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Biomedical subjects

B A Pruitt

Publications and source records attributed to B A Pruitt.

At least 55 records · Page 3Linked to original sources
PubMed1995

Enhanced survival of autoepidermal-allodermal composite grafts in allosensitized animals by use of silver-nylon dressings and direct current.

OBJECTIVE: Observe the effect of silver-nylon (SN) dressing and direct electric current on healing of meshed autoepidermal/allodermal composite skin grafts (MCSGs) in allosensitized rats. MATERIALS AND METHODS: MCSGs were placed on experimental animals 28 to 30 days after placement of sensitizing allografts. MCSGs and control allografts were covered with either Vaseline gauze (VG) or SN; direct current, 40 microA, was applied for 5 days to some of the SN-dressed wounds (SNDCs). MEASUREMENTS AND MAIN RESULTS: Second set rejection of MCSG was not observed. SN- and SNDC-treated grafts showed expansion of the meshed autoepidermis with complete epithelialization within 3 weeks. VG-covered wounds developed areas of open granulation and were not completely epithelialized at 3 months. Both SN and SNDC reduced wound contraction when compared to VG (SN versus VG p < 0.02, SNDC versus VG p < 0.008). MCSG was found to be of low alloantigenicity in that it did not induce second set rejection of subsequent skin allograft. CONCLUSIONS: SN dressings enhanced survival of meshed composite skin grafts.

Animals↗
PubMed1995

Effects of nitric oxide synthase inhibition on regional blood flow in a porcine model of endotoxic shock.

The results of early studies suggest that nitric oxide (NO) synthesis inhibition may be therapeutic in sepsis, but recent data indicate that NO inhibition may be harmful. This study investigates the effects of NO synthesis inhibition with N-nitro-L-arginine methyl ester (NAME) on regional blood flow following endotoxemia. Anesthetized, instrumented swine were randomly divided into four groups. Controls received normal saline resuscitation (NSR) at 1 cc/kg/min beginning at T0. The lipopolysaccharide group (LPS) received NSR and Escherichia coli LPS, 200 micrograms/kg at T0. The LPS+NAME group received NSR and LPS at T0, plus NAME (50 micrograms/kg/min) starting at T1. The NAME group received only NSR and NAME. Hemodynamic data, regional blood flow, and gastric intramucosal pH (pHi) were measured hourly. LPS increased renal and carotid blood flow consistent with a hyperdynamic state. Mesenteric blood flow was decreased. Treatment of endotoxic animals with NAME decreased renal and carotid blood flow. Mesenteric blood flow and gastric pHi were improved by NAME. NO inhibition in endotoxic shock results in decreased carotid and renal blood flow, by decreasing cardiac output. Mesenteric blood flow and perfusion were improved; however, this requires further study for validation.

Amino Acid Oxidoreductases↗
PubMed1995

Burn center care for patients with toxic epidermal necrolysis.

BACKGROUND: Toxic epidermal necrolysis (TEN) is a life threatening exfoliative disorder that is most commonly precipitated by the administration of a medication. Efforts to reduce morbidity and improve survival have brought into question the use of corticosteroids and recommend the transfer of patients to a burn center to facilitate wound care. STUDY DESIGN: This study evaluated the correlation of measures of disease severity and impact of treatment strategies on morbidity and mortality in patients with TEN. The records of all patients with TEN admitted to the United States Army Institute of Surgical Research during a 12 year period were reviewed. Patient characteristics, etiologic agents, time to referral of patients to the burn center, corticosteroid therapy, and other demographic features were studied. Univariate and multivariate analyses were used to determine the significance of these factors with respect to outcome. RESULTS: The sulfonamides and phenytoin were the most frequently identified etiologic agents. Patients at the extremes of age had a higher mortality rate. The period of hospitalization was longer in patients transferred to the burn center more than seven days after skin slough. Percent of epidermalysis, white blood cell count nadir, and corticosteroid administration for more than 48 hours were independently associated with mortality. CONCLUSIONS: These data indicate that the sulfonamides and phenytoin are the most common etiologic agents, expeditious transfer to a burn center reduces morbidity, and corticosteroid administration dramatically increases mortality.

Adrenal Cortex Hormones↗
PubMed1994

Detrimental hemodynamic effects of nitric oxide synthase inhibition in septic shock.

OBJECTIVE: To investigate the physiologic effects of nitric oxide synthase inhibition with N-nitro-L-arginine methyl ester in an acute resuscitated model of porcine septic shock. DESIGN: Randomized control trial. SETTING: Animal research facility. STUDY SUBJECTS: Domestic Yorkshire swine. INTERVENTIONS: Twenty-four animals were randomly divided into one of four treatment groups as follows: normal saline resuscitation (NSR) (control group); NSR plus 200 micrograms/kg of lipopolysaccharide (LPS) at 1 hour after baseline (LPS group); NSR, LPS, and a continuous infusion of 50 micrograms/kg per minute of N-nitro-L-arginine methyl ester (NAME) at 1 hour after baseline (LPS/NAME group); and NSR and NAME (NAME group). All animals received NSR at 1 mL/kg per minute starting at baseline. MAIN OUTCOME MEASURES: Mean arterial pressure (MAP), systemic vascular resistance index (SVRI), mean pulmonary arterial pressure (MPAP), and pulmonary vascular resistance index (PVRI) were measured at baseline and hourly for 4 hours. Values at baseline and 3 hours are given below as mean (+/- SE). RESULTS: All variables remained unchanged in the control group. The administration of LPS produced a systemic hyperdynamic response characterized by a decrease in MAP and SVRI from 66.0 +/- 3.9 to 55.0 +/- 2.8 mm Hg (P < .05) and from 422.0 +/- 22.0 to 272.0 +/- 29.0 mm Hg.min.kg/L (P < .05), respectively. The administration of LPS produced an increase in MPAP and PVRI from 16.3 +/- 0.8 to 30.0 +/- 1.3 mm Hg (P < .05) and from 37.0 +/- 5.3 to 119.0 +/- 13.0 mm Hg.min.kg/L (P < .05), respectively. In the LPS/NAME group, NAME infusion normalized MAP and increased SVRI from 506.0 +/- 40.0 to 642.0 +/- 72.0 mm Hg.min.kg/L (P < .05). Infusion of NAME potentiated LPS-induced pulmonary hypertension, increasing MPAP and PVRI from 16.8 +/- 0.6 to 36.0 +/- 2.8 mm Hg (P < .05) and from 59.0 +/- 3.5 to 319.0 +/- 64.0 mm Hg.min.kg/L (P < .05), respectively. Infusion of NAME alone increased MAP from 74.0 +/- 1.3 to 100.0 +/- 4.1 mm Hg (P < .05) and had no significant effect on MPAP and PVRI. CONCLUSIONS: The potentiation of LPS-induced pulmonary hypertension following NAME infusion suggests that inhibition of nitric oxide synthase may have a limited role in the treatment of septic shock.

Amino Acid Oxidoreductases↗
PubMed1994

The pulmonary effect of nitric oxide synthase inhibition following endotoxemia in a swine model.

OBJECTIVE: To evaluate the pulmonary effect of treatment with N-nitro-L-arginine methyl ester (NAME) with and without inhaled nitric oxide (NO) in a swine model of endotoxemia. DESIGN: Randomized controlled trial. SETTING: Laboratory. INTERVENTIONS: Following a 20-minute intravenous infusion of Escherichia coli lipopolysaccharide (LPS) (200 micrograms/kg), animals were resuscitated with saline solution (1 mL/kg per minute) and observed for 3 hours while mechanically ventilated (fraction of inspired oxygen [FIO2], 0.6; tidal volume, 12 mL/kg; positive end-expiratory pressure, 5 cm H2O). Group 1 (LPS, n = 6) received no additional treatment; group 2 (NAME, n = 5) received NAME (3 mg/kg per hour) for the last 2 hours; group 3 (NO, n = 6) received NAME (3 mg/kg per hour) and inhaled NO (40 ppm) for the last 2 hours; and group 4 (control, n = 5) received only saline solution without LPS. MAIN OUTCOME MEASURES: Cardiopulmonary variables and blood gases were measured serially. The multiple inert gas elimination technique was performed at 3 hours. The wet-to-dry lung weight ratio was measured following necropsy. RESULTS: Administration of LPS resulted in pulmonary arterial hypertension, pulmonary edema, and hypoxemia with increased ventilation perfusion ratio mismatching. None of these changes were attenuated by NAME treatment alone but all were significantly improved by the simultaneous administration of inhaled NO. CONCLUSIONS: Systemic NO synthase inhibition failed to restore hypoxic pulmonary vasoconstriction following LPS administration. The deleterious effects of endotoxemia on pulmonary function can be improved by inhaled NO but not by systemic inhibition of NO synthase.

Administration, Inhalation↗
PubMed1994

A decade of reduced gram-negative infections and mortality associated with improved isolation of burned patients.

OBJECTIVE: To compare the incidence of gram-negative bacteremia (GNB) and mortality in patients with large burns (> or = 20% of total body surface) hospitalized in either an open ward (OW) or a single-bed isolation (IW) environment. DESIGN: Retrospective cohort study. SETTING: The US Army Institute of Surgical Research, Burn Center, Ft Sam Houston, Tex. PATIENTS: Two thousand five hundred nineteen consecutive patients with large burns divided into two 10-year cohorts. Patients in the first cohort period were treated under OW conditions; patients in the second cohort period, under IW conditions. Infection (bacteremia) data were from a laboratory database. A microbial surveillance system was used to monitor patient isolation. Mortality was compared with predicted mortality derived by logistic regression of outcome, burn size, and age of patients without bacteremia in the study. MAIN OUTCOME MEASURES: Presence of GNB and survival. RESULTS: The incidence of GNB was higher in the OW cohort (31.2%) than the IW cohort (12.0%) (P < .001). The postinjury time of first GNB was delayed in the IW vs the OW cohort (28.9 days vs 11.8 days, respectively) (P < .001). For patients who had GNB in the OW cohort, mortality was higher than predicted (observed-predicted mortality ratio, 1.61) (P < .001). Such increased mortality was not present in the IW cohort. Multiple antibiotic-resistant gram-negative pathogens were endemic in the OW cohort. There was no evidence of cross infection or endemic conditions with multiple antibiotic-resistant gram-negative pathogens in the IW cohort. CONCLUSION: Improvements in isolation of burned patients were associated with decreased incidence of GNB, delayed postinjury time of GNB, and improved survival. Improved survival is likely related to decreased susceptibility as a result of longer exposure to the benefits of treatment and wound closure. These results suggest that, in patients with severe burn injuries, gram-negative infections and the related mortality can largely be prevented.

Adult↗
PubMed1994

The effects of pentoxifylline on pulmonary function following smoke inhalation.

Bronchopulmonary injury secondary to smoke inhalation is a significant comorbid factor following major thermal trauma. The present study evaluates the effects of pentoxifylline (PTX) on pulmonary function in an ovine model of inhalation injury. Following smoke exposure to produce a moderate inhalation injury, 16 animals were divided into two groups. Group 1 animals (n = 8) were untreated; Group 2 animals (n = 8) were treated continuously with pentoxifylline following smoke exposure. The animals were observed in the unintubated, awake state for 48 hr. Cardiopulmonary variables and blood gases were measured serially. Ventilation perfusion distribution (VA/Q), analyzed using the multiple inert gas elimination technique, and bronchoalveolar lavage (BAL) were performed at 48 hr. The wet to dry lung weight ratio was measured following necropsy. In Group 2, the progressive hypoxemia observed following smoke inhalation was attenuated with less VA/Q mismatching than in Group 1 (P < 0.05). Pulmonary hypertension secondary to increased vascular resistance was also attenuated in Group 2 (P < 0.05). In BAL fluid, polymorphonuclear leukocytes, total protein content, and conjugated dienes were less in Group 2 than in Group 1 (P < 0.05). Plasma-conjugated diene levels were also lower in Group 2 at 48 hr. Extravascular lung water and decrease in lung compliance were greater in Group 1. There was less morphologic evidence of airway injury in Group 2 compared to Group 1. The improvement of pulmonary function following treatment with PTX suggests that this agent may be useful in the management of smoke inhalation injury.

Animals↗
PubMed1994

Predicting ventilation failure in children with inhalation injury.

Despite advances in mechanical ventilatory support for patients with smoke inhalation injury, including the use of high-frequency flow-interruption ventilators such as the VDR, inhalation injury alone may increase mortality by as much as 20% in patients with thermal injury, and up to 60% when pneumonia occurs. Inhalation injury causes a primary large and small airway epithelial insult that results in ventilation abnormalities, rather than a primary alveolar lesion that results in oxygenation abnormalities as occur in multiple-system organ failure. Patients with inhalation injury requiring high ventilatory pressures experience complications of barotrauma and frequently succumb to necrotizing tracheobronchitis and oxygenation abnormalities after 2 to 4 weeks of mechanical ventilation. Ventilatory indexes obtained early in the postburn period allow the development of accurate predictive formulae that identify patients who will not be adequately supported by mechanical ventilation after smoke inhalation injury. Early identification of such patients will allow rapid conversion to other methods of ventilatory support that effect gas exchange, with minimal risk of further barotrauma, while inhalation injury healing occurs. Such predictors may be developed for other disease processes that are characterized by severe pulmonary ventilatory dysfunction.

Adolescent↗
PubMed1994

Insulin-like growth factor-1 lowers protein oxidation in patients with thermal injury.

OBJECTIVE: The effect of insulin-like growth factor-1 (IGF-1) on energy expenditure and protein and glucose metabolism in a group of patients with thermal injury was determined. SUMMARY BACKGROUND DATA: Accelerated protein catabolism is a constant feature of the hypermetabolic response to thermal injury. Insulin-like growth factor-1 has been reported to minimize protein catabolism and normalize energy expenditure in animal models of thermal injury. METHODS: To determine the efficacy of IGF-1 in human burn patients, resting energy expenditure (metabolic cart), whole body protein kinetics (N15 Lysine), and glucose disposal (glucose tolerance test) were assessed in eight burn patients before and after a 3-day infusion of IGF-1 (20 micrograms/kg/hr). All patients were fluid-resuscitated uneventfully and were without obvious infection at the time of study. Enteral nutrition was administered at a constant rate before and during the IGF-1 infusion. RESULTS: Resting energy expenditure was not altered by IGF-1 (40.3 +/- 2.2 vs. 39.1 +/- 2.3 kcal/kg/day). However, glucose uptake was promoted, and protein oxidation decreased significantly (0.118 +/- 0.029 vs. 0.087 +/- 0.021 g/kg/d, p < 0.05) by IGF-1. In addition, insulin secretion, in response to a glucose challenge, was blunted. CONCLUSIONS: Insulin-like growth factor-1 therapy has a beneficial effect in preserving lean body mass during severe stress conditions by minimizing the flux of amino acids toward oxidation.

Adult↗
PubMed1994

Intracompartmental sepsis in burn patients.

An uncommon cause of sepsis in patients with large burns is occult intracompartmental infection. A multi-institution review of 1171 burn admissions identified 5 patients (0.4%) who developed intracompartmental sepsis presenting with fever and purulent drainage or fever, erythema, and swelling on clinical examination. Contributing factors may have included high-volume resuscitation, delayed escharotomy, extravasated intraosseous infusion, cannulation-related arterial injury, and splinting or positioning difficulties. A high index of suspicion and an aggressive surgical approach facilitate successful management of this unusual problem.

Adult↗
PubMed1994

Comparison of acid neutralizing and non-acid neutralizing stress ulcer prophylaxis in thermally injured patients.

We have compared the effectiveness of non-acid neutralizing stress ulcer prophylaxis (SUC) with sucralfate (n = 48) with that of acid neutralizing prophylaxis (AN) utilizing antacids and cimetidine (n = 48) in the prevention of stress ulcer bleeding and nosocomial pneumonia (PN) in thermally injured patients. In the subset of intubated patients, the incidence of PN was 17.8% and 42.8% in the AN and SUC groups, respectively (p < 0.05) despite a similar postburn time of onset of pneumonia. Ten patients in each group died. Three patients in the SUC group developed upper GI bleeding with one requiring gastrectomy. Bacterial colonization of the upper airway occurred in virtually all patients, whereas 83% (SUC) and 96% (AN) had colonization of gastric contents. Gram-negative colonization rates for the upper airway were not different (70%) whereas 48% of SUC patients compared with 60% of AN patients had gram-negative gastric colonization. In conclusion, SUC therapy was efficacious in the prevention of stress ulcer bleeding but did not alter the rate of bacterial colonization of the airway or gastric contents, and was associated with a higher incidence of nosocomial pneumonia in intubated patients.

Adult↗
PubMed1994

A longitudinal study of resting energy expenditure in thermally injured patients.

We have recently developed a new burn-specific equation that satisfactorily estimates initial caloric requirements for thermally injured patients. In the present study, we compared these estimates with resting energy expenditures (REE) (n = 141) measured weekly by indirect calorimetry in 20 patients between postburn days 3 and 348. In this group, mean initial burn size was 46.7% (range, 21-88) and mean age 31.3 years (range, 19-61). Serial measurements were continued until the burn wounds were closed or the patient was discharged. Multiple regression analysis indicated a relationship between REE, initial burn size, and postburn day in these patients (r = 0.65). This analysis indicated a general trend of decline in REE toward normal values 100 to 150 days postburn in patients with smaller burns (20%-40%) and roughly 250 days postinjury in those with larger burns (> 75%). The initial predictive equation appeared adequate for estimating caloric needs during the first postburn month, but beyond 30 days postburn indirect calorimetric measurements became necessary for accurate estimation of caloric requirements.

Adult↗
PubMed1994

The effect of inhaled nitric oxide on smoke inhalation injury in an ovine model.

Smoke inhalation is a significant comorbid factor in thermal trauma. The effect of inhaled nitric oxide (NO) on smoke inhalation injury was evaluated in an ovine model. Following smoke exposure, group 1 animals (n = 9) spontaneously breathed room air, and group 2 animals (n = 8) breathed 20 parts per million of NO in air for 48 hours. Cardiopulmonary variables and blood gases were serially measured; bronchoalveolar lavage (BAL) was performed and wet-to-dry lung weight ratios (W/D) determined at 48 hours. Pulmonary vasoconstriction following smoke inhalation was significantly attenuated by inhaled NO (p < 0.05), which exerted no apparent effect on the systemic circulation. In group 2, the serial decline in pulmonary oxygenation was less than in group 1, consistent with a smaller physiologic shunt (p < 0.05). There were no significant differences in W/D, lung compliance, BAL fluid analysis results, or histologic evaluation findings between the two groups. These results suggest that inhaled NO exerted beneficial effects on pulmonary arterial hypertension and oxygenation following smoke inhalation without apparent amelioration of airway inflammation.

Administration, Inhalation↗
PubMed1994

The effect of inhaled nitric oxide on pulmonary ventilation-perfusion matching following smoke inhalation injury.

BACKGROUND: We previously reported that inhaled nitric oxide (NO) improved pulmonary function following smoke inhalation. This study evaluates the physiologic mechanism by which inhaled NO improves pulmonary function in an ovine model. METHODS: Forty-eight hours following wood smoke exposure to produce a moderate inhalation injury, 12 animals were anesthetized and mechanically ventilated (FIO2, 0.40; tidal volume, 15 mL/kg; PEEP, 5 cm H2O) for 3 hours. For the first and third hours, each animal was ventilated without NO: for the second hour, all animals were ventilated with 40 ppm NO. Cardiopulmonary variables and blood gases were measured every 30 minutes. The multiple inert gas elimination technique (MIGET) was performed during the latter 30 minutes of each hour. The data were analyzed by ANOVA. RESULTS: Pulmonary arterial hypertension and hypoxemia following smoke inhalation were significantly attenuated by inhaled NO compared with the values without NO (p < 0.05, ANOVA). Smoke inhalation resulted in a significant increase in blood flow distribution to low VA/Q areas (VA/Q < 0.10) with increased VA/Q dispersion. These changes were only partially attenuated by the use of inhaled NO. The SF6 (sulfur hexafluoride) retention ratio was also decreased by inhaled NO. Peak inspiratory pressures and pulmonary resistance values were not affected by inhaled NO. CONCLUSIONS: Inhaled NO moderately improved VA/Q mismatching following smoke inhalation by causing selective pulmonary vasodilation of ventilated areas in the absence of bronchodilation. This modest effect appears to be limited by the severe inflammatory changes that occur as a consequence of smoke exposure.

Analysis of Variance↗
PubMed1994

Effect of inhaled nitric oxide on pulmonary function after sepsis in a swine model.

BACKGROUND: Inhaled nitric oxide (NO) has been shown to improve sepsis induced pulmonary dysfunction. This study evaluated the mechanism by which inhaled NO improves pulmonary function in a porcine sepsis model. METHODS: After an infusion of Escherichia coli lipopolysaccharide (LPS, 200 micrograms/kg), animals were resuscitated with saline solution (1 ml/kg/min) and observed for 3 hours while mechanically ventilated (fraction of inspired oxygen, 0.6; tidal volume, 12 ml/kg; positive end-expiratory pressure, 5 cm H2O). Group 1 (LPS, n = 6) received no additional treatment. Group 2 (NO, n = 6) received inhaled NO (40 ppm) for the last 2 hours. Group 3 (control, n = 5) received only saline solution without LPS. Cardiopulmonary variables and blood gases were measured serially. Multiple inert gas elimination technique was performed at 3 hours. Wet to dry lung weight ratio was measured after necropsy. RESULTS: Lipopolysaccharide resulted in pulmonary arterial hypertension, pulmonary edema, and hypoxemia. Multiple inert gas elimination technique analysis indicated a significant increase in blood flow to true shunt and high ventilation perfusion distribution (VA/Q) areas with an increased dispersion of VA/Q distribution. All of these changes were significantly attenuated by NO. CONCLUSIONS: Inhaled NO significantly improved LPS induced VA/Q mismatching by decreasing both true shunt and high VA/Q areas, by decreasing pulmonary edema, and by redistributing blood flow from true shunt to ventilated areas.

Administration, Inhalation↗
PubMed1993

Improved survival of burned patients with inhalation injury.

OBJECTIVE: To study a cohort of patients treated at the same institution and to compare that patient population with that of a previous report documenting the comorbidity of inhalation injury and pneumonia. Specifically, we wanted to determine whether there had been an improvement in survival of patients suffering inhalation injury. DESIGN: A retrospective review. SETTING: The US Army Institute of Surgical Research, Ft Sam Houston, Tex, a 40-bed burn intensive care referral unit. SUBJECTS: One thousand two hundred fifty-six thermally injured patients treated between January 1985 and December 1990. MAIN OUTCOME MEASURE: A comparison of pneumonia frequency and ultimate survival of the current cohort of patients as compared with a previously generated stepwise logistic analysis predicting mortality on the basis of 1980 to 1984 patient data. RESULTS: Of 1256 burned patients admitted between 1985 and 1990, there were 330 identified as having inhalation injury. These patients were older (35.0 vs 26.6 years) and had more extensive burns (41.1% vs 18.3%) and a higher mortality (29.4% vs 5.0%) than did the patients without inhalation injury. When compared with a mortality predictor generated from 1980 through 1984 patient data, patients in the most recent period had a lower mortality than predicted (29.4% vs 41.4%). Patients with less severe injury (positive xenon scan, negative results of bronchoscopy; n = 85), although having a similar incidence of pneumonia (13.1% vs 19.5%) as the same group from 1980 through 1984, accounted for the most improvement in survival. The 3.6% mortality was significantly less than the predicted rate of 15.7%. Patients with positive results of bronchoscopy (n = 245) also showed some improvement in outcome from that predicted (38.3% vs 50.2%) despite no change in the rate of pneumonia (46.9% vs 48.5%). Further improvement in survival was realized in those patients supported with high-frequency ventilation. Although their age (33.9 vs 36.3 years), burn size (46.0% vs 45.5%), and duration of intubation (16.8 vs 15.1 days) were similar to those of conventionally treated patients, mortality was significantly less than predicted (16.4% vs 40.9%) and less than that in patients treated with conventional ventilation (16.4% vs 42.7%). CONCLUSIONS: The improvement in survival of patients with inhalation injury represents the aggregate effects of the general improvement and outcome of all burned patients, the prevention of pneumonia by high-frequency ventilation, and the reduced mortality from the pneumonias that did occur.

Adult↗
PubMed1993

Leukocyte responses to injury.

Injury elicits a response from all cells of the immune system in which cytokines and other metabolic products of activated leukocytes can act either beneficially to provide for enhanced host resistance or deleteriously to depress the function of remote organs and cause what has been termed systemic inflammation. These at times antithecal responses of leukocytes that appear to integrate postinjury changes in the neuroendocrine, immune, and coagulation systems have been implicated as principal causative factors in multiple systems organ failure. Numerous investigators have evaluated a variety of therapeutic agents to prevent and control infection by restoring leukocyte function, while others have evaluated antagonists and monoclonal antibodies as a means of controlling the exaggerated and persistent actions of leukocytes and cytokines caused by systemic inflammation. The redundancies of the cell populations and the cytokines and other metabolites produced by the cells predictably limit the effectiveness of any single agent and make clinical evaluation of such agents difficult.

Antibodies, Monoclonal↗