Streptase Side Effects
Generic name: streptokinase
Medically reviewed by Drugs.com. Last updated on May 18, 2024.
Note: This document provides detailed information about Streptase.
Applies to streptokinase: injectable powder for injection.
General
The production of the general body symptom, fever, has also been associated with urokinase, which is not antigenic. While the mechanism of fever is not known, this suggests that fever may be due to breakdown products of thrombi rather than to thrombolytic drugs.[Ref]
Hypersensitivity
In the 8,592 patients in the ISIS-2 trial who received SK there were no confirmed incidences of anaphylactic shock. The GISSI study 7 incidents of nonfatal anaphylactic reactions among 5,860 patients who had received SK (0.1%), though 99 patients (1.7%) had allergic reactions severe enough to discontinue therapy and another 42 (0.7%) were identified retrospectively. Skin testing immediately before SK therapy appears to be a practical, sensitive, and specific tool to help identify patients at risk for anaphylaxis.[Ref]
The overall incidence of hypersensitivity reactions to SK from the ISIS-2, GISSI-1 and GISSI-2 data ranged from 1.6% to 4.4%. Smaller studies have reported an incidence of 2% to 6%. Acute allergic reactions to SK ranged from minor dyspnea, urticaria, pruritus, flushing, nausea, headache, or musculoskeletal pain to severe anaphylaxis, bronchospasm, or periorbital or angioneurotic edema. SK-induced fever has been reported in 30% to 50% of patients. Severe acute hypersensitivity reactions have usually required discontinuation of therapy, antihistamines, and/or corticosteroids. In rare cases, adrenergic agents have been required to treat anaphylactic shock.[Ref]
Cardiovascular
Since cardiovascular side effects may be more likely among the population of patients in whom SK in indicated, a cause-and-effect relationship to the drug is not always clear. Transient hypotension has been reported during SK therapy in approximately 40% of patients (anterior or inferior wall MI). Hypotension has been associated with reperfusion, which has been associated with decreased in-hospital mortality. Reperfusion of the myocardium has resulted in arrhythmias in 80% of patients who experience reperfusion. The most common reperfusion arrhythmia is a transient accelerated idioventricular rhythm, which is typically clinically benign. Premature ventricular depolarizations during reperfusion do not necessarily predict severe ventricular arrhythmias.
Dyspnea, cyanosis, rare cases of hemorrhagic myocardial infarction, serious ventricular arrhythmias, hemopericardium, and death from cardiogenic shock have been associated with thrombolytic therapy, in general.
Rare cases of cholesterol embolization syndrome have been associated with SK and other thrombolytic agents.[Ref]
Cholesterol embolization, a rare syndrome that typically presents with painful ischemia or necrosis of the digits, myalgias, skin changes of livedo reticularis and often progresses to renal failure and death, has occurred. Other findings have included cyanosis, ulcers, gangrene of the hands and feet, myalgias, intestinal infarction or eosinophilia. The exact mechanism is not known, but is believed to be due to physical disruption of atheromatous plaques by lysis of platelet-fibrin thrombi.[Ref]
Renal
New or worsened renal impairment has been associated with SK-induced immune complex disease. Rare cases of mild and transient acute renal insufficiency with proteinuria without evidence of hypersensitivity have been described after SK therapy.[Ref]
The differential diagnosis of acute renal failure following SK therapy includes ischemic injury, immunologic injury, and postrenal obstruction. Ischemia may be due to low cardiac output or hypotension secondary to acute myocardial infarction (if present), a direct effect of SK, reperfusion-induced hypotension, or hemorrhagic shock. These conditions may cause acute tubular necrosis. Ischemia may also be due to emboli from mural thrombi (if present), cholesterol emboli syndrome, or myoglobinuria.
Immunologic injury to the kidney may be related to SK-induced serum sickness, Schonlein-Henoch purpura, or immune complex nephritis.
Retroperitoneal hemorrhage or ureter thrombosis during or following SK therapy can cause postrenal obstruction.[Ref]
Nervous system
Hemorrhagic stroke, a potentially serious nervous system side effect, has affected approximately 0.1% to 1.0% of patients. Extremely rare cases of Guillain-Barre syndrome have been associated with the use of SK.[Ref]
In one case of Guillain-Barre syndrome (GBS) associated with SK oligoclonal IgG bands in the cerebrospinal fluid and serum were shown to be specific for streptokinase. Clinical symptoms of GBS were thought to result from SK-antibody complex-mediated damage to the local blood-nerve barrier.[Ref]
Gastrointestinal
Gastrointestinal side effects have been rare. Hemorrhagic gastritis has been associated with the thrombolytic state. Nausea or vomiting has been reported during thrombolytic therapy. Unusual cases of hemorrhagic splenic rupture and subcapsular hepatic hematoma have occurred.[Ref]
Hepatic
Rare cases of SK-induced hepatic dysfunction have been reported . Some experts believe that mild, transient liver function test elevations indicative of cholestasis do not appear to be caused by toxic or allergic effects of SK itself, but by the high activities of the proteolytic enzymes, plasminogen activator and plasmin. Rare cases of jaundice have been reported.[Ref]
In a prospective study of 24 nonselected patients with peripheral arterial occlusions undergoing SK therapy, 18 had significant liver enzyme elevations typical of cholestasis and impaired hepatocellular integrity and function, but none became jaundiced.[Ref]
Musculoskeletal
Rare cases of musculoskeletal back pain have been reported. In some cases bleeding into the iliopsoas muscles was discovered, but in most reported cases, there was no evidence of allergy, aortic dissection, worsened myocardial infarction or retroperitoneal hemorrhage.[Ref]
Genitourinary
A genitourinary concern for menstruating women who are considered for thrombolytic therapy has been whether SK can safely be used during menses. The drug has been used safely during menses, perhaps because hemostasis of the uterine endothelium after the first day of menses depends on arteriolar vasoconstriction more than the formation of fibrin.[Ref]
Respiratory
Adult respiratory distress syndrome (ARDS) has been rarely associated with the use of SK. ARDS is a known complication of hypersensitivity to SK.[Ref]
Dermatologic
Dermatologic side effects have included rare cases of dermal microemboli. Some cases have progressed to dermal necrosis.[Ref]
Immunologic
SK is antigenic and may induce the formation of antibodies. Delayed hypersensitivity reactions may result in the development of immune complex disease, presenting as fever, vasculitic or purpuric rashes, abnormal renal and liver function tests, arthralgias, serum sickness, and/or a syndrome resembling adult respiratory distress syndrome. A case of SK-induced direct antiglobulin test-positive hemolysis has been reported.[Ref]
Hematologic
Hematologic side effects of streptokinase (the active ingredient contained in Streptase) (SK) have included minor and major bleeding. The risk of bleeding appears to be significantly increased when plasma fibrinogen levels fall below 250 mg/dl. Minor bleeding has occurred in up to 67% of patients, presenting as venipuncture or arterial cutdown site oozing, microscopic hematuria, hemoptysis, or hematemesis. Local bleeding usually has been controlled by manual compression for 20 to 30 minutes. Serious or major bleeding, including gastrointestinal, genitourinary, joint, retroperitoneal or intracerebral hemorrhage, has occurred in 0.3% to 6.0% of patients. Adjuvant heparin, but not aspirin, therapy appears to increase the risk of bleeding.
Intracranial hemorrhage in 0.1% to 1.0% of patients and rare cases of intramyocardial hemorrhage have been reported. Several fatalities due to intracranial or retroperitoneal hemorrhage have occurred during thrombolytic therapy.
Rare cases of embolization and anti-SK-mediated platelet aggregation during or after SK therapy have been reported. There is speculation that fibrinolysis could increase pericatheter thrombosis, which can result in local or distal thromboembolism.[Ref]
Predisposing risk factors for the development of intracranial hemorrhage during thrombolytic therapy for myocardial infarction have included body weight less than 70 kg, age greater than 65 years old, and preexisting anticoagulant therapy. The authors of GISSI concluded that the risk of hemorrhagic stroke is also directly related to Killip classification.
A meta-analysis of 30 studies dealing with proximal lower extremity deep vein thrombosis (DVT) has revealed the following relative risks for patients who received SK + heparin versus heparin alone: any major bleeding, 2.9; central nervous system (CNS) bleeding, 4.5; mortality from CNS bleeding, 4.0; pulmonary embolism (PE), 1.0; mortality from PE, 1.0; postphlebitic syndrome, 0.4 Side Effects associated with streptokinase. Some dosage forms listed on this page may not apply specifically to the brand name Streptase.
Applies to streptokinase: injectable powder for injection.
General
The production of the general body symptom, fever, has also been associated with urokinase, which is not antigenic. While the mechanism of fever is not known, this suggests that fever may be due to breakdown products of thrombi rather than to thrombolytic drugs.[Ref]
Hypersensitivity
In the 8,592 patients in the ISIS-2 trial who received SK there were no confirmed incidences of anaphylactic shock. The GISSI study 7 incidents of nonfatal anaphylactic reactions among 5,860 patients who had received SK (0.1%), though 99 patients (1.7%) had allergic reactions severe enough to discontinue therapy and another 42 (0.7%) were identified retrospectively. Skin testing immediately before SK therapy appears to be a practical, sensitive, and specific tool to help identify patients at risk for anaphylaxis.[Ref]
The overall incidence of hypersensitivity reactions to SK from the ISIS-2, GISSI-1 and GISSI-2 data ranged from 1.6% to 4.4%. Smaller studies have reported an incidence of 2% to 6%. Acute allergic reactions to SK ranged from minor dyspnea, urticaria, pruritus, flushing, nausea, headache, or musculoskeletal pain to severe anaphylaxis, bronchospasm, or periorbital or angioneurotic edema. SK-induced fever has been reported in 30% to 50% of patients. Severe acute hypersensitivity reactions have usually required discontinuation of therapy, antihistamines, and/or corticosteroids. In rare cases, adrenergic agents have been required to treat anaphylactic shock.[Ref]
Cardiovascular
Since cardiovascular side effects may be more likely among the population of patients in whom SK in indicated, a cause-and-effect relationship to the drug is not always clear. Transient hypotension has been reported during SK therapy in approximately 40% of patients (anterior or inferior wall MI). Hypotension has been associated with reperfusion, which has been associated with decreased in-hospital mortality. Reperfusion of the myocardium has resulted in arrhythmias in 80% of patients who experience reperfusion. The most common reperfusion arrhythmia is a transient accelerated idioventricular rhythm, which is typically clinically benign. Premature ventricular depolarizations during reperfusion do not necessarily predict severe ventricular arrhythmias.
Dyspnea, cyanosis, rare cases of hemorrhagic myocardial infarction, serious ventricular arrhythmias, hemopericardium, and death from cardiogenic shock have been associated with thrombolytic therapy, in general.
Rare cases of cholesterol embolization syndrome have been associated with SK and other thrombolytic agents.[Ref]
Cholesterol embolization, a rare syndrome that typically presents with painful ischemia or necrosis of the digits, myalgias, skin changes of livedo reticularis and often progresses to renal failure and death, has occurred. Other findings have included cyanosis, ulcers, gangrene of the hands and feet, myalgias, intestinal infarction or eosinophilia. The exact mechanism is not known, but is believed to be due to physical disruption of atheromatous plaques by lysis of platelet-fibrin thrombi.[Ref]
Renal
New or worsened renal impairment has been associated with SK-induced immune complex disease. Rare cases of mild and transient acute renal insufficiency with proteinuria without evidence of hypersensitivity have been described after SK therapy.[Ref]
The differential diagnosis of acute renal failure following SK therapy includes ischemic injury, immunologic injury, and postrenal obstruction. Ischemia may be due to low cardiac output or hypotension secondary to acute myocardial infarction (if present), a direct effect of SK, reperfusion-induced hypotension, or hemorrhagic shock. These conditions may cause acute tubular necrosis. Ischemia may also be due to emboli from mural thrombi (if present), cholesterol emboli syndrome, or myoglobinuria.
Immunologic injury to the kidney may be related to SK-induced serum sickness, Schonlein-Henoch purpura, or immune complex nephritis.
Retroperitoneal hemorrhage or ureter thrombosis during or following SK therapy can cause postrenal obstruction.[Ref]
Nervous system
Hemorrhagic stroke, a potentially serious nervous system side effect, has affected approximately 0.1% to 1.0% of patients. Extremely rare cases of Guillain-Barre syndrome have been associated with the use of SK.[Ref]
In one case of Guillain-Barre syndrome (GBS) associated with SK oligoclonal IgG bands in the cerebrospinal fluid and serum were shown to be specific for streptokinase. Clinical symptoms of GBS were thought to result from SK-antibody complex-mediated damage to the local blood-nerve barrier.[Ref]
Gastrointestinal
Gastrointestinal side effects have been rare. Hemorrhagic gastritis has been associated with the thrombolytic state. Nausea or vomiting has been reported during thrombolytic therapy. Unusual cases of hemorrhagic splenic rupture and subcapsular hepatic hematoma have occurred.[Ref]
Hepatic
Rare cases of SK-induced hepatic dysfunction have been reported . Some experts believe that mild, transient liver function test elevations indicative of cholestasis do not appear to be caused by toxic or allergic effects of SK itself, but by the high activities of the proteolytic enzymes, plasminogen activator and plasmin. Rare cases of jaundice have been reported.[Ref]
In a prospective study of 24 nonselected patients with peripheral arterial occlusions undergoing SK therapy, 18 had significant liver enzyme elevations typical of cholestasis and impaired hepatocellular integrity and function, but none became jaundiced.[Ref]
Musculoskeletal
Rare cases of musculoskeletal back pain have been reported. In some cases bleeding into the iliopsoas muscles was discovered, but in most reported cases, there was no evidence of allergy, aortic dissection, worsened myocardial infarction or retroperitoneal hemorrhage.[Ref]
Genitourinary
A genitourinary concern for menstruating women who are considered for thrombolytic therapy has been whether SK can safely be used during menses. The drug has been used safely during menses, perhaps because hemostasis of the uterine endothelium after the first day of menses depends on arteriolar vasoconstriction more than the formation of fibrin.[Ref]
Respiratory
Adult respiratory distress syndrome (ARDS) has been rarely associated with the use of SK. ARDS is a known complication of hypersensitivity to SK.[Ref]
Dermatologic
Dermatologic side effects have included rare cases of dermal microemboli. Some cases have progressed to dermal necrosis.[Ref]
Immunologic
SK is antigenic and may induce the formation of antibodies. Delayed hypersensitivity reactions may result in the development of immune complex disease, presenting as fever, vasculitic or purpuric rashes, abnormal renal and liver function tests, arthralgias, serum sickness, and/or a syndrome resembling adult respiratory distress syndrome. A case of SK-induced direct antiglobulin test-positive hemolysis has been reported.[Ref]
Hematologic
Hematologic side effects of streptokinase (the active ingredient contained in Streptase) (SK) have included minor and major bleeding. The risk of bleeding appears to be significantly increased when plasma fibrinogen levels fall below 250 mg/dl. Minor bleeding has occurred in up to 67% of patients, presenting as venipuncture or arterial cutdown site oozing, microscopic hematuria, hemoptysis, or hematemesis. Local bleeding usually has been controlled by manual compression for 20 to 30 minutes. Serious or major bleeding, including gastrointestinal, genitourinary, joint, retroperitoneal or intracerebral hemorrhage, has occurred in 0.3% to 6.0% of patients. Adjuvant heparin, but not aspirin, therapy appears to increase the risk of bleeding.
Intracranial hemorrhage in 0.1% to 1.0% of patients and rare cases of intramyocardial hemorrhage have been reported. Several fatalities due to intracranial or retroperitoneal hemorrhage have occurred during thrombolytic therapy.
Rare cases of embolization and anti-SK-mediated platelet aggregation during or after SK therapy have been reported. There is speculation that fibrinolysis could increase pericatheter thrombosis, which can result in local or distal thromboembolism.[Ref]
Predisposing risk factors for the development of intracranial hemorrhage during thrombolytic therapy for myocardial infarction have included body weight less than 70 kg, age greater than 65 years old, and preexisting anticoagulant therapy. The authors of GISSI concluded that the risk of hemorrhagic stroke is also directly related to Killip classification.
A meta-analysis of 30 studies dealing with proximal lower extremity deep vein thrombosis (DVT) has revealed the following relative risks for patients who received SK + heparin versus heparin alone: any major bleeding, 2.9; central nervous system (CNS) bleeding, 4.5; mortality from CNS bleeding, 4.0; pulmonary embolism (PE), 1.0; mortality from PE, 1.0; postphlebitic syndrome, 0.4.
The risk of hemorrhagic side effects from streptokinase can be minimized with patient selection. Major risk factors for intracranial hemorrhage have included known intracranial tumor, prior neurosurgery, stroke within the past six months, head trauma within the past month. Other significant risk factors included severe, uncontrolled hypertension, a remote stroke known not to be hemorrhagic, recent transient ischemic attacks, advanced age, and female gender.[Ref]
References
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79. Kelly MP, Bielawska C (1991) "Recurrence of a reactive arthritis following streptokinase therapy." Postgrad Med J, 67, p. 402
80. Glassock RJ, Ritz E, Bommer J, Andrassy K, Waldherr R (1984) "Acute renal failure, hypertension and skin necrosis in a patient with streptokinase therapy." Am J Nephrol, 4, p. 193-200
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88. Bednarczyk EM, Sherlock SC, Farah MG, Green JA (1989) "Anaphylactic reaction to streptokinase with first exposure: case report and review of the literature." DICP, 23, p. 869-72
89. Green C (1993) "Antistreptokinase titres after topical streptokinase." Lancet, 341, p. 1602-3
90. Birnbaum Y, Strasberg B, Rechavia E, Neuman Y, Stahl B (1993) "Acute renal failure following intravenous streptokinase infusion for acute myocardial infarction." West J Med, 158, p. 406-9
91. Lynch M, Pentecost BL, Littler WA, Stockley RA (1993) "Why do patients develop reactions to streptokinase?" Clin Exp Immunol, 94, p. 279-85
92. Lee HS, Yule S, McKenzie A, Cross S, Reid T, Davidson R, Jennings K (1993) "Hypersensitivity reactions to streptokinase in patients with high pre- treatment antistreptokinase antibody and neutralisation titres." Eur Heart J, 14, p. 1640-3
93. Cross DB (1994) "Should streptokinase be readministered? insights from recent studies of antistreptokinase antibodies." Med J Aust, 161, p. 100-1
94. Gray MY, Lazarus JH (1994) "Iritis after treatment with streptokinase." BMJ, 309, p. 97
95. Lantin JP, Gattesco S, Duclos A, Zanchi A, Schaller MD, Pecoud A, Aubert V (1994) "Anaphylactoid purpura like vasculitis following fibrinolytic therapy - role of the immune response to streptokinase." Clin Exp Rheumatol, 12, p. 429-33
96. Cooper JP, Quarry DP, Beale DJ, Chappell AG (1994) "Life-threatening, localized angio-oedema associated with streptokinase." Postgrad Med J, 70, p. 592-3
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98. Mcgrath K, Hogan C, Hunt D, Omalley C, Green N, Dauer R, Dalli A (1995) "Neutralising antibodies after streptokinase treatment for myocardial infarction: a persisting puzzle." Br Heart J, 74, p. 122-3
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100. DiMuzio A, DiGuglielmo G, Feliciani C, DeLuca G, DiMuzio M, Uncini A (1997) "Inflammatory myopathy after intravenous streptokinase." Muscle Nerve, 20, p. 619-21
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102. Ridker PM, Michel T (1989) "Streptokinase therapy and cholesterol embolization." Am J Med, 87, p. 357-8
103. Zatuchni J (1988) "Postthrombolytic high-risk syndrome." Angiology, 39, p. 773-4
104. Alexopoulos D, Collins R, Adamopoulos S, Peto R, Sleight P (1991) "Holter monitoring of ventricular arrhythmias in a randomised, controlled study of intravenous streptokinase in acute myocardial infarction." Br Heart J, 65, p. 9-13
105. Richardson SG, Allen DC, Morton P, Murtagh JG, Scott ME, O'Keeffe DB (1989) "Pathological changes after intravenous streptokinase treatment in eight patients with acute myocardial infarction." Br Heart J, 61, p. 390-5
106. Pirson Y, Honhon B, Cosyns JP, van Ypersele C (1988) "Cholesterol embolism in a renal graft after treatment with streptokinase." Br Med J (Clin Res Ed), 296, p. 394-5
107. Blankenship JC, Almquist AK (1989) "Cardiovascular complications of thrombolytic therapy in patients with a mistaken diagnosis of acute myocardial infarction." J Am Coll Cardiol, 14, p. 1579-82
108. Schwartz MW, McDonald GB (1987) "Cholesterol embolization syndrome. Occurrence after intravenous streptokinase therapy for myocardial infarction." JAMA, 258, p. 1934-5
109. Pochmalicki G, Feldman L, Meunier P, Rougeot C, Weschler J, Jan F (1992) "Cholesterol embolisation syndrome after thrombolytic therapy for myocardial infarction." Lancet, 339, p. 58-9
110. Cercek B, Horvat M (1985) "Arrhythmias with brief, high-dose intravenous streptokinase infusion in acute myocardial infarction." Eur Heart J, 6, p. 109-13
111. Herlitz J, Hartford M, Aune S, Karlsson T (1993) "Occurrence of hypotension during streptokinase infusion in suspected acute myocardial infarction, and its relation to prognosis and metoprolol therapy." Am J Cardiol, 71, p. 1021-4
112. Gemmill JD, Hogg KJ, Douglas JT, Dunn FG, Lowe GD, Rae AP, Hillis WS (1993) "The incidence and mechanism of hypotension following thrombolytic therapy for acute myocardial infarction with streptokinase-containing agents--lack of relationship to pretreatment streptokinase resistance." Eur Heart J, 14, p. 819-25
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115. Payne ST, Hosker HS, Allen MB, Bradbury H, Page RL (1989) "Transient impairment of renal function after streptokinase therapy." Lancet, 2, p. 1398
116. Pickett TM, Hilton PJ (1993) "Proteinuria and streptokinase." Lancet, 341, p. 1538
117. Lynch M, Pentecost BL, Littler WA, Stockley RA (1993) "Proteinuria with streptokinase." Lancet, 341, p. 1024
118. Lang EK (1985) "Streptokinase therapy: complications of intra-arterial use." Radiology, 154, p. 75-7
119. Birnbaum Y, Barash D, Rechavia E, Regev A, Stahl B, Mager A (1993) "Acute iritis and transient renal impairment following thrombolytic therapy for acute myocardial infarction." Ann Pharmacother, 27, p. 1539-40
120. Zilliox AP, Domoto DT, Hutcheson PS, Tsai CC, Slavin RG (1993) "Henoch-Schoenlein purpura due to streptokinase." J Clin Immunol, 13, p. 415-23
121. Birnbaum Y, Hasdai D, Stahl B (1994) "Renal adverse effects of streptokinase therapy." Int J Cardiol, 46, p. 1-6
122. Lynch M, Hoffmann NV, Aroney CN (1995) "Thrombolytic treatment and proteinuria." Br Heart J, 74, p. 354-7
123. Maggioni AP, Franzosi MG, Santoro E, White H, Van de Werf F, Tognoni G (1992) "The risk of stroke in patients with acute myocardial infarction after thrombolytic and antithrombotic treatment. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico II (GISSI-2), andThe International Study Group." N Engl J Med, 327, p. 1-6
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125. Chrysanthopoulos C, Kounis N (1992) "Rhabdomyolysis due to combined treatment with lovastatin and cholestyramine." BMJ, 304, p. 1225
126. Leaf DA, MacDonald I, Kliks B, Wilson R, Jones SR (1984) "Streptokinase and the Guillain-Barre syndrome." Ann Intern Med, 100, p. 617
127. Arrowsmith JB, Milstien JB, Kuritsky JN, Murano G (1985) "Streptokinase and the Guillain-Barre syndrome." Ann Intern Med, 103, p. 302
128. Maggioni AP, Franzosi MG, Farina ML, Santoro E, Celani MG, Ricci S, Tognoni G (1991) "Cerebrovascular events after myocardial infarction: analysis of the GISSI trial. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI)." BMJ, 302, p. 1428-31
129. Kinshuck D (1992) "Bilateral hypopyon and streptokinase." BMJ, 305, p. 1332
130. Aldrich MS, Sherman SA, Greenberg HS (1985) "Cerebrovascular complications of streptokinase infusion." JAMA, 253, p. 1777-9
131. Kaiser R, Kaufmann R, Czygan M, Lang H, Lucking CH (1993) "Guillain-Barre syndrome following streptokinase therapy." Clin Investig, 71, p. 795-801
132. Freimark D, Leor R, Hod H, Elian D, Kaplinsky E, Rabinowitz B (1991) "Impaired hepatic function tests after thrombolysis for acute myocardial infarction." Am J Cardiol, 67, p. 535-7
133. Mager A, Birnbaum Y, Zlotikamien B, Strasberg B, Rechavia E, Sagie A, Sclarovsky S (1991) "Streptokinase-induced jaundice in patients with acute myocardial infarction." Am Heart J, 121, p. 1543-4
134. Polkey MI, Oliver RM, Walker JM (1992) "Hepatic dysfunction induced by streptokinase." Am J Gastroenterol, 87, p. 1062
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137. Pipek R, Avizohar O, Levy Y (1994) "Transient hepatic dysfunction in two brothers receiving heparin and streptokinase: a genetic predisposition?" Int J Cardiol, 46, p. 299-301
138. Gilutz H, Cohn G, Battler A (1996) "Jaundice induced by streptokinase." Angiology, 47, p. 281-4
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140. Shah M, Taylor RT (1990) "Low back pain associated with streptokinase." BMJ, 301, p. 1219
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142. Lear J, Rajapakse R, Pohl J (1992) "Low back pain associated with streptokinase." Lancet, 340, p. 851
143. Simel DL, Moorman JR, Pryor SL, Piscitelli JT, Sharma GV (1984) "Is streptokinase safe during menses?" Arch Intern Med, 144, p. 841-2
144. Powers JC (1992) "Is menstruation a contraindication to thrombolytic therapy?." Clin Cardiol, 15, p. 875
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147. Abraham JS, Wilson M, Scripcariu V, Barnes PC, Marcuson RW (1994) "Microembolism from aortic aneurysm and ventricular thrombus: a complication of intravenous streptokinase." Postgrad Med J, 70, p. 756-8
148. Juhlin P, Bostrom PA, Torp A, Bredberg A (1999) "Streptokinase antibodies inhibit reperfusion during thrombolytic therapy with streptokinase in acute myocardial infarction." J Intern Med, 245, p. 483-8
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