CORRESPONDENCE

Inhibition of Wydase® by human serum

To the editor: The possibility that blood contains a hyaluronidase inhibitor was suggested as early as 1933 by Duran-Reynals.1 Several groups confirmed this hypothesis and it was later shown that human blood contained a thermolabile inhibitor of bovine testicular hyaluronidase.2'3 Experimental studies indicated that hyaluronidase could be useful in minimizing the death of tissue following coronary artery occlusion.4 Clinical trials have since demonstrated electrocardiographic evidence in support of these proposals,5 and have prompted my study of the effects of human serum on the activity of Wydase®, which is bovine testicular hyaluronidase; it has been used extensively in many clinical studies. Preliminary results with the use of a colorimetric method6 have confirmed those of earlier studies and have demonstrated that human seContributions to the Correspondence section are welcomed and if considered suitable will be published as space permits. They should be typewritten double-spaced and, except for case reports, should be no longer than 1½ manuscript pages.

rum inhibits the activity of Wydase®. Since Alidase® (not currently marketed in Canada) is also bovine testicular hyaluronidase, one would expect similar findings in studies with this preparation. These results appear to contradict the hypothesis predicting a role for bovine testicular hyaluronidase in the management of acute myocardial infarction. A further complication in using this enzyme is that it is strongly inhibited by heparin;7 therefore heparin cannot be used in conjunction with Wydase® or Alidase®. I acknowledge the skilful technical assistance of Mrs. Pat Hersack. This study was supported by the special services and research committee of the University of Alberta Hospital. MARK L. SALKIE, MB

University of Alberta Hospital Edmonton, Alta.

References 1. DURAN-REYNALS F: Studies on a certain spreading factor existing in bacteria and its significance for bacterial invasiveness. J Exp Med 58: 161, 1933 2. DORFMAN A, OTT ML, WHITNEY R:

The hyaluronidase inhibitor of human blood. J Biol Chem 174: 621, 1948 3. MCCLEAN D: The in-vivo decapsulation of streptococci by hyaluronidase. J Pathol Bacteriol 54: 284, 1942

The Canadian Medical Associatlonfl'Association m6dlcaIo canadienne 1867 AIta Vista Dr., Ottawa, Ont. KIG 3Y6; (613) 7314331 President/pr6sldent: D.L. Wilson. MD. FRCP.C. bc.'itary gsoersljeecr6talre g6niral: R.G. Wilson, MD Director £.f communlcatlons/dlrectour d.a coinmunlcatlon.: GA. Geekie, SPHE. 0P14

OMA' Joit.naI/JournaI de lAUC Scientific edltorfr6clacteur sclentlftque: NJ.B. Wiggin, MD. MSc, PhD News end featurSe edltor/rddscteur des nouvelles et reportagea: J. Garner Associate scientific editor/r4dacteur scientifique aaaoci6: P.P. Morgan. MD, DPift, DEPid Seeder ssistant edltor/r6dectrice adjointe en chef: A. Bolster, BA A stunt edI.ge.s/r6dactrlces adlointes: L.D. MacDougall, J. Whitney, BSc Ornltvtbutlng edtorsfcollateorateurs: 0.. Roi.fIlard, PhD; C.t. Jarrett, PhD, MD; M.O. Landry, BA; D.T. W.is, MD. PhD, MPH; 0. Woods DitectOr of advertising saleaf Irecttner dv is pubilcit6: N. Hutton Ptoductlon mMgar/ohef du servicede i. production: RM. Slnnott

4. MAROKO PR, LIBBY P, BLOOR CM,

et al: Reduction by hyaluronidase of myocardial necrosis following coronary artery occlusion. Circulation 46: 430, 1972 5. MAROKO PR, HILLIs LD, MULLER JE: Hyaluronidase effect on ECG evidence of necrosis in myocardial infarction. N Engi J Med 296: 898,

1977 6. SALKIE ML, HANNAH CL: saminoglycan

metabolism

Glycoin

preg-

nancy. Enzyme 22: 151, 1977 7. MATHEWS MB, DORFMAN A: Inhibi-

tion of hyaluronidase. Physiol Rev 35: 381, 1955

Acute intermiffent porphyria associated with postural hypotension To the editor: The relation between psychiatric symptoms and acute intermittent porphyria is well established.1'2 It has also been noted that temporary spells of hypertension may occur in patients with acute intermittent porphyria,3 but no instances have been reported of severe attacks of postural hypotension, which is surprising since hyponatremia has been recorded.3 We report two cases that are interesting because postural hypotension led to the diagnosis of acute intermittent porphyria; however, it could be argued that the diagnosis was so obvious that it should not have required this additional feature. The Canadian Medical Association Journal Is published twice a month by the Canadian Iviedical Association. P0 Box 865., Ottawa. Ont. KIG OG. and is printed by Herpeli's Press Cooperative, Gardenveie. P0 HOA t.O. Subscription rates and information for contributors of manuscripts are published in the first issue of each volume. All reproduction .*g1*s are rserved.

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CMA JOURNAL/OCTOBER 6, 1979/VOL. 121 845

Case 1 A 34-year-old woman with a number of vague somatic complaints and depression was admitted to hospital after being referred to the psychiatric department by a physician. She had a history of intermittent disabling abdominal complaints, and an appendectomy scar was present. During a ward round she bemoaned her fate and claimed that she was unable to walk, while being propped up on both sides by nurses. One of us (M.S.), who has reported a series of four patients with Addison's disease and depression,4 checked her blood pressure, especially as she had a moderate degree of hyponatremia. It was 90/55 mm Hg while she was standing. Therefore, this patient was the fifth with Addison's disease associated with depression. A 24-hour urine collection was ordered to assess the excretion of 17-ketosteroids. The following day the urine specimen was an unusual colour and acute intermittent porphyria was subsequently confirmed. Case 2 A 27-year-old woman presented with depression. She had had a therapeutic abortion at 6 weeks' gestation because of persistent abdominal pain and vomiting. However, she claimed that her depression was not connected with the abortion. Three years previously an episode of abdominal pain had been investigated in hospital, but no cause was found. In view of the patient's present distress and general agitation, barbiturates were prescribed; however, they had no beneficial effect. The patient was mildly hypertensive and was therefore given a small dose of a rauwolfia agent for 3 days, after which her blood pressure settled. She then complained of fainting spells during which she had fallen and bruised her legs, a lack of energy and the need for support while walking. She was referred for psychiatric consultation. The patient was pale (hemoglobin concentration 14 g/dl) and her pulse rate was 96 beats/mm. Her blood pressure was recorded daily and was constant at 120/80 mm Hg. The clinical picture was so similar to that of the previous pa-

tient that the blood pressure was checked while the patient was standing: it was found to be 80/40 mm Hg. Intermittent porphyria was again suspected; the following day a urine specimen was strongly positive for porphobilinogen. Comment Acute intermittent porphyria has a variety of clinical features; each in itself is not diagnostic, but taken together they are presumptive evidence of the condition. Postural hypotension is easily determined and should now be considered a feature of the disease. In the first case it led to the diagnosis accidentally, and in the second case it was a useful factor in the clinical diagnosis. It should therefore be sought whenever acute intermittent porphyria is suspected; if present it makes further investigations mandatory. MYRE SIM, MD (EDIN), FRCP, FRC PSYCH, FRCP[C], DPM

Professor of psychiatry Faculty of health sciences University of Ottawa Royal Ottawa Hospital RAYMOND HUDON, MD

Grace Hospital Ottawa, Ont.

References 1. WHITTAKER

SRF,

WHITEHEAD

TP:

Acute and latent porphyria. Lancet 1: 547, 1956 2. ACKNER B, COOPER JE, GRAY CH,

et al: Excretion of porphobilinogen and 'y-aminolaevulinic acid in acute porphyria. Lancet 1: 1256, 1961 3. SCHMID R: Porphyria, in Textbook of Medicine, 13th ed, BEESON PB, MCDERMOTT W (eds), Saunders, Philadelphia, 1971, p 1704 4. Si. M: Guide to Psychiatry, rev 3rd ed, Churchill-Livingstone, Edinburgh, 1974, p 217

Abortion of fetuses with spina bifida? To the editor: Dr. A.T. Kerigan asks "whether anyone has ever asked sufferers of spina bifida what value they put on their own life" (Can Med Assoc J 120: 913, 1979). Forrester1 has reported the results of a survey in which children with spina bifida were asked how they would feel if their mother was again pregnant with a fetus with spina bifida.

846 CMA JOURNAL/OCTOBER 6, 1979/VOL. 121

The children surveyed attended a day school for physically handicapped children run by the Wigan Area Education Authority. Approximately 50% of the 160 enrolled pupils suffered from spina bifida that was sufficiently severe to keep them out of the normal stream of education. A group of about 15 children aged 13 to 15 years were shown a television program about the ethics of saving fetuses with spina bifida. They were then asked, "If you knew that your mother was having another baby, and that it could be foretold that it had spina bifida, would you suggest that she go ahead with the pregnancy or that it be terminated?" Their reply was clear-cut and unanimous: they would advise abortion.1 The children further stated: "We are here and that can't be helped, but we would not wish this state on anybody else" (R.M. Forrester: personal communication, 1979). All these children had had good medical and surgical care since birth and were receiving full-time education in a very good day school near their homes. Individuals who champion the rights of a fetus with a neural tube defect should objectively assess the outlook for such individuals. Not only should it be asked "what value they put on their own life", but also how many are able to answer the question. The prospects of a child with anencephaly are self-evident but these children are often ignored by opponents of the screening process. Of all fetuses with neural tube defects 50% are either stillborn or die within 3 days of birth; a further 25% die by the age of 5 years, and of the remainder half are mentally retarded and have physical handicaps of various degrees.2 A study was recently performed in which infants born with neural tube defects were immediately transferred to a tertiary care hospital.3 Of the 67% of the infants who were able to undergo an operation immediately 10% died, and of the 12% who were able to undergo an operation subsequently 8% died; the remaining 21 % had inoperable conditions, and within 8 months 81% had died. Thus, approximately 60% of the total group were alive at the

Acute intermittent porphyria associated with postural hypotension.

CORRESPONDENCE Inhibition of Wydase® by human serum To the editor: The possibility that blood contains a hyaluronidase inhibitor was suggested as ea...
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