STREPTOKINASE

Drugs in Pregnancy and Lactation.

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Name: STREPTOKINASE
Class: Thrombolytic
Risk Factor:    CM

Fetal Risk Summary

No reports linking the use of streptokinase with congenital defects have been located. Animal reproductive studies have not been conducted with streptokinase (1).

Only minimal amounts cross the placenta and are not sufficient to cause fibrinolytic effects in the fetus (2,3,4,5,6,7 and 8). Although the passage of streptokinase is blocked by the placenta, streptokinase antibodies do cross to the fetus (6). This passive sensitization would have clinical importance only if the neonate required streptokinase therapy. A 1970 review briefly mentioned the use of streptokinase in 12 pregnant women with deep vein thrombosis and in one case of placental insufficiency, but no fetal or neonatal data were given (9).

Fetal death occurred in one case shortly after the start of streptokinase for massive pulmonary embolism in a 24-year-old multipara at 34 weeks' gestation (4). An autopsy found no evidence of fetal hemorrhage and the loss was attributed to maternal hypoxia.

In one study, 24 patients were treated in the 2nd and 3rd trimesters without fetal complications (6). Use in the 1st trimester for maternal thrombophlebitis has also been reported (7). No adverse effects were observed in the infant born at term.

A 1970 report described the use of streptokinase in a 35-year-old pregnant woman with recurrent embolism of the left middle cerebral artery (10,11). At 33 weeks' gestation, low-dose streptokinase was infused at 10,000 IU/hour for 2 hours, then 5000 IU/hour for 4 hours. Warfarin (50 mg IV) was given during the infusion and heparin was started following streptokinase. Complete resolution of carotid occlusion was documented on angiogram with improvement of the patient's symptoms. Rupture of the membranes occurred 9 hours after the start of streptokinase followed 1 hour later by delivery of premature triplets (1.7, 1.5, and 1.7 kg). No complications of streptokinase were observed in the mother or newborns, although one of the triplets died 5 days later of respiratory distress syndrome.

Two women were treated with streptokinase (60,000 IU for 30 minutes, then 100,000 IU/hour for approximately 3–7 days) for iliofemoral thrombi in the left leg at 3 and 6 months' gestation (12). No other specific data were given except that the women had no complications and both had normal deliveries.

An abstract published in 1981 briefly summarized the results of treating acute thrombotic occlusion of one or both iliofemoral veins in 122 pregnant women (13). Gestational ages varied between 14 and 38 weeks' gestation. Dosage was 1.0–1.5 million IU for 30 minutes followed by an hourly infusion of not more than 250,000 IU/hour for 24–48 hours. The complications included premature rupture of membranes (1), abruptio placentae (1) with fetal death, and severe maternal hemorrhage during treatment necessitating emergency delivery by cesarean section (2).

A 21-year-old woman presented in her 26th week of pregnancy with premature labor and a marginal placental abruption (without retroplacental clot) (14). She was treated with two courses of tranexamic acid (an antifibrinolytic agent) and started on terbutaline. At 28 weeks' gestation, the patient developed acute massive pulmonary embolism and was started on heparin therapy. She continued to deteriorate and, after 40 hours, therapy was changed to streptokinase, 100,000 IU for 30 minutes followed by an infusion of 100,000 IU/hour for 10 hours. Therapy was stopped at this time because of the return of regular uterine contractions. A spontaneous vaginal delivery of a breech, preterm, 1140-g male infant occurred 75 minutes later. No complications of therapy were noted in the infant. The mother, who was restarted on streptokinase 8 hours after delivery, had postpartum hemorrhage that required transfusion and eventual discontinuance of therapy after a total treatment time of 29 hours.

A 28-year-old patient at 28 weeks' gestation was treated with streptokinase, 250,000 IU for 30 minutes then 100,000 IU/hour for 24 hours, for prosthetic mitral valve obstruction secondary to a thrombus (15). Treatment resulted in the complete resolution of her symptoms and the return of normal valve function. Heparin infusion was started following streptokinase therapy and continued until the onset of labor 7 days later. A premature 1.4-kg infant was delivered vaginally who did well except for neonatal jaundice that responded to phototherapy.

A 1995 Reference reviewed the treatment of 166 women with streptokinase (24 case reports including those described above, the majority of which have occurred in Germany), for deep vein thrombosis, pulmonary embolus, thrombosed prosthetic heart valve, axillary vein thrombosis, and cerebral arterial embolism (16). Gestational lengths varied from 9 to 38 weeks. Complications included maternal hemorrhage (N=13), maternal death (N=2), preterm delivery (N=6), and pregnancy loss (N=9) (16). The fetal and neonatal deaths included fetal loss because of maternal death (N=2), spontaneous abortion and/or intrauterine fetal death without further details (N=3), spontaneous abortion at 13 weeks' gestation (N=1), neonatal death secondary to respiratory distress syndrome (N=1), fetal death secondary to abruptio placentae during therapy (N=1), and intrauterine fetal death occurring 8 hours after start of therapy (N=1). No direct relationship between thrombolytic therapy and fetal death was apparent in seven of the losses, but a causal association cannot be excluded in the latter two cases (16). The theoretical concern that thrombolytic therapy before 14 weeks' gestation may interfere with placental implantation cannot be answered from the available reports. Four women were treated with streptokinase prior to 14 weeks, one of whom had a spontaneous abortion (16). No congenital anomalies were reported after streptokinase therapy, including the five cases in which treatment occurred during the 1st trimester.

In summary, streptokinase does not appear to present a major direct or indirect risk to the fetus, especially if treatment is withheld during the intrapartum period. Fetal losses have occurred that may have been related to therapy, but fetal hemorrhage and teratogenicity as a result of streptokinase have not been reported and are not expected because of the minimal placental transfer. Sensitization of the newborn to streptokinase from antibodies received in utero is a complication only if the neonate required therapy. The effect of thrombolytic therapy on placental implantation early in pregnancy has not been determined, but no increased risk of preterm rupture of membranes, premature labor, or placental hemorrhage is apparent (16). Based on these data, streptokinase can be used during gestation if the mother's condition requires this therapy.

Breast Feeding Summary

No data are available. Because of the nature of the indications for this agent and its very short half-life (approximately 23 minutes for the streptokinase-plasminogen complex), the opportunities for its use during lactation and potential exposure of the nursing infant are minimal.

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References

  1. Product information. Streptase. Astra USA, 1996.
  2. Pfeifer GW. Distribution and placental transfer of 131I streptokinase. Aust Ann Med 1970;19(Suppl):17–8.
  3. Hall RJC, Young C, Sutton GC, Campbell S. Treatment of acute massive pulmonary embolism by streptokinase during labour and delivery. Br Med J 1972;4:647–9.
  4. McTaggart DR, Ingram TG. Massive pulmonary embolism during pregnancy treated with streptokinase. Med J Aust 1977;1:18–20.
  5. Benz JJ, Wick A. The problem of fibrinolytic therapy in pregnancy. Schweiz Med Wochenschr 1973;103:1359–63.
  6. Ludwig H. Results of streptokinase therapy in deep venous thrombosis during pregnancy. Postgrad Med J 1973;49(Suppl 5):65–7.
  7. Walter C, Koestering H. Therapeutische thrombolyse in der neunten schwangerschalftswoche. Dtsch Med Wochenschr 1969;94:32–4.
  8. Witchitz S, Veyrat C, Moisson P, Scheinman N, Rozenstajn L. Fibrinolytic treatment of thrombus on prosthetic heart valves. Br Heart J 1980;44:545–54.
  9. Pfeifer GW. The use of thrombolytic therapy in obstetrics and gynaecology. Aust Ann Med 1970;19(Suppl):28–31.
  10. Amias AG. Cerebral vascular disease in pregnancy. 2. Occlusion. J Obstet Gynaecol Br Commonw 1970;77:312–25.
  11. Amias AG. Streptokinase, cerebral vascular disease—and triplets. Br Med J 1977;1:1414–5.
  12. Johansson E, Ericson K, Zetterquist S. Streptokinase treatment of deep venous thrombosis of the lower extremity. Acta Med Scand 1976;199:89–74.
  13. Ludwig H, Genz HJ. Thrombolytic treatment during pregnancy. Thromb Haemost 1981;46:438.
  14. Fagher B, Ahlgren M, Ästedt B. Acute massive pulmonary embolism treated with streptokinase during labor and the early puerperium. Acta Obstet Gynecol Scand 1990;69:659–62.
  15. Ramamurthy S, Talwar KK, Saxena A, Juneja R, Takkar D. Prosthetic mitral valve thrombosis in pregnancy successfully treated with streptokinase. Am Heart J 1994;127:446–8.
  16. Turrentine MA, Braems G, Ramirez MM. Use of thrombolytics for the treatment of thromboembolic disease during pregnancy. Obstet Gynecol Surv 1995;50:534–41.

Index

Q&A about Streptokinase

tandra_b...
Why doesn't injection of streptokinase cause a streptococcal infecton?
How do we know the streptokinase will digest fibrin only and not good tissues? if bacterial enzyme sreptokinase is used to digest fibrin in patients with atherosclerosis.
N E
Eric B
The bacterial enzyme streptokinase is used to digest fibrin (blood clots) in patients with atherosclerosis.?
The bacterial enzyme streptokinase is used to digest fibrin (blood clots) in patients with atherosclerosis. Why doesn’t injection of streptokinase cause a streptococcal infection? Why does the streptokinase only affect fibrin and not beneficial tissues around it?
Patrion
Streptokinase actually indirectly breaks down blood clots via the activation of another enzyme known as plasminogen which ultimately cleaves into plasmin which is the "action taker" in breaking down clots. Since streptokinase is only an enzyme and not a weaken pathogen such as vaccines, streptococcus won't invade the host.
valerie h
how do we know that streptokinase will digest fibrin only and not good tisues?
goldwing
It is an enzyme, all enzymes have specific targets due to protein makeup of the molecule. This enzyme is secreted to disolve clots which inhibit the spread of strep in the body.