763
finding of a 54% frequency of HLGR led us to adopt the of routinely screening all enterococcal blood isolates for HLGR. Appropriate infection control measures are used for patients infected with these organisms to attempt to prevent intrahospital spread of these resistant isolates. The
policy
Department of Infection Control, and Clinical Microbiology Laboratory, Division of Infectious Diseases, Maimonides Medical Center, Brooklyn, New York 11219, USA
JEREMY D. GRADON SUZANNE LUTWICK LARRY I. LUTWICK MICHAEL H. LEVI
1. Gradon JD, Lutwick S, Lutwick LI, Levi MH. The incidence of high-level gentamicin resistance among enterococci isolated from blood cultures in a community hospital in New York. NY State Med J 1991; 91: 321-22. 2. Watanakunakorn C. The prevalence of high level aminoglycoside resistance among enterococci isolated from blood cultures during 1980-1988. J Antimicrob Chemother 1989; 24: 63-68.
Laboratory monitoring of antifungal chemotherapy SIR,—The British Society for Antimicrobial Chemotherapy Working Party (June 29, p 1577) discusses the value and necessity of monitoring serum concentrations of flucytosine during treatment. The bioassay seems to be recommended mainly because it can be done in non-specialised laboratories. We noted that flucytosine interfered with the two-slide enzymic assay for creatinine, with the Kodak ’Ektachem’ analyser. Discovery of this interference enabled us to design a procedure, using the Kodak analyser and its reagent system, that facilitated measurement of 5-fluorocytosine concentrations in blood. This assay was shown to correlate very well with the microbiological one.1 Huang et al2 reported a procedure that used the same basic principle but a different reagent system that did not require use of the Kodak ektachem analyser. Their procedure was slightly modified to operate in rate mode (rather than endpoint) for use with our Cobas ’Fara’ analyser. This modification reduced the reaction incubation time from 20 min to about 2 min. We have used this assay for the past two years and found its performance satisfactory. It is simple to use, economical, and has a short turnaround time (results are obtained in less than 10 min). Additionally, interpretation of results does not require the skill and experience that is necessary with the microbiological assay. The enzymic assay can easily be adopted by most non-specialised clinical laboratories; therefore, it warrants mention as a useful method for determination of serum flucytosine levels. Department of Laboratory Medicine, University Hospital, UBC Site, Vancouver, British Columbia V6T 2B5, Canada
A. SHIVJI M. A. NOBLE M. BERNSTEIN
MA, Harper B, Grant AG, Bernstein M. Rapid determination of 5fluorocytosine levels in blood J Clin Microbiol 1984; 20: 996-97 2. Huang CM, Kroll MH, Ruddel M, Washburn RG, Bennett JE. An enzymatic method for 5-fluorocytosine. Clin Chem 1988; 34: 59-62. 1. Noble
Development after exposure to mifepristone in early pregnancy outcome has been reported for pregnancies in three who decided to have babies despite having taken mifepristone.’ Postnatal examination of the infants revealed no abnormality and they continued to develop normally a few months later. We present two patients who decided to continue to term, despite having taken mifepristone for induced abortion. Patient 1-A 30-year-old woman (para 3 + 0) was given mifepristone (400 mg) at 6 weeks of amenorrhea. She decided not to proceed with termination. Ultrasound scans showed normal fetal morphology. The patient delivered a healthy boy weighing 3030 g at 41 weeks’ gestation. Postnatal examination of the infant revealed no
SiR,—The
women
abnormality. Patient 2-A 25-year-old primigravida was given mifepristone (400 mg) at 5 weeks’ gestation. Before prostaglandin administration, the patient indicated that she did not wish to proceed with termination. At 17 weeks’ gestation ultrasound scan showed a complete lack of amniotic sac, and stomach, gallbladder, and urinary tract were not seen. The pregnancy was terminated at 18
weeks’ gestation by prostaglandin administration. The 190 g fetus was malformed with typical sirenomelia: the lower limbs were fused with a single flexed foot. Seven toes were present. No external genitalia were seen and there were no anal or urethral openings. The fetus had a cleft palate and a cleft lip. The lungs were hypoplastic. Internal reproductive organs, lower urinary tract, and kidneys were absent. The ending of the left colon was blind. Sirenomelia (sympodia, or caudal regression syndrome) results from a primary defect in the mid-posterior axis mesoderm. The embryonic defect dates back to the primitive streak stage during the third week of gestation, before the development of the allantois.2 The cleft palate and cleft lip in our case was not related to caudal regression syndrome since the timing of induction of this syndrome is around 36 days of gestation.2 It is now generally recognised that mifepristone has teratogenic effects in the rabbit, but not in other species.3 Initial reported cases suggest that human fetuses that have been exposed to mifepristone and that are not subsequently aborted continue to develop normally. The number of cases reported is small. On the basis of our second case, however, a deleterious effect of mifepristone cannot be ruled out. Departments of Obstetrics and Gynaecology and Pathology, Antoine Beclere Hospital,
JEAN-CLAUDE PONS
Clamart 92141, France
MARIE-CLAIRE IMBERT
University Paris VI, CRAT, Saint-Antoine Hospital, Paris
ELISABETH ELEFANT CHARLES ROUX
Department of Obstetrics and Gynaecology, Etampes Hospital, Etampes
PAULE HERSCHKORN
Department of Obstetrics and University René Descartes, Cochin Hospital, Paris
EMILE PAPIERNIK
Gynaecology,
1. Lim
BH, Lees DAR, Bjornsson S, et al. Normal development after exposure to mifepristone in early pregnancy. Lancet 1990; 336: 257-58. 2. Jones KL. Smith’s recognizable patterns of human malformation Philadelphia: Saunders, 1988 3. Jost A. Animal reproduction-new date on the animal requirement of the pregnant rabbit: partial pregnancies and fetal anomalies resulting from treatment with a hormonal antagonist given at a sub-abortive dosage. CR Acad Sci 1986; 7: 281-84.
Nifedipine and hypotension SiR,—In your July 27 editorial you recommend sublingual nifedipine for severe, life-threatening hypertension in preference to sublingual captopril. You suggest that the vasodilator side-effects of this agent are only a minor drawback, and that previous reports of severe hypotension’ were probably largely the result of prematurely repeated doses. Four other cases have been recorded, however, 2,3 in which the administration of one 10 mg dose of sublingual nifedipine to patients with severe hypertension resulted in profound hypotension and myocardial ischaemia. Three of these patients (with initial diastolic blood pressures of 120 mm Hg or more) had myocardial infarctions. We have treated a 52-year-old man who we believe had cerebral damage from nifedipine-induced hypotension. He initially presented with a retinal artery thrombosis and a blood pressure of 230/135 mm Hg; he had no history of hypertension. He was admitted and his hypertension was controlled with atenolol 100 mg and hydrochlorthiazide 25 mg. No underlying cause was found and he was discharged well. On attendance at his general practitioner one week after discharge his blood pressure had risen to 213/117. Nifedipine (’Adalat retard’) 20 mg twice daily was prescribed, and he took the first dose at home and went to bed. Two hours later he awoke with a dense right hemiparesis. Since his blood pressure at home was unknown we cannot be certain that his stroke was related to a hypotensive episode. However, the timing of the event was coincident with the peak concentration of this dose of nifedipine;4- computed tomography showed a cerebral infarction, not haemorrhage, and his blood pressure was lower (213/117) than on his previous admission. As Capewell and CapewelF pointed out, most, if not all, antihypertensive agents can cause pronounced hypotension, and
finding of a 54% frequency of HLGR led us to adopt the of routinely screening all enterococcal blood isolates for HLGR. Appropriate infection control measures are used for patients infected with these organisms to attempt to prevent intrahospital spread of these resistant isolates. The
policy
Department of Infection Control, and Clinical Microbiology Laboratory, Division of Infectious Diseases, Maimonides Medical Center, Brooklyn, New York 11219, USA
JEREMY D. GRADON SUZANNE LUTWICK LARRY I. LUTWICK MICHAEL H. LEVI
1. Gradon JD, Lutwick S, Lutwick LI, Levi MH. The incidence of high-level gentamicin resistance among enterococci isolated from blood cultures in a community hospital in New York. NY State Med J 1991; 91: 321-22. 2. Watanakunakorn C. The prevalence of high level aminoglycoside resistance among enterococci isolated from blood cultures during 1980-1988. J Antimicrob Chemother 1989; 24: 63-68.
Laboratory monitoring of antifungal chemotherapy SIR,—The British Society for Antimicrobial Chemotherapy Working Party (June 29, p 1577) discusses the value and necessity of monitoring serum concentrations of flucytosine during treatment. The bioassay seems to be recommended mainly because it can be done in non-specialised laboratories. We noted that flucytosine interfered with the two-slide enzymic assay for creatinine, with the Kodak ’Ektachem’ analyser. Discovery of this interference enabled us to design a procedure, using the Kodak analyser and its reagent system, that facilitated measurement of 5-fluorocytosine concentrations in blood. This assay was shown to correlate very well with the microbiological one.1 Huang et al2 reported a procedure that used the same basic principle but a different reagent system that did not require use of the Kodak ektachem analyser. Their procedure was slightly modified to operate in rate mode (rather than endpoint) for use with our Cobas ’Fara’ analyser. This modification reduced the reaction incubation time from 20 min to about 2 min. We have used this assay for the past two years and found its performance satisfactory. It is simple to use, economical, and has a short turnaround time (results are obtained in less than 10 min). Additionally, interpretation of results does not require the skill and experience that is necessary with the microbiological assay. The enzymic assay can easily be adopted by most non-specialised clinical laboratories; therefore, it warrants mention as a useful method for determination of serum flucytosine levels. Department of Laboratory Medicine, University Hospital, UBC Site, Vancouver, British Columbia V6T 2B5, Canada
A. SHIVJI M. A. NOBLE M. BERNSTEIN
MA, Harper B, Grant AG, Bernstein M. Rapid determination of 5fluorocytosine levels in blood J Clin Microbiol 1984; 20: 996-97 2. Huang CM, Kroll MH, Ruddel M, Washburn RG, Bennett JE. An enzymatic method for 5-fluorocytosine. Clin Chem 1988; 34: 59-62. 1. Noble
Development after exposure to mifepristone in early pregnancy outcome has been reported for pregnancies in three who decided to have babies despite having taken mifepristone.’ Postnatal examination of the infants revealed no abnormality and they continued to develop normally a few months later. We present two patients who decided to continue to term, despite having taken mifepristone for induced abortion. Patient 1-A 30-year-old woman (para 3 + 0) was given mifepristone (400 mg) at 6 weeks of amenorrhea. She decided not to proceed with termination. Ultrasound scans showed normal fetal morphology. The patient delivered a healthy boy weighing 3030 g at 41 weeks’ gestation. Postnatal examination of the infant revealed no
SiR,—The
women
abnormality. Patient 2-A 25-year-old primigravida was given mifepristone (400 mg) at 5 weeks’ gestation. Before prostaglandin administration, the patient indicated that she did not wish to proceed with termination. At 17 weeks’ gestation ultrasound scan showed a complete lack of amniotic sac, and stomach, gallbladder, and urinary tract were not seen. The pregnancy was terminated at 18
weeks’ gestation by prostaglandin administration. The 190 g fetus was malformed with typical sirenomelia: the lower limbs were fused with a single flexed foot. Seven toes were present. No external genitalia were seen and there were no anal or urethral openings. The fetus had a cleft palate and a cleft lip. The lungs were hypoplastic. Internal reproductive organs, lower urinary tract, and kidneys were absent. The ending of the left colon was blind. Sirenomelia (sympodia, or caudal regression syndrome) results from a primary defect in the mid-posterior axis mesoderm. The embryonic defect dates back to the primitive streak stage during the third week of gestation, before the development of the allantois.2 The cleft palate and cleft lip in our case was not related to caudal regression syndrome since the timing of induction of this syndrome is around 36 days of gestation.2 It is now generally recognised that mifepristone has teratogenic effects in the rabbit, but not in other species.3 Initial reported cases suggest that human fetuses that have been exposed to mifepristone and that are not subsequently aborted continue to develop normally. The number of cases reported is small. On the basis of our second case, however, a deleterious effect of mifepristone cannot be ruled out. Departments of Obstetrics and Gynaecology and Pathology, Antoine Beclere Hospital,
JEAN-CLAUDE PONS
Clamart 92141, France
MARIE-CLAIRE IMBERT
University Paris VI, CRAT, Saint-Antoine Hospital, Paris
ELISABETH ELEFANT CHARLES ROUX
Department of Obstetrics and Gynaecology, Etampes Hospital, Etampes
PAULE HERSCHKORN
Department of Obstetrics and University René Descartes, Cochin Hospital, Paris
EMILE PAPIERNIK
Gynaecology,
1. Lim
BH, Lees DAR, Bjornsson S, et al. Normal development after exposure to mifepristone in early pregnancy. Lancet 1990; 336: 257-58. 2. Jones KL. Smith’s recognizable patterns of human malformation Philadelphia: Saunders, 1988 3. Jost A. Animal reproduction-new date on the animal requirement of the pregnant rabbit: partial pregnancies and fetal anomalies resulting from treatment with a hormonal antagonist given at a sub-abortive dosage. CR Acad Sci 1986; 7: 281-84.
Nifedipine and hypotension SiR,—In your July 27 editorial you recommend sublingual nifedipine for severe, life-threatening hypertension in preference to sublingual captopril. You suggest that the vasodilator side-effects of this agent are only a minor drawback, and that previous reports of severe hypotension’ were probably largely the result of prematurely repeated doses. Four other cases have been recorded, however, 2,3 in which the administration of one 10 mg dose of sublingual nifedipine to patients with severe hypertension resulted in profound hypotension and myocardial ischaemia. Three of these patients (with initial diastolic blood pressures of 120 mm Hg or more) had myocardial infarctions. We have treated a 52-year-old man who we believe had cerebral damage from nifedipine-induced hypotension. He initially presented with a retinal artery thrombosis and a blood pressure of 230/135 mm Hg; he had no history of hypertension. He was admitted and his hypertension was controlled with atenolol 100 mg and hydrochlorthiazide 25 mg. No underlying cause was found and he was discharged well. On attendance at his general practitioner one week after discharge his blood pressure had risen to 213/117. Nifedipine (’Adalat retard’) 20 mg twice daily was prescribed, and he took the first dose at home and went to bed. Two hours later he awoke with a dense right hemiparesis. Since his blood pressure at home was unknown we cannot be certain that his stroke was related to a hypotensive episode. However, the timing of the event was coincident with the peak concentration of this dose of nifedipine;4- computed tomography showed a cerebral infarction, not haemorrhage, and his blood pressure was lower (213/117) than on his previous admission. As Capewell and CapewelF pointed out, most, if not all, antihypertensive agents can cause pronounced hypotension, and
