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)

A 77-year-old man developed a fever up to 38.4 degrees C, with diarrhoea, acute renal failure (creatinine up to 8.7 mg/dl; urea up to 308 mg/dl) and marked jaundice (total bilirubin up to 24.3 mg/dl). In addition there was thrombocytopenia, conjunctivitis and epistaxis, as well as cerebral symptoms with somnolence and general slowing up. At first he was thought to have cholangitis resulting from previously diagnosed gall-stones, and he was therefore treated with ampicillin, 2 g two times daily, and metronidazole, 0.5 g two times daily. The fewer regressed, but the renal failure required haemodialysis and haemofiltration under strict fluid control. Endoscopy excluded obstructive jaundice, but a suspicion of inflammatory liver disease or possibly cirrhosis was raised in the differential diagnosis. Serology revealed an increased titre for Leptospira interrogans var. sejroe (1:200, later 1:1600). Liver biopsy finding was compatible with the diagnosis of leptospirosis. Because of the high inflammatory activity in the liver, 2 mega units of penicillin G were administered three times daily for six days. Gradually the renal functions and jaundice improved and, on discharge on the 36th day, the patient was again in generally good health, although creatinine and bilirubin values were still slightly elevated (1.7 mg/dl each).
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PMID:[A severe course of leptospirosis with acute kidney failure and extensive icterus (Weil disease)]. 840 98

There are conflicting reports on the ability of aspirin as a single agent to cause acute or chronic renal failure in experimental animals. Chronic administration of aspirin alone over 18 to 68 weeks in doses of 120 to 500 mg/kg/d has been reported to cause renal papillary necrosis in rats. However, some investigators have been unable to produce renal papillary necrosis in other species or in rats given lower divided doses comparable to therapeutic doses used in humans. In a variety of rat strains, aspirin administered as a single high dose intravenously or by oral gavage produces acute tubular necrosis of proximal tubules, rarely accompanied by renal papillary necrosis in susceptible strains. Several human studies have addressed the chronic nephrotoxicity of aspirin alone or relative risk of end-stage renal disease in association with aspirin use after correction for other analgesics. With the exception of one case control study demonstrating a low, but statistically significant risk of end-stage renal disease in association with aspirin use, all other case control studies and several prospective studies have been unable to identify a significant risk of chronic renal failure in patients using aspirin alone in therapeutic doses. In healthy adults, short-term aspirin administration in therapeutic doses has no effect on creatinine clearance, urine volume, osmolar clearance, or sodium and potassium excretion. However, in predisposed individuals with glomerulonephritis, cirrhosis, and chronic renal insufficiency, and in children with congestive heart failure, short-term aspirin use in therapeutic doses may precipitate reversible acute renal failure. Acute aspirin intoxication (>300 mg/kg) frequently causes acute renal failure and doses of 500 mg/kg may be lethal. Chronic salicylate intoxication has been reported to cause reversible or irreversible acute renal failure in association with a pseudosepsis syndrome.
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PMID:Does aspirin cause acute or chronic renal failure in experimental animals and in humans? 866 25

Nonsteroidal anti-inflammatory drugs (NSAIDs) are one of the most valuable groups of available medications because of their effectiveness in relieving pain, particularly that associated with rheumatoid arthritis. They are also among the most commonly prescribed drugs and, because of their availability over-the-counter, they are among the most widely consumed agents, especially by elderly people. Older individuals are more predisposed to the renal adverse effects of NSAIDs, because of: (i) age-associated changes in renal function; (ii) the prevalence of comorbid conditions (congestive heart failure, hypertension, hepatic cirrhosis, renal insufficiency); and (iii) the pervasive use of concomitant drugs that affect kidney function (diuretics, antihypertensives). However, because the incidence of NSAID-induced acute renal failure (ARF) is relatively low, and because it occurs in an identifiable and therefore preventable setting, the benefits of limited NSAID use outweigh the risks of this adverse effect. Using NSAIDs for a restricted period of time at the lowest effective dosage, and informing patients of the conditions in which ARF can occur, should minimise the risk of this effect. If the use of an NSAID in a patient at potential risk of ARF is necessary, close monitoring of renal function should further reduce the already low risk:benefit ratio for this adverse effect.
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PMID:Nonsteroidal anti-inflammatory drugs and acute renal failure in the elderly. A risk-benefit assessment. 892 61

Acute renal and hepatic failure can occur for many reasons. The hepatorenal syndrome is acute renal failure of unknown cause developing in a patient with chronic liver disease, usually cirrhosis. The pathogenesis is functional in nature due to a combination of redistribution of fluid between compartments and intrarenal events reducing renal blood flow (activation of the renin-angiotensin system, increased renal sympathetic activity, and a decrease in vasodilating and increase in vasoconstricting prostaglandins). Management of combined renal and hepatic failure consists of measures to control the uraemia and the effects of hepatic dysfunction. Haemodialysis is accompanied by a number of specific problems such as maintenance of cerebral perfusion and anticoagulation. At present the best dialysis mode is continuous haemodiafiltration using a biocompatible membrane. The prognosis of the hepatorenal syndrome is poor and depends on recovery of hepatic function. Liver transplantation may be required.
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PMID:Hepatorenal failure. 904 37

While the relative incidence of serious nephrotoxicities in the population consuming nonsteroidal anti-inflammatory drugs (NSAIDs) is very low, the frequency of adverse events in patients at risk has considerably increased due to the rising popularity of the use of the drugs in recent years. Under normal conditions, NSAIDs have relatively little effect on the kidney because of low renal production of prostaglandins. However, in the presence of renal hypoperfusion in which local synthesis of vasodilator prostaglandins is increased to protect the glomerular hemodynamics and to maintain appropriate renal tubular transport of fluid and electrolytes, inhibition of prostaglandin synthesis by NSAIDs can lead to vasoconstrictive acute renal failure as well as fluid and electrolyte disorders such as sodium retention and resistance to diuretics, hyponatremia and hyperkalemia. Conditions that increase the risk for NSAID-induced nephrotoxicities include volume depletion from diuretics and other causes, edematous states such as congestive heart failure and cirrhosis of the liver, old age and underlying renal disease, especially in the presence of renal functional impairment. In addition, renal parenchymal diseases may develop in susceptible patients taking NSAIDs. These include acute tubulointerstitial nephritis, frequently associated with nephrotic syndrome, and chronic progressive renal disease, with or without renal papillary necrosis. Rare cases of vasculitis and glomerulonephritis have also been reported. Finally, NSAIDs may aggravate hypertension by interacting with antihypertensive drugs, especially with diuretics and beta-blockers. Withdrawal of NSAIDs in patients at risk can frequently reverse or improve the nephrotoxicities. It is recommended that physicians be aware of the clinical settings that increase the risk for NSAID-induced nephrotoxicities and take preventive or therapeutic measures accordingly.
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PMID:Nephrotoxicities of nonsteroidal anti-inflammatory drugs. 908 Jul 53

Apart from the initially described vasoconstriction, endothelins have been shown to cause a variety of biological activities in non-vascular tissues. A rapidly growing body of data supports the concept of endothelin as a paracrine acting hormone. In this review, we will discuss the impact of this local endothelin system for various cardiovascular pathophysiological states, especially atherosclerotic vascular disease, restenosis, myocardial infarction, congestive heart failure, and arterial hypertension. In addition, the endothelin system is a modulator of renal function via its binding to abundant receptors in renal tissue and by the ability of renal endothelial and epithelial cells to synthesize and release endothelin. In the kidney, endothelin may function as a paracrine/autocrine factor in the regulation of renal blood flow, glomerular haemodynamics, and sodium and water homeostasis. The renal endothelin system is involved in kidney diseases such as impaired renal function in liver cirrhosis, cyclosporin toxicity, acute renal failure and renal glomerular and interstitial fibrosis. Therapeutic approaches with new orally active endothelin receptor antagonists are also discussed.
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PMID:The paracrine endothelin system: pathophysiology and implications in clinical medicine. 929 57

Cirrhosis encompasses a range of pathophysiological changes that may alter drug disposition. Drugs that are dependent primarily on the liver for their systemic clearance are more likely to be subject to reduced elimination and subsequent accumulation. Drug accumulation may lead to excessive plasma drug concentrations and adverse effects, if the adverse effects of the drug are concentration-dependent. The effects of hepatic insufficiency on the pharmacokinetics of drugs are not consistent or predictable. Furthermore, the influence of hepatic disease on the disposition of various drugs can vary, even though those drugs may share the same apparent metabolic pathway. Problems in forecasting drug kinetic behaviour are further enhanced by the additional impairment of kidney function (frequently encountered in patients with advanced liver disease) and by the unpredictability of the glomerular filtration rate using customary methods in patients with cirrhosis. Accordingly, dosages are generally adapted empirically, with the help of serum drug concentrations, when applicable. However, drugs eliminated predominantly by hepatic metabolism are not among those most commonly inducing adverse drug reactions or causing severe complications in patients with cirrhosis. Electrolyte disturbances and the hepatorenal syndrome produced by furosemide (frusemide)-the disposition of which is not substantially modified in liver disease-appear to be the most frequent adverse drug reactions in patients with liver disease. Furthermore, clinically significant alterations in the action of medications at concentrations generally considered to be in the normal therapeutic range are not uncommon. Tissue responsiveness to the pharmacological action of some drugs may be modified, as evidenced by the increased susceptibility of the brain in patients with cirrhosis to the action of many psychoactive agents. Another example is the greater susceptibility of such patients to the nephrotoxic potential of aminogly-cosides, which should not be used in this patient group. Drugs may also interfere with adaptive physiological processes induced by liver disease. ACE inhibitors and nonsteroidal anti-inflammatory drugs counteract the enhanced activity of the renin-angiotensin system in advanced liver disease, thereby generating a high risk of excessive hypotension or acute renal failure, respectively. These drugs are best avoided in patients with cirrhosis. Finally, there may be pharmacological effects that overlap with some pathophysiological modifications related to the process of liver disease, such as increased portal pressure produced by some calcium antagonists, or hypoprothrombinaemia related to the inhibition of synthesis of vitamin K-dependent clotting factors by some beta-lactam antibacterials (especially moxalactam and cefamandole). Accordingly, the use of these drugs should be avoided in advanced liver disease. It is noteworthy that reduced drug metabolism in patients with liver disease does not seem to have a significant impact on the frequency of hepatotoxicity. Special caution should be exercised, however, in patients with alcoholic liver disease because excessive alcohol intake may potentiate the hepatotoxic effect of paracetamol (acetaminophen).
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PMID:Drug administration in chronic liver disease. 925 30

Acute cholecystitis is a common disease which may carry the risk of complications, including empyema, perforation, abscess, peritonitis and sepsis. Percutaneous transhepatic drainage of the gallbladder (PTGBD) with antibiotics can provide prompt decompression of gallbladder in acute cholecystitis and interrupt the natural history of the disease effectively. From July 1986 to June 1996, 154 patients with acute cholecystitis were reviewed retrospectively in Kaohsiung Medical College Hospital. The chief symptoms and signs were pain (98.1%), fever (57.1%) and jaundice (37.7%). WBC count more than 10,000 was noted in 116 (75.3%) patients. Associated diseases included empyema: 42 (27.3%), septic shock: 14 (9.1%), diabetes mellitus: 13 (8.4%), pancreatitis: 10 (6.5%), perforation: 7 (4.5%), liver cirrhosis: 6 (3.9%) and respiratory failure: 1 (0.6%). All of them underwent ultrasound-guided PTGBD immediately after the diagnosis was established. The symptoms and signs disappeared soon after this procedure. Bacterial culture was found positive in 104 (67.5%) of 154 patients in which Escherichia coli (51.9%) was the most common organism, followed by Klebsiella pneumonia (20.2%). After acute stage, 138 patients obtained the cholangiography via PTGBD tube. Gallbladder stones were only noted in 56 (40.6%) patients, gallbladder stone concomitant with common bile duct stone in 26 (18.8%), cystic duct obstruction in 25 (18.1%), acalculous cholecystitis in 21 (15.2%), gallbladder perforation in 1 (0.7%), choledochocyst in 1 (0.7%), and cholecystocolonic fistula in 1 (0.7%). There were 135 patients to undergo surgery after the clinical condition was stable. The operative findings included gallbladder stones only in 88 (65.2%), gallbladder stone concomitant with common bile duct stone in 34 (25.2%), acalculous cholecystitis in 13 (9.6%), choledochocyst in 1 (0.7%), and cholecysto-colonic fistula in 1 (0.7%). The postoperative complications included wound infection 8 (5.9%), UGI bleeding 3 (2.2%), acute renal failure 1 (0.7%) and acute respiratory failure 1 (0.7%). The postoperative mortality rate was 0.7% (1/135), which was much lower than those of previous reports, which not undergoing PTGBD initially. It led us to conclude that PTGBD, as an initial preoperative modality to treat acute cholecystitis, is effective in decreasing postoperative morbidity and mortality.
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PMID:Ultrasound-guided percutaneous transhepatic drainage of gallbladder followed by cholecystectomy for acute cholecystitis--10 years' experience. 951 85

Nonsteroidal antiinflammatory drugs (NSAIDs), including various chemical families of drugs, inhibit prostaglandin synthesis and act on the central nervous system. Prostaglandins are involved in regulation of regional circulations, cell turn-over in the gastrointestinal tract, and in primary haemostasis. The patterns of action of NSAIDs result in analgesic properties, but also in adverse effects. NSAIDs are increasingly used perioperatively, alone or associated with opioids or local anaesthetics, because of their analgesic and opioid sparing properties. Some of their adverse effects, especially ischaemic acute renal failure and gastrointestinal complications, can be life-threatening, and increased haemorrhagic risk is an issue for spinal or epidural anaesthesia in patients taking aspirin. Safe use of NSAIDs is possible in consideration of contraindications (elderly patient, hypovolaemia, cirrhosis, congestive heart failure, renal failure, active gastrointestinal ulcer, bleeding diathesis, pregnancy), and requires close monitoring of renal function if they must be used in patients at risk for renal failure. NSAIDs are not ulcerogenic in the short-term in healthy subjects. They must be used with caution in patients with a preexisting haemostatic defect or undergoing haemorrhagic surgical procedures.
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PMID:[Role of non-steroidal anti-inflammatory agents in the perioperative period. Usefulness and limitations]. 975 Jun 5

Acutely increased intraabdominal pressure can lead to multisystem organ dysfunction. Organ dysfunction consists of acute pulmonary failure secondary to compressive atelectasis and associated with high peak inspiratory pressures and impaired gas exchange, acute renal failure with marked oliguria without hypernaturia, intestinal and hepatic ischemia possibly leading to bacterial translocation or necrosis with peritonitis, increased intracranial pressures which may cause brain dysfunction or aggravate head injury edema, venous thrombosis and thromboembolism, and abdominal wall ischemia or necrosis. The diagnosis is made clinically in a patient with high peak inspiratory pressures, oliguria and an apparently tight abdomen, although urinary bladder pressure > or = 20 cm H2O pressure is suggestive. However, chronically increased intraabdominal pressure as is seen in the morbidly obese, pregnancy and cirrhosis may be misleading. As to treatment, once the diagnosis is made, the patient's abdomen should be opened and the tension relieved. The intestinal contents need to be protected and evaporative water loss minimized by either closing the skin and not the fascia or, if this is not possible, using an impermeable protective dressing. If the abdomen is difficult to close at the primary operation, it is best to prevent the development of an acute abdominal compartment syndrome by closing only the skin or leaving it open and using an impermeable dressing. In conclusion, the acute abdominal compartment syndrome has become increasingly recognized as a cause for multisystem organ failure. Recognition of the problem or prevention is mandatory for optimal patient survival.
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PMID:Multisystem organ failure secondary to increased intraabdominal pressure. 1144 Mar 93


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