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Paradoxical effect of inhaled nitric oxide in a newborn with pulmonary hypertension
Letters to the Editor
Non-haemolytic transfusion reactions after platelet substitution
1
2
SiR-Life-threatening non-haemolytic transfusion reactions (NHTR) after platelet substitution vary from urticarial to severe anaphylactic reactions and occur with a frequency of 1-2%.1 We have investigated factors possibly associated with these reactions, such as total complement activity (CH100) as an indicator for complement activation and total serum IgE and specific IgE antibodies against common aero-allergens and food-allergens as diagnostic markers for allergic events.3 We analysed 57 NHTR of unknown cause after platelet substitution. HLA-antibodies in the platelet concentrate and in the recipients’ sera, or bacterial contamination of the concentrate were excluded. Because of a previous report,4 the reactions were divided into three groups by symptoms: febrile (fever and chill), allergic (rash, itching, urticaria, or concomitant circulatory distress), and circulatory (circulatory distress with no signs of allergic events). Most of the NHTR after platelet concentrate substitution were allergic (51 %), followed by febrile (32%), and circulatory (17%). We included five patients who had multiple allergic NHTR after platelet concentrate transfusion. Whilst the first NHTR were mostly mild (rash, itching), those after repeated transfusion occurred almost immediately and with an increasing severity (ie, shock). Similar observations have been made after transfusion of fresh frozen plasma.5 No major alterations in laboratory variables were detected in the platelet concentrate itself. Specific IgE antibodies were found in 2 (4%) of the 57 concentrates. CH100 and total serum IgE were normal. By contrast, these variables did alter in the recipients’ serum. Most patients who had circulatory distress after platelet-concentrate transfusion had complement activation ; allergic NHTR were not associated with decreased complement activity. However, the frequency of specific IgE antibodies was associated with allergic NHTR. 93% of all patients with allergic transfusion reactions had these antibodies, whereas only about 20% of sera of patients with febrile reactions or circulatory distress symptoms had these antibodies. Total serum IgE in recipients’ sera was of minor diagnostic value, probably because of large individual variances (table).
*Mean
(SD). Table: Complement activity, serum IgE, and antibodies in recipients’ sera after NHTR
specific IgE
Atopic patients have a higher risk of hypersensitivity NHTR platelet substitution than non-atopic recipients. Therefore, we suggest allergy investigation for all patients who require multiple platelet transfusion. Additionally, a diagnosis of allergy should be considered in patients who have a first NHTR, even if the reaction was only mild. after
D
Wilhelm, M Klouche, A Fiebelkorn, S Görg, H Klüter, H Kirchner
Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, D-23538 Lübeck, Germany
364
3 4
5
Kevy SV, Schmidt PJ, et al.
Febrile nonhemolytic transfusion reactions and the limited role of leukoagglutinins in their etiology. Transfusion 1962; 2: 71. Miletic VD, Popovich O. Complement activation in stored platelet concentrates. Transfusion 1993; 33: 150-54. Johansson SGO. The clinical impact of the discovery of IgE. Ann Allergy 1982; 48: 325-30. Buck SA, Kickler TS, McGuire M, et al. The utility of platelet washing using an automated procedure for severe platelet allergic reactions. Transfusion 1987; 27: 391-93. Mollison PL, Engelfried CP, Contreras M. Blood transfusion in clinical medicine. 8th ed. Oxford: Blackwell, 1988: 16: 737.
Paradoxical effect of inhaled nitric oxide in newborn with pulmonary hypertension
a
SiR-Inhaled nitric oxide (NO) has selective pulmonary vasodilatory effects in animals and humans.’ Inhaled NO has been reported to increase oxygenation in persistent pulmonary hypertension of the newborn (PPHN).2 We report a case of acute oxygen desaturation in a newborn with PPHN during the inhalation of NO. A female twin of 36 weeks was born with an Apgar score of 1 at 1 min and required mechanical ventilation with a fraction of inspired oxygen (Fi02) of 10. Her mother had received indomethacin for hydramnios and threatened premature birth during the last week of pregnancy. PPHN was confirmed by a preductal oxygen saturation (Sp02) of 60% and a right-to-left shunt across the foramen ovale. Echocardiography showed an almost complete closure of the ductus arteriosus, a dilated right ventricle with a rightward deviation of the ventricular septum, and tricuspid regurgitation. Group B streptococcus was isolated from tracheal secretions and she received amoxycillin. Because of the persisting hypoxaemia (preductal Sp02 82%) with arterial oxygen pressure in the descending aorta (postductal) of 4-11 kPa, and despite mechanical ventilation at high rates, inotropic support (dopamine, dobutamine, and norepinephrine), and sedation, we decided to try NO inhalation. Parental informed consent was obtained. During NO inhalation at 7 ppm (Fi02 0-97) and then at 15 ppm (Fi02 0-93), the preductal Sp02 dropped to 34% within 2 min without any change in mean systemic arterial pressure. NO inhalation and norepinephrine infusion were immediately discontinued and the Sp02 rose to 80% within 5 min. 4 hours later a second inhalation of NO at 7 ppm was given during echocardiography. The preductal Sp02 dropped from 86% to 63% within 3 min associated with a marked increase of right-to-left shunting and returned to 85% in 7 min, with a decrease of the right-to-left shunt after stopping NO inhalation. Mean systemic arterial pressure fell from 41 to 35 mm Hg under NO inhalation and went back to 38 mm Hg after its discontinuation. A few hours later, the child died of persisting hypoxaemia. The autopsy showed hyperplasia of the pulmonary arteriolar wall. The other twin had the same echocardiographic findings with a less severe
hypoxia. Indomethacin treatment during late pregnancy can induce ductal constriction,3modifications of the pulmonary arteriolar wall in fetuses,4 and PPHN. Furthermore, indomethacinand inhaled NO’ have been reported to reverse early-phase group B streptococcus-induced pulmonary hypertension in piglets. In our case, acute hypoxaemia during NO inhalation was not due
and does not seem to be in decrease systemic arterial pressure. only related is Pulmonary vasoconstriction unlikely to have been caused by the decrease of Fi02 which was small. To our knowledge, no paradoxical effect of inhaled NO has been described before. NO inhalation has been recently reported to induce pulmonary vasodilation in a ligated ductus arteriosus animal.8 We speculate in-utero indomethacin may be responsible for this paradoxical response to NO inhalation. to
ventilation/perfusion mismatch, to a
Denis Oriot, Thierry Boussemart, Michel Berthier, Dominique Bonneau, Damien Coisne
The elevation of ventricular and atrial thresholds after carbamazepine accords with observations that the drug has class I antiarrhythmic properties.’ This class increases myocardial stimulation threshold.2,4 Attention should be paid to stimulus amplitude in patients with pace-makers before
starting carbamazepine. Pierre Ambrosi, Gérard
1
Departments of Pediatrics and Cardiology, University Hospital of Poitiers, 2
818-19. 3 Eronen M. The hemodynamic effects of antenatal indomethacin and a &bgr;-sympathomimetic agent on the fetus and the newborn: a randomized study. Pediatr Res 1993; 33: 615-19. 4 Levin DL, Mills LJ, Weinberg AG. Hemodynamic, pulmonary vascular, and myocardial abnormalities secondary to pharmacologic construction of the fetal ductus arteriosus. Circulation 1979; 60:
360-64. 5 Manchester D, Mayolis HS, Sheldon RE. Possible associaton between maternal indomethacin therapy and primary hypertension of the newborn. Am J Obstet Gynecol 1976; 126: 467-69. 6 Runkle B, Goldberg RN, Streitfeld MM, et al. Cardiovascular changes in group B streptococcal sepsis in the piglet: response to indomethacin and the relationship to prostacyclin and thromboxane A2. Pediatr Res 1984; 15: 899-904. 7 Berger JI, Gibson RL, Redding GJ, et al. Effect of inhaled nitric oxide during group B streptococcal sepsis in piglets. Am Rev Respir Dis 1993; 147: 1080-86. 8 Zayek M, Cleveland D, Morin FC. Treatment of persistent pulmonary hypertension in the newborn lamb by inhaled nitric oxide. J Pediatr 1993; 122: 743-50.
Carbamazepine and pacing threshold SiR-Carbamazepine can cause sinus node depression and atrioventricular blocks.1 We describe an abrupt rise in stimulation threshold causing failure of a functioning pacer in a 59-year-old man who had an aortic valve replacement for aortic regurgitation. A complete heart block followed the operation and the patient received a permanent dual-chamber pacemaker (DDDR-Synergist, Medtronic). He was also treated with lithium for mania. 2 years later, because left ventricular function had progressively worsened, we decided to replace lithium by carbamazepine. The day before the start of carbamazepine, the pace-maker was checked. An electrocardiogram (ECG) showed normal atrial and ventricular pacing; telemetry revealed that atrial and ventricular pulse amplitudes were 2-5 V and the battery was normal. After 5 days of carbamazepine the patient was admitted because of dizziness. ECG showed that atrial and ventricular stimuli were ineffective without sensory failure. Atrial and ventricular capture occurred when ventricular and atrial pulse amplitudes were increased to 5 V. Usual causes of stimulation-threshold elevation were exc1uded.2 Glucose and potassium were normal; chest radiography showed a good position of the leads. Lithium could have contributed to threshold elevation since it can depress the sinus node and prolong atrioventricular conduction; however this was unlikely 5 days after stopping lithium (half-life, 24 hours).3 Plasma carbamazepine was 21 [tmol/L and the drug was continued. 2 months later the patient received a heart transplant. Examination of the heart showed absence of myocardial infarction, cellular hypertrophy, and mild myocardial fibrosis.
Louis
Poggi, Roger Luccioni
G, Bergfeldt L, Vallin H, Tomson T, Edhag O. Electrophysiologic effects and clinical hazard of carbamazepine treatment for neurologic disorders in patients with abnormalities of the cardiac conduction system. Am Heart J 1991; 121: 1421-29. Dohrmann ML, Goldschlager N. Metabolic and pharmacologic effects on myocardial stimulation threshold in patients with cardiac pacemakers. In: Barold S, ed. Modern cardiac pacing. New York:
Kennebäck
86000-Poitiers, France
1 Pepke-Zaba J, Higenbottam TW, Dinh-Xuan AT, et al. Inhaled nitric oxide as a cause of selective pulmonary vasodilatation in pulmonary hypertension. Lancet 1991; 338: 1173-74. 2 Roberts JD, Polaner DM, Lang P, et al. Inhaled nitric oxide in persistent pulmonary hypertension of the newborn. Lancet 1992; 340:
Faugère,
Service de cardiologie, Hôpital de la Timone, Marseille, France
Futura, 1985: 161-69. Singer I, Rotenberg D. Mechanisms of lithium action. N Engl J Med 1973; 289: 254-60. 4 Bianconi L, Boccadamo R, Toscano S, et al. Effects of oral propafenone therapy on chronic myocardial threshold. PACE 1992; 15:
3
148-54.
Albuminuria with
or
without streptokinase
SIR—Lynch and colleagues (April 17, p 1024) suggest that streptokinase was a causative factor for proteinuria in patients with acute myocardial infarction (AMI). However, Pickett and Hilton (June 12, p 1538) and others1 have recorded proteinuria in the early phase of AMI in patients who did not receive streptokinase. Similarly, findings in a series of patients with AMI treated in one institution with or without streptokinase suggest that proteinuria was probably due to a neurohormonal activation in the early phase of an AMI rather than to
thrombolysis.2,3 We investigated prospectively 22 patients with AMI for urinary concentration of albumin (U-ALB; indicating glomerular dysfunction) and retinol-binding protein (U-RBP; indicating dysfunction of the proximal tubuli). Streptokinase was given to 12 patients admitted within 6 h of onset of symptoms, but not to 7 patients admitted later than 24 h after this time. The two groups did not differ significantly with respect to clinical characteristics such as sex (10 men, 2 women vs 5 men, 2 women), age (median age at AMI 62 years vs 65), and maximum serum lactate dehydrogenase-1 activity (median 489 vs 1122
U/L). U-ALB and U-RBP were measured on day of admission, the following days, and on the fifth day. Initially, U-ALB and U-RBP were often raised, but values fell to near normal in the following days.2 Patients admitted within 6 h of onset of symptoms had higher U-ALB and U-RBP concentrations than did the other group (table). We also compared U-ALB and U-RBP at similar points in the clinical course from the onset of
two
All values= median
(range). *Day 2
streptokinase vs
no
= second day after onset of symptoms. tU-RBP, streptokinase, p=004 (Mann-WhitneyU test, two-tailed) ; all other compansons were non-significant. Table: Urinary albumin and retinol-binding protein concentrations at admission and In relation to onset of symptoms of AMI
365
Non-haemolytic transfusion reactions after platelet substitution
1
2
SiR-Life-threatening non-haemolytic transfusion reactions (NHTR) after platelet substitution vary from urticarial to severe anaphylactic reactions and occur with a frequency of 1-2%.1 We have investigated factors possibly associated with these reactions, such as total complement activity (CH100) as an indicator for complement activation and total serum IgE and specific IgE antibodies against common aero-allergens and food-allergens as diagnostic markers for allergic events.3 We analysed 57 NHTR of unknown cause after platelet substitution. HLA-antibodies in the platelet concentrate and in the recipients’ sera, or bacterial contamination of the concentrate were excluded. Because of a previous report,4 the reactions were divided into three groups by symptoms: febrile (fever and chill), allergic (rash, itching, urticaria, or concomitant circulatory distress), and circulatory (circulatory distress with no signs of allergic events). Most of the NHTR after platelet concentrate substitution were allergic (51 %), followed by febrile (32%), and circulatory (17%). We included five patients who had multiple allergic NHTR after platelet concentrate transfusion. Whilst the first NHTR were mostly mild (rash, itching), those after repeated transfusion occurred almost immediately and with an increasing severity (ie, shock). Similar observations have been made after transfusion of fresh frozen plasma.5 No major alterations in laboratory variables were detected in the platelet concentrate itself. Specific IgE antibodies were found in 2 (4%) of the 57 concentrates. CH100 and total serum IgE were normal. By contrast, these variables did alter in the recipients’ serum. Most patients who had circulatory distress after platelet-concentrate transfusion had complement activation ; allergic NHTR were not associated with decreased complement activity. However, the frequency of specific IgE antibodies was associated with allergic NHTR. 93% of all patients with allergic transfusion reactions had these antibodies, whereas only about 20% of sera of patients with febrile reactions or circulatory distress symptoms had these antibodies. Total serum IgE in recipients’ sera was of minor diagnostic value, probably because of large individual variances (table).
*Mean
(SD). Table: Complement activity, serum IgE, and antibodies in recipients’ sera after NHTR
specific IgE
Atopic patients have a higher risk of hypersensitivity NHTR platelet substitution than non-atopic recipients. Therefore, we suggest allergy investigation for all patients who require multiple platelet transfusion. Additionally, a diagnosis of allergy should be considered in patients who have a first NHTR, even if the reaction was only mild. after
D
Wilhelm, M Klouche, A Fiebelkorn, S Görg, H Klüter, H Kirchner
Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, D-23538 Lübeck, Germany
364
3 4
5
Kevy SV, Schmidt PJ, et al.
Febrile nonhemolytic transfusion reactions and the limited role of leukoagglutinins in their etiology. Transfusion 1962; 2: 71. Miletic VD, Popovich O. Complement activation in stored platelet concentrates. Transfusion 1993; 33: 150-54. Johansson SGO. The clinical impact of the discovery of IgE. Ann Allergy 1982; 48: 325-30. Buck SA, Kickler TS, McGuire M, et al. The utility of platelet washing using an automated procedure for severe platelet allergic reactions. Transfusion 1987; 27: 391-93. Mollison PL, Engelfried CP, Contreras M. Blood transfusion in clinical medicine. 8th ed. Oxford: Blackwell, 1988: 16: 737.
Paradoxical effect of inhaled nitric oxide in newborn with pulmonary hypertension
a
SiR-Inhaled nitric oxide (NO) has selective pulmonary vasodilatory effects in animals and humans.’ Inhaled NO has been reported to increase oxygenation in persistent pulmonary hypertension of the newborn (PPHN).2 We report a case of acute oxygen desaturation in a newborn with PPHN during the inhalation of NO. A female twin of 36 weeks was born with an Apgar score of 1 at 1 min and required mechanical ventilation with a fraction of inspired oxygen (Fi02) of 10. Her mother had received indomethacin for hydramnios and threatened premature birth during the last week of pregnancy. PPHN was confirmed by a preductal oxygen saturation (Sp02) of 60% and a right-to-left shunt across the foramen ovale. Echocardiography showed an almost complete closure of the ductus arteriosus, a dilated right ventricle with a rightward deviation of the ventricular septum, and tricuspid regurgitation. Group B streptococcus was isolated from tracheal secretions and she received amoxycillin. Because of the persisting hypoxaemia (preductal Sp02 82%) with arterial oxygen pressure in the descending aorta (postductal) of 4-11 kPa, and despite mechanical ventilation at high rates, inotropic support (dopamine, dobutamine, and norepinephrine), and sedation, we decided to try NO inhalation. Parental informed consent was obtained. During NO inhalation at 7 ppm (Fi02 0-97) and then at 15 ppm (Fi02 0-93), the preductal Sp02 dropped to 34% within 2 min without any change in mean systemic arterial pressure. NO inhalation and norepinephrine infusion were immediately discontinued and the Sp02 rose to 80% within 5 min. 4 hours later a second inhalation of NO at 7 ppm was given during echocardiography. The preductal Sp02 dropped from 86% to 63% within 3 min associated with a marked increase of right-to-left shunting and returned to 85% in 7 min, with a decrease of the right-to-left shunt after stopping NO inhalation. Mean systemic arterial pressure fell from 41 to 35 mm Hg under NO inhalation and went back to 38 mm Hg after its discontinuation. A few hours later, the child died of persisting hypoxaemia. The autopsy showed hyperplasia of the pulmonary arteriolar wall. The other twin had the same echocardiographic findings with a less severe
hypoxia. Indomethacin treatment during late pregnancy can induce ductal constriction,3modifications of the pulmonary arteriolar wall in fetuses,4 and PPHN. Furthermore, indomethacinand inhaled NO’ have been reported to reverse early-phase group B streptococcus-induced pulmonary hypertension in piglets. In our case, acute hypoxaemia during NO inhalation was not due
and does not seem to be in decrease systemic arterial pressure. only related is Pulmonary vasoconstriction unlikely to have been caused by the decrease of Fi02 which was small. To our knowledge, no paradoxical effect of inhaled NO has been described before. NO inhalation has been recently reported to induce pulmonary vasodilation in a ligated ductus arteriosus animal.8 We speculate in-utero indomethacin may be responsible for this paradoxical response to NO inhalation. to
ventilation/perfusion mismatch, to a
Denis Oriot, Thierry Boussemart, Michel Berthier, Dominique Bonneau, Damien Coisne
The elevation of ventricular and atrial thresholds after carbamazepine accords with observations that the drug has class I antiarrhythmic properties.’ This class increases myocardial stimulation threshold.2,4 Attention should be paid to stimulus amplitude in patients with pace-makers before
starting carbamazepine. Pierre Ambrosi, Gérard
1
Departments of Pediatrics and Cardiology, University Hospital of Poitiers, 2
818-19. 3 Eronen M. The hemodynamic effects of antenatal indomethacin and a &bgr;-sympathomimetic agent on the fetus and the newborn: a randomized study. Pediatr Res 1993; 33: 615-19. 4 Levin DL, Mills LJ, Weinberg AG. Hemodynamic, pulmonary vascular, and myocardial abnormalities secondary to pharmacologic construction of the fetal ductus arteriosus. Circulation 1979; 60:
360-64. 5 Manchester D, Mayolis HS, Sheldon RE. Possible associaton between maternal indomethacin therapy and primary hypertension of the newborn. Am J Obstet Gynecol 1976; 126: 467-69. 6 Runkle B, Goldberg RN, Streitfeld MM, et al. Cardiovascular changes in group B streptococcal sepsis in the piglet: response to indomethacin and the relationship to prostacyclin and thromboxane A2. Pediatr Res 1984; 15: 899-904. 7 Berger JI, Gibson RL, Redding GJ, et al. Effect of inhaled nitric oxide during group B streptococcal sepsis in piglets. Am Rev Respir Dis 1993; 147: 1080-86. 8 Zayek M, Cleveland D, Morin FC. Treatment of persistent pulmonary hypertension in the newborn lamb by inhaled nitric oxide. J Pediatr 1993; 122: 743-50.
Carbamazepine and pacing threshold SiR-Carbamazepine can cause sinus node depression and atrioventricular blocks.1 We describe an abrupt rise in stimulation threshold causing failure of a functioning pacer in a 59-year-old man who had an aortic valve replacement for aortic regurgitation. A complete heart block followed the operation and the patient received a permanent dual-chamber pacemaker (DDDR-Synergist, Medtronic). He was also treated with lithium for mania. 2 years later, because left ventricular function had progressively worsened, we decided to replace lithium by carbamazepine. The day before the start of carbamazepine, the pace-maker was checked. An electrocardiogram (ECG) showed normal atrial and ventricular pacing; telemetry revealed that atrial and ventricular pulse amplitudes were 2-5 V and the battery was normal. After 5 days of carbamazepine the patient was admitted because of dizziness. ECG showed that atrial and ventricular stimuli were ineffective without sensory failure. Atrial and ventricular capture occurred when ventricular and atrial pulse amplitudes were increased to 5 V. Usual causes of stimulation-threshold elevation were exc1uded.2 Glucose and potassium were normal; chest radiography showed a good position of the leads. Lithium could have contributed to threshold elevation since it can depress the sinus node and prolong atrioventricular conduction; however this was unlikely 5 days after stopping lithium (half-life, 24 hours).3 Plasma carbamazepine was 21 [tmol/L and the drug was continued. 2 months later the patient received a heart transplant. Examination of the heart showed absence of myocardial infarction, cellular hypertrophy, and mild myocardial fibrosis.
Louis
Poggi, Roger Luccioni
G, Bergfeldt L, Vallin H, Tomson T, Edhag O. Electrophysiologic effects and clinical hazard of carbamazepine treatment for neurologic disorders in patients with abnormalities of the cardiac conduction system. Am Heart J 1991; 121: 1421-29. Dohrmann ML, Goldschlager N. Metabolic and pharmacologic effects on myocardial stimulation threshold in patients with cardiac pacemakers. In: Barold S, ed. Modern cardiac pacing. New York:
Kennebäck
86000-Poitiers, France
1 Pepke-Zaba J, Higenbottam TW, Dinh-Xuan AT, et al. Inhaled nitric oxide as a cause of selective pulmonary vasodilatation in pulmonary hypertension. Lancet 1991; 338: 1173-74. 2 Roberts JD, Polaner DM, Lang P, et al. Inhaled nitric oxide in persistent pulmonary hypertension of the newborn. Lancet 1992; 340:
Faugère,
Service de cardiologie, Hôpital de la Timone, Marseille, France
Futura, 1985: 161-69. Singer I, Rotenberg D. Mechanisms of lithium action. N Engl J Med 1973; 289: 254-60. 4 Bianconi L, Boccadamo R, Toscano S, et al. Effects of oral propafenone therapy on chronic myocardial threshold. PACE 1992; 15:
3
148-54.
Albuminuria with
or
without streptokinase
SIR—Lynch and colleagues (April 17, p 1024) suggest that streptokinase was a causative factor for proteinuria in patients with acute myocardial infarction (AMI). However, Pickett and Hilton (June 12, p 1538) and others1 have recorded proteinuria in the early phase of AMI in patients who did not receive streptokinase. Similarly, findings in a series of patients with AMI treated in one institution with or without streptokinase suggest that proteinuria was probably due to a neurohormonal activation in the early phase of an AMI rather than to
thrombolysis.2,3 We investigated prospectively 22 patients with AMI for urinary concentration of albumin (U-ALB; indicating glomerular dysfunction) and retinol-binding protein (U-RBP; indicating dysfunction of the proximal tubuli). Streptokinase was given to 12 patients admitted within 6 h of onset of symptoms, but not to 7 patients admitted later than 24 h after this time. The two groups did not differ significantly with respect to clinical characteristics such as sex (10 men, 2 women vs 5 men, 2 women), age (median age at AMI 62 years vs 65), and maximum serum lactate dehydrogenase-1 activity (median 489 vs 1122
U/L). U-ALB and U-RBP were measured on day of admission, the following days, and on the fifth day. Initially, U-ALB and U-RBP were often raised, but values fell to near normal in the following days.2 Patients admitted within 6 h of onset of symptoms had higher U-ALB and U-RBP concentrations than did the other group (table). We also compared U-ALB and U-RBP at similar points in the clinical course from the onset of
two
All values= median
(range). *Day 2
streptokinase vs
no
= second day after onset of symptoms. tU-RBP, streptokinase, p=004 (Mann-WhitneyU test, two-tailed) ; all other compansons were non-significant. Table: Urinary albumin and retinol-binding protein concentrations at admission and In relation to onset of symptoms of AMI
365