Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

It has been suggested that enalaprilat inhibits the renin-angiotensin-aldosterone system in plasma and tissue; it may therefore reduce portal vascular pressure owing to secondary hyperaldosteronism in patients with liver cirrhosis. In order to evaluate this concept, 20 patients with hepatitis B surface antigen (HBsAg)-positive liver cirrhosis and portal hypertension received an intravenous infusion of 2.5 mg of enalaprilat. Wedged hepatic venous pressure, free hepatic venous pressure and cardiac index were measured before, immediately after, and then 15 min, 30 min and 1 h after intravenous enalaprilat infusion. The mean pressure gradient between wedged hepatic venous pressure and free hepatic venous pressure was significantly decreased, by 13% immediately after, 18% at 15 min, 23% at 30 min and 13% at 1 h after infusion of enalaprilat. Thirteen patients experienced a decrease of hepatic venous pressure gradient (HVPG) greater than 5 mmHg, another three 3-5 mmHg and the remaining four patients exhibited no significant change in HVPG. Systemic haemodynamic indices, including pulmonary arterial pressure, pulmonary capillary wedge pressure and central venous pressure, decreased significantly at 15 and 30 min after enalaprilat infusion (P < 0.01). Liver function, renal function and blood routine before and after enalaprilat infusion showed no significant change. There were no adverse effects during or after enalaprilat infusion. We conclude that enalaprilat infusion can quickly and safely reduce the hepatic venous pressure gradient in patients with HBsAg-positive cirrhosis.
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PMID:Haemodynamic effects of enalaprilat on portal hypertension in patients with HBsAg-positive cirrhosis. 754

We evaluated the dynamic response of renin, aldosterone, and vasopressin to intravenous water loading (20 ml 5% glucose/kg b.w.) in 12 children (aged 7-18 years) with postinflammatory liver cirrhosis after hepatitis B virus (HBV) infection. All of the patients had early-stage liver cirrhosis; according to Child's classification, nine patients had group A; three, group B cirrhosis. A group of 17 children with chronic persistent hepatitis served as the control. The diagnoses were confirmed in all of the patients by liver biopsy. The patients followed a diet containing 3 mmol NaCl/kg/day, maximum 100 mmol per day for 6 days. Water loading was performed in recumbency over approximately 45 min. Renin, aldosterone, and vasopressin, assayed by radioimmunoassay (RIA), were determined before, 1 h, and 5 h after starting the water load. Prestudy hormone levels were within normal range in both groups. Renin and aldosterone concentration change patterns were similar in both groups and characterized by suppression of hormone activity caused by central volume expansion and recovery to prestudy levels after 5 h. However, the pattern of change of vasopressin concentrations differed in the control and study groups. In contrast to that of the controls, volume expansion did not suppress vasopressin in the group with liver cirrhosis. We conclude that failure to suppress vasopressin activity after central volume expansion may be one of the early mechanisms responsible for water-electrolyte imbalance in liver cirrhosis in children.
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PMID:The renin-angiotensin-aldosterone system and vasopressin in early-stage liver cirrhosis after HBV infection in children. 787 98

Agents that produce their effects through an antisense mechanism offer the possibility of developing highly specific alternatives to traditional pharmacological antagonists, thereby providing a novel class of therapeutic agents, ones which act at the level of gene expression. Among the antisense compounds, antisense RNA produced intracellularly by an expression vector has been used extensively in the past several years. This review considers the advantages of the antisense RNA approach over the use of antisense oligodeoxynucleotides, the different means by which one may deliver and produce antisense RNA inside cells, and the experimental criteria one should use to ascertain whether the antisense RNA is acting through a true antisense mechanism. Its major emphasis is on exploring the potential therapeutic use of antisense RNA in several areas of medicine. For example, in the field of oncology antisense RNA has been used to inhibit several different target proteins, such as growth factors, growth factor receptors, proteins responsible for the invasive potential of tumor cells and proteins directly involved in cell cycle progression. In particular, a detailed discussion is presented on the possibility of selectively inhibiting the growth of tumor cells by using antisense RNA expression vectors directed to the individual calmodulin transcripts. Detailed consideration is also provided on the development and potential therapeutic applications of antisense RNA vectors targeted to the D2 dopamine receptor subtype. Studies are also summarized in which antisense RNA has been used to develop more effective therapies for infections with certain viruses such as the human immunodeficiency virus and the virus of hepatitis B, and data are reviewed suggesting new approaches to reduce elevated blood pressure using antisense RNA directed to proteins and receptors from the renin-angiotensin system. Finally, we outline some of the problems which the studies so far have yielded and some outstanding questions which remain to be answered in order to develop further antisense RNA vectors as therapeutic agents.
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PMID:Antisense RNA gene therapy for studying and modulating biological processes. 1022 54

We report a 66-year-old man with hepatocellular carcinoma who was positive for hepatitis B surface antigen, and was hospitalized because of hypoglycemia and hypertension. His plasma renin activity was normal (2.3 ng/ml per h), but concentrations of angiotensin I (>2500 pg/ml) and II (86 pg/ml) were high. Increased angiotensin I level at sites proximal and distal from the confluence of the hepatic vein and the inferior vena cava indicated that the hypertension was provoked by overproduction of angiotensin I from the hepatocellular carcinoma. Previous reports of patients with hepatocellular carcinoma with hypertension due to abnormality of renin-angiotensin system are reviewed.
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PMID:Hypertension as a paraneoplastic syndrome in hepatocellular carcinoma. 1045 90

Chronic renal failure represents a major problem of public health. Incidence for patients arrived at the terminal stage of the disease is in France 126.4/million inhabitants and the cost of medical care reaches 2 % of the expenses of the National Health Insurance. The progression of the disease is divided into 5 stages that are defined by the level of creatinine clearance from the stage of renal diseases with a normal renal function (clearance>90 ml/min) to the terminal stage (clearance <15 ml/min). Prevalence of patients at this ultimate stage is around 50,000. Prevalence for the totality of patients with a renal disease is evaluated between 2 and 3 millions. Renal diseases must be screened because they are silent and because an early pre-dialysis nephrological care allows renal replacement therapy to be delayed and the number of cardiovascular accidents to be diminished. Screening must be performed in the high-risk populations, essentially patients with diabetes, hypertension, coronary ischemia, renal tract diseases and all subjects treated with drugs toxic for the kidneys. Screening in the total population seems inadequate because of a high cost to benefit ratio. Screening is based on testing for the presence of proteinuria, quantifying the number of formed elements and plasma creatinine determination, the latter allowing, together with age and weight, glomerular filtration rate to be evaluated according to Cockcroft's formula. Prevention of renal diseases in the whole population necessitates the same life style as that recommended for prevention of cardiac and metabolic diseases. In the high-risk populations, one must control glycemia, blood pressure and cholesterol plasma level. In patients that have been already screened, renal function decay has to be slowed down by blocking the renin angiotensin system with converting enzyme inhibitors, controlling plasma cholesterol with statins and diminishing dietary proteins. In the light of these various data, the National Academy of medicine recommends: 1 - in the field of public health, to extend to the whole country the registries containing data on patients with terminal chronic renal failure, to support the creation of medical networks for the screening of renal diseases, to vaccine the patients against hepatitis B, flue and pneumococcal infections and to verify whether a low birth weight is associated with a greater risk of renal diseases in adulthood; 2 - in the field of teaching and research, to stop the decrease in the number of nephrologists, to promote research in genetics, to evaluate the efficacy of antifibrosis drugs and the possible renal toxicity of all new drugs.
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PMID:[Prevention and screening of chronic renal failure]. 1591 71

Hepatitis B virus (HBV) infection is the most prevalent cause of fulminant hepatic failure (FHF) in the Far East. HBV-associated FHF is characterised by rapidly progressive end organ dysfunction/failure and a very poor prognosis. To investigate how molecular adsorbent recirculating system (MARS) treatment impacts multiple organ system function in HBV-associated FHF. Ten consecutive patients were treated with MARS in a period of 12 months. Clinical, biochemical and haemodynamic parameters were assessed before and after MARS. Various disease severity scoring systems including model for end-stage liver disease, APACHE II, APACHE III, sequential organ failure assessment and organ system failure scores were also assessed. There were significant improvements in hepatic encephalopathy grading (p < 0.001), mean arterial pressure (p < 0.001), plasma renin activity (p = 0.027), bilirubin (p < 0.001), ammonia (p = 0.001) and creatinine levels (p < 0.001). There were also significant improvements in all the scoring systems evaluated. Meanwhile, platelet count was significantly decreased (p < 0.001). One patient was successfully bridged to liver transplantation. Three patients were alive at 3 months of follow-up. MARS can improve multiple organ functions in HBV-associated FHF. On the basis of these findings, randomised controlled studies are indicated and justified.
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PMID:Extracorporal liver support with molecular adsorbents recirculating system in patients with hepatitis B-associated fulminant hepatic failure. 1623 82

We present the case of a young patient with hypertension and unprovoked symptomatic hypokalemia. His workup uncovered secondary aldosteronism, moderate proteinuria, and, quite unusually, concurrent chronic hepatitis B. Detailed investigations, including renal angiography, renal vein sampling, and kidney biopsy, showed unilateral renin hypersecretion due to intrarenal arterial stenoses and mesangioproliferative glomerulonephritis, presumed to be secondary to hepatitis B infection. Targeted pharmacotherapy reversed all clinical manifestations, normalizing blood pressure and serum potassium level and achieving full remission of proteinuria and loss of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg), and a dramatic decrease in viral load.
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PMID:Hypertension and symptomatic hypokalemia in a patient with simultaneous unilateral stenoses of intrarenal arteries and mesangioproliferative glomerulonephritis. 2215 39

The various types of glomerulonephritis, including many forms of vasculitis, are responsible for about 15% of cases of end-stage renal disease (ESRD). Arterial hypertension represents a frequent finding in patients suffering from glomerulonephritis or vasculitis and hypertension also serves as an indicator for these severe types of diseases. In addition, there are symptoms and signs like hematuria, proteinuria and renal failure. Especially, rapidly progressive glomerulonephritis (RPGN) constitutes a medical emergency and must not be missed by treating physicians. This disease can either occur limited to the kidneys or in the context of a systemic inflammatory disorder, like a vasculitis. If left untreated, RPGN can lead to a necrotizing destruction of glomeruli causing irreversible kidney damage within several months or even weeks. With respect to the immunologically caused vasculitis, there are - depending upon the severity and type of organ involved - many clinical warning signs to be recognized, such as arterial hypertension, hemoptysis, arthalgias, muscle pain, palpable purpura, hematuria, proteinuria and renal failure. In addition, constitutional signs, such as fever and loss of body weight may occur concurrently. Investigations of glomerulonephritis or vasculitis must contain a careful and complete examination of family history and medications used by the respective patient. Thereafter, a thorough clinical examination must follow, including skin, joints and measurement of arterial blood pressure. In addition, a spectrum of laboratory analyses is required in blood, such as full blood screen, erythrocyte sedimentation rate, CRP, creatinine, urea and glucose, and in urine, including urinalysis looking for hematuria, red cell casts and proteinuria. Importantly, proteinuria needs to be quantified by the utilization of a random urine sample. Proteinuria > 3g/d is diagnostic for a glomerular damage. These basic tests are usually followed by more specialized analyses, such as a screening for infections, including search for HIV, hepatitis B or C and various bacteria, and for systemic inflammatory diseases, including tests for antibodies, such as ANA, anti-dsDNA, ANCA, anti-GBM and anti-CCP. In cases of membranous nephropathy, antibodies against phospholipase-A2-receptor need to be looked for. Depending upon the given clinical circumstances and the type of disease, a reasonable tumor screening must be performed, especially in cases of membranous and minimal-change nephropathy. Finally, radiological examinations will complete the initial work-up. In most cases, at least an ultrasound of the kidney is mandatory. Thereafter, in most cases a renal biopsy is required to establish a firm diagnosis to define all treatment options and their chance of success. The elimination of a specific cause for a given glomerulonephritis or vasculitis, such as an infection, a malignancy or a drug-related side-effect, remains the key principle in the management of these diseases. ACE-inhibitors, angiotensin receptor-blockers, aldosteron antagonists and renin-inhibitors remain the mainstay in the therapy of arterial hypertension with proteinuria. Only in cases of persistently high proteinuria, ACE-inhibitors and angiotensin receptor blockers can be prescribed in combination. Certain types of glomerulonephritis and essentially all forms of vasculitis require some form of more specific anti-inflammatory therapy. Respective immunosuppressive drug regimens contain traditionally medications, such as glucocorticoids (e. g. prednisone), cyclosporine A, mycophenolate mofetil, cyclophosphamide, and azathioprine. With respect to more severe forms of glomerulonephritis and vasculitis, the antibody rituximab represents a new and less toxic alternative to cyclophosphamide. Finally, in certain special cases, like Goodpasture's syndrome or severe ANCA-positive vasculitis, a plasma exchange will be useful and even required.
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PMID:[Glomerulonephritis and vasculitis as causes of arterial hypertension]. 2254 60


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