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PubMed1994

Involvement of liver in the decompensation of hemorrhagic shock.

In a hemorrhagic shock model without adequate volume resuscitation we investigated the question whether a biochemical stabilization of liver function by applying 2-mercaptopropionyl-glycine (2MPG) may influence the shock dynamics especially the transition from compensated to decompensated shock and the development of multiple organ failure (MOF). The application of a bolus of 10 mg/kg 2MPG just after hemorrhage had significantly beneficial effects on shock dynamics. All measured blood parameters demonstrate a less severe liver dysfunction. We found a decisive recovery of systemic pH, prolonged high levels of blood glucose, a better ammonia detoxification, arterial ketone ratios (acetoacetate/beta-OH-butyrat) above about 0.25, and a significantly increased survival time from 200 +/- 10 min to more than 240 min after hemorrhage. Decompensation of the 2MPG group started about 60 min after decompensation of the shock group. The transition to decompensation was combined in the shock group as well as in the 2MPG group with a severe liver dysfunction indicated by an arterial ketone ratio below .25. Decreasing levels of blood thiobarbituric reactive material in compensated shock of both groups demonstrate that production of free radicals did not primarily cause decompensation, but increasing levels of thiobarbituric reactive material during decompensation seems to be one of the factors mediating MOF. Our data support the hypothesis of the liver being a barrier against decompensation of shock and MOF.

Acetoacetates↗

PubMed2007

Spectrum of liver histology in presumed decompensated alcoholic liver disease.

BACKGROUND: In presumed decompensated alcoholic liver disease (ALD; liver decompensation, heavy alcohol intake, and negative results of noninvasive screening for other causes), liver biopsy is often performed to assess severity of liver injury and to rule out other liver diseases. AIM: The aim of the study is to describe the spectrum of liver histology in such patients. METHODS: We reviewed all patients with presumed decompensated ALD seen between 1998 and 2004, in whom liver tissue was available for histology (N = 110). RESULTS: A total of 104 of the 110 patients had at least one of the histological features suggestive of ALD: fat, Mallory's hyalin, neutrophilic infiltrate, and hepatocyte ballooning. These features were more prevalent in tissue obtained within a month after presentation with decompensation than in that obtained before decompensation or more than 1 month after. These features were also associated with more severe liver dysfunction. Histology revealed a major additional diagnosis (Budd-Chiari syndrome) in only one case. In 41 patients biopsied within a month of first presentation with decompensation, Child score and Maddrey discriminant function (DF), but none of the histological features, were predictive of survival by Cox multivariate analysis. Of the 26 of these 41 patients with a Maddrey DF >32, 22 (85%) had alcoholic hepatitis. CONCLUSIONS: In patients with presumed decompensated ALD, other liver diseases are uncommon. Routine liver biopsy is of limited added value but biopsy should be considered in those in whom the noninvasive workup, or failure to recover despite abstinence, raises the possibility of other liver diseases.

Adult↗

PubMed2002

Pharmacologic therapies for acutely decompensated heart failure.

The management of acutely decompensated heart failure in the emergency medical setting poses a major clinical challenge. Acutely decompensated heart failure is characterized by hemodynamic abnormalities and neuroendocrine activation that contribute to heart failure symptoms, end-organ dysfunction, arrhythmias, and progressive cardiac failure. The therapeutic goals in patients presenting with acutely decompensated heart failure are to stabilize the patient, reverse acute hemodynamic abnormalities, rapidly reverse dyspnea and/or hypoxemia caused by pulmonary edema, and initiate treatments that will decrease disease progression and improve survival. Pharmacologic therapies to impact the hemodynamic abnormalities and symptoms in patients with acutely decompensated heart failure include diuretics, inotropic agents, vasodilators, and natriuretic peptides. In patients with acutely decompensated heart failure, it has recently been demonstrated that elevation in left ventricular filling pressure is the hemodynamic abnormality that most directly impacts heart failure symptoms and is highly predictive of increased risk of fatal decompensation and sudden death. Measures of systemic perfusion, arterial pressure, and vascular resistance have not been predictive of symptoms or clinical outcomes. An ideal agent for acute decompensated heart failure would be one that rapidly reduces pulmonary wedge pressure, results in balanced arterial and venous dilation, promotes natriuresis, lacks direct positive inotropic effects, and does not result in reflex neuroendocrine activation.

Cardiotonic Agents↗

PubMed2000

Hepatic decompensation in patients with cirrhosis during infection with influenza A.

BACKGROUND: Patients with chronic liver disease can develop hepatic decompensation during systemic infections. Although gram-negative and gram-positive bacteria are well recognized as causes of decompensation, the effect of influenza virus infection on patients with chronic liver disease is poorly documented. METHODS: Retrospective analysis of patients with positive viral cultures who were seen at a liver transplantation clinic in a tertiary care referral center during the 1997-1998 influenza A (H3N2) epidemic in San Diego, Calif. RESULTS: Three patients with end-stage liver disease (1 with Wilson disease and 2 with alcoholic liver disease) developed hepatic decompensation and required hospitalization during infection with influenza A. Two patients had biochemical and clinical evidence of hepatic decompensation, including ascites, hepatic encephalopathy, and peripheral edema, and the third had acute hepatocellular damage, with elevated levels of aminotransferases. Viral hepatitis serologic test results, acetaminophen levels, drug and alcohol screening findings, and bacterial and fungal cultures were negative in all 3 patients. Hepatic decompensation resolved without the need for transplantation in the 2 patients with liver failure, and all patients recovered to their baseline liver function levels within 1 month of onset of acute illness. CONCLUSIONS: Influenza A infection can cause hepatic decompensation and hospitalization in patients having cirrhosis or who are awaiting liver transplantation. Effective prevention with vaccination and early recognition and treatment of influenza are strongly recommended in these individuals.

Adult↗

PubMed1999

Serial circulating concentrations of C-reactive protein, interleukin (IL)-4, and IL-6 in patients with acute left heart decompensation.

BACKGROUND: Interleukin (IL)-6 has recently been shown to have negative inotropic effects, and several studies have reported increases in circulating concentrations of this cytokine in patients with depressed left ventricular ejection fraction and chronic left heart failure. However, most previous clinical studies have measured cytokines in compensated chronic heart failure. HYPOTHESIS: The purpose of this study was to examine the temporal evolution of circulating concentrations of C-reactive protein (CRP) and cytokines in patients with cardiomyopathy and acute cardiac decompensation, free of infection and unstable angina. METHODS: The time course of circulating concentrations of CRP, an anti-inflammatory cytokine interleukin (IL)-4, and a proinflammatory cytokine IL-6 were studied in eight patients with cardiomyopathy and acute cardiac decompensation in the absence of infection or unstable angina. Control samples were obtained from eight age-matched asymptomatic subjects. RESULTS: Increased circulating concentrations of CRP (2.6 +/- 0.8 mg/dl), IL-4 (164.6 + 36.5 pg/ml), and IL-6 (17.1 +/- 5.1 pg/ml) were found in all eight patients during acute cardiac decompensation; these values decreased significantly with the resolution of symptoms of cardiac decompensation (0.5 +/- 0.1 mg/dl, 77.8 +/- 23.6 pg/ml, 2.3 +/- 0.1 pg/ml, respectively, p < 0.05 for both). There was a significant correlation between peak CRP and peak IL-6 (p < 0.05). CONCLUSIONS: In patients with acute left heart decompensation in the absence of infection or coronary events, CRP, IL-4, and IL-6 increased and returned toward normal levels as the symptoms of heart failure resolved. Since the changes in concentrations of CRP, IL-4, and IL-6 in patients with heart failure are dynamic, the distinction between compensated and decompensated state is important when discussing the significance of acute reactive proteins or cytokines in the pathogenesis of heart failure.

Aged↗

PubMed1982

The compensated and the decompensated form of benign nephrosclerosis.

Decompensated benign nephrosclerosis, a disease which was briefly described by Theodor Fahr in 1925, defended by him in 1934, and then forgotten, is reported and differentiated from compensated benign nephrosclerosis. Decompensated benign nephrosclerosis can be differentiated from compensated benign nephrosclerosis by the frequent appearance of interstitial cortical fibrosis and glomerular alterations in the sense of hypertensive glomerulopathy. Hypertensive glomerulopathy results in ascending obliteration of the glomeruli, i.e., their transformation into PAS-positive hyaline globules. In compensated benign nephrosclerosis, interstitial fibrosis, if present at all, can usually be identified only in the subcapsular areas. In decompensated benign nephrosclerosis, however, a pyramid-like structure with its base at the corticomedullary border is formed. The severity of preglomerular vascular alterations does not differ in compensated and decompensated benign nephrosclerosis. Clinically, there is no significant difference between the degree of hypertension and the development of the disease. The nephritic symptoms are more pronounced in decompensated benign nephrosclerosis, which predominantly affects middle-aged men (male:female, 5.7:1), than in compensated benign nephrosclerosis. As a result, decompensated benign nephrosclerosis is frequently diagnosed and treated as chronic glomerulonephritis.

Chronic Disease↗

PubMed2004

Clinical value of increased serum creatinine concentration as predictor of short-term outcome in decompensated cirrhosis.

BACKGROUND: The purpose of this study was to assess whether serum creatinine concentration alone or associated with other biological parameters was an independent predictor of short-term mortality in patients with decompensated cirrhosis. METHODS: A total of 212 consecutive episodes of decompensated cirrhosis in patients admitted to the hospital between January 1999 and December 2001 were reviewed retrospectively. Depending on a serum creatinine concentration equal to or greater than 1.5 mg/dL at the time of admission, patients were divided into decompensated cirrhosis with renal failure (101 episodes in 59 patients, aged 69.8 +/- 10 years) and without renal failure (111 episodes in 61 patients, aged 64.5 +/- 13 years). Outcome (alive, death) during the episode of decompensation of liver disease and outcome at 90 days after admission were assessed. RESULTS: Differences in the frequency of variables according to outcome in the overall episodes of decompensated cirrhosis with and without renal failure showed significant differences between patients who died and those who were alive both at hospital discharge and at 90 days in serum bilirubin, Child-Pugh score, MELD (model for end-stage liver disease) score, and serum creatinine levels. In the multivariate analysis, serum creatinine was not an independent predictor of outcome. The prediction accuracy according to the area under the ROC (receiver operating characteristic) curve was greater for the MELD scale than for serum creatinine. CONCLUSIONS: Serum creatinine concentration is a parameter that should be included in the prognostic assessment of patients with decompensated cirrhosis, but should be combined with other specific parameters of liver function, such as bilirubin, albumin, and the international normalized ratio (INR) for prothrombin time.

Aged↗

PubMed1996

Geometric analysis of coronal decompensation in idiopathic scoliosis.

STUDY DESIGN: Frontal plane geometry of postoperative curves was analyzed using a geometric model to investigate the relationship between coronal decompensation and postoperative apical shifts from the center sacral line for various thoracic and lumbar Cobb angles. OBJECTIVE: To determine if a balanced spinal configuration is possible when the postoperative lumbar curve is larger than the thoracic curve, and to determine the limits on the postoperative magnitude of the lumbar curve relative to the thoracic curve beyond which a spinal configuration with acceptable balance cannot be achieved. SUMMARY OF BACKGROUND DATA: Previous studies have suggested that overcorrection of the primary thoracic curve may be the principal cause of coronal decompensation after selective thoracic correction and fusion in King Type II curves. Also, other causative factors, such as inappropriate selection of fusion levels and hook patterns, have been implicated as possible reasons for decompensation after Cotrel-Dubousset instrumentation for idiopathic scoliosis. METHODS: Postoperative thoracic curves of 20 degrees, 25 degrees, and 30 degrees were simulated on a model spine. For each thoracic Cobb angle, three left lumbar curves were simulated with the lumbar curve larger than thoracic by 5 degrees, 10 degrees, and 15 degrees. For each combination of thoracic and lumbar Cobb angles, spinal configurations corresponding to different lateral shifts of the thoracic and lumbar apical vertebrae from the center sacral line were obtained. RESULTS: For a given combination of postoperative thoracic and lumbar Cobb angles, there is an optimal range of postoperative lateral distance between the thoracic and lumbar apices (relative apical distance) that will maintain acceptable balance (decompensation < or = 10 mm). Smaller values of the relative apical distance will decompensate the spine. For a constant postoperative thoracic Cobb angle, the postoperative distance between the thoracic and lumbar apices needed to maintain a balanced spine increases with increasing postoperative lumbar Cobb angle. Similarly, for a constant difference between the postoperative thoracic and lumbar Cobb angles, the postoperative distance between the thoracic and lumbar apices needed to maintain a balance spine increases with increasing postoperative thoracic Cobb angle. For postoperative thoracic curves of 20 degrees-30 degrees, acceptable balance can be achieved when the magnitude of the postoperative lumbar curve is up to twice the thoracic curve as long as adequate postoperative relative apical distance can be maintained. CONCLUSIONS: Decompensation does not appear to be caused by the relative magnitudes of the postoperative thoracic and lumbar curves, but is a result of inadequate relative distance between the thoracic and lumbar apical vertebrae in the postoperative geometry.

Humans↗

PubMed1997

Physiologic and molecular characterization of the role of nitric oxide in hemorrhagic shock: evidence that type II nitric oxide synthase does not regulate vascular decompensation.

To determine the role of nitric oxide (NO) in decompensated and irreversible hemorrhagic shock, rats were subjected to hemorrhagic shock (HS) for 3 or 5 h. Lung, liver, and plasma samples were studied for evidence of NO formation using Northern analysis and immunohistochemistry for Type II NOS, as well as measurement of plasma nitrite/nitrate, cyclic GMP, and nitrosylated hemoglobin levels. Comparisons were made with similarly instrumented time-matched sham rats. Type II NOS mRNA and protein were detectable in lung and liver only in the irreversible phase of HS (5 h). A large accumulation of nitrosylated hemoglobin and nitrite/nitrate appeared in the irreversible phase. Significant accumulation of cyclic GMP or nitrite/nitrate was not detectable in the decompensation phase. Despite the hemodynamic decompensation at 3 h of HS, Type II NOS mRNA and protein expression, as well as NO metabolites were not elevated. To assess whether NO plays a physiologically significant role in decompensation, rats in the decompensation phase and sham animals were subjected to nonspecific NOS inhibition. Both groups displayed a similar magnitude and duration of blood pressure elevation. Hemodynamic decompensation in HS is not mediated by Type II NOS induction. NO production increases only after prolonged HS; significant NO production is observed only in severe, irreversible HS.

Animals↗

PubMed2006

Sagittal thoracic decompensation following long adult lumbar spinal instrumentation and fusion to L5 or S1: causes, prevalence, and risk factor analysis.

STUDY DESIGN: Retrospective study. OBJECTIVE: To analyze the causes, prevalence of, and risk factors for sagittal thoracic decompensation in adult lumbar spinal instrumentation and fusion (from distal thoracic or upper lumbar spine) to L5 or S1. SUMMARY OF BACKGROUND DATA: To our knowledge, no studies on sagittal thoracic decompensation following long adult lumbar spinal instrumentation and fusion (from distal thoracic or upper lumbar spine) to L5 or S1 have been published. METHODS: A clinical and radiographic assessment of 99 patients with adult lumbar spinal deformity (average age 56.7 years) who underwent long (> or = 4 vertebrae; range 4-10/average 6.7) spinal instrumentation and fusion (from lower thoracic or upper lumbar spine to L5 or S1) at a single institution between 1985 and 2003 with a minimum 2-year follow-up (average 4.5 years) was performed. We defined sagittal thoracic decompensation as a progressive kyphotic deformity of the thoracic spine without pseudarthrosis after a long lumbar fusion, which subsequently resulted in a C7 plumb relative to the posterior aspect of the L5-S1 disc > or = 8 cm. RESULTS: The prevalence of sagittal thoracic decompensation after long adult lumbar spinal instrumentation and fusion (from distal thoracic or upper lumbar spine) to L5 or S1 was 23% (23/99 cases). The etiologies were 14 acute sharp angular kyphoses and 9 long sweeping kyphoses above the instrumented fusion. Of the 14 sharp angular kyphoses, 10 occurred from severe disc degeneration and 4 were caused by compression fractures at the uppermost instrumented vertebra. CONCLUSION: Risk factors for sagittal thoracic decompensation developing were sagittal imbalance at 8 weeks postoperatively (> or = 5 cm), smaller lumbar lordosis compared with thoracic kyphosis (< 10 degrees) at 8 weeks postoperatively, preoperative sagittal imbalance (> or = 5 cm), age at surgery (older than 55 years), and associated comorbidities. Sagittal thoracic decompensation adversely affected Scoliosis Research Society 24 outcomes scores.

Adult↗

PubMed2005

Blood-brain barrier changes during compensated and decompensated hemorrhagic shock.

Dysfunction of the blood-brain barrier (BBB) can be associated with a large number of central nervous system and systemic disorders. The aim of the present study was to determine BBB changes during different phases of hemorrhagic shock. The experiments were carried out on male Wistar rats anaesthetized with urethane. To produce compensated or decompensated hemorrhagic shock, mean arterial pressure was decreased from the normotensive control values to 40 mmHg by a standardized method of blood withdrawal from the femoral artery. Cerebral blood flow changes were followed by laser-Doppler flowmetry, and arterial blood gas values were monitored over the whole procedure. Cortical blood flow was significantly reduced in compensated and in decompensated hemorrhagic shock compared with the normotensive rats. As the shock shifted to the decompensated phase, the blood flow reduction was more pronounced. BBB permeability studies using sodium fluorescein (molecular weight of 376) and Evan's Blue albumin (molecular weight of 67,000) have revealed a significant increase of the BBB permeability for sodium fluorescein in the decompensated stage of hemorrhagic shock. Western blot analysis of brain capillaries showed that the expression of the transmembrane tight junction protein occludin was reduced in response to hemorrhagic shock, and the decrease of occludin was more pronounced in the decompensated phase. A similar expression pattern was shown by the transmembrane adherens junction protein cadherin as well. Our results suggest that the decompensated phase of hemorrhagic shock is associated with disturbances of the BBB, which may be explained by the dysfunction of interendothelial junctions caused by decreased occludin and cadherin levels.

Adherens Junctions↗

PubMed2001

The treatment targets in acute decompensated heart failure.

Acute decompensated heart failure is characterized by hemodynamic abnormalities as well as neuroendocrine activation, which contribute to heart failure symptoms, progressive cardiac dysfunction, and sudden death. The therapeutic goals in patients hospitalized with decompensated heart failure are to reverse acute hemodynamic abnormalities, relieve symptoms, and initiate treatment that will slow disease progression and improve long-term survival. Traditional hemodynamic targets in acute heart failure have been reduction in left and right ventricular filling pressures, reduction in systemic vascular resistance, and increase in cardiac output. Treatments aimed at these targets in patients with acute decompensated heart failure include diuretics, vasodilators, and inotropic agents. In patients hospitalized with acute decompensated heart failure, persistently elevated left ventricular filling pressure has been shown to be highly predictive of an increased risk of fatal decompensation and sudden death. Measures of systemic perfusion, arterial pressure, and vascular resistance have not. Thus, there is a more compelling physiologic rationale for the use of vasodilators than for inotropic agents in these patients. An ideal agent for acute decompensated heart failure would be one that rapidly reduces pulmonary wedge pressure, results in balanced arterial and venous dilation, promotes natriuresis, lacks direct positive inotropic effects, and does not result in reflex neuroendocrine activation.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2006

Acutely decompensated heart failure: characteristics of hospitalized patients and opportunities to improve their care.

UNLABELLED: Heart failure (HF) remains a major public health problem in western countries, despite the enormous progress in its diagnosis and treatment. Acute and chronic decompensated HF are leading medical causes of hospitalization among people aged over 65 years in European countries, the USA, Australia and New Zealand. However, there have been few studies on acute and chronic decompensated HF and the European Society of Cardiology (ESC) guidelines on this subject have only just been published. AIM: To evaluate the overall prevalence of hospitalization due to HF according to its subtypes, comorbidities, and decompensating factors, in the Medical Department of a central teaching hospital in an urban area. METHODS: We performed a retrospective observational study of patients admitted consecutively to the Medical Department via the emergency room between January and June 2001. Discharge casenotes on 1038 admissions were reviewed. Those with a diagnosis of HF or cardiovascular conditions associated with or precursors of HF were analyzed. Cases with a final diagnosis of HF according to the criteria of the ESC guidelines were included in the study. We evaluated the overall prevalence of HF and subtypes of cardiac dysfunction, etiological risk factors, patients' demographic characteristics, decompensating factors, comorbidity, mean length of hospital stay, and in-hospital mortality rate. RESULTS: We identified 180 patients with HF (17.4%), mean age 74.6 +/- 14; 87 were male (48%), aged 73.7 +/- 14.2, and 93 female (52%), aged 75.6 +/- 14. Left ventricular systolic dysfunction (LVSD) was present in 42.2% of cases, preserved left ventricular systolic function in 32.6%, and valvular heart disease in 10.6%. Hypertension and coronary artery disease were the main etiological risk factors (62.2% and 42.8% respectively). Atrial fibrillation was recorded in 43.4% of the patients, diabetes was diagnosed in 21.6%, and anemia and chronic obstructive pulmonary disease in about one third. Infection, predominantly respiratory, was the main factor triggering decompensation, followed by uncontrolled hypertension and supraventricular tachyarrhythmia. At admission, 42.2% of the patients were in NYHA class III and 44.8% in NYHA class IV. HF patients had a mean hospital stay of 13.8 days, slightly shorter than the mean overall stay of patients admitted to the Medical Department in the same period (14.5 days). In-hospital mortality for HF patients was 7.7%, with HF being the first cause of admission to the Medical Department, followed by stroke (10.6%). CONCLUSIONS: This study confirms the high prevalence of acute or chronic decompensated HF in patients hospitalized in the Medical Department of a central teaching hospital in an urban area. The patients were mainly elderly, of both genders, with a slightly higher proportion of HF due to LVSD. Most patients were in NYHA classes III and IV. Mean hospital stay was no longer than that of all patients admitted in the same period. The in-hospital mortality rate was low. The age-group affected and the high prevalence of multiple comorbidities emphasize the need to establish HF clinics with multidisciplinary teams to manage these patients, and health authorities must be made aware of the burden of this syndrome.

Acute Disease↗

PubMed1990

[Decompensated diabetes mellitus and circadian rhythm of plasma TSH].

The plasmatic levels of TSH in 2 group of diabetic patients (7 decompensated and 8 decompensated, but in treatment) were measured at 9:30 and 23:30 hours. The mean glycemia levels were of 280 +/- 45 and 150 +/- 30 mg/dl (p less than 0.0005). There was no significant difference between daily TSH and nocturnal TSH in any of the groups, but there was a tendency for the nocturnal TSH to be higher in decompensated patients. There was no difference when comparing the TSH of the first group to the TSH of the 2nd group. The mean TSH N/TSH D was superior by 1 (1.36 in decompensated and 1,095 in treated patients). The correlation between glycemia and TSH D was negligible in all groups. The data suggests the tendency that the circadian rhythm of TSH in maintained in diabetes decompensation with shorter rhythm registered in treated patients. This shows a certain normality in the suprahypophysary area in charge of the rhythm and is similar to the minor liberation of TSH after TRH stimulus that other authors have described as happening in the decompensation of diabetes mellitus.

Adult↗

PubMed1995

Occurrence of hepatocellular carcinoma and decompensation in western European patients with cirrhosis type B. The EUROHEP Study Group on Hepatitis B Virus and Cirrhosis.

To examine the morbidity of compensated cirrhosis type B, a cohort of 349 Western European, white patients (86% men; mean age, 44 years) with biopsy-proven cirrhosis was followed up for a mean period of 73 months and was studied for occurrence of hepatocellular carcinoma (HCC) and decompensation. At entry into the study all patients were tested for hepatitis B e antigen (HBeAg; 34% of patients were HBeAg-positive) and antibody to hepatitis delta virus (anti-HDV; 20% of patients were anti-HDV-positive); 48% of 252 patients tested were hepatitis B virus (HBV)-DNA-positive. During follow-up HCC developed in 32 (9%) of the 349 patients and decompensation was observed in 88 (28%) of 317 tumor-free patients. Five years after diagnosis, the probability of HCC appearance was 6% and the probability of decompensation was 23%. After the first episode of decompensation the probability of survival was 35% at 5 years. Cox's regression analysis identified three variables that independently correlated with HCC: age, serum levels of platelets, and liver firmness on physical examination. HBV (HBeAg or HBV-DNA) and HDV (anti-HDV) markers at presentation had no prognostic value for the development of HCC. In conclusion, a high proportion of patients with HBsAg-positive compensated cirrhosis do not experience worsening of their condition for several years, but once decompensation occurs life expectancy is poor. European, white patients with compensated cirrhosis type B are at consistent risk for HCC. Prognostic factors for HCC reflect an advanced stage of cirrhosis and support the hypothesis that development of a tumor could be the likely consequence of long-standing hepatic disease.

Aged↗

PubMed2003

Focal hypoxia of the obstructed rabbit bladder wall correlates with intermediate decompensation.

AIMS: We showed that partial obstruction of the rabbit bladder outlet caused decreases in detrusor blood flow that were directly proportional to the level of decompensation present. Bladder decompensation is characterized by decreases in detrusor contractility, mitochondrial function, and sarco/endoplasmic reticulum calcium ATPase (SERCA) activity in obstructed rabbits. The current study was designed to create bladder decompensation and to relate its characteristic dysfunctions to the presence or absence of hypoxia in the obstructed rabbit bladder wall. Tissue hypoxia was visualized immunohistochemically after administration of a hypoxia probe in vivo. METHODS: Twelve New Zealand White rabbits were separated into two groups. The rabbits in group 1 received sham operations; the rabbits in group 2 received partial outlet obstructions by standard methods. Four weeks after surgery, each rabbit received an intraperitoneal injection of aqueous Hypoxyprobe-1, which forms protein adducts in cells having O(2) concentrations less than 14 microM. Two hours after injection, the rabbit was anesthetized and the bladder exposed through a midline incision. One full-thickness bladder strip was cut and immediately placed in fixative for immunohistochemical recognition and visualization of Hypoxyprobe-1-protein adducts. The remaining bladder was then excised, and three additional strips were cut for contractility studies. The remainder of the bladder was frozen for biochemical and slot-blot analyses. RESULTS: Bladder weight was increased fourfold after obstruction, and significant contractile and biochemical dysfunctions were observed that indicated an intermediate level of decompensation. Immunohistochemical visualization revealed focal areas of moderate to severe hypoxia in the detrusor smooth muscle (SM) and subserosal regions of these bladders. No hypoxia was observed in the obstructed bladder mucosa, consistent with the absence of biochemical dysfunction in this compartment, or in unobstructed bladders. Slot-blot analyses confirmed the presence of significant Hypoxyprobe-1-protein adducts in the detrusor of the obstructed bladder, whereas none were present in the control bladder detrusors. CONCLUSIONS: Partial outlet obstruction of rabbit bladders resulted in focal areas of moderate to severe hypoxia in the detrusor SM and subserosal regions concomitant with increased bladder mass, decreased contractile function, and selective metabolic dysfunctions of the SM consistent with an intermediate stage of decompensation. The metabolic characteristics of the normoxic mucosa were normal a were those of unobstructed bladders.

Adenosine Triphosphate↗

PubMed2004

Connexin 43 expression and distribution in compensated and decompensated cardiac hypertrophy in patients with aortic stenosis.

OBJECTIVES: Gap junctions (GJ) are important determinants of conduction. In advanced heart failure alterations of the major ventricular GJ protein, connexin 43 (Cx43) are found. However, changes in Cx43 expression during the progression from compensated cardiac hypertrophy to heart failure, especially in humans, have not been studied extensively. The aim of the present study was to investigate changes in Cx43 expression and distribution in compensated and decompensated left ventricular (LV) hypertrophy in pressure-overloaded human hearts with valvular aortic stenosis (AS). METHODS: We measured Cx43 levels by Western blot and quantitative immunoconfocal microscopy of LV septum biopsies from three groups of patients with AS (group I (n=9): ejection fraction (EF)>50%; group II (n=12): EF 30-50%; group III (n=9): EF<30%). LV biopsies from six patients with mitral valve stenosis and two donor hearts served as controls. RESULTS: Only the early phase of LV hypertrophy (AS-I) was characterized by extensive Cx43 lateral staining. As compared to controls, the AS-I group showed a 44.3% increase in Cx43 protein, which was reflected in an augmented number of GJs per 100 microm(2) intercalated disc area (control: 62.5+/-6.4 vs. AS-I: 79.8+/-4, p<0.001) and an increased GJ surface density (control: 0.00547 vs. AS-I: 0.00724 microm(2)/microm(3), p<0.01). Decompensated LV hypertrophy (AS-III) was specified by reduced percentage of the Cx43 signal per myocyte area (control: 1.74% vs. AS-III: 1.31%, p<0.01) or per intercalated disc (control: 18.3% vs. AS-III: 11.3%, p<0.005). Mean GJ area and GJ number per intercalated discs in the AS-III group were decreased significantly by, respectively, 42.5% and 36.4% as compared to control. In addition, decompensated LV myocardium showed a markedly heterogeneous spatial distribution of Cx43. CONCLUSION: The quantity and spatial distribution of Cx43 differs markedly between compensated and decompensated LV hypertrophy in human patients with AS. Upregulation of Cx43 in compensated hypertrophy may represent the immediate adaptive response to increased load, whereas diminished and heterogeneous Cx43 distribution in decompensated hypertrophy may play maladaptive roles culminating in heart failure and ventricular arrhythmias.

Aged↗

PubMed2006

Hepatitis E virus (HEV) infection in patients with cirrhosis is associated with rapid decompensation and death.

BACKGROUND/AIMS: India is hyper-endemic for hepatitis E virus (HEV). HEV infection in cirrhosis may cause high mortality. Prospective study evaluating HEV infection in cirrhotics is scarce. METHODS: Consecutive patients with cirrhosis and healthy controls were included. Cirrhotics were categorized to 3 groups, (Group I - rapid decompensation, Group II - chronically decompensated, Group III - cirrhotics without decompensation). Sera from cirrhotics and controls were tested for HEV-RNA (RT-PCR). HEV-RNA positivity among cirrhotics and controls was compared. Natural course and mortality rate between HEV infected and non-infected cirrhotics were assessed during a 12-month follow-up. RESULTS: 107 cirrhotics and 200 controls were included. 30 (28%) cirrhotics and 9 (4.5%) controls had detectable HEV-RNA (p<0.001). HEV- RNA positivity among Group I (n=42), II (n=32) and III (n=33) cirrhotics was 21 (50%), 6 (19%) and 3 (10%), respectively (p=0.002). 70% (21/30) with HEV infection and 27% (21/77) without it had rapid decompensation (p=0.001). Mortality between HEV infected and non-infected cirrhotics at 4 weeks (43% vs. 22%, p=0.001) and 12 month (70% vs. 30%, p=0.001) was different. Multivariate analysis identified HEV infection, Child-Pugh's score, renal failure, and sepsis as independent factors for mortality. CONCLUSIONS: In India, cirrhotics were prone to HEV infection, which was associated with rapid decompensation and death.

Adult↗