649 not find a higher proportion of low serum-folate in the samples taken at booking of women who subsequently delivered babies with major malformations. I report here the 11 c.N.s. malformation cases in that study in greater detail. None of these women had had folic acid!

Gestation at

Type of malformation Anencephaly

booking Serum-folate (wk) (ng/ml) at booking 25

1.9

29 27 15 14

9.5 4.6 4-77 6.22

Parity

Hydrocephaly/ meningocele

Hydrocephaly Meningocele Anencephaly Hydrocephaly/ memngomyelocele Memngomyelocele Anencephaly

0 0 3 0

ponding to C. welchii"). The results were as follows: Group (1) Normal weight Low-birth-weight (2) Special care Lying-in ward (3) Bottle fed Breast fed

(4) Vaginal delivery

Caesarean

section

Total

24 12 24 12 17 18

Encephalocele Occult

spina bifida Anencephaly

9.33 11.22 6.22 7.4 5 7 3.11

2 6 1 0 4 1

The mean booking serum-folate is 6.35ng/ml compared with the mean booking level for all primigravidae in this study of 6.60 (S.D. 2.88) and the multigravid mean of 6.72 (s.D. M8). Only 6 out of 11 women booked before 20 weeks, but since the serum-folate falls as pregnancy advances4 this makes it more clear that there is no difference between these women and those without malformations, since the late bookers would probably have had even higher serum-folate levels at booking. I suggest that this study, which was of a complete year’s bookings in the City of Aberdeen, represents the real situation (i.e., that folic acid deficiency is not the cause of c.N.s. malformation) more reliably than do studies such as that of Smithells et al. where patients were recruited "on a voluntary basis" before 13 weeks. Their "controls" must have included a disproportionate number of women who were receiving more antenatal care than do most women, and whose nutritional state may be different from that of the pregnant population as a whole. Department of Obstetrics University of Aberdeen,

McClung and Toabe9 for use in toxigenicity testing with specific antiserum (Burroughs Wellcome Clostridium perfringens type A). All positive results obtained were also Naglar positive (i.e., toxigenic strains of perfringens type A, corresof

and

Gynaecology,

MARION H. HALL

Aberdeen AB9 2ZD

No. No. positive 76 51 (77%) 27 51 (67%) 69 43 (62%) 34 29 (85%) 75 55 (73%) 28 17 (61%) 74 50 (67%) 29 22 (75%) 103 72 (70%)

In group 3 the breast-fed babies did receive complementary feeds of artificial milk. A mixed diet tends to produce a flora akin to that of an artificially fed baby. 11I The results show that there is a high enough frequency of clostridial colonisation to validate that part of the Pedersen hypothesis. Colonisation is not the same as invasion, however. The lack of difference in the percentage of positive specimens between the low-birth-weight and normal-weight groups and between the special-care baby unit and lying-in ward groups suggests that another factor (or factors) must be sought to explain the peak incidence ofN.E.c. at weights below 1600 g.4 A. D. KINDLEY P. J. ROBERTS Liverpool Maternity Hospital, W. H. TULLOCH Liverpool L7 7B

AMNIOTIC-FLUID ALPHA-FETOPROTEIN IN TURNER SYNDROME

SIR,-There have been conflicting reports about the level of amniotic-fluid a-fetoprotein (A.F.P.) when a fetus has Turner syndrome.’2 We have studied a pregnancy in which Turner syndrome was diagnosed antenatally. The pregnancy was terminated by hysterotomy at 20 weeks’ gestation, and the intact gestation sac was removed (Dr R. Wurm) and transported to the laboratory within an hour. Cord-blood lymphocyte culture confirmed the fetal karyotype to be 45,X.

NEONATAL NECROTISING ENTEROCOLITIS

SIR,-Neonatal necrotising enterocolitis (N.E.C.) has lately been the subject of a hypothesiss an editorialand a letter7 in The Lancet. Pedersen et al.5 suggested that necrotising enterocolitis could be caused by clostridial invasion of bowel damaged by anoxia. They commented that clostridial colonisation of the neonatal intestine had not been examined in detail. They cited a survey of breast-fed babies in rural Guatemala who, in their first week, had mainly an anaerobic flora. We have examined the faeces of 103 babies on their fifth day of life. This day was chosen because the mean time of onset of the N.E.c. is day 4.8 These babies were unselected-some coming from a lying-in ward and some from the special-care baby unit. The weight, type of delivery, type of feed, and ward of origin of each baby was noted. Fsces were cultured anaerobically on blood and neomycin blood agar plates as well as in Robertson’s cooked-meat medium for 24 h at 37°C. The Robertson’s cooked-meat samples were then subcultured and reincubated anaerobically. The plates were examined for clostridia at each stage. A half antitoxin Naglar plate was prepared by the method 4

Hall, M. H., Pirani, B. B. K., Campbell, D. Br. J. Obstet. Gynœc. 1976, 83,

132 5 Pedersen, P. V. Lancet, 1976, ii, 715. 6 ibid 1977, i, 459. 7 Flynn, D. H., and others, ibid. p. 545. 8 Mizrahi, A., and others. J. Pediat. 1965,

66, 697.

Fetus with Turner syndrome after ated from left cervical pouch.

30 ml of fluid had been aspir-

During collection of amniotic fluid from the sac one of the large fetal cervical pouches was inadvertently punctured, and 30 ml of clear amber liquid which looked like amniotic fluid was obtained without difficulty. Subsequent inspection of the 9. McClung, S. L., Toabe, R. J. Bact. 1947, 53, 139. 10. Cowan, S. T. Manual for Identification of Medical Bacteria; p. 67. London, 1974. 11. Fraser Williams, R. in Scientific Foundations of Pædiatrics (edited by J. A. Davis and J. Dobbing); chap. 44. London, 1974. 1. Hunter, A., Hammerton, J. L., Baskett, T., Lyons, E. Lancet, 1976, i, 596. 2. Seller, M. J. ibid. p. 807.

650 cervical pouches showed a needle mark in the left pouch but little apparent decrease in size (see figure). Amniotic fluid was obtained from the sac. Analyses of the amniotic and pouch fluids are shown in the table. The cord-blood A.F.P. was 1045 mg/1. Cells from both fluids grew in culture to show 45,X karyotypes, although only the pouch fluid had a raised macrophage-count.3 Neither fluid was macroscopically bloodstained. The A.F.P. level in the fluid obtained at the diagnostic amniocentesis at 15 weeks’ gestation was 16 mg/1 (normal range 5-32 mg/1). We suggest that the high levels of amniotic-fluid A.F.P. reported in some instances of Turner syndrome’ may result COMPOSITION OF AMNIOTIC AND CERVICAL-POUCH FLUID AT

20

WEEKS’ GESTATION

from aspiration of the fetal cervical pouches at amniocentesis. The fluid obtained would macroscopically and chemically resemble amniotic fluid. Fluid from a cervical pouch may have an increased macrophage-count and A.F.P. level as in this case. There is no reason to suggest that the pouches leak4 A.F.P. into the fluid, because they are covered with skin.

described as short, non-motile rods, often foundin pairs, and flourishing best in a temperature range of 35-40"C-and that is all. It seems unlikely that we shall ever know the true identity of Frisch’s bacillus. We have examined biopsy material from patients presenting with clinical signs of rhinoscleroma, the nasal form of the discases were

Characteristic foam or "Mikulicz" cells were demonstrated microscopically in all, while ten of them yielded strains of non-motile gram-negative rods which produced mucoid colonies on blood agar. Their biochemical properties were studied by use of the API system 20E and the results confirmed at the Computer Trials Laboratory, Colindale, London. Capsular antigens were identified using the immunofluorescence method of Riser et al.2 Our results are set out in the table. Clearly Frisch’s bacillus is not a single entity, and any of three species of Klebsiella is likely to be involved in rhinoscleroma. Further studies may well reveal additional types. ease.

Institute of Laryngology and London WC1X 8EE

Otology,

T. A. REES MONICA M. GREGORY

MITOCHONDRIAL CALCIUM OVERLOAD, A CAUSE OF ESSENTIAL HYPERTENSION?

suggestedthat some diseases of skeletal cardiac muscle may be related to unidentified defects in the sarcolemma or cell membrane which allow an excessive intracellular influx of calcium ions. The calcium overload causes hypercontraction of the affected cells and may eventually destroy them. The intracellular calcium overload is prevented by calcium antagonists such as verapamil. The medical treatment of essential hypertension is currently based almost exclusively on sympatholytic drugs of one kind or another on the assumption that the disease is caused by overactivity of the sympathetic nervous system. The assumption is usually not supported by signs of sympathetic activity other than the hypertension, which suggests that sympathetic stimulation may not be the cause in all patients. Sympathetic nervous function is depressed in patients with low-renin essential hypertension.4 Volume-pulse plethysmography5 often detects dilatation of the alpha-adrenoceptor blood-vessels of the fingers and constriction of the beta-adrenoceptor blood-vessels of the skeletal musculature in patients with treated or untreated essential hypertension, which indicates failure in the conductivity of the efferent sympathetic pathways. The treatment of essential hypertension with sympatholytic drugs is not always impressive, and the fact that the hypertension may be resistant to beta-adrenoceptor blockade indicates that sympathetic stimulation of the heart is not always the basis of the disease but may be an aggravating factor. Three drugs used in clinical anwsthesia consistently cause arterial hypotension in patients with essential hypertensionhalothane, d-tubocurarine, and verapamil. They depress the myocardium by a competitive and reversible antagonism of the positive inotropic function of calcium ions. This negative inotropy is reversed by intravenous injections of calcium ions. Details of this work in relation to clinical anaesthesia will be reported elsewhere. The cardiovascular effects of ketamine in manmimic the SIR,-It has been

Cytogenetic Unit, Department of Histopathology, Adelaide Children’s Hospital, North Adelaide, South Australia 5006

GRANT R. SUTHERLAND

Department of Chemical Pathology, Adelaide Children’s Hospital

DENISE HOLT

Genetics Research Unit, Royal Children’s Hospital Research Foundation Melbourne

JOHN G. ROGERS

or

CAUSATIVE ORGANISMS IN RHINOSCLEROMA

SIR,-Scleroma is a chronic granulomatous disease of the upper respiratory tract occurring most commonly in the nose and endemic in many parts of the world, including South America, Egypt, Czechoslovakia, the U.S.S.R., and India. The aetiological agent is thought to be a bacterium, known as Frisch’s bacillus after the Viennese doctor who first proposed BACTERIOLOGICAL FINDINGS IN CASES OF RHINOSCLEROMA

a bacterial aetiology in 1882.’ Most accounts of scleroma equate this bacillus with Klebsiella rhinoscleromatis. All too often, however, the mere isolation of a mucoid gram-negative bacillus from a patient with clinical and histological signs of

Sutherland, G. R., Brock, D. J. H., Scrimgeour, J. B. J. med. Genet. 1975, 12, 135. 4. Seller, M. J., Creasy, M. R., Alberman, E. D. Br. med. J. 1974, n, 524. 1. von Frisch, A. Wiener med. Wschr. 1882, 32, 971. 3.

the disease is sufficient to lead the investigator to report that Frisch’s bacillus has been found. Supporting bacteriological studies seldom permit proper identification of the organism. von Frisch’s observations were made before Gram described his staining method, and the bacteria isolated from his twelve

2.

Riser, E., Noone, P., Poulton, T. A. J. clin. Path. 1976, 29, 296. 3. Wrogemann, K., Penn, S. D. J. Lancet, 1976, i, 672. 4. Esler, M., Zweifler, A., Randall, O., Julius, S., Bennett, J., Rydelek, P., Cohen, E., DeQuattro, V. ibid. 1976, ii, 115. 5. Johnstone, M Anæsthesia, Rounds 10: Adult Preoperative Medication. Imperial Chemical Industries Ltd (Pharmaceuticals Division), Macclesfield, 1976 6. Johnstone, M. Anæsthesia, 1976, 31, 873.

Amniotic-fluid alpha-fetoprotein in Turner syndrome.

649 not find a higher proportion of low serum-folate in the samples taken at booking of women who subsequently delivered babies with major malformatio...
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