hepato-renal syndrome is defined as potentially reversible functional renal failure associated with acute fulminant hepatitis or, more often, with advanced chronic liver failure. It is characterized by oliguria, azotemia, retention of sodium and water with formation of ascites, and hyponatremia. While urinary sodium concentration of less than 10 mEq/l reflects intact tubular sodium absorption, the kidney lacks the ability for adequate free-water generation. This condition must be separated from specific renal diseases which may arise during the course of intra-or extrahepatic diseases and which must be classified accordingly. Pathophysiological aspects of the hepa-to-renal syndrome include hemodynamic factors, such as changes in intrarenal blood flow distribution in the presence of elevated intrarenal and reduced peripheral vascular resistance. The functional relationship of vasoconstrictor, sodium retaining, and anti-diuretic hormones (e.g., renin-angiotensin, aldosterone, and vasopressin) to vasodilator, diuretic, and natriuretic hormonal factors (e.g., prostaglandins, kinins, and natriuretic hormone) may be altered as well. Finally, a pre- and intrahepatic spillover resulting in decreased endotoxin clearance must be considered. Due to the lack of understanding of their complex interactions, so far pharmacological and therapeutic approaches remained ineffective to correct at least some of these factors. Today, recovery from hepato-renal syndrome will, therefore, mainly depend on the course of the underlying liver disease.
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PMID:[Hepato-renal syndrome (author's transl)]. 727 84

Recent association and linkage studies suggested that angiotensinogen may play an important role in the pathogenasis of essential hypertension. However, there is little information in human concerning a relationship between plasma angiotensinogen levels and the angiotensinogen mRNA expression in the liver, which is the main production site of angiotensinogen. Therefore, the aim of this study was to examine whether hepatic angiotensinogen gene expression determines the level of circulating angiotensinogen and the activity of the renin-angiotensin system in humans. The subjects were 36 patients with chronic hepatitis. Blood was collected from each patients for estimation of plasma renin activity, plasma angiotensinogen and angiotensin II concentrations and several parameters of liver function. In addition, total RNA was isolated from liver biopsy specimens, which were then used to measure angiotensinogen mRNA with Northern blot analysis. Levels of angiotensinogen mRNA were detected easily in the liver biopsy specimens in all of the patients. Hepatic angiotensinogen mRNA levels were positively correlated with plasma angiotensinogen levels (r=0.41, P=0.013). In contrast, hepatic angiotensinogen mRNA levels did not show any significant relationship with plasma renin activity, plasma angiotensin II concentration, histological subgroup of hepatitis, histological activity index and parameters of liver function tests. The present study demonstrated, for the first time, that hepatic angiotensinogen mRNA levels correlated with plasma angiotensinogen concentration in humans.
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PMID:Relationship between hepatic angiotensinogen mRNA expression and plasma angiotensinogen in patients with chronic hepatitis. 912 85

The relative importance of molecular biology in clinical practice is often underestimated. However, numerous procedures in clinical diagnosis and new therapeutic drugs have resulted from basic molecular research. Furthermore, understanding of the physiological and physiopathological mechanisms underlying several human diseases has been improved by the results of basic molecular research. For example, cloning of the gene encoding leptin has provided spectacular insights into the understanding of the mechanisms involved in the control of food intake and body weight maintenance in man. In cystic fibrosis, the cloning and identification of several mutations in the gene encoding the chloride channel transmembrane regulator (CFTR) have resolved several important issues in clinical practice: cystic fibrosis constitutes a molecular defect of a single gene. There is a strong correlation between the clinical manifestations or the severity of the disease (phenotype) with the type of mutations present in the CFTR gene (genotype). More recently, identification of mutations in the gene encoding a subunit of the renal sodium channel in the Liddle syndrome has provided important insight into the physiopathological understanding of mechanisms involved in this form of hereditary hypertension. Salt retention and secondary high blood pressure are the result of constitutive activation of the renal sodium channel by mutations in the gene encoding the renal sodium channel. It is speculated that less severe mutations in this channel could result in a less severe form of hypertension which may correspond to patients suffering from high blood pressure with low plasma renin activity. Several tools, most notably PCR, are derived from molecular research and are used in everyday practice, i.e. in prenatal diagnosis and in the diagnosis of several infectious diseases including tuberculosis and hepatitis. Finally, the production of recombinant proteins at lower cost and with fewer side effects is used in everyday clinical practice. Gene therapy remains an extraordinary challenge in correcting severe hereditary or acquired diseases. The use of genetically modified animal cell lines producing growth factors, insulin or erythropoetin, which are subsequently encapsulated and transferred to man, represents an attractive approach for gene therapy.
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PMID:[Is molecular biology useful to the practitioner?]. 919 Jun 68

The mesenteric hemodynamic response to circulatory shock is characteristic and profound; this vasoconstrictive response disproportionately affects both the mesenteric organs and the organism as a whole. Vasoconstriction of post-capillary mesenteric venules and veins, mediated largely by the alpha-adrenergic receptors of the sympathetic nervous system, can effect an "autotransfusion" of up to 30% of the total circulating blood volume, supporting cardiac filling pressures ("preload"), and thereby sustaining cardiac output at virtually no cost in nutrient flow to the mesenteric organs. Under conditions of decreased cardiac output caused by cardiogenic or hypovolemic shock, selective vasoconstriction of the afferent mesenteric arterioles serves to sustain total systemic vascular resistance ("afterload"), thereby maintaining systemic arterial pressure and sustaining the perfusion of non-mesenteric organs at the expense of mesenteric organ perfusion (Cannon's "flight or fight" response). This markedly disproportionate response of the mesenteric resistance vessels is largely independent of the sympathetic nervous system and variably related to vasopressin, but mediated primarily by the renin-angiotensin axis. The extreme of this response can lead to gastric stress erosions, nonocclusive mesenteric ischemia, ischemic colitis, ischemic hepatitis, ischemic cholecystitis, and/or ischemic pancreatitis. Septic shock can produce decreased or increased mesenteric perfusion, but is characterized by an increased oxygen consumption that exceeds the capacity of mesenteric oxygen delivery, resulting in net ischemia and consequent tissue injury. Mesenteric organ injury from ischemia/reperfusion due to any form of shock can lead to a triggering of systemic inflammatory response syndrome, and ultimately to multiple organ dysfunction syndrome. The mesenteric vasculature is therefore a major target and a primary determinant of the systemic response to circulatory shock.
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PMID:The mesenteric hemodynamic response to circulatory shock: an overview. 1133 91


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