***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: CONTEXT The hypothalamic-pituitary-adrenal axis is a major determinant of the host response to stress . The relationship between its activation and patient outcome is not known . OBJECTIVE To evaluate the prognostic value of cortisol levels and a short corticotropin stimulation test in patients with septic shock . DESIGN AND SETTING Prospect i ve inception cohort study conducted between October 1991 and September 1995 in 2 teaching hospital adult intensive care units in France . PARTICIPANTS A total of 189 consecutive patients who met clinical criteria for septic shock . INTERVENTION A short corticotropin stimulation test was performed in all patients by intravenously injecting 0.25 mg of tetracosactrin ; blood sample s were taken immediately before the test ( T0 ) and 30 ( T30 ) and 60 ( T60 ) minutes afterward . MAIN OUTCOME MEASURES Twenty-eight-day mortality as a function of variables collected at the onset of septic shock , including cortisol levels before the corticotropin test and the cortisol response to corticotropin ( delta max , defined as the difference between T0 and the highest value between T30 and T60 ) . RESULTS The 28-day mortality was 58 % ( 95 % confidence interval [ CI ] , 51%-65 % ) and median time to death was 17 days ( 95 % CI , 14 - 27 days ) . In multivariate analysis , independent predictors of death ( P < or = .001 for all ) were McCabe score greater than 0 , organ system failure score greater than 2 , arterial lactate level greater than 2.8 mmol/L , ratio of PaO2 to fraction of inspired oxygen no more than 160 mm Hg , cortisol level at T0 greater than 34 microg/dL and delta max no more than 9 microg/dL. Three groups of patient prognoses were identified : good ( cortisol level at T0 < or = 34 microg/dL and delta max > 9 microg/dL ; 28-day mortality rate , 26 % ) , intermediate ( cortisol level at T0 34 microg/dL and delta max < or = 9 microg/dL or cortisol level at T0 > 34 microg/dL and delta max > 9 microg/dL ; 28-day mortality rate , 67 % ) , and poor ( cortisol level at T0 > 34 microg/dL and delta max < or = 9 microg/dL ; 28-day mortality rate , 82 % ) . CONCLUSION Our data suggest that a short corticotropin test has a good prognostic value and could be helpful in identifying patients with septic shock at high risk for death We conducted a multicenter r and omized , double-blind , placebo-controlled trial of early short-term , high-dose methylprednisolone sodium succinate in 223 patients with clinical signs of systemic sepsis and a normal sensorium ( 112 received glucocorticoid and 111 placebo ) . Patients also received antibiotics and intravenous fluids . Glucocorticoid or placebo was administered intravenously by a bolus ( 30 mg per kilogram of body weight over 15 minutes ) followed by infusion of 5 mg per kilogram per hour for nine hours . The average time between the diagnosis of sepsis and infusion was 2.8 hours . The principal end point was 14-day mortality , which was similar in the placebo ( 22 percent ) and glucocorticoid ( 21 percent ) groups ( P = 0.97 ) . Mortality was also not significantly different between those receiving placebo and those receiving glucocorticoid in subgroups with evidence of sepsis ( 21 vs. 19 percent ) , gram-negative bacteremia ( 27 vs. 7 percent ) , gram-positive bacteremia ( 18 vs. 26 percent ) , or all gram-negative infections ( 25 vs. 17 percent ) . Resolution of secondary infection within 14 days was significantly higher in patients receiving placebo ( 12 of 23 ) than in those receiving glucocorticoid ( 3 of 16 ) ( P = 0.03 ) , but mortality rates were similar in both treatment groups for those with unresolved infection ( 36 vs. 31 percent ) . We conclude that early high-dose glucocorticoid therapy does not reduce mortality significantly in patients with systemic sepsis who have a normal sensorium , and therefore should not be used as adjunctive therapy Within the last few years , increasing evidence of relative adrenal insufficiency in septic shock evoked a re assessment of hydrocortisone therapy . To evaluate the effects of hydrocortisone on the balance between proinflammatory and antiinflammation , 40 patients with septic shock were r and omized in a double-blind crossover study to receive either the first 100 mg of hydrocortisone as a loading dose and 10 mg per hour until Day 3 ( n = 20 ) or placebo ( n = 20 ) , followed by the opposite medication until Day 6 . Hydrocortisone infusion induced an increase of mean arterial pressure , systemic vascular resistance , and a decline of heart rate , cardiac index , and norepinephrine requirement . A reduction of plasma nitrite/nitrate indicated inhibition of nitric oxide formation and correlated with a reduction of vasopressor support . The inflammatory response ( interleukin-6 and interleukin-8 ) , endothelial ( soluble E-selectin ) and neutrophil activation ( expression of CD11b , CD64 ) , and antiinflammatory response ( soluble tumor necrosis factor receptors I and II and interleukin-10 ) were attenuated . In peripheral blood monocytes , human leukocyte antigen-DR expression was only slightly depressed , whereas in vitro phagocytosis and the monocyte-activating cytokine interleukin-12 increased . Hydrocortisone withdrawal induced hemodynamic and immunologic rebound effects . In conclusion , hydrocortisone therapy restored hemodynamic stability and differentially modulated the immunologic response to stress in a way of antiinflammation rather than immunosuppression We conducted a 9-month prospect i ve cohort study of 2,527 patients with systemic inflammatory response syndrome in three intensive care units and three general wards in a tertiary health care institution . Markov models were developed to predict the probability of movement to and from more severe stages -- sepsis , severe sepsis , or septic shock -- at 1 , 3 , and 7 days . For patients with sepsis , severe sepsis , and septic shock , the probabilities of remaining in the same category after 1 day were .65 , .68 , and .61 , respectively . The probability for progression after 1 day was .09 for sepsis to severe sepsis and .026 for severe sepsis to shock . The probability of patients with sepsis , severe sepsis , and septic shock dying after 1 day was .005 , .009 , and .079 , respectively . The model can be used to predict the reduction in end organ dysfunction and mortality with use of increasingly effective antisepsis agents CONTEXT No pharmacological therapeutic protocol has been found effective in modifying the clinical course of acute respiratory distress syndrome ( ARDS ) and mortality remains greater than 50 % . OBJECTIVE To determine the effects of prolonged methylprednisolone therapy on lung function and mortality in patients with unresolving ARDS . DESIGN R and omized , double-blind , placebo-controlled trial . SETTING Medical intensive care units of 4 medical centers . PARTICIPANTS Twenty-four patients with severe ARDS who had failed to improve lung injury score ( LIS ) by the seventh day of respiratory failure . INTERVENTIONS Sixteen patients received  methylprednisolone and 8 received placebo . Methylprednisolone dose was initially 2 mg/kg per day and the duration of treatment was 32 days . Four patients whose LIS failed to improve by at least 1 point after 10 days of treatment were blindly crossed over to the alternative treatment . MAIN OUTCOME MEASURES Primary outcome measures were improvement in lung function and mortality . Secondary outcome measures were improvement in multiple organ dysfunction syndrome ( MODS ) and development of nosocomial infections . RESULTS Physiological characteristics at the onset of ARDS were similar in both groups . At study entry ( day 9 [ SD , 3 ] of ARDS ) , the 2 groups had similar LIS , ratios of PaO2 to fraction of inspired oxygen ( FIO2 ) , and MODS scores . Changes observed by study day 10 for methylprednisolone vs placebo were as follows : reduced LIS ( mean [ SEM ] , 1.7 [ 0.1 ] vs 3.0 [ 0.2 ] ; P<.001 ) ; improved ratio of PaO2 to FIO2 ( mean [ SEM ] , 262 [ 19 ] vs 148 [ 35 ] ; P<.001 ) ; decreased MODS score ( mean [ SEM ] , 0.7 [ 0.2 ] vs 1.8 [ 0.3 ] ; P<.001 ) ; and successful extubation ( 7 vs 0 ; P=.05 ) . For the treatment group vs the placebo group , mortality associated with the intensive care unit was 0 ( 0 % ) of 16 vs 5 ( 62 % ) of 8 ( P=.002 ) and hospital-associated mortality was 2 ( 12 % ) of 16 vs 5 ( 62 % ) of 8 ( P=.03 ) . The rate of infections per day of treatment was similar in both groups , and pneumonia was frequently detected in the absence of fever . CONCLUSIONS In this study , prolonged administration of methylprednisolone in patients with unresolving ARDS was associated with improvement in lung injury and MODS scores and reduced mortality Naloxone and methylprednisolone sodium succinate ( MPSS ) may act in synergy to improve hemodynamics in patients with septic shock by enhancement of sympathomedullary discharge . This r and omized double-blind study describes the effect of various dosing regimens of naloxone and MPSS upon hemodynamics and plasma catecholamines in patients with septic shock ( n = 57 ) . Consecutive bolus doses of naloxone were given 30 minutes apart ( 10 micrograms/kg;-100 micrograms/kg ) and a single dose of MPSS ( 30 mg/kg ) ; bolus doses of 5 % dextrose in water solution plus single dose of MPSS as above ; bolus dose of naloxone ( 30 micrograms/kg ) followed by continuous infusion ( 30 micrograms/kg/hr for 1 hour ) with single dose of MPSS as above ; a bolus and continuous infusion of naloxone as above without MPSS ; MPSS alone and st and ard therapy alone . In patients treated with bolus doses of naloxone in combination with MPSS , plasma levels of epinephrine and norepinephrine were increased approximately five-to tenfold . In patients treated with bolus plus continuous infusion of naloxone given with or without MPSS , only plasma epinephrine levels were increased . Systolic blood pressure and left ventricular stroke work index were improved within 15 minutes in groups which received naloxone and corticosteroids regardless of dose . In those groups , there were no changes in heart rate or filling pressure . Systemic vascular resistance improved significantly only in the group which received low dose bolus and continuous infusion of naloxone and MPSS . Naloxone and MPSS quickly improved cardiac function in patients with septic shock by enhanced sympathomedullary discharge and may be useful as an adjunct in the therapy of this disorder Objective To determine the incidence , cost , and outcome of severe sepsis in the United States . Design Observational cohort study . Setting All nonfederal hospitals ( n = 847 ) in seven U.S. states . Patients All patients ( n = 192,980 ) meeting criteria for severe sepsis based on the International Classification of Diseases , Ninth Revision , Clinical Modification . Interventions None . Measurements and Main Results We linked all 1995 state hospital discharge records ( n = 6,621,559 ) from seven large states with population and hospital data from the U.S. Census , the Centers for Disease Control , the Health Care Financing Administration , and the American Hospital Association . We defined severe sepsis as documented infection and acute organ dysfunction using criteria based on the International Classification of Diseases , Ninth Revision , Clinical Modification . We vali date d these criteria against prospect i ve clinical and physiologic criteria in a subset of five hospitals . We generated national age- and gender-adjusted estimates of incidence , cost , and outcome . We identified 192,980 cases , yielding national estimates of 751,000 cases ( 3.0 cases per 1,000 population and 2.26 cases per 100 hospital discharges ) , of whom 383,000 ( 51.1 % ) received intensive care and an additional 130,000 ( 17.3 % ) were ventilated in an intermediate care unit or cared for in a coronary care unit . Incidence increased > 100-fold with age ( 0.2/1,000 in children to 26.2/1,000 in those > 85 yrs old ) . Mortality was 28.6 % , or 215,000 deaths nationally , and also increased with age , from 10 % in children to 38.4 % in those > 85 yrs old . Women had lower  age-specific incidence and mortality 
    Output:
    
For all trials , regardless of duration of treatment and dose , use of corticosteroids did not significantly affect mortality .
With long courses of low doses of corticosteroids , however , mortality at 28 days and hospital morality was reduced