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PubMed1990

Effect of acute hemodynamic decompensation on electrical inducibility of ventricular arrhythmias in patients with dilated cardiomyopathy and complex nonsustained ventricular arrhythmias.

In patients with dilated cardiomyopathy, hemodynamic decompensation has been postulated to increase vulnerability to reentrant ventricular arrhythmias. To test this hypothesis, we performed programmed ventricular stimulation with three extrastimuli on nine patients with dilated cardiomyopathy and asymptomatic complex ventricular arrhythmias during a period of acute hemodynamic decompensation; programmed ventricular stimulation was then repeated following hemodynamic improvement with nitroprusside. These patients did not have a history of documented or suspected sustained ventricular tachycardia or fibrillation. The mean left ventricular ejection fraction was 0.21 +/- 0.04 (range 0.15 to 0.26). In the baseline state, mean right atrial pressure was 8 +/- 4 mm Hg, pulmonary artery wedge pressure was 20 +/- 3 mm Hg, and cardiac index was 3.2 +/- 0.5 L/min/m2. Following acute hemodynamic decompensation, mean right atrial pressure increased to 16 +/- 5 mm Hg and pulmonary artery wedge pressure to 33 +/- 8 mm Hg; cardiac index decreased to 2.1 +/- 0.5 L/min/m2. In this decompensated state, programmed ventricular stimulation failed to induce sustained or nonsustained ventricular arrhythmias in any patient. Following nitroprusside administration (mean dose 1.5 +/- 1.1 micrograms/kg/min), there were significant decreases in mean right atrial pressure (11 +/- 3 mm Hg) and pulmonary artery wedge pressure (16 +/- 3 mm Hg), and a significant increase in cardiac index (3.1 +/- 1.1 L/min/m2) (p less than 0.05 for all values versus the decompensated state). In the improved hemodynamic state, programmed ventricular stimulation induced nonsustained ventricular tachycardia (six beats) in only one patient, and sustained arrhythmias in none.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗

PubMed2003

Decompensated heart failure: symptoms, patterns of onset, and contributing factors.

PURPOSE: To examine the time course, contributing factors, and patient responses to decompensated heart failure. METHODS: We studied consecutive patients admitted to a public general hospital with a diagnosis of heart failure. Using a timeline follow-back technique, a nurse interviewer administered a questionnaire shortly after admission, exploring knowledge of a heart failure diagnosis, the symptoms and time course of decompensation, and patient responses to worsening symptoms. RESULTS: Of 87 patients, 83 (95%) consented to be interviewed. Only 49 (59%) were aware of the diagnosis of heart failure. Symptoms associated with decompensation included dyspnea in 81 patients (98%), edema in 64 patients (77%), and weight gain in 34 patients (41%). Onset of worsening of these symptoms was noted a mean (+/- SD) of 12.4 +/-1.4 days before admission for edema, 11.3 +/-1.6 days for weight gain, and 8.4 +/- 0.9 days for dyspnea. Forty-two patients (57%) reported missing or skipping medication because of various factors, particularly missed outpatient appointments. CONCLUSION: Using a timeline follow-back interview, we identified a period of days to weeks between the onset of worsening symptoms and hospital admission for heart failure decompensation. This pattern suggests that there is a time window between symptom exacerbation and admission during which earlier access and intervention might prevent hospitalization in these patients. Medication lapses continue to be an important preventable cause of decompensation leading to admission.

Aged↗

PubMed1992

Late decompensation of neobladder.

We report on 6 patients in whom we constructed detubularized ileocolonic neobladders in conjunction with cystectomy to treat invasive transitional cell carcinoma of the bladder. The patients had delayed complete or partial decompensation of the neobladder after an initial interval of normal voiding. Two patients experienced complete decompensation with inability to empty in the absence of urodynamic, cystoscopic or radiographic evidence of outlet obstruction. The other 4 patients had greater than 400 cc residual urine without evidence of outlet obstruction. The mean interval to decompensation after the initial period of normal voiding was 12.8 months (range 4 to 21). All 6 patients had a reservoir capacity of greater than 800 cc. We also constructed neobladders in 3 other patients for similar indications. These 3 patients have a neobladder capacity of less than 800 cc and all are voiding to completion with followup of 19 to 32 months. We hypothesize that neobladder decompensation is due either to creation of an excessively large pouch alone or in combination with a poor Valsalva ability. Until we know the neobladder capacity required for continence that will simultaneously allow for complete emptying, all patients should be advised of the possible need for intermittent self-catheterization. Urological followup should include monitoring of post-void residual urine volume to detect failure to empty early before irreversible decompensation occurs.

Adult↗

PubMed2000

The role of thoracic ultrasonography for evaluation of patients with decompensated chronic heart failure.

OBJECTIVES: This study examined the usefulness of thoracic ultrasonography for evaluation of fluid accumulation in patients with decompensated chronic heart failure (CHF) in comparison with physical signs, upright posteroanterior chest X-ray and echocardiography. BACKGROUND: Decompensated CHF is frequently accompanied by pleural effusion, suggesting that pleural effusion is a useful marker for confirming the diagnosis of the uncontrolled stage of CHF. Thoracic ultrasonography seems to be adequate for this purpose. METHODS: Patients with uncontrolled CHF and an interpretable physical examination, chest X-ray, ultrasonogram for the heart and thorax and thoracic X-ray computed tomographic (CT) scan were enrolled in the study (n = 60). Patients free from thoracic and cardiovascular diseases served as a control (n = 22). Thoracic CT scan was used as the gold standard for the presence or absence of pleural effusion. Variables used to predict body fluid accumulation included the following: pulmonary rales, jugular venous distension or peripheral edema, roentgenographic evidence of pulmonary edema or pleural fluid, pericardial or pleural effusion on ultrasonographic study. RESULTS: The reported incidence of pleural effusion detected by thoracic ultrasonography was high (91%). The incidence of physical signs and roentgenographic signs of body fluid accumulation, however, was modest (56%) to low (33%). The best clinical variable for identifying patients with decompensated CHF was the detection of pleural fluid by thoracic ultrasonography (91% predictive accuracy). This variable also had high interobserver agreement (95% overall agreement, kappa = 0.70). There was only 41% to 65% predictive accuracy of other clinical variables, with 72% to 95% agreement (kappa = 0.400-0.848). CONCLUSIONS: Thoracic ultrasonography is a simple, sensitive and accurate method for the evaluation of body fluid accumulation in patients with decompensated CHF. This technique can be used to assist in making the diagnosis of decompensated CHF if other causes of pleural effusion have been clinically ruled out.

Aged↗

PubMed1999

Nitric oxide metabolites in decompensated liver cirrhosis.

High levels of nitric oxide are thought to be the cause of some of the complications associated with decompensated end-stage liver disease. To assess nitric oxide metabolism in cirrhotic patients, we measured the levels of nitric oxide metabolites (nitrosohemoglobin, methemoglobin, nitrate, and nitrite) in normal subjects, in patients with decompensated cirrhosis, in patients with renal failure (model for impaired NO metabolites excretion), and in patients with mononitrates-treated anginal syndrome (model for exogenous nitric oxide). When compared to controls, patients with decompensated cirrhosis exhibited elevated levels of nitrate only. A significant increase of nitrate was also noted in patients receiving exogenous nitrates, whereas patients with impaired excretion had significantly elevated levels of both nitrite and nitrate. In conclusion, nitric oxide metabolism in patients with decompensated cirrhosis is similar to that of patients receiving nitric oxide from an exogenous source. Renal impairment, whether alone or associated with cirrhosis, causes a change in nitric oxide metabolism. These findings may have clinical implications for nitrates treatment in patients with decompensated cirrhosis.

Adult↗

PubMed2003

[Psychosomatic stress factors in compensated and decompensated tinnitus].

AIMS: In modern medical practice, chronic decompensated tinnitus is defined as a complex psychosomatic process in which mental and social factors are considered to have a determining effect on the patient's subjective response to the impairment of otological or other somatic functions attributed to tinnitus. What is still largely unknown is the interaction of the individual factors and their impact on the patient's ability to cope with tinnitus. The impact of psycho-social and somatic factors on the subjective experience of patients with compensated and decompensated tinnitus is evaluated. PATIENTS AND METHODS: 53 patients with chronic tinnitus were divided into two groups, compensated and decompensated, on the basis of their subjective experience of the disorder, established according to the tinnitus questionnaire published by Goebel and Hiller. Self-assessment instruments and a survey of symptoms of somatic stress disorders were used to compare the two groups in terms of differences in the patients' mental and psycho-social behaviour, in their strategies for coping with tinnitus and in the incidence of co-morbidity. RESULTS: The patients with decompensated tinnitus suffered from more pronounced mental and social disabilities, were more prone to depression and used less effective techniques to cope with their illness. The principal difference between the two groups, however, appeared to lie in a significantly higher degree of somatic multi-morbidity, where a particularly strong correlation was found between tinnitus and the incidence of cardiovascular diseases and hypacusis. 81 percent of the total sample of patients suffered from impaired hearing. Patients with decompensated tinnitus experienced greater communication difficulties as a result of their auditory impairment. CONCLUSIONS: In the diagnosis and therapy of tinnitus, in addition to psychic and psycho-social aspects greater attention ought to be paid to somatic factors, influencing the patient's ability to cope with the disorder.

Adult↗

PubMedDate not supplied

Survival and prognostic indicators in patients with hepatitis B virus-related cirrhosis after onset of hepatic decompensation.

GOALS: To determine the 2-year survival and prognostic indicators of hepatitis B virus-related cirrhosis after the onset of hepatic decompensation. BACKGROUND: Chronic hepatitis B (CHB) patients with cirrhosis and resultant hepatic decompensation have reduced survival. However, the natural history of these patients has not been well characterized in previous studies. Better understanding of survival and prognostic indicators is essential in management of these patients, especially in determining who should be candidates for orthotopic liver transplantation. STUDY: This is a retrospective longitudinal study of 96 patients with CHB-related cirrhosis after the onset of hepatic decompensation. The overall survival was ascertained, and clinical and laboratory variables were analyzed. Significant prognostic indicators for survival at 2 years were determined using univariate and multivariate analyses with Cox regression model. RESULTS: The overall survival was 80% at 2 years after onset of decompensation. With univariate and multivariate analyses, hepatic encephalopathy and hypoalbuminemia less than 2.8 g/dL were significant prognostic indicators of poor survival probability. The hazard ratios were 5.22 (95% confidence interval, 1.67-16.3) and 8.57 (95% confidence interval, 1.94-37.8), respectively. Patients with hypoalbuminemia less than 2.8 g/dL had a 2-year survival of only 62%. CONCLUSIONS: Our study showed that of CHB patients who developed the first episode of hepatic decompensation, those with hepatic encephalopathy or significant hypoalbuminemia or both have worse prognoses. They should be considered potential candidates for liver transplantation.

Female↗

PubMed2005

Determinants of early mortality and benefits of lamivudine therapy in patients with hepatitis B virus-related decompensated liver cirrhosis.

Chronic hepatitis B infection (HBV) is a major health problem worldwide. The prognosis is grave for patients with HBV-related decompensated liver cirrhosis (LC). We evaluated the effectiveness and the determinants of early mortality of lamivudine treatment in patients with HBV-related decompensated LC. Thirty patients with HBV-related decompensated LC and active viral replication were treated with lamivudine 100 mg daily for a median duration of 9 months. Among these patients, five patients died within 3 months. Two patients were lost to follow-up at week 8 and 9. One patient was treated for <6 months. Twenty-two patients were treated over 6 months. Univariate analysis revealed that the total bilirubin (P = 0.008), prothrombin time (P = 0.004), Child-Turcotte-Pugh score (P = 0.005), the model of efd-stage liver disease score (P = 0.004) and stage III hepatic encephalopathy (P = 0.001) were predictive factors of early mortality. Multivariate analysis revealed that the independent factor associated with early mortality was stage III encephalopathy. Among 22 patients, liver function improved markedly after lamivudine therapy. Of the nine hepatitis B e antigen (HBeAg)-positive patients, three had HBeAg seroconversion. Two patients had YMDD mutant and virological breakthrough at 41 and 46 weeks. One of the two had hepatocellular carcinoma and died of hepatic failure at week 125; the other received adefovir and is doing well. Lamivudine appeared to have benefits in viral suppression and significant improvement in liver function in patients with HBV-related decompensated LC. As noted in prior studies, poor baseline liver function is associated with a poor prognosis in Asian patients with decompensated HBV cirrhosis treated with lamivudine.

Adenine↗

PubMed2003

Diabetes mellitus is a risk factor for hepatic decompensation in patients with hepatocellular carcinoma undergoing resection: a longitudinal study.

OBJECTIVES: Patients with hepatocellular carcinoma (HCC) frequently have diabetes mellitus (DM) due to coexisting liver cirrhosis. The aim of this study was to assess the long-term impact of DM on the hepatic regenerative ability of HCC patients undergoing surgical resection. METHODS: We retrospectively studied 245 HCC patients (210 male; age, 61 +/- 13 yr) with well-preserved liver functions undergoing resection. Forty (16%) of them were diabetic and were controlled with hypoglycemic agents. The Child-Pugh scoring system was used to evaluate the postoperative liver regeneration ability. The endpoint was the occurrence of hepatic decompensation, defined as a sustained increase in the Child-Pugh score of 2 or more points or the development of tumor recurrence. RESULTS: Seventy-five patients (31%) developed hepatic decompensation during a follow-up period of 27 +/- 18 months (range, 3-75). DM (p = 0.001), large (>3 cm) tumor size (p = 0.044), and age > 65 yr (p = 0.058) were the factors associated with hepatic decompensation in univariate analysis. Multivariate Cox regression model analysis confirmed that DM (relative risk [RR] = 2.3, 95% CI = 1.4-3.7, p = 0.001) and tumor size > 3 cm (RR = 1.7, 95% CI = 1.1-2.7, p = 0.046) were independent prognostic predictors associated with the occurrence of hepatic decompensation; the respective 3- and 5-yr cumulative rates were 53% and 64% versus 27% and 50% for diabetic and nondiabetic patients, and 24% and 41% versus 38% and 60% for patients with small (< or =3 cm) versus large (>3 cm) tumors. CONCLUSION: HCC patients with DM or large tumor size are at a cumulative increased risk for postoperative hepatic decompensation.

Adult↗

PubMed1998

Preventable causative factors leading to hospital admission with decompensated heart failure.

OBJECTIVE: To determine the distribution and importance of various factors, especially the preventable ones, that contribute to cardiac decompensation and subsequent hospital admission for heart failure. METHODS: During a one year period patients were prospectively recruited and evaluated during their hospital stay by means of a structured personal interview by trained medical staff and through clinical examination and laboratory investigation. SETTING: The cardiological department at a teaching affiliated general community hospital in Berlin, Germany. PATIENTS: Consecutive sample of 179 patients admitted to hospital with acute decompensation of pre-existing heart failure. MAIN OUTCOME MEASURES: Proportional distribution of causative factors leading to hospital admission for heart failure; relative importance of preventable factors; details of patient compliance with diet and medication, and knowledge about medication. RESULTS: Mean (SD) age was 75.4 (9.9) years. Potential causative factors for decompensated heart failure were identified in 85.5% of patients. Lack of adherence to the medical regimen was the most commonly identified factor and was regarded as the cause of the cardiac decompensation in 41.9% of cases. Non-compliance with drugs was found in 23.5% of patients. Other factors related to hospital admission were coronary ischaemia (13.4%), cardiac arrhythmias (6.1%), uncontrolled hypertension (5.6%), and inadequate preadmission treatment (12.3%). In all, 54.2% of admissions could be regarded as preventable. CONCLUSIONS: Many hospital admissions for decompensation of chronic heart failure in patients at a district hospital in Berlin are preventable. Measures are necessary to improve this situation and evaluation of programmes that include patient education, patient follow up, and physician training is needed.

Aged↗

PubMed2004

Quantitative hepatic phosphorus-31 magnetic resonance spectroscopy in compensated and decompensated cirrhosis.

Few studies have examined the physiological/biochemical status of hepatocytes in patients with compensated and decompensated cirrhosis in situ. Phosphorus-31 magnetic resonance spectroscopy ((31)P MRS) is a noninvasive technique that permits direct assessments of tissue bioenergetics and phospholipid metabolism. Quantitative (31)P MRS was employed to document differences in the hepatic metabolite concentrations among patients with compensated and decompensated cirrhosis as well as healthy controls. All MRS examinations were performed on a 1.5-T General Electric Signa whole body scanner. The concentration of hepatic phosphorylated metabolites among patients with compensated cirrhosis (n = 7) was similar to that among healthy controls (n = 8). However, patients with decompensated cirrhosis (n = 6) had significantly lower levels of hepatic ATP compared with patients with compensated cirrhosis and healthy controls (P < 0.02 and P < 0.009, respectively) and a higher phosphomonoester/phosphodiester ratio than controls (P < 0.003). The results of this study indicate that metabolic disturbances in hepatic energy and phospholipid metabolism exist in patients with decompensated cirrhosis that are not present in patients with compensated cirrhosis or healthy controls. These findings provide new insights into the pathophysiology of hepatic decompensation.

Adenosine Triphosphate↗

PubMed2004

Endothelial cell activation in patients with decompensated heart failure.

BACKGROUND: Vascular endothelial functions, other than nitric oxide (NO)-mediated control of vasomotor tone, are poorly characterized in patients with chronic heart failure (CHF). Veins and arteries are exposed to the same circulating proinflammatory mediators in patients with CHF. The present study tested whether endothelial cell activation occurs in veins of patients with decompensated CHF and whether activation, if present, subsides with return to a clinically compensated state. METHODS AND RESULTS: Fifteen patients with decompensated CHF requiring transient inotropic support and 6 age-matched, healthy controls were studied. Endothelial cells and blood were collected from a forearm vein, and brachial artery flow-mediated dilation (FMD) was measured before and 24 hours after discontinuation of short-term inotropic therapy, when patients had returned to a steady compensated state. Nitrotyrosine immunoreactivity (an intracellular marker of oxidative stress), cyclooxygenase-2 (COX-2), and inducible NO synthase (iNOS) expression were significantly higher in venous endothelial cells of patients in clinical decompensation when compared with healthy subjects. Return to a compensated state resulted in a significant reduction in nitrotyrosine immunoreactivity, COX-2, and iNOS expression. Concomitantly, a significant increase in FMD and a decline in plasma total 8-isoprostane and bicycloprostaglandin E2 levels were observed. Venous endothelial NOS expression was unaffected by clinical decompensation. CONCLUSIONS: Clinical decompensation in CHF is associated with activation of the venous endothelium. Return to a compensated state after short-term inotropic therapy results in a significant reduction in endothelial nitrotyrosine formation, COX-2, and iNOS expression.

Adult↗

PubMed2003

Levosimendan: a review of its use in the management of acute decompensated heart failure.

UNLABELLED: Levosimendan (Simdax) is a calcium-sensitising drug that stabilises the troponin molecule in cardiac muscle, thus prolonging its effects on contractile proteins, with concomitant vasodilating properties. Intravenous levosimendan (12-24 microg/kg loading dose followed by 0.1-0.2 microg/kg/min for 24 hours, adjusted for response and tolerability) is approved for the short-term treatment of acute severe decompensated heart failure. Cardiac output increased by about 30% and pulmonary capillary wedge pressure and systemic vascular resistance decreased by about 17-29% in patients with decompensated heart failure receiving intravenous levosimendan. In large, well controlled trials in patients with decompensated heart failure, intravenous levosimendan was significantly more effective than placebo or dobutamine for overall haemodynamic response rate (primary endpoint). Significant benefits were also seen for mortality (versus placebo or dobutamine) and for the combined risk of worsening heart failure or death (versus dobutamine). Improvements in key symptoms (dyspnoea and fatigue) have not been consistently demonstrated. Hospitalisation costs were similar for levosimendan and dobutamine; the total incremental (hospitalisation plus drug) cost per life-year saved (extrapolated to 3 years) for levosimendan relative to dobutamine was estimated at Euro 3205 (year of costing 2000). Levosimendan is generally well tolerated, with an adverse event profile at recommended dosages similar to that in patients receiving placebo. Cardiac rate/rhythm disorders and headache were the most common events. At higher dosages, patients receiving levosimendan had higher rates of sinus tachycardia than those in placebo recipients. More patients receiving dobutamine than those receiving levosimendan experienced angina pectoris/chest pain/myocardial ischaemia or rate/rhythm disorders. CONCLUSION: Intravenous levosimendan is an effective calcium-sensitising drug with vasodilatory and inotropic effects, and superior efficacy/tolerability to those of intravenous dobutamine in patients with acute decompensated heart failure. It may be associated with reduced mortality compared with both placebo and dobutamine. Levosimendan is generally well tolerated and may have less potential for cardiac rate/rhythm disorders than dobutamine. While evidence from well designed trials confirming the improved mortality over dobutamine and investigating haemodynamic efficacy and mortality versus other positive inotropes is required, intravenous levosimendan appears to be a useful addition to the treatment options for acute decompensated heart failure in patients with low cardiac output.

Acute Disease↗

PubMed2001

Drug treatment of patients with decompensated heart failure.

Decompensated heart failure (HF) may be defined as sustained deterioration of at least one New York Heart Association functional class, usually with evidence of sodium retention. Episodes of decompensation are most commonly precipitated by sodium retention, often associated with medication noncompliance. Our therapeutic approach to hospitalized patients is based on the documented hemodynamic responses to vasodilator therapy, with redistribution of mitral regurgitant flow to forward cardiac output and decompression of the left atrium. Invasive hemodynamic monitoring is seldom required for the effective management of patients with HF and there are risks associated with pulmonary artery catheterization. The currently available parenteral vasoactive drugs for decompensated heart failure include: (i) vasodilators such as nesiritide, nitroprusside and nitroglycerin (glyceryl trinitrate); (ii) catecholamine inotropes, primarily dobutamine; and (iii) inodilators such as milrinone, a phosphodiesterase inhibitor. Vasodilators are most appropriate for those patients who are primarily volume-overloaded, but with adequate peripheral perfusion. In this class of agents, nesiritide (recombinant human B-type natriuretic peptide) offers advantages over currently available drugs. Nesiritide produces rapid and sustained decreases in right atrial and pulmonary capillary wedge pressures, with reduction in pulmonary and systemic vascular resistance and increases in cardiac index. The hemodynamic effects of nesiritide infusion were sustained over a duration of 1 week and the drug may be used without intensive monitoring in patients with decompensated HF. Treatment with dobutamine is indicated in patients in whom low cardiac output rather than elevated pulmonary pressure is the primary hemodynamic aberration. However, milrinone reduces left atrial congestion more effectively than dobutamine, and is well tolerated and effective when used in patients receiving beta-blockers. In-patient therapy for decompensated HF is a short term exercise for symptom relief and provides an opportunity to re-assess management in the continuum of care.

Cardiac Output, Low↗

PubMed1985

Furosemide absorption altered in decompensated congestive heart failure.

We assessed whether patients with decompensated congestive heart failure had altered absorption of oral furosemide. Pharmacokinetic and pharmacodynamic responses were studied in 11 patients receiving their usual oral dose of furosemide while decompensated, and after attaining normal weight. Seven patients also received 25 g of oral D-xylose to further assess intestinal absorption. A 57% decrease in lag time (p = 0.033), a 27% decrease in time to peak serum concentration (p = 0.041), and a 29% increase in the peak serum furosemide concentration (p = 0.008) were seen in compensated as compared to decompensated patients. No significant change was seen in absorption or elimination half-lives, area under the serum concentration versus time curves for furosemide, or in absorption of D-xylose. Although the pharmacodynamics of furosemide were reduced compared to normal subjects, there was little difference in the compensated and decompensated states. Our results show an alteration in furosemide absorption in decompensated congestive heart failure.

Adult↗

PubMed2005

Efficacy of lamivudine therapy for decompensated liver cirrhosis due to hepatitis B virus with or without hepatocellular carcinoma.

The prognosis for patients with decompensated hepatitis B virus (HBV) related liver cirrhosis (LC-B), especially for those with LC-B complicated with hepatocellular carcinoma (HCC), is poor. We investigated the effects of lamivudine in patients with decompensated LC-B, with and without HCC. Decompensated LC-B patients (n=55) with Child-Pugh classification scores (CPS) >7 points were enrolled. All were admitted to the hospitals of the authors between January 1997 and December 2004. Decompensated cases due to a severe exacerbation of hepatitis with CH-B and patients with HCC showing an extra hepatic metastasis or portal vein tumor thrombus were excluded. Some 19 cases (including 5 cases complicated with HCC at the start of therapy) were treated with lamivudine at 100 mg/day (L group), and 36 (including 7 cases with HCC at time of admittance) were treated without lamivudine (non-L group). The median of CPS points in the L group was higher than that of non-L group (11 points versus 9 points, p<0.02). Prothrombin time (%), albumin, ascites, CPS, and HBV-DNA quantity were each significantly improved after 6 months in the L group (p<0.05). A mutation in the YMDD motif was observed in 5 patients in the L group, however liver function did not deteriorate. Further, the survival rate was significantly higher in the L group (p<0.05). HCC was found in 3 L group and 4 non-L group patients during the study. In the L group, all patients complicated with HCC were treated repeatedly or until cured, whereas 91% of those in the non-L group could not be treated (p<0.01). Our results suggest that lamivudine is a useful and important therapy for patients with decompensated LC-B with and without HCC, as well as those who are restricted from having liver transplantation.

Adult↗

PubMed2006

Lamivudine treatment of decompensated hepatitis B virus-related cirrhosis.

BACKGROUND: Patients with decompensated hepatitis B virus (HBV)-related cirrhosis tend to have low or undetectable HBV replication. However, some patients continue to have high levels of HBV replication and effective suppression of HBV replication with antiviral agents may potentially decrease hepatic necroinflammation and improve or stabilize liver function. This review was to understand the efficacy and safety of lamivudine in the treatment of decompensated HBV cirrhosis. DATA SOURCES: An English-language literature search (MEDLINE January 1988-July 2005) was performed, and a total of 52 articles/abstracts relevant to the issue were selected. After review of the selected papers, the meaningful results and conclusions were extracted using scientific criteria. The papers reviewed pertained mainly to the efficacy and safety profiles of lamivudine treatment for decompensated HBV cirrhosis. RESULTS: The ultimate treatment of decompensated HBV cirrhosis is liver transplantation, but lamivudine treatment may lead to rapid suppression of viral replication and improvement of biochemical and clinical parameters, reduced morbidity and hospitalization for complications of liver disease, increased pre-transplant survival as well as reduced need for transplantation. However, viral resistance can develop after prolonged treatment with lamivudine, and breakthrough hepatitis may be fatal in few patients. Adefovir is effective for lamivudine-resistant HBV mutants. CONCLUSIONS: Antiviral therapy with lamivudine for decompensated HBV cirrhosis can be effective. However, some patients may experience a hepatitis flare with the emergence of YMDD mutants resulting in progressive worsening of liver disease, and should be referred for "rescue" therapy with other nucleoside/nucleotide analogues such as adefovir dipivoxil.

Hepatitis B↗

PubMed1986

A procedure of vestibular decompensation for clinical diagnosis. I. Animal experiments.

Vestibular lesions are often so effectively compensated that their diagnosis may be difficult. Certain chemicals can decompensate the central vestibular system and thus uncover symptoms present before compensation. This study attempts to devise a procedure which can utilize such decompensation for the benefit of clinical diagnosis. Unilateral labyrinthectomies were performed in rats. Pathological movements and body positions due to the vestibular loss were compensated within about one week. Systemic application of cholinomimetic drugs (physostigmine and nicotine) led to consistent decompensation which lasted, however, too long and was accompanied by too severe side effects to be considered for clinical diagnostic purposes. Local application of these drugs into the middle ear of the healthy side were without effect. Brief inhalation of nitrous oxide (up to 79 vol.%) caused decompensation during the first four postoperative weeks but not consistently at longer survival times. Inhalation of halothane in N2O and O2 for 90 seconds caused a reliable decompensation at all times during the six month postoperative observation period. It is concluded that a brief halothane-N2O anesthesia may prove to be useful in a diagnostic search for compensated vestibular deficits.

Adaptation, Physiological↗