51 P.T.H. and calcitonin secretion in ursemic patients. Further studies are needed to assess their long-term effects on the secretion of these hormones and on renal osteodystrophy. The contrast between the significant effect of propranolol and the non-significant effect of metoprolol on P.T.H. and plasma-calcitonin supports the idea that P.T.H. and calcitonin secretion is modulated by specific &bgr;2 receptors. Our results thus accord with those of Aurbach et al.’1 A. FOURNIER B. COEVOET J. F. DE FREMONT J. GUERIS G. CAILLENS Service d’Hémodialyse du C.H.U., C. DESPLAN Amiens Hôpital Nord, C. CALMETTE 8000 Amiens, France M. S. MOUKHTAR et I.N.S.E.R.M. U 18 et U 113, Paris
Platelet-count
ASPIRIN FOR THE TREATMENT OF RECURRENT TOXÆMIA woman was seen in 1976 at the SacraMedical Center in her 29th week of pregnancy. She had
SIR,-A 31-year-old mento
hypertension (180/110 mm Hg), thrombocytopenia (pla000/jjd), and was delivered by cassarean section at approximately the 30th week. The infant weighted 870 g and died after 4 days with ascites, thrombocytopenia, and renal failure (mirror syndrome).2 The patient’s first pregnancy, managed elsewhere, had run a similar course. Between pregnancies her platelet-counts were normal, as were all other laboratory tests and physical findings. In the 15th week of gestation of her third pregnancy, her platelet-count was 59 000/ul and her hxmatocrit was 40%. Bone-marrow and peripheral-blood smear suggested peripheral consumption of platelets. There was no other laboratory suggestion of microangiopathic anxmia or consumption coagulopathy throughout her pregancy. She was treated with heparin 5000 units three times a day for 4 weeks with no appreciable effect on platelet-count. At the 22nd week, aspirin 600 mg three times a day was started, with gradual improve-’ ment in platelet-count (figure). The aspirin was discontinued in the 32nd week because of the fear of creating a closed fetal ductus. She then began to severe
during pregnancy.
Arrows represent dexamethasone 12 mg.
normotensive with sedation and bedrest. However,
at
her 33rd
hypertension (160/100 mm Hg) appeared, and platelet-count decreased to 50 000/1 and her haematocrit
week,
severe
her increased. The ultrasonic B scans had shown normal fetal growth and amniotic fluid up to the 28th week, but with the toxxmia fetal growth apparently ceased and amniotic fluid dis-
appeared.
again given aspirin and her platelet-count returned normal in the 34th week. Twice she was given dexamethasone to mature fetal lungs. The non-stress fetal heartrate test pattern showed variable decelerations, and we were unable to obtain further amniotic fluid for analysis. She was delivered by caesarean section of a 1410 g growth-retarded male fetus (placental weight 305 g) who showed no respiratory distress. The baby’s platelet-count was 180 000/1 and he did well. Post partum, the patient’s platelet-count remained normal, as did her blood-pressure. She showed a marked haemodilution in the post-partum period with a 30% fall in haematocrit. This case demonstrates the thrombocytopenia seen with some cases of recurrent toxxmia, as well as the possible beneficial effects of aspirin therapy. Aspirin may benefit thrombocvtopenia in children with the haemolytic ursemic syndrome.3 It She
was
to near
G. D., and others, Calc. Tissue Res. 1977, suppl. 22, 117. R., Cotton, D., Haesslein, H. Am J. Obstet. Gynec. in the 3. Arenson, E., August, C. J. Pediat. 1975, 86, 957.
1. Aurbach, 2. Goodlin,
press
aspinn.
may also ameliorate this type of recurrent toxasmia, which may be related to the post-partum haemolytic renal failure syndrome.
telet-count 40
experience painful uterine contractions and for the first time in this pregnancy, had mildly increased blood-pressure (150/88 to 150/92 mm Hg). She was admitted to hospital and became
,
ASA=
Sacramento Medical Center, Sacramento, California 95817, U.S.A. Glenn Memorial Hospital Willows, California
R. C. GOODLIN H. O. HAESSLEIN
J. FLEMING
COBALT IN URÆMIC CARDIOMYOPATHY
SIR,-Two years agol we presented a case with progressive renal failure and heart enlargement in association with a high serum concentration of cobalt. After kidney transplantation the heart size became normal as did the serum-cobalt, and urinary cobalt excretion was high. Among possible ursemic toxins to the heart (i.e., toxins producing uraemic cardiomyopathy with or without pericardial effusion) we have paid special attention to trace elements such as cobalt. Cobalt excretion depends on renal function. Cobalt is toxic to the myocardium. 1-4 Although the setiology of Quebec beer drinkers’ cardiomyopathy is considered multicausal, cobalt is thought to be the prime factor, and this has been supported by experimental evidence.5,6 Mohiuddin et al. have described an animal model for cobalt-induced cardiac disease which possesses the features of the disease as it occurs in man. We have now studied the cobalt concentration in the myocardium in four cases with progressive renal failure. At necropsy in all cases the myocardium was stiff and hypertrophied, especially the wall of the left ventricle and the septum which showed the features of a hypertrophic non-obstructive cardiomyopathy. The concentrations of cobalt in uraemic and normal heart tissue, measured by neutron-activation analysis, are presented in the table. All patients had high cobalt concentrations in the myocardium ranging from 3 to 23 times (mean 10 times) over the upper limit of normal concentrations as determined in the twenty normal controls presented by Wester.8 None of the patients had received treatment with cobalt, which we consider contraindicated in renal failure. 1. Lins, L. E., Pehrsson, K. Lancet, 1976, i, 1191. 2. Lamarche, M. Arnould, P., Koracev, V. Koracev, R. Biol. c. r. 1957, 157, 1415. 3. Jalavisto, E., Makkonen, E., Makkonen, H., Pallasvua, M. R. Ann. Acad.
Sci. fenn. 1965, 115, 1. 4. Semenova, L. A., Martyniuk, R. A., Martsinovich, V. P. Cor Vasa, 1975, 17, 145. 5. Sullivan, J., Woodbury, J., Degan, J. J. Lab. clin. Med. 1967, 70, 814. 6. Sullivan, J., Parker, M., Carson, S. B. ibid. 1968, 71, 813. 7. Mohiuddin, S., Taskar, P. K., Rheault, M., Roy, P-E., Chenard, J., Mosin, Y. Am Heart J. 1970, 80, 532. 8. Wester, P. O. Acta med. scand. 1965, suppl. 439.
Platelet-count
ASPIRIN FOR THE TREATMENT OF RECURRENT TOXÆMIA woman was seen in 1976 at the SacraMedical Center in her 29th week of pregnancy. She had
SIR,-A 31-year-old mento
hypertension (180/110 mm Hg), thrombocytopenia (pla000/jjd), and was delivered by cassarean section at approximately the 30th week. The infant weighted 870 g and died after 4 days with ascites, thrombocytopenia, and renal failure (mirror syndrome).2 The patient’s first pregnancy, managed elsewhere, had run a similar course. Between pregnancies her platelet-counts were normal, as were all other laboratory tests and physical findings. In the 15th week of gestation of her third pregnancy, her platelet-count was 59 000/ul and her hxmatocrit was 40%. Bone-marrow and peripheral-blood smear suggested peripheral consumption of platelets. There was no other laboratory suggestion of microangiopathic anxmia or consumption coagulopathy throughout her pregancy. She was treated with heparin 5000 units three times a day for 4 weeks with no appreciable effect on platelet-count. At the 22nd week, aspirin 600 mg three times a day was started, with gradual improve-’ ment in platelet-count (figure). The aspirin was discontinued in the 32nd week because of the fear of creating a closed fetal ductus. She then began to severe
during pregnancy.
Arrows represent dexamethasone 12 mg.
normotensive with sedation and bedrest. However,
at
her 33rd
hypertension (160/100 mm Hg) appeared, and platelet-count decreased to 50 000/1 and her haematocrit
week,
severe
her increased. The ultrasonic B scans had shown normal fetal growth and amniotic fluid up to the 28th week, but with the toxxmia fetal growth apparently ceased and amniotic fluid dis-
appeared.
again given aspirin and her platelet-count returned normal in the 34th week. Twice she was given dexamethasone to mature fetal lungs. The non-stress fetal heartrate test pattern showed variable decelerations, and we were unable to obtain further amniotic fluid for analysis. She was delivered by caesarean section of a 1410 g growth-retarded male fetus (placental weight 305 g) who showed no respiratory distress. The baby’s platelet-count was 180 000/1 and he did well. Post partum, the patient’s platelet-count remained normal, as did her blood-pressure. She showed a marked haemodilution in the post-partum period with a 30% fall in haematocrit. This case demonstrates the thrombocytopenia seen with some cases of recurrent toxxmia, as well as the possible beneficial effects of aspirin therapy. Aspirin may benefit thrombocvtopenia in children with the haemolytic ursemic syndrome.3 It She
was
to near
G. D., and others, Calc. Tissue Res. 1977, suppl. 22, 117. R., Cotton, D., Haesslein, H. Am J. Obstet. Gynec. in the 3. Arenson, E., August, C. J. Pediat. 1975, 86, 957.
1. Aurbach, 2. Goodlin,
press
aspinn.
may also ameliorate this type of recurrent toxasmia, which may be related to the post-partum haemolytic renal failure syndrome.
telet-count 40
experience painful uterine contractions and for the first time in this pregnancy, had mildly increased blood-pressure (150/88 to 150/92 mm Hg). She was admitted to hospital and became
,
ASA=
Sacramento Medical Center, Sacramento, California 95817, U.S.A. Glenn Memorial Hospital Willows, California
R. C. GOODLIN H. O. HAESSLEIN
J. FLEMING
COBALT IN URÆMIC CARDIOMYOPATHY
SIR,-Two years agol we presented a case with progressive renal failure and heart enlargement in association with a high serum concentration of cobalt. After kidney transplantation the heart size became normal as did the serum-cobalt, and urinary cobalt excretion was high. Among possible ursemic toxins to the heart (i.e., toxins producing uraemic cardiomyopathy with or without pericardial effusion) we have paid special attention to trace elements such as cobalt. Cobalt excretion depends on renal function. Cobalt is toxic to the myocardium. 1-4 Although the setiology of Quebec beer drinkers’ cardiomyopathy is considered multicausal, cobalt is thought to be the prime factor, and this has been supported by experimental evidence.5,6 Mohiuddin et al. have described an animal model for cobalt-induced cardiac disease which possesses the features of the disease as it occurs in man. We have now studied the cobalt concentration in the myocardium in four cases with progressive renal failure. At necropsy in all cases the myocardium was stiff and hypertrophied, especially the wall of the left ventricle and the septum which showed the features of a hypertrophic non-obstructive cardiomyopathy. The concentrations of cobalt in uraemic and normal heart tissue, measured by neutron-activation analysis, are presented in the table. All patients had high cobalt concentrations in the myocardium ranging from 3 to 23 times (mean 10 times) over the upper limit of normal concentrations as determined in the twenty normal controls presented by Wester.8 None of the patients had received treatment with cobalt, which we consider contraindicated in renal failure. 1. Lins, L. E., Pehrsson, K. Lancet, 1976, i, 1191. 2. Lamarche, M. Arnould, P., Koracev, V. Koracev, R. Biol. c. r. 1957, 157, 1415. 3. Jalavisto, E., Makkonen, E., Makkonen, H., Pallasvua, M. R. Ann. Acad.
Sci. fenn. 1965, 115, 1. 4. Semenova, L. A., Martyniuk, R. A., Martsinovich, V. P. Cor Vasa, 1975, 17, 145. 5. Sullivan, J., Woodbury, J., Degan, J. J. Lab. clin. Med. 1967, 70, 814. 6. Sullivan, J., Parker, M., Carson, S. B. ibid. 1968, 71, 813. 7. Mohiuddin, S., Taskar, P. K., Rheault, M., Roy, P-E., Chenard, J., Mosin, Y. Am Heart J. 1970, 80, 532. 8. Wester, P. O. Acta med. scand. 1965, suppl. 439.
