- Email: [email protected]
CONTROLLED TRIAL OF AN ELECTROSTATIC PRECIPITATOR IN CHILDHOOD ASTHMA
559 abnormal DNCB response. Ideally, a faster method than the skin test should be developed; perhaps circulating lymphocytes should be used. Notwithstanding our argument that cutaneous cancers seen in PUVA patients may appear as a result of a pseudopromotor activity of PUVA, it is very likely that PUVA will prove also to be an initiator of carcinogenesis, as has already been demonstrated in the mouse.20,21 Such an effect would not be expected to appear in man for some time, PUVA having been in widespread use only for about 4 years. It would, however, be expected to interact synergistically, perhaps in a rather dramatic way, with the postulated pseudopromotor action if PUVA therapy were to be maintained. Finally, the clearly documented effects on lymphocytes raise the possibility of malignant disease being initiated among these cells. In this connection the lymphatic leukaemia arising in a PUVA-treated xeroderma pigmentosum patient,’and the "preleukasmia or hematopoietic dysplasia" with "excess,myeloblasts" in the marrow22 and acute myeloid leukxmia 21 that have been reported in PUVA-treated psoriatics, may prove to be important. an
G.H.S. was supported by the Cancer Research Campaign. We thank Dr A. Craven for statistical help.
REFERENCES
Bridges BA. Possible long term hazards of photochemotherapy with psoralens and near ultraviolet light. Clin Exp Dermatol 1978; 3: 349-53. 2 Stern RS et al. Risk of cutaneous carcinoma in patients treated with oral methoxsalen photochemotherapy for psoriasis. N Engl J Med 1979; 300: 809-13. 3 Bridges BA, Strauss GH. Possible hazards of photochemotherapy for psoriasis. Nature 1980; 283: 523-24. 4. Strauss GH et al 6-Thioguanine resistant peripheral blood lymphocytes in humans following psoralen, long-wave ultraviolet light (PUVA) therapy. J Invest Dermatol 1
1979; 73: 211-16. 5 Vella-Briffa D, Rogers S, Greaves MW, Narks
J, Shuster S, Warm APC. A randomized, controlled clinical trial comparing photochemotherapy with dithranol in the initial treatment of chronic plaque psoriasis. Clin Exp Dermatol 1978; 3: 339. 6 Catalona WJ, Chretien PB. Abnormalities of quantitative dinitrochlorobenzene sensitizaton in cancer patients: Correlation with tumour stage and histology. Cancer 1972; 31: 353-56. 7 Catalona WJ, Taylor PT, Chretien PB. Quantitative dinitrochlorobenzene contact sensitization in a normal population. Clin Exp Immunol 1972; 12: 325-33. 8. Simo-Camps E, et al. Immunologic impairment in patients with non-lymphoid cancer; correlation with tumoral stage, response to treatment and survival. Cancer 1976; 37: 724-27 9. Kraemer HH, Weinstein GD Decreased thymidine incorporation m circulating leukocytes after treatment of psoriasis with psoralen and long-wave ultraviolet light. J Invest Dermatol 1977; 69: 211-14. 10. Lischka G, Bohnert E, Bachtold G, Jung EG. Effects of 8-methoxypsoralen (8-MOP) and UVA on human lymphocytes. Arch Dermatol 1977; 259: 293-98. 1 . Roberts LK, Schmitt M, Daynes RA. Tumour susceptibility generated in mice treated with sub-carcinogenic doses of 8-methoxypsoralen and long-wave ultraviolet light. J Invest Dermatol 1979; 72 (6). 306-309. 12 Kripke ML, et al. Further characterization of immunological unresponsiveness induced in mice by ultraviolet radiation. Transplantation 1979; 28 (3): 212-17. 13 Spellman CW, Woodward JG, Daynes RA. Modification of immunological potential by ultraviolet radiation. I. Immune status of short-term UV-irradiated mice. Transplantation 1977; 24 (2): 112-26 14
Moller R, Howitz J Methoxsalen and multiple basal-cell carcinomas. J Arch Dermatol 1976; 112: 1613-14. RS, Zierler S, Parrish JA. Skin carcinoma in patients with psoriasis treated with topical tar and artificial ultraviolet radiation. Lancet 1980; i. 732-35. Reed WD Treatment of psoriasis with oral psoralens and long-wave ultraviolet light. Acta Dermato-vener 1976; 56: 315-18. Reed WB, Sugarman GI, Mathis RA. De-Sanctis-Cacchione syndrome. A case report with autopsy findings. Arch Dermatol 1977; 113: 1561-63. Walder BK, et al. Skin cancer and immunosuppression. Lancet 1971; ii: 1282. Kmlen L, et al. Collaborative United Kingdom/Australasian study of cancer in patients
15 Stern 16 17.
18 19
treated with immunosuppressive drugs. Br Med J 1979; ii: 1461. 20. Griffin AC Methoxsalen in ultraviolet carcinogenesis in the mouse. J Invest Dermatol 1959, 32: 367-72. 21 Urbach FJ. Modification of ultraviolet carcinogenesis by photoactive agents. J Invest Dermatol 1959; 32: 373-78. 22 Wagner J, Manthorpe R, Philips P, Frost F. Preleukemia (hematopoietic dysplasia) developing in a patient with psoriasis treated with 8-methoxypsoralen and ultraviolet light (PUVA treatment) Scand J Haematol 1978, 22: 57-60. 23 Hanson NE. Development of acute myeloid leukaemia in a patient with psoriasis treated with oral 8-methoxypsoralen and longwave ultraviolet light. Scan J Haematol 1979;
22: 57-60.
CONTROLLED TRIAL OF AN ELECTROSTATIC PRECIPITATOR IN CHILDHOOD ASTHMA E. A. MITCHELL
R. B. ELLIOTT
Department of Pædiatrics, School of Medicine, University of Auckland, Auckland, New Zealand A cross-over trial was conducted on 10 children with moderate to severe who had asthma, positive skin tests to Dermatophagoides pteronyssinus and nocturnal wheeze. An electrostatic precipitator was used during the night to remove airborne particles from the bedroom. During use of the
Summary
precipitator peak expiratory flow
rates were no
better
than in a control period. Introduction
provoke asthmatic attacks, and one major allergenic components is the house mite Dermatophagoides pteronyssinus.1,2 Other allergens in house dust include animal danders and mould spores.3 The mite is widely distributed in household dust throughout New Zealand4 and high levels are found in domestic mattresses.2,5 The mite population can be reduced by simple measures such as vacuum-cleaning mattresses and enclosing them in plastic sheets, using synthetic blankets and regularly washing them, and removing soft toys from the bedroom. 6, Such anti-mite HousE dust
can
of the
have reduced the incidence of asthmatic attacks in some patients,5,S but not in others.9 Bronchial allergy to house dust is common in moderate to severe asthma.10,11 The failure of anti-mite measures to produce dramatic improvement in most patients with mite-sensitive asthma suggests either that the-usual anti-mite measures are not sufficiently effective or that bronchial allergy to house dust and mite is not the major cause of their asthmatic attacks. Although the most important source of mites is the mattress, clearly the mite must be inhaled if it is to produce bronchospasm. We therefore conducted a controlled trial to study the effects of removal of airborne particles by an electrostatic precipitator, at night, in the bedroom of children with moderate to severe asthma. measures
Materials and
Methods
10 children (4 boys and 6 girls) aged between 6-9and 13.5 yr with asthma were studied. Criteria for entry into the study were (a) nocturnal wheeze; (b) positive skin tests to house dust, D. pteronyssinus, and D. farinae; and (c) moderate to severe asthma requiring regular prophylactic medication and intermittent use of aerosol bronchodilators. Table i gives the clinical details. The type and dose of the drugs used for prophylaxis were kept constant throughout the trial. A controlled cross-over trial was conducted in the patient’s
home. The
study consisted of two consecutive 4-week periods. period an electrostatic precipitator was used in the child’s bedroom; the other period served as the control. The order was randomised. Throughout the 8-week trial standard mite-avoidance measures were practised as previously recommended.6 Patients were studied consecutively throughout 1 During
one
year. The ’Micronaire p-500’ electrostatic precipitator contains a fan which draws the particle-laden air through a prefilter which removes the larger particles. The remaining smaller airborne particles then pass to the ioniser area, where they are
570
denly and drastically reduce the myocardial blood supply. They showed that ischaemia can occur without any preceding change in myocardial oxygen requirements and by angiography they displayed coronary artery "spasm" during these episodes of pain, whether the ST segment was raised or depressed.’The rehabilitation of spasm as a respectable explanation is complete. But is spasm the right word to describe what may be normal degrees of vasoconstriction? Prinzmetal et al.,’in their original description, concluded that variant angina "results from a temporary occlusion of a large diseased artery with a narrow lumen due to a normal increase in of the vessel wall". For, as Pickering8 pointed out, "there is no contention here that vessels do not contract and expand" but it is not necessary to assume "that arteries behave like whimsical children ... and react violently to a perfectly ordinary stimulus or to none at all". Normal coronary arteries can change their size spontaneously and dilate by as much as 163% after nitroglycerine.9 Clearly in areas where organic stenoses are present a normal amount of vasoconstriction will reduce the lumen considerably. MacAlpin’" has looked at this fundamental point. Simple geometry predicts that the lumen of a segment of coronary artery with a 50% stenosis (which is pliable or eccentric) will be occluded completely if the outer circumference is reduced by 9%; this is well within the range of normal variation of size. Furthermore, MacAlpin has found that in 90% of cases spasm occurs at the site of an organic lesion." Therefore, in most patients, a normal amount of vasoconstriction can produce severe ischaemia if it happens in an already stenosed segment of the artery. This should probably not be called spasm. In the few patients, with angiographically normal coronary arteries, true spasm may be a factor. What we need to know is the cause of this fluctuating vasoconstriction that presumably results in unstable angina. One attractive idea is that thromboxane A2, a potent vasoconstrictor, is released from agglutinated platelets. Mehta and co-workers12 report that platelets clump more readily after passing through an atherosclerotic coronary artery. 12 Autonomic nervous mechanisms may also be important. 13 If vasoconstriction is the underlying mechanism in unstable angina then the ideal treatment is to paralyse the coronary artery with nitrates and calcium blocking drugs. Plotnick14 has outlined a management plan. All tonus
patients should have intensive medical treatment in a coronary care unit, and this will successfully relieve the pain in about 85%. Nitrates are given in high doses as isosorbide dinitrate orally, topical nitroglycerin ointment, or intravenous nitroglycerin, until the onset of headache or a drop in systolic blood pressure. Verapamil and nifedipine both reduce the frequency of attacks.15,16 Nifedipine can be combined with beta blocking drugs. Theoretically, beta-blockers, by promoting alpha activity, may make vasoconstriction more likely, but there is no evidence that this happens. Doses should be increased until the resting heart rate is 50 to 60 beats per minute, systolic blood pressure is below 105 mm Hg, or heart failure develops. Anticoagulants have been recommended,17 although there has not been a good trial in this condition. The value of surgery has been clarified by the National Co-operative Study Group. 18, 19 There is no place for immediate surgery. Conti20 has reviewed all published trials (random and non-random), and the results point to a higher myocardial infarction rate with surgical treatment and no difference in mortality rate. Furthermore, fewer surgical patients return to work.21 However, if intensive medical treatment does not alleviate the pain after 48 h, surgery is indicated. In Yaco6b’s series 99% of such patients had a main stem or severe left anterior descending artery stenosis.22 In this group the benefits of intra-aortic ballon pumping outweigh the risks of complications, because pain is con-, sistently relieved and cardiac catheterisation is safer .21 For most of these patients surgery is successful and pain is removed.22,24 Each unit needs to know its own figures to assess the risks properly: not everyone will be able to reproduce an operative mortality of 4.2% and a graft patency rate of 91%.22 But medical treatment is now effective for most patients with unstable angina. The question remains: why are some people’s coronary arteries so apt to vasoconstrict? Perhaps cardiologists should look to the bronchial tree for an analogy.
-
5. Maseri A.
Pathogenetic
mechanism of
Heart J 1980; 43: 648-60. 6. Maseri A, L’Abbate A, Pesola A, toris. Lancet 1977; i: 713-17.
et
angina pectoris: expanding
al.
Coronary
views.
Br
vasospasm in angina pec-
7. Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris I: a variant form of angina pectoris. Am J Med 1959; 27: 375-88. 8. Pickering GW. Vascular spasm. Lancet 1951; ii: 845-50. 9. Gensini GG, Kelly AE, Da Costa BCB, Huntingdon PP. Quantitative angiography: the measurements of coronary vasomobility in the intact animal and man. Chest 1971; 60: 522-30. 10. MacAlpin RN. Contribution of dynamic vascular wall thickening to luminal narrowing during coronary arterial constriction. Circulation 1980, 61: 296-301. 11. MacAlpin RN. Relation of coronary arterial spasm to site of organic stenosis.
Am J Cardiol 1980; 46: 143-54. J, Mehta P, Pepine CJ. Platelet aggregation in aortic and coronary venous blood in patients with and without coronary disease, 3: Role of tachycardia stress and propranolol. Circulation 1978; 58: 881-86. 13. Mudge GH, Grossman W, Mills RM, Lesch M, Braunwald E. Reflex increase in coronary vascular resistance in patients with ischæmic heart disease. N Engl J Med 1976; 295: 1333-37. 14. Plotnick GD. Approach to the management of unstable angina. Am Heart J 1979; 98: 243-55. 12. Mehta
15. Parodi O, Maseri A, Simonetti I. Management of unstable angina at rest by verapamil. A double-blind cross-over study in a coronary care unit. Br 16.
Heart J 1979; 41: 167-74. Goldberg S, Reichek N, Wilson J, Hirschfeld J, Muller J, Kastor J. Nifedipine in the treatment of Prinzmetal’s (variant) angina. Am J Cardiol 1979; 44: 804-08.
17. Wood P. Acute and subacute coronary insufficiency. Br Med J 1961; i: 1779-82. 18. National Co-operative Study Group. Unstable angina pectoris: National Cooperative study group to compare surgical and medical therapy. II in-hospital experience and initial follow-up results in patients with one, two and three vessel disease. Am J Cardiol 1978; 42: 839-48. 19. National Co-operative Study Group. Unstable angina pectoris: National Cooperative study group to compare surgical and medical therapy. III results in patient with ST segment elevation during pain. Am J Cardiol 1980, 45: 819-24. 20. Conti CR. Initial management of patients hospitalised because of angina pectoris. Proceedings of the VIII European Congress of Cardiology. 1980, p. 256. 21. Russell RO, Wayne JB, Kronenfeld J, et al. Surgical versus medical therapy for treatment of unstable angina: changes in work status and family income. Am J Cardiol 1980; 45: 134-40. 22. Ahmed M, Thompson R, Seabra-Gomes R, Rickards A, Yacoub M. Unstable angina: a clinicoarteriographic correlation and long term results of early myocardial vascularisation. J. Thorac Cardiovasc Surg 1980; 79: 606-16. 23. Gold HK, Leinbac RC, Sanders CA, Buckley MJ, Mundth ED, Austen WG. Intra-aortic balloon pumping for control of recurrent myocardial ischemia. Circulation 1973; 47: 1197-1203. 24. Weintraub RM, Aroesty JM, Paulin S, Levine FH, Markis JE, LaRaia PJ, Cohen SI, Kurland GF. Medically refractory unstable angina pectoris. 1. Long term follow up of patients undergoing intraortic balloon counterpulsation and operation. Am J Cardiol 1979; 43: 877-82.
561 anti-mite measures are effective in reducing the incidence of asthmatic attacks. This study has shown that addition of an electrostatic precipitator to standard anti-mite measures and prophylactic asthmatic drugs does not significantly improve asthma in children.
simple
The ’Micronaire p-500’ electrostatic precipitator (Dome Laboratones, Division of Miles Laboratories, Australia) was kindly loaned through Ebos Dental and Surgical Supplies Limited, Christchurch, new Zealand. REFERENCES 1. Voorhorst
R, Spieksma-Boezeman MI, Spieksma FT. Is a mite (Dermatophathe producer of the house dust allergen? Allerg Asthma 1964;
goides sp.)
10: 329-34. 2. Maunsell K, Wraith DG, Cunningham AM. Mites and house dust allergy in bronchial asthma. Lancet 1968; i: 1267-70. 3. Virehow C, Roth A, Möller E. IgE antibodies to house dust, mite, animal allergens and molds in house dust hypersensitivity. Clin Allergy 1976; 6: 147-54. 4. Cornere BM. House dust mites: a national survey. NZ Med J 1972; 76: 270-71. 5. Sarsfield JK. Role of house-dust mites in childhood asthma. Arch Dis Childh
1974; 49: 711-15. JK, Gowland G, Troy R, Norman ALE. Mite-sensitive asthma of childhood: trial of avoidance measures. Arch Dis Childh 1974; 49:
6. Sarsfield
716-21.
Blythe ME, Al Ubaydi F, Williams JD, Smith JM. Study of dust mites in three Birmingham Hospitals. Br Med J 1975; i: 62-64. 8. Maunsell K, Hughes AM, Wraith DG. Mite asthma. Practitioner 1970; 205: 7.
779-83. 9. Burr ML, St. Leger AS, Neale E. Antimite measures in mite sensitive adult asthma A controlled trial. Lancet 1976; i: 333-35. 10 Aas K. Bronchial provocation test in asthma. Arch Dis Childh 1970; 45: 221-28. 11 Warner JO. Significance of late reactions after bronchial challenge with house dust mite. Arch Dis Childh 1976; 51: 905-11. BM. A miniature Wright peak-flow meter. Br Med J 1978; ii: 1627-28. 13. Godfrey S, Kamburoff PL, Nairn JR, Connolly NMC, Davis J, Packham E, Samuels CS. Spirometry, lung volumes and airway resistance in normal children aged 5-18 years. Br J Dis Chest 1970; 64: 15-25. 14. Warner JO. Mites and asthma in children. Br J Dis Chest 1978; 72: 79-87. 15. Burr ML, St. Leger AS, Neale E. Nocturnal wheeze and mite sensitivity. Lancet 1976; i: 972-73.
12. Wright
Preliminary
Communication
PARTIAL SUPPLEMENTATION WITH EXPRESSED BREAST-MILK FOR PREVENTION OF INFECTION IN LOW-BIRTH-WEIGHT INFANTS
K. PRAKASH R. K. VERMA
INDIRA NARAYANAN SHASHI BALA V. V.
GUJRAL
Kalawati Saran Children’s Hospital, Lady Hardinge Medical College, New Delhi, India
prospective controlled study the antiproperties of breast-milk were evaluated in 70 high-risk low-birth-weight infants. 32 babies (group I) were given fresh expressed breast-milk during the day and milk formula at night. 38 infants (group II) received only milk formula and served as controls. The two groups
Summary
In
a
infective
were matched
for other factors that could influence the occurof infection. The incidence of infections was significantly less (p<0·01) in babies who received breast-milk. rence
INTRODUCTION
THE progressive decline in century is rather unfortunate,
breast-feeding during this particularly in view of its
unique properties.’-9 Most of the research work, however, has involved estimation of factors in human milk, in-vitro analyses of the cellular components, or experimental , animals. 4-9 Clinical evaluation of infants at high-risk has been limited. 10-12 In developing countries, urbanisation has meant that although most women still begin breast-feeding, many tend to stop early with disastrous results.13,14 Whereas more widespread feeding of normal babies requires mainly better motivation of mothers and birth attendants, giving breast milk to high-risk infants, such as low-birth-weight babies, who are unable to suck directly from the breast is more complicated. There are numerous problems involved in providing expressed human milk in a developing country with uneducated mothers from the low socioeconomic group. In fact, theoretically at least, it may even have a greater risk of introducing
infection. This planned prospective controlled study was undertaken to evaluate the effect of giving expressed breast-milk on the incidence of infection in the high-risk newborn infant. It was part of a more extensive project on the influence of varying quantities of colostrum and mature breast-milk on the prevention of infection in low-birth-weight infants -
(Narayanan et al. Unpublished observations).
MATERIALS AND METHODS
The study involved 70 high-risk newborn infants who had been delivered in hospital and transferred to the nursery which catered for babies born to mothers who were actually or likely to be infected. These included women who had obvious infections, those who had prolonged rupture of membranes or leaking for more than 24 h, and those who had had an unhygienic vaginal examination by one of the untrained indigenous "dias" (traditional birth attendant). The women belonged to the low socioeconomic and educational status. Babies of such mothers were selected for this study because they had the highest risk of acquiring infection (Narayanan I. Unpublished observations). The actual indications for admission to the nursery included low birth-weight (<2000 gm), prematurity, birth asphyxia, delivery by Caesarian section, and so on. Babies in the other nursery and all the normal low-risk infants who stayed with their mothers in the maternity wards were not included in this study. Collection of breast-milk from donors was supervised by trained personnel. It was manually expressed directly into autoclaved feeding bottles. In most instances the mothers were called to an outer room in the nursery. When the mother could not come, the staff went to the maternity wards to collect the milk and transported it in ice in an insulated container. Many of the samples were fed to the babies within 30 minutes and all within 60 minutes of collection. Whenever possible, babies were given milk from their own mother, but in some instances supplementation from other donors was required. Milk was not taken from women who had any signs of infection or from those who were on drugs. Random samples of milk were sent for culture. The babies were divided into two groups :Group L-Infants in this group were given fresh expressed milk from 9 A.M. to 9 P.M. and at night they had the milk formula (Lactodex-Raptakos and Brett Limited) given in the nursery to lowbirth-weight babies. This was to avoid the problems of preserving the breast-milk at night. Group fl.-Infants were given only milk formula (control infants). The total volume of milk given each day was based on the weight, gestation, degree of intrauterine growth retardation, and age, 15 and was similar in both groups. Babies were divided into the two groups by a randomised block design. Each was matched for various other factors which were identified on admission into the nursery. These included birthweight, prolonged labour, prolonged rupture of membranes or
’
G.H.S. was supported by the Cancer Research Campaign. We thank Dr A. Craven for statistical help.
REFERENCES
Bridges BA. Possible long term hazards of photochemotherapy with psoralens and near ultraviolet light. Clin Exp Dermatol 1978; 3: 349-53. 2 Stern RS et al. Risk of cutaneous carcinoma in patients treated with oral methoxsalen photochemotherapy for psoriasis. N Engl J Med 1979; 300: 809-13. 3 Bridges BA, Strauss GH. Possible hazards of photochemotherapy for psoriasis. Nature 1980; 283: 523-24. 4. Strauss GH et al 6-Thioguanine resistant peripheral blood lymphocytes in humans following psoralen, long-wave ultraviolet light (PUVA) therapy. J Invest Dermatol 1
1979; 73: 211-16. 5 Vella-Briffa D, Rogers S, Greaves MW, Narks
J, Shuster S, Warm APC. A randomized, controlled clinical trial comparing photochemotherapy with dithranol in the initial treatment of chronic plaque psoriasis. Clin Exp Dermatol 1978; 3: 339. 6 Catalona WJ, Chretien PB. Abnormalities of quantitative dinitrochlorobenzene sensitizaton in cancer patients: Correlation with tumour stage and histology. Cancer 1972; 31: 353-56. 7 Catalona WJ, Taylor PT, Chretien PB. Quantitative dinitrochlorobenzene contact sensitization in a normal population. Clin Exp Immunol 1972; 12: 325-33. 8. Simo-Camps E, et al. Immunologic impairment in patients with non-lymphoid cancer; correlation with tumoral stage, response to treatment and survival. Cancer 1976; 37: 724-27 9. Kraemer HH, Weinstein GD Decreased thymidine incorporation m circulating leukocytes after treatment of psoriasis with psoralen and long-wave ultraviolet light. J Invest Dermatol 1977; 69: 211-14. 10. Lischka G, Bohnert E, Bachtold G, Jung EG. Effects of 8-methoxypsoralen (8-MOP) and UVA on human lymphocytes. Arch Dermatol 1977; 259: 293-98. 1 . Roberts LK, Schmitt M, Daynes RA. Tumour susceptibility generated in mice treated with sub-carcinogenic doses of 8-methoxypsoralen and long-wave ultraviolet light. J Invest Dermatol 1979; 72 (6). 306-309. 12 Kripke ML, et al. Further characterization of immunological unresponsiveness induced in mice by ultraviolet radiation. Transplantation 1979; 28 (3): 212-17. 13 Spellman CW, Woodward JG, Daynes RA. Modification of immunological potential by ultraviolet radiation. I. Immune status of short-term UV-irradiated mice. Transplantation 1977; 24 (2): 112-26 14
Moller R, Howitz J Methoxsalen and multiple basal-cell carcinomas. J Arch Dermatol 1976; 112: 1613-14. RS, Zierler S, Parrish JA. Skin carcinoma in patients with psoriasis treated with topical tar and artificial ultraviolet radiation. Lancet 1980; i. 732-35. Reed WD Treatment of psoriasis with oral psoralens and long-wave ultraviolet light. Acta Dermato-vener 1976; 56: 315-18. Reed WB, Sugarman GI, Mathis RA. De-Sanctis-Cacchione syndrome. A case report with autopsy findings. Arch Dermatol 1977; 113: 1561-63. Walder BK, et al. Skin cancer and immunosuppression. Lancet 1971; ii: 1282. Kmlen L, et al. Collaborative United Kingdom/Australasian study of cancer in patients
15 Stern 16 17.
18 19
treated with immunosuppressive drugs. Br Med J 1979; ii: 1461. 20. Griffin AC Methoxsalen in ultraviolet carcinogenesis in the mouse. J Invest Dermatol 1959, 32: 367-72. 21 Urbach FJ. Modification of ultraviolet carcinogenesis by photoactive agents. J Invest Dermatol 1959; 32: 373-78. 22 Wagner J, Manthorpe R, Philips P, Frost F. Preleukemia (hematopoietic dysplasia) developing in a patient with psoriasis treated with 8-methoxypsoralen and ultraviolet light (PUVA treatment) Scand J Haematol 1978, 22: 57-60. 23 Hanson NE. Development of acute myeloid leukaemia in a patient with psoriasis treated with oral 8-methoxypsoralen and longwave ultraviolet light. Scan J Haematol 1979;
22: 57-60.
CONTROLLED TRIAL OF AN ELECTROSTATIC PRECIPITATOR IN CHILDHOOD ASTHMA E. A. MITCHELL
R. B. ELLIOTT
Department of Pædiatrics, School of Medicine, University of Auckland, Auckland, New Zealand A cross-over trial was conducted on 10 children with moderate to severe who had asthma, positive skin tests to Dermatophagoides pteronyssinus and nocturnal wheeze. An electrostatic precipitator was used during the night to remove airborne particles from the bedroom. During use of the
Summary
precipitator peak expiratory flow
rates were no
better
than in a control period. Introduction
provoke asthmatic attacks, and one major allergenic components is the house mite Dermatophagoides pteronyssinus.1,2 Other allergens in house dust include animal danders and mould spores.3 The mite is widely distributed in household dust throughout New Zealand4 and high levels are found in domestic mattresses.2,5 The mite population can be reduced by simple measures such as vacuum-cleaning mattresses and enclosing them in plastic sheets, using synthetic blankets and regularly washing them, and removing soft toys from the bedroom. 6, Such anti-mite HousE dust
can
of the
have reduced the incidence of asthmatic attacks in some patients,5,S but not in others.9 Bronchial allergy to house dust is common in moderate to severe asthma.10,11 The failure of anti-mite measures to produce dramatic improvement in most patients with mite-sensitive asthma suggests either that the-usual anti-mite measures are not sufficiently effective or that bronchial allergy to house dust and mite is not the major cause of their asthmatic attacks. Although the most important source of mites is the mattress, clearly the mite must be inhaled if it is to produce bronchospasm. We therefore conducted a controlled trial to study the effects of removal of airborne particles by an electrostatic precipitator, at night, in the bedroom of children with moderate to severe asthma. measures
Materials and
Methods
10 children (4 boys and 6 girls) aged between 6-9and 13.5 yr with asthma were studied. Criteria for entry into the study were (a) nocturnal wheeze; (b) positive skin tests to house dust, D. pteronyssinus, and D. farinae; and (c) moderate to severe asthma requiring regular prophylactic medication and intermittent use of aerosol bronchodilators. Table i gives the clinical details. The type and dose of the drugs used for prophylaxis were kept constant throughout the trial. A controlled cross-over trial was conducted in the patient’s
home. The
study consisted of two consecutive 4-week periods. period an electrostatic precipitator was used in the child’s bedroom; the other period served as the control. The order was randomised. Throughout the 8-week trial standard mite-avoidance measures were practised as previously recommended.6 Patients were studied consecutively throughout 1 During
one
year. The ’Micronaire p-500’ electrostatic precipitator contains a fan which draws the particle-laden air through a prefilter which removes the larger particles. The remaining smaller airborne particles then pass to the ioniser area, where they are
570
denly and drastically reduce the myocardial blood supply. They showed that ischaemia can occur without any preceding change in myocardial oxygen requirements and by angiography they displayed coronary artery "spasm" during these episodes of pain, whether the ST segment was raised or depressed.’The rehabilitation of spasm as a respectable explanation is complete. But is spasm the right word to describe what may be normal degrees of vasoconstriction? Prinzmetal et al.,’in their original description, concluded that variant angina "results from a temporary occlusion of a large diseased artery with a narrow lumen due to a normal increase in of the vessel wall". For, as Pickering8 pointed out, "there is no contention here that vessels do not contract and expand" but it is not necessary to assume "that arteries behave like whimsical children ... and react violently to a perfectly ordinary stimulus or to none at all". Normal coronary arteries can change their size spontaneously and dilate by as much as 163% after nitroglycerine.9 Clearly in areas where organic stenoses are present a normal amount of vasoconstriction will reduce the lumen considerably. MacAlpin’" has looked at this fundamental point. Simple geometry predicts that the lumen of a segment of coronary artery with a 50% stenosis (which is pliable or eccentric) will be occluded completely if the outer circumference is reduced by 9%; this is well within the range of normal variation of size. Furthermore, MacAlpin has found that in 90% of cases spasm occurs at the site of an organic lesion." Therefore, in most patients, a normal amount of vasoconstriction can produce severe ischaemia if it happens in an already stenosed segment of the artery. This should probably not be called spasm. In the few patients, with angiographically normal coronary arteries, true spasm may be a factor. What we need to know is the cause of this fluctuating vasoconstriction that presumably results in unstable angina. One attractive idea is that thromboxane A2, a potent vasoconstrictor, is released from agglutinated platelets. Mehta and co-workers12 report that platelets clump more readily after passing through an atherosclerotic coronary artery. 12 Autonomic nervous mechanisms may also be important. 13 If vasoconstriction is the underlying mechanism in unstable angina then the ideal treatment is to paralyse the coronary artery with nitrates and calcium blocking drugs. Plotnick14 has outlined a management plan. All tonus
patients should have intensive medical treatment in a coronary care unit, and this will successfully relieve the pain in about 85%. Nitrates are given in high doses as isosorbide dinitrate orally, topical nitroglycerin ointment, or intravenous nitroglycerin, until the onset of headache or a drop in systolic blood pressure. Verapamil and nifedipine both reduce the frequency of attacks.15,16 Nifedipine can be combined with beta blocking drugs. Theoretically, beta-blockers, by promoting alpha activity, may make vasoconstriction more likely, but there is no evidence that this happens. Doses should be increased until the resting heart rate is 50 to 60 beats per minute, systolic blood pressure is below 105 mm Hg, or heart failure develops. Anticoagulants have been recommended,17 although there has not been a good trial in this condition. The value of surgery has been clarified by the National Co-operative Study Group. 18, 19 There is no place for immediate surgery. Conti20 has reviewed all published trials (random and non-random), and the results point to a higher myocardial infarction rate with surgical treatment and no difference in mortality rate. Furthermore, fewer surgical patients return to work.21 However, if intensive medical treatment does not alleviate the pain after 48 h, surgery is indicated. In Yaco6b’s series 99% of such patients had a main stem or severe left anterior descending artery stenosis.22 In this group the benefits of intra-aortic ballon pumping outweigh the risks of complications, because pain is con-, sistently relieved and cardiac catheterisation is safer .21 For most of these patients surgery is successful and pain is removed.22,24 Each unit needs to know its own figures to assess the risks properly: not everyone will be able to reproduce an operative mortality of 4.2% and a graft patency rate of 91%.22 But medical treatment is now effective for most patients with unstable angina. The question remains: why are some people’s coronary arteries so apt to vasoconstrict? Perhaps cardiologists should look to the bronchial tree for an analogy.
-
5. Maseri A.
Pathogenetic
mechanism of
Heart J 1980; 43: 648-60. 6. Maseri A, L’Abbate A, Pesola A, toris. Lancet 1977; i: 713-17.
et
angina pectoris: expanding
al.
Coronary
views.
Br
vasospasm in angina pec-
7. Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris I: a variant form of angina pectoris. Am J Med 1959; 27: 375-88. 8. Pickering GW. Vascular spasm. Lancet 1951; ii: 845-50. 9. Gensini GG, Kelly AE, Da Costa BCB, Huntingdon PP. Quantitative angiography: the measurements of coronary vasomobility in the intact animal and man. Chest 1971; 60: 522-30. 10. MacAlpin RN. Contribution of dynamic vascular wall thickening to luminal narrowing during coronary arterial constriction. Circulation 1980, 61: 296-301. 11. MacAlpin RN. Relation of coronary arterial spasm to site of organic stenosis.
Am J Cardiol 1980; 46: 143-54. J, Mehta P, Pepine CJ. Platelet aggregation in aortic and coronary venous blood in patients with and without coronary disease, 3: Role of tachycardia stress and propranolol. Circulation 1978; 58: 881-86. 13. Mudge GH, Grossman W, Mills RM, Lesch M, Braunwald E. Reflex increase in coronary vascular resistance in patients with ischæmic heart disease. N Engl J Med 1976; 295: 1333-37. 14. Plotnick GD. Approach to the management of unstable angina. Am Heart J 1979; 98: 243-55. 12. Mehta
15. Parodi O, Maseri A, Simonetti I. Management of unstable angina at rest by verapamil. A double-blind cross-over study in a coronary care unit. Br 16.
Heart J 1979; 41: 167-74. Goldberg S, Reichek N, Wilson J, Hirschfeld J, Muller J, Kastor J. Nifedipine in the treatment of Prinzmetal’s (variant) angina. Am J Cardiol 1979; 44: 804-08.
17. Wood P. Acute and subacute coronary insufficiency. Br Med J 1961; i: 1779-82. 18. National Co-operative Study Group. Unstable angina pectoris: National Cooperative study group to compare surgical and medical therapy. II in-hospital experience and initial follow-up results in patients with one, two and three vessel disease. Am J Cardiol 1978; 42: 839-48. 19. National Co-operative Study Group. Unstable angina pectoris: National Cooperative study group to compare surgical and medical therapy. III results in patient with ST segment elevation during pain. Am J Cardiol 1980, 45: 819-24. 20. Conti CR. Initial management of patients hospitalised because of angina pectoris. Proceedings of the VIII European Congress of Cardiology. 1980, p. 256. 21. Russell RO, Wayne JB, Kronenfeld J, et al. Surgical versus medical therapy for treatment of unstable angina: changes in work status and family income. Am J Cardiol 1980; 45: 134-40. 22. Ahmed M, Thompson R, Seabra-Gomes R, Rickards A, Yacoub M. Unstable angina: a clinicoarteriographic correlation and long term results of early myocardial vascularisation. J. Thorac Cardiovasc Surg 1980; 79: 606-16. 23. Gold HK, Leinbac RC, Sanders CA, Buckley MJ, Mundth ED, Austen WG. Intra-aortic balloon pumping for control of recurrent myocardial ischemia. Circulation 1973; 47: 1197-1203. 24. Weintraub RM, Aroesty JM, Paulin S, Levine FH, Markis JE, LaRaia PJ, Cohen SI, Kurland GF. Medically refractory unstable angina pectoris. 1. Long term follow up of patients undergoing intraortic balloon counterpulsation and operation. Am J Cardiol 1979; 43: 877-82.
561 anti-mite measures are effective in reducing the incidence of asthmatic attacks. This study has shown that addition of an electrostatic precipitator to standard anti-mite measures and prophylactic asthmatic drugs does not significantly improve asthma in children.
simple
The ’Micronaire p-500’ electrostatic precipitator (Dome Laboratones, Division of Miles Laboratories, Australia) was kindly loaned through Ebos Dental and Surgical Supplies Limited, Christchurch, new Zealand. REFERENCES 1. Voorhorst
R, Spieksma-Boezeman MI, Spieksma FT. Is a mite (Dermatophathe producer of the house dust allergen? Allerg Asthma 1964;
goides sp.)
10: 329-34. 2. Maunsell K, Wraith DG, Cunningham AM. Mites and house dust allergy in bronchial asthma. Lancet 1968; i: 1267-70. 3. Virehow C, Roth A, Möller E. IgE antibodies to house dust, mite, animal allergens and molds in house dust hypersensitivity. Clin Allergy 1976; 6: 147-54. 4. Cornere BM. House dust mites: a national survey. NZ Med J 1972; 76: 270-71. 5. Sarsfield JK. Role of house-dust mites in childhood asthma. Arch Dis Childh
1974; 49: 711-15. JK, Gowland G, Troy R, Norman ALE. Mite-sensitive asthma of childhood: trial of avoidance measures. Arch Dis Childh 1974; 49:
6. Sarsfield
716-21.
Blythe ME, Al Ubaydi F, Williams JD, Smith JM. Study of dust mites in three Birmingham Hospitals. Br Med J 1975; i: 62-64. 8. Maunsell K, Hughes AM, Wraith DG. Mite asthma. Practitioner 1970; 205: 7.
779-83. 9. Burr ML, St. Leger AS, Neale E. Antimite measures in mite sensitive adult asthma A controlled trial. Lancet 1976; i: 333-35. 10 Aas K. Bronchial provocation test in asthma. Arch Dis Childh 1970; 45: 221-28. 11 Warner JO. Significance of late reactions after bronchial challenge with house dust mite. Arch Dis Childh 1976; 51: 905-11. BM. A miniature Wright peak-flow meter. Br Med J 1978; ii: 1627-28. 13. Godfrey S, Kamburoff PL, Nairn JR, Connolly NMC, Davis J, Packham E, Samuels CS. Spirometry, lung volumes and airway resistance in normal children aged 5-18 years. Br J Dis Chest 1970; 64: 15-25. 14. Warner JO. Mites and asthma in children. Br J Dis Chest 1978; 72: 79-87. 15. Burr ML, St. Leger AS, Neale E. Nocturnal wheeze and mite sensitivity. Lancet 1976; i: 972-73.
12. Wright
Preliminary
Communication
PARTIAL SUPPLEMENTATION WITH EXPRESSED BREAST-MILK FOR PREVENTION OF INFECTION IN LOW-BIRTH-WEIGHT INFANTS
K. PRAKASH R. K. VERMA
INDIRA NARAYANAN SHASHI BALA V. V.
GUJRAL
Kalawati Saran Children’s Hospital, Lady Hardinge Medical College, New Delhi, India
prospective controlled study the antiproperties of breast-milk were evaluated in 70 high-risk low-birth-weight infants. 32 babies (group I) were given fresh expressed breast-milk during the day and milk formula at night. 38 infants (group II) received only milk formula and served as controls. The two groups
Summary
In
a
infective
were matched
for other factors that could influence the occurof infection. The incidence of infections was significantly less (p<0·01) in babies who received breast-milk. rence
INTRODUCTION
THE progressive decline in century is rather unfortunate,
breast-feeding during this particularly in view of its
unique properties.’-9 Most of the research work, however, has involved estimation of factors in human milk, in-vitro analyses of the cellular components, or experimental , animals. 4-9 Clinical evaluation of infants at high-risk has been limited. 10-12 In developing countries, urbanisation has meant that although most women still begin breast-feeding, many tend to stop early with disastrous results.13,14 Whereas more widespread feeding of normal babies requires mainly better motivation of mothers and birth attendants, giving breast milk to high-risk infants, such as low-birth-weight babies, who are unable to suck directly from the breast is more complicated. There are numerous problems involved in providing expressed human milk in a developing country with uneducated mothers from the low socioeconomic group. In fact, theoretically at least, it may even have a greater risk of introducing
infection. This planned prospective controlled study was undertaken to evaluate the effect of giving expressed breast-milk on the incidence of infection in the high-risk newborn infant. It was part of a more extensive project on the influence of varying quantities of colostrum and mature breast-milk on the prevention of infection in low-birth-weight infants -
(Narayanan et al. Unpublished observations).
MATERIALS AND METHODS
The study involved 70 high-risk newborn infants who had been delivered in hospital and transferred to the nursery which catered for babies born to mothers who were actually or likely to be infected. These included women who had obvious infections, those who had prolonged rupture of membranes or leaking for more than 24 h, and those who had had an unhygienic vaginal examination by one of the untrained indigenous "dias" (traditional birth attendant). The women belonged to the low socioeconomic and educational status. Babies of such mothers were selected for this study because they had the highest risk of acquiring infection (Narayanan I. Unpublished observations). The actual indications for admission to the nursery included low birth-weight (<2000 gm), prematurity, birth asphyxia, delivery by Caesarian section, and so on. Babies in the other nursery and all the normal low-risk infants who stayed with their mothers in the maternity wards were not included in this study. Collection of breast-milk from donors was supervised by trained personnel. It was manually expressed directly into autoclaved feeding bottles. In most instances the mothers were called to an outer room in the nursery. When the mother could not come, the staff went to the maternity wards to collect the milk and transported it in ice in an insulated container. Many of the samples were fed to the babies within 30 minutes and all within 60 minutes of collection. Whenever possible, babies were given milk from their own mother, but in some instances supplementation from other donors was required. Milk was not taken from women who had any signs of infection or from those who were on drugs. Random samples of milk were sent for culture. The babies were divided into two groups :Group L-Infants in this group were given fresh expressed milk from 9 A.M. to 9 P.M. and at night they had the milk formula (Lactodex-Raptakos and Brett Limited) given in the nursery to lowbirth-weight babies. This was to avoid the problems of preserving the breast-milk at night. Group fl.-Infants were given only milk formula (control infants). The total volume of milk given each day was based on the weight, gestation, degree of intrauterine growth retardation, and age, 15 and was similar in both groups. Babies were divided into the two groups by a randomised block design. Each was matched for various other factors which were identified on admission into the nursery. These included birthweight, prolonged labour, prolonged rupture of membranes or
’