SEARCH · PubMed Health

Results for “decompensation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed1984

Corneal grafts for endothelial decompensation: the influence of intraocular lenses on corneal graft survival.

Re-examination of the fate of 136 corneal grafts for bullous keratopathy (secondary endothelial decompensation) revealed a decreased, but not significant, graft survival of those grafts compared to the total of 572 grafts in patients with a diagnosis other than bullous keratopathy, as well as a decreased graft survival when compared to the survival of the grafts for Fuchs dystrophy (primary endothelial decompensation). A statistically significant decreased graft survival (P = 0.015) was observed when corneal grafts performed in pseudophakic eyes with secondary endothelial decompensation were compared to those performed in aphakic eyes with secondary endothelial decompensation. An immunological explanation for this difference was not detected. The influence of an intraocular lens on corneal corneal graft survival was analyzed. Indications for removing or retaining the intraocular lens at the time of graft surgery are reported.

Aged↗

PubMed1984

Splanchnic and renal elimination and release of catecholamines in cirrhosis. Evidence of enhanced sympathetic nervous activity in patients with decompensated cirrhosis.

Plasma noradrenaline (NA) and adrenaline (A) concentrations were determined in different vascular areas in 32 patients with cirrhosis and in nine controls during a right sided heart, liver, and renal vein catheterisation. The patients were divided into four groups: (I) Compensated (without ascites); (II) Recompensated on diuretic treatment because of former ascites; (III) Decompensated (with ascites) without treatment and (IV) Decompensated on diuretic treatment. Median arterial noradrenaline concentrations were 1.48, 1.07, 2.66, 4.14 and 2.50 nmol/l in controls, group I, II, III, and IV, respectively, the three last mentioned values being significantly raised (p less than 0.01). Median arterial adrenaline concentrations were not significantly increased. In patients arterial-hepatic venous extraction ratios of noradrenaline and adrenaline were on the average 25% (p less than 0.01) and 20% (p less than 0.02) less than those of the controls, indicating a slightly reduced splanchnic elimination of catecholamines in cirrhoses. In controls and group I significant renal venous-arterial noradrenaline differences were absent (0.00 and 0.03 nmol/l) while renal venous-arterial noradrenaline differences were significantly increased in groups II, III and IV (0.47, 0.53 and 0.68 nmol/l, p less than 0.01), indicating a significant net release of noradrenaline from the kidneys in recompensated and decompensated patients. Renal extraction of adrenaline was normal. In conclusion, increased arterial noradrenaline in decompensated and recompensated cirrhosis is only to a limited extent owing to reduced net splanchnic elimination. More likely the increase is caused by release of noradrenaline from the kidneys and possibly other organs indicating enhanced sympathetic nervous tone in these conditions.

Adult↗

PubMed1998

Troponin I phosphorylation and myofilament calcium sensitivity during decompensated cardiac hypertrophy.

We have measured myocyte cell shortening, troponin-I (Tn-I) phosphorylation, Ca2+ dependence of actomyosin adenosinetriphosphatase (ATPase) activity, adenosine 3',5'-cyclic monophosphate (cAMP) levels, and myofibrillar isoform expression in the spontaneously hypertensive rat (SHR) during decompensated cardiac hypertrophy (76 wk old) and in age-matched Wistar-Kyoto rat (WKY) controls. The decreased inotropic response to beta-adrenergic stimulation previously observed in myocytes from 26-wk-old SHR was further reduced at 76 wk of age. In response to beta-adrenergic stimulation, Tn-I phosphorylation was greater in the 76-wk-old SHR than in the WKY, although cAMP-dependent protein kinase A (PKA)-dependent Tn-I phosphorylation in the SHR did not increase with progression from compensated (26 wk) to decompensated (76 wk) hypertrophy. We also observed a dissociation between the increased PKA-dependent Tn-I phosphorylation and decreased cAMP levels in the 76-wk-old SHR versus WKY during beta-adrenergic stimulation. Baseline Tn-I phosphorylation was significantly reduced in 76-wk-old SHR versus WKY and was associated with decreased basal cAMP levels and increased Ca2+ sensitivity of actomyosin ATPase activity. The change in myofilament Ca2+ sensitivity during beta-adrenergic stimulation in the 76-wk-old SHR (0.65 pCa units) was over twofold greater than in the 76-wk-old WKY (0.30 pCa units). We also determined whether embryonic troponin T isoforms were reexpressed in decompensated hypertrophy and observed significant reexpression of the embryonic cardiac troponin T isoforms in the 76-wk-old SHR. The significant decrease in Ca2+ sensitivity with beta-adrenergic stimulation in 76-wk-old SHR may contribute to the severely impaired inotropic response during decompensated hypertrophy in the SHR.

Actin Cytoskeleton↗

PubMed2026

Dysregulation of the serum and IgG N-glycome in decompensated cirrhosis and its association with Model for End-Stage Liver Disease-Sodium (MELD-Na).

BACKGROUND AND AIMS: N-glycans modulate glycoprotein structure and function and are altered during chronic inflammation. We sought to define the extent of serum and IgG N-glycan disruption in patients with decompensated liver cirrhosis from alcohol-related liver disease (ALD), primary sclerosing cholangitis (PSC), and ALD-related hepatocellular carcinoma (HCC). Finally, we aimed to examine whether serum and IgG glycosylation is associated with changes in Model for End-stage Liver Disease-Sodium (MELD-Na) scores, a clinical marker used to prioritise liver transplantation. METHODS: Serum samples were obtained from patients with ALD (n = 17), PSC (n = 7), ALD-related HCC (n = 4), and healthy controls (n = 10). N-glycans were released, fluorescently labelled, and profiled by hydrophilic interaction ultra performance liquid chromatography (HILIC-UPLC). Chromatograms were integrated into 46 and 23 glycan peaks for serum and IgG respectively. These peaks and their associated glycosylation traits were statistically compared with healthy controls using age- and sex-adjusted linear regression models. RESULTS: In serum, decompensated cirrhosis shows statistically significant shifts toward less complex, agalactosylated and asialylated biantennary glycans, accompanied by significant losses of highly branched, galactosylated and sialylated structures. IgG mirrored this pattern, which is characteristic of a pro-inflammatory signature, with increased agalactosylation and bisected glycan levels, along with reduced levels of digalactosylated and sialylated species. N-glycan profiles showed significant associations with MELD-Na scores, indicating that inflammatory processes in decompensated liver cirrhosis continue to reshape serum glycoproteins. CONCLUSION: Decompensated liver cirrhosis shows profound remodelling of serum and IgG N-glycans. These data establish a reference framework for terminal glycomic disruption in liver disease and highlight the potential value of incorporating glycosylation analysis into broader assessments of liver disease progression.

Humans↗

PubMed2004

History of depression as a predictor of adverse outcomes in patients hospitalized for decompensated heart failure.

STUDY OBJECTIVE: To evaluate the prevalence and impact of depression on the risk of in-hospital death or need for cardiopulmonary resuscitation (CPR) in patients admitted for decompensated heart failure. DESIGN: Observational single-center study. SETTING: Coronary care unit and cardiac intermediate-care unit of a tertiary referral center. PATIENTS: One hundred seventy-one patients hospitalized with decompensated heart failure who were included in the Acute Decompensated Heart Failure Registry (ADHERE). MEASUREMENTS AND MAIN RESULTS: The 34 patients with a history of depression had a higher likelihood of experiencing the combined end point of in-hospital death or CPR compared with the 137 patients without a history of depression (17.7% vs 6.6%, p<0.05). A history of depression (odds ratio 3.3, 95% confidence interval 1.01-10.6, p<0.05) was still predictive of in-hospital death or CPR in a multivariate analysis after adjusting for predictors of the combined end point. CONCLUSIONS: This study suggests that a history of depression is associated with an increased risk of in-hospital mortality or CPR in patients hospitalized for decompensated heart failure. Our results require confirmation in larger trials.

Antidepressive Agents↗

PubMed2001

Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with decompensated liver cirrhosis.

Hepatic encephalopathy is one of the major complications in decompensated liver cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in liver cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or decompensated liver cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with decompensated liver cirrhosis were found to be significantly lower than the levels in controls and patients with compensated liver cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.

Ammonia↗

PubMed2003

Nesiritide: a review of its use in acute decompensated heart failure.

UNLABELLED: Nesiritide (Natrecor) is a recombinant form of human B-type (brain) natriuretic peptide that has beneficial vasodilatory, natriuretic, diuretic and neurohormonal effects. The drug is administered intravenously for the management of patients with decompensated congestive heart failure (CHF). In the Vasodilation in the Management of Acute Congestive Heart Failure (VMAC) study, patients hospitalised with acute decompensated CHF who received nesiritide had significantly greater mean reductions from baseline in pulmonary capillary wedge pressure 3 hours after starting treatment than nitroglycerin or placebo recipients (-5.8 vs -3.8 and -2 mm Hg, respectively); all patients also received standard therapy (e.g. intravenous diuretics). Improvements in other haemodynamic parameters were also seen in nesiritide recipients. In addition, significantly more nesiritide than placebo recipients reported an improvement in dyspnoea after 3 hours' treatment in VMAC, whereas there was no significant difference between nitroglycerin and placebo recipients. Improvements in global clinical status, dyspnoea and fatigue were also seen with nesiritide in another active-comparator study and in a placebo-controlled study. In VMAC, there was no significant difference between nesiritide and nitroglycerin recipients in 6-month mortality. In the other active-comparator trial, 6-month mortality was significantly lower in recipients of nesiritide 0.015 micro g/kg/min than in dobutamine recipients (although mortality was not a prespecified endpoint and this result should be interpreted with caution). In this same study, the 21-day all-cause hospital readmission rate was significantly lower with nesiritide 0.015 micro g/kg/min than with dobutamine and the duration of active drug treatment was significantly shorter with nesiritide than with dobutamine. Nesiritide is generally well tolerated. In VMAC, significantly more adverse events occurred with nitroglycerin than with nesiritide. The most common adverse events reported during the first 24 hours of therapy in nesiritide and nitroglycerin recipients included general pain, abdominal pain, catheter-related pain, headache, nausea, asymptomatic and symptomatic hypotension, nonsustained ventricular tachycardia and angina pectoris. Most episodes of symptomatic hypotension resolved spontaneously or after an intravenous volume challenge of </=250 ml. In addition, nesiritide does not appear to be proarrhythmic. CONCLUSION: Short-term intravenous infusion of nesiritide is associated with haemodynamic and symptomatic improvements in patients with acutely decompensated CHF. Nesiritide may offer tolerability and practical advantages over currently used vasodilators, inodilators and inotropes in this condition; in particular, nesiritide does not appear to have proarrhythmic effects. Nesiritide also appears to be effective and well tolerated in patients receiving concomitant beta-blocker therapy and in patients with renal insufficiency. Thus, nesiritide is a suitable first-line option for the treatment of patients with acutely decompensated CHF and is a welcome addition in an area where intravenous agents are few.

Acute Disease↗

PubMed1991

Increased levels of fibrinolysis reaction products (D-dimer) in patients with decompensated alcoholic liver cirrhosis.

We studied the activation of coagulation and fibrinolysis in the blood of patients with compensated (n = 25) and decompensated (n = 25) liver cirrhosis. We observed increased blood concentrations of thrombin-antithrombin III (TAT) complexes (p less than 0.001) and of D-dimer (p less than 0.001) in both groups of patients compared with healthy volunteers (n = 25). The blood levels of tissue-type plasminogen activator (t-PA) activity (p less than 0.001) and the concentrations of t-PA antigen (p less than 0.001) were also significantly raised in both groups of patients compared with controls, whereas plasminogen activator inhibitor did not deviate. There were no significant differences in the determined variables between the two groups of patients except that the concentrations of D-dimer were significantly higher (p less than 0.001) in patients with decompensated liver cirrhosis. The ratio between D-dimer and TAT did not deviate between patients with compensated liver cirrhosis and healthy volunteers but was significantly increased in patients with decompensated liver cirrhosis. These observations indicate that efflux from the extravascular space (for example, ascitic fluid) contributes to the high concentrations of fibrin degradation products (D-dimer) in patients with decompensated liver cirrhosis. In addition, we conclude that patients with liver cirrhosis have an enhanced activation of both coagulation and fibrinolysis but that the balance between these two systems is not significantly displaced compared with healthy volunteers.

Aged↗

PubMed2005

MELD vs Child-Pugh and creatinine-modified Child-Pugh score for predicting survival in patients with decompensated cirrhosis.

AIM: Model of End-stage Liver Disease (MELD) score has recently gained wide acceptance over the old Child-Pugh score in predicting survival in patients with decompensated cirrhosis, although it is more sophisticated. We compared the predictive values of MELD, Child-Pugh and creatinine-modified Child-Pugh scores in decompensated cirrhosis. METHODS: A cohort of 102 patients with decompensated cirrhosis followed-up for a median of 6 mo was studied. Two types of modified Child-Pugh scores estimated by adding 0-4 points to the original score using creatinine levels as a sixth categorical variable were evaluated. RESULTS: The areas under the receiver operating characteristic curves did not differ significantly among the four scores, but none had excellent diagnostic accuracy (areas: 0.71-0.79). Child-Pugh score appeared to be the worst, while the accuracy of MELD was almost identical with that of modified Child-Pugh in predicting short-term and slightly better in predicting medium-term survival. In Cox regression analysis, all four scores were significantly associated with survival, while MELD and creatinine-modified Child-Pugh scores had better predictive values (c-statistics: 0.73 and 0.69-0.70) than Child-Pugh score (c-statistics: 0.65). Adjustment for gamma-glutamate transpeptidase levels increased the predictive values of all systems (c-statistics: 0.77-0.81). Analysis of the expected and observed survival curves in patients subgroups according to their prognosis showed that all models fit the data reasonably well with MELD probably discriminating better the subgroups with worse prognosis. CONCLUSION: MELD compared to the old Child-Pugh and particularly to creatinine-modified Child-Pugh scores does not appear to offer a clear advantage in predicting survival in patients with decompensated cirrhosis in daily clinical practice.

Adult↗

PubMed1975

The decompensated back.

There is no single circumstance or combination of circumstances which precipitate all clinical instances of back discomfort. This simple statement should be so obvious that one must question the finality and accuracy of the diagnostic effort in those reports which relate to large series of patients treated by one method. There is no thought of impugning the basic honesty of the reporting physician in this statement, but rather of raising the fair question of whether the "slipped disc" (or whatever the etiological diagnosis) is all that happened to produce the symptoms, and whether its removal (or whatever) is all that occurred in accomplishing clinical cure improvement. If there is doubt that the answer to both questions is in the affirmative, then serious consideration must be given to those other factors, if the medical profession is ever to be a science instead of a trade. The back structures are different from comparable structures elsewhere in the body, principally in their neurological organization and controlmthere is the specific, discrete, segmental arrangement of both sensory and motor functions of muscular and nonmuscular structures via the posterior primary rami of the spinal nerves. Coupled with this is a different mechanism of segmental innervation of the vascular and nonmuscular structures which line the vertebral canal, via the sinu-vertebral nerves. Both are modulated by higher level influences. The sinu-vertebral nerves, through the sympathetic chain, may provide an additional avenue of response which may avoid or alter the influence of higher levels. The Melzack-Wall hypothesis would seem to provide an acceptable explanation for the need to modulate nociceptive afferent stimuli before they evoke pain perception and response. Since this modulation mechanism decompensates under numerous conditions, pain perception and responses do occur. Among those responses are the alterations in normal function of the low back structures, perhaps the disastrously effective one of which is decompensation of the muscular strength necessary to accomplish the demands of daily use. This problem is not so simply solved by a handout sheet of exercises. The primary consideration is to modify or relieve pain by a careful evaluation of its source and the employment in combination of those therapeutic efforts which a logical treatment plan indicates. If these be accomplished, the final and most important consideration, then, is the improvement of neuromuscular function to the level compatible with normal activities by a carefully guided activity program. There is no method for instant reversal of the status of the decompensated heart--nor the decompensated back.

Adult↗

PubMed2002

[Therapeutic efficacy of lamivudine in patients with hepatitis B virus-related decompensated cirrhosis in Korea].

BACKGROUND/AIMS: Although several clinical trials have suggested that lamivudine treatment can be very effective in patients with decompensated HBV-associated cirrhosis, its role and clinical efficacy are still uncertain because of the study designs. The aim of this study is to evaluate the efficacy of lamivudine in consecutively enrolled patients with decompensated cirrhosis. METHODS: Twenty-four patients with decompensated HBV-associated cirrhosis (Child-Pugh score > or =8) were enrolled consecutively and treated with lamivudine 100 mg or 150 mg daily for 2-51 months (median: 16 months). They were all positive for HBV DNA and 21 were positive for serum HBeAg. Eight were Child-Pugh class B and 16 were class C. Clinical improvement was defined as a decrease of Child-Pugh score of at least 2 points. RESULTS: At 6(th) month after lamivudine, all the patients cleared serum HBV DNA. The cumulative rates for HBeAg loss were 28.6% at 6(th) and 46.6% at 12(th) month. The cumulative viral breakthrough rates at 12(th) and 24(th) month were 20.0% and 37.5%. Fourteen patients (60.8%) showed clinical improvement, while 8 (34.8%) showed no change and 1 got worse, at 6(th) month after lamivudine. Most clinical improvement developed within the initial 6 months. The cumulative mortality rates were 20.8% at 1 year and 37.5% at 2 year. CONCLUSIONS: These data suggest that lamivudine can result in clinical improvement in about 60% of patients with HBV-related decompensated cirrhosis. Because most improvement occurs within 6 months after starting lamivudine, liver transplantation should be actively considered in cases which do not show clinical improvement despite 6-month lamivudine treatment.

Adult↗

PubMed2002

[Efficacy and safety of long-term lamivudine therapy in the patients with decompensated liver cirrhosis secondary to hepatitis B].

BACKGROUND/AIMS: Lamivudine use in patients with decompensated cirrhosis B has been reported to improve the hepatic function and often delay the need for liver transplantation. In the present study, we evaluated the efficacy and safety of long-term lamivudine therapy in patients with decompensated cirrhosis by comparative study using a matched, untreated cohort. METHODS: 41 patients with decompensated cirrhosis B were included for this study (31 male and 10 female; mean age, 50 years; mean observation period, 18 months). They were divided into two groups: a lamivudine treatment group and an untreated control group. 21 patients in the treatment group were treated with lamivudine 75 or 150 mg daily for at least 12 months. Biochemical and serologic markers were evaluated at two to three-month intervals for all patients. Clinical improvement was defined by a decrease in the Child-Pugh score of at least 2 points. RESULTS: During the observation period, 62% (13/21) was responders, 33% (7/21) was breakthrough, and 5% (1/21) was non-responder in the treated group. The mean Child-Pugh score was significantly improved from 8.6 to 6.0 in the treatment group, but aggravated from 8.7 to 10.0 in the control group during the follow-up. The HBeAg seroconversion rate was 31% in the treatment group (5/16) and none in the control group (0/14). Clinical improvement was observed in fifteen of 21 in the treatment group (71%) and only one of 20 in the control group (5%). According to the treatment responses, clinical improvement was observed in ten of 13 responders (77%), four of 7 breakthrough (57%), and one non-responder. CONCLUSIONS: The long-term administration of lamivudine for patients with decompensated cirrhosis B is effective and safe, although breakthrough and non-response occurred in some patients.

Adult↗

PubMedDate not supplied

Hepatitis E virus is responsible for decompensation of chronic liver disease in an endemic region.

BACKGROUND: Hepatitis A virus infection in patients with previously stable chronic liver disease is associated with liver decompensation. Whether infection with hepatitis E virus (HEV) also does so is not known. METHODS: We studied 32 patients with decompensated liver disease and definite evidence of underlying cirrhosis for evidence of recent HEV infection. RESULTS: Of 32 patients, 14 (44%) had detectable IgM anti-HEV in their serum. In comparison, only 3 of 48 (6%) patients with stable cirrhosis and no recent decompensation had such antibodies (p<0.0001). Of the 14 patients with evidence of recent HEV infection, 11 had history of prodrome. The etiology of cirrhosis in these patients was: hepatitis B 6, hepatitis C 2, both hepatitis B and C 2, Wilson's disease 1, autoimmune 1 and cryptogenic 2. Two of these 14 patients died. Twelve patients survived, as compared to 9 of 18 patients without evidence of recent HEV infection (p<0.01). CONCLUSION: HEV infection is a frequent cause of decompensation in patients with liver cirrhosis in HEV-endemic regions.

Adolescent↗

PubMed2004

Pessimistic mood in decompensated narcissistic patient.

We report the negative emotional state as pessimistic mood of a case with narcissistic personality disorder during the period of narcissistic decompensation. In addition, we identified the clinical differences between pessimistic mood and depressive disorder. An 28-year-old unmarried woman experienced herself, her life and the external object as futile and disappointing after repeated failure to satisfy her grandiose fantasies about the search for ideal love. The patient then gave up her formerly gratifying activities, and fell into a prolonged state of negative emotions and passivity dominated by pessimistic mood characterized by an overwhelming sense of futility. The patient did not respond to medical treatment with antidepressants firstly. However after a 2-year course of intensive psychotherapy, the patient was able to restore her zest to find a new boyfriend with a more rational and realistic attitude. Clinically, decompensated narcissistic patients do not exhibit the typical attitude of worthlessness or guilty feelings, and are devoid of certain specific depressive emotions (e.g., sadness, sorrow, etc.). In contrast, decompensated narcissistic patients with pessimistic mood exhibit a dominant sense of futility and other negative emotions presented as outrage and disappointment. The purpose of this case report was to emphasize the importance to recognize clinical features of pessimistic mood for the differential diagnosis and management of the decompensated narcissistic patient.

Adult↗

PubMedDate not supplied

Prolonged activation of tumor necrosis factor (TNF)-alpha and its soluble receptors in chronic heart failure patients both in the compensated and decompensated state. Interplay between their levels and metalloproteinase-3.

INTRODUCTION: Recent clinical and experimental studies indicate that upregulation of the TNF system can contribute to the progression of cardiac remodeling and heart failure decompensation, by promoting alterations in cardiomyocyte biology and extracellular matrix metabolism. Extracellular matrix turnover is regulated by the matrix metalloproteinases (MMPs), which are endogenous enzymes responsible for extracellular collagen degradation. The present study investigates the fluctuation of serum levels of TNF-alpha, soluble TNF receptor-1 (sTNFR1) and -2 (sTNFR2), in patients with chronic heart failure both during acute decompensation and the stable state of the syndrome. The second goal of this study was to determine if a relationship exists between serum MMPs profiles (MMP-1, MMP-2, MMP-3) and circulating TNF-alpha or its soluble receptors. METHODS: Our patient group consisted of 52 patients with chronic heart failure (NYHA III-IV; mean age: 65 +/- 4 years; hypertensive cardiomyopathy: 20, ischemic cardiomyopathy: 17, dilated cardiomyopathy: 10, valvular disease: 5), who were hospitalized for acute decompensation of the syndrome. Our control group consisted of 30 healthy subjects (mean age: 57 +/- 6 years). Serum levels of TNF-alpha, sTNFR1, sTNFR2 and MMP-1,-2,-3 were measured in heart failure patients by ELISA at admission and after one month as follow-up. Values are expressed as medians and interquartile ranges. RESULTS: In our patient group, we observed a statistically significant increase in the levels of sTNFR1 and sTNFR2 at admission (sTNFR1: 5.15 ng\mL, 4.49-8.90 ng\mL, P < 0.001, sTNFR2: 13.40 ng\mL, 6.10-21.50 ng\mL, P < 0.001), and at one-month follow-up (sTNFR1: 5.30 ng\mL, 4.61-6.90 ng\mL, P < 0.001, sTNFR2: 21.80 ng\mL, 11.50-25.20 ng\mL, P < 0.001), compared to the control group (sTNFR1: 3.83 ng\mL, 3.70-3.95 ng\mL, sTNFR2: 4.00 ng\mL, 3.40-5.40 ng\mL). There was a statistically significant difference in the levels of sTNFR2 between admission and follow-up (P < 0.05). Significant correlations between serum MMP-3 and sTNFR2 levels both at admission and follow up (r -/+ 0.460, P -/+ 0.005 and r -/+ 0.338, P -/+ 0.044, respectively) were also found. CONCLUSIONS: Soluble TNF receptors are elevated in heart failure patients both in acute decompensation and stable phase. We have detected higher levels of soluble TNFR2 during the compensated phase of heart failure, suggesting that TNFR2 receptors appear to stabilize the cytokine and thereby prolong its half-life and biological functions. Finally, TNF system-mediated cardiac remodeling may exist through the activation of MMP-3 signaling pathways.

Aged↗

PubMed2004

Optimizing treatment of chronic decompensated heart failure in the outpatient setting.

Chronic decompensated heart failure (HF) is costly to manage because of frequent episodes of acute decompensation that result in hospitalization. Patients with chronic decompensated HF may have inadequate hemodynamic responses or limited tolerance of oral HF medications and therefore may require parenteral administration of vasoactive agents. Intermittent infusions of inotropic agents are no longer recommended, but preliminary data suggest that intermittent nesiritide may be a safe and effective adjunct to oral drug therapy for select patients at risk for further episodes of decompensation. In other patients, nonpharmacologic approaches used in combination with drug therapy may help improve functional status and reduce mortality.

Ambulatory Care↗

PubMed2006

Danshao huaxian capsule in treatment of decompensated cirrhosis resulting from chronic hepatitis B.

BACKGROUND: The prognosis of decompensated cirrhosis resulting from chronic hepatitis B is poor, and the benefits of treatment with interferon are outweight serious side-effects and the risk of fatal exacerbation of disease. Danshao huaxian capsule rapidly reduces hepatitis B virus (HBV)-DNA in serum to undetectable levels. METHODS: A total of 35 patients with chronic hepatitis B and decompensated cirrhosis were treated with danshao huaxian 1.2 g. p.o. tid daily. Before the treatment, HBV-DNA in serum was positive in all patients. Ten patients had Child-Pugh class B and 25, class C hepatitis B. Seven patients underwent liver transplantation within 6 months of initial treatment. Of the 10 patients of class B, 5 died within 6 months, and the other 5 did not complete the treatment for some reasons; the 25 patients of class C were treated for at least 6 months (mean=19 months). RESULTS: In most of the 25 patients, liver function was improved slowly but markedly after 9 months of treatment, showing a decreased level of serum bilirubin from 67+/-13 to 30+/-4 micromol/L (P<0.05, baseline vs. 6 months), an increased level of serum albumin from 27+/-1 to 34+/-1 g/L (P<0.05) and a decreased level of Child-Pugh score from 10.3+/-0.4 to 7.5+/-0.5 (P<0.05). Three patients developed resistance to danshao huaxian because of a mutation in the YMDD motif, but liver function was not deteriorated. Inhibition of viral replication with danshao huaxian resulted in a significant improvement of liver function in patients with decompensated HBV cirrhosis, but the long-term results remain uncertain. CONCLUSION: Danshao huaxian capsule is effective in inhibiting viral DNA replication in patients with decompensated cirrhosis and making clinical improvement.

Capsules↗

PubMedDate not supplied

Antiviral therapy of decompensated cirrhosis due to hepatitis C viral infection.

BACKGROUND: For decompensated HCV cirrhosis, liver transplantation is the only available treatment. Only a few studies in world literature have used antiviral therapy in this situation. METHODS: During a 4-year period, we gave closely monitored antiviral therapy to all consecutive patients of HCV-related cirrhosis with episodes of decompensation. Patients who were excluded from the standard Interferon trials were treated. Patients were started on low dose Interferon alpha-2b (1 MIU tiw) and Ribavirin (800 mg/day) combination therapy or low-dose Interferon alpha- 2b (1 MIJ tiw) monotherapy (in the presence of renal failure) for 6 months to 1 year. Dose of Interferon was escalated gradually to a maximum dose of 3 MIU tiw according to clinical follow-up. RESULTS: A total of 18 patients (mean age = 51.6 +/- 9.8 years; male: female ratio= 10: 8) were treated. At baseline, mean Child-Pugh score was 9.4 +/- 0.8 (range = 7-12). Interferon monotherapy was given to 4 (22.2%) and combination therapy to 14 (77.8%) patients after clinical recovery from an episode of decompensation. Though 16 (88.9%) patients noticed some adverse events, 15 (83.3%) patients completed the treatment schedule. Premature discontinuation was warranted in 3 (16.7%) patients. Out of the 15 patients who completed the treatment schedule, mean maximum tolerated dose of Interferon was 1.73 +/- 0.6 MIU tiw, 10 patients had genotype II or III and 2 patients had genotype I. Of these, end-of-treatment virological response was seen in 11 (73.3 %) and sustained virological response (at 6 months) in 7 (46.6 %) patients. All these patients were followed up for a mean duration of 1.3 +/- 0.6 years (6 month to 3.5 years). During follow up, 7 non-responders had further episodes of decompensation, of whom 4 died. CONCLUSION: Although there is high intolerance to the treatment, closely-monitored low dose escalating Interferon and/ or Ribavirin therapy achieves good results.

Adult↗