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

The paper is concerned with the results of hormonal studies on virus hepatitis in 84 children aged 2 to 14, of them 28 had a mild form of disease, 50--medium grave and 6--a severe form of disease. A study was made of the blood content of ACTH, STH, TSH, cortisol, aldosterone, T3, T4, prolactin, and alpha-fetoprotein. The hormones were determined by a radioimmunoassay using Sorin kits (France). A considerable increase in the blood content of ACTH, cortisol, aldosterone and a moderate increase in STH, TSH and T4 concentrations were noted at the height of virus hepatitis. The above changes were interpreted as a result of combined manifestation of a stress reaction and a decrease in the catabolism of some liver hormones. An assumption has been made of a possibility of the effect of late hormonal shifts on the outcome of virus hepatitis of development of chronic hepatitis.
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PMID:[Endocrine changes in children with acute viral hepatitis]. 343 65

In a group of 50 patients with liver cirrhosis compared with a group of 50 clinically healthy subjects serum magnesium levels were determined. The patients were divided according the aetiology of liver cirrhosis and to the presence or not of ascite and cholestasis. The serum magnesium levels were related to the main laboratory tests used in liver cirrhosis. The patients present a significant decrease of serum magnesium levels in comparison to controls. The patients with alcoholic cirrhosis of the liver and with ascite have significant lower magnesium levels in comparison with the patients with post-hepatitis cirrhosis and with patients without ascite. There is a significant correlation between serum magnesium levels and serum levels of aldosterone, albumin, gamma-glutamyl transpeptidase and total pool of bile acids. Direct and indirect effects of alcohol, a secondary hyperaldosteronism, the use of diuretics, and hypoalbuminaemia could account for magnesium serum level decrease in liver cirrhosis.
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PMID:[Serum levels of magnesium in hepatic cirrhosis]. 344 90

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

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

FK506 is an immunosuppressant that is thought to be less nephrotoxic than cyclosporine A. However, complications due to renal tubular acidosis (RTA) have recently been reported. We report a case of RTA secondary to FK506 administration in liver transplantation. A 6-month-old girl was treated with FK506 after undergoing living donor liver transplantation for fulminant hepatitis. On postoperative day 17, she demonstrated hyperkalaemia and metabolic acidosis; she was diagnosed to have hyperkalaemic distal RTA with aldosterone deficiency (type IV). Intravenous sodium bicarbonate and furosemide, and intrarectal calcium polystyrenesulfonate were administered to correct the acidosis and promote potassium secretion. Thereafter, the FK506 concentration in whole blood gradually decreased, and the hyperkalaemia and metabolic acidosis following RTA improved. RTA is one type of nephrotoxicity induced by FK506, and it is reversible in mild cases when appropriately treated. The mechanism of RTA induced by FK506 has not yet been clearly elucidated. Surgeons and physicians should therefore be aware of the potential for RTA to occur with FK506 after any organ transplantation. The treatment for acidosis and hyperkalaemia should be started as soon as RTA is diagnosed, and the dosage of FK506 should also be reduced if possible.
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PMID:Renal tubular acidosis secondary to FK506 in living donor liver transplantation: a case report. 1453 Jan 8

We present a case of a 39-year-old G8P6 Pacific Islander woman who at 15+5 weeks' gestation had an out-of-hospital cardiac arrest secondary to profound hypokalaemia which was associated with severe hyperemesis gravidarum (HG). Her clinical course after arrest was complicated by a second 5-minute cardiac arrest in the Intensive Care Unit (ICU) (pre-arrest potassium 1.8), anuric renal failure requiring dialysis, ischaemic hepatitis, and encephalopathy and unfortunately fetal demise and a spontaneous miscarriage on day 2 of admission. Despite these complications, she was discharged home 4 weeks later with a full recovery. Following a plethora of inpatient and outpatient investigations, the cause of her cardiac arrest was determined to be profound hypokalaemia. The hypokalaemia was presumed second to a perfect storm of HG with subsequent nutritional deficiencies causing electrolyte wasting, extracellular fluid (ECF) volume reduction, and activation of the renin-angiotensin-aldosterone axis (RAAS). This combined with the physiological changes that promote potassium wasting in pregnancy including volume expansion, increased renal blood flow, increased glomerular filtration rate, and increase in cortisol contributed to the patient having a profoundly low total body potassium level. This diagnosis is further strengthened by the fact that her pre- and post-pregnancy potassium levels were within normal limits in the absence of supplementary potassium. This case highlights the potentially life-threatening electrolyte imbalances that can occur with HG and the importance of recognising the disease, comprehensive electrolyte monitoring, and aggressive management in pregnancy.
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PMID:Profound Hypokalaemia Resulting in Maternal Cardiac Arrest: A Catastrophic Complication of Hyperemesis Gravidarum? 3015 Dec 87


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