MUCH MORE LIGHT ON PORT-WINE STAINS

MUCH MORE LIGHT ON PORT-WINE STAINS

626 absorbed,l7,18 which leads to less than adequate of premature infants. This difficulty is seldom encountered in the UK since most infants receiv...

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626

absorbed,l7,18 which leads

to less than adequate of premature infants. This difficulty is seldom encountered in the UK since most infants receive their own mother’s milk raw. Human milk confers some immunological advantage to the infant, but in developed countries there is very little evidence that breast milk confers significant additional protection to premature babies. Avoidance of nonhuman protein is an additional theoretical advantage of breast milk but there are few indications of adverse effects of cow’s milk formulas in most premature infants. Conversely, some studies assessing the effect of high-protein formula feeds have documented rates of growth in premature infants exceeding that expected for the fetus;the longer-term effects of overnutrition must be considered carefully. What conclusions can be drawn from these studies? There is no doubt that breast milk does not provide adequate substrate for normal bone mineralisation and there are no agreed guidelines as to the appropriate supplementation of human milk with phosphorus and calcium. Human milk engineering has been attempted, but the report of the Royal College of Obstetricians and Gynaecologists on problems associated with AIDS21 recommends screening of all mothers donating breast milk; such a policy would sharply reduce the supply of milk available for such processing. When a mother wishes to breast feed her own premature infant it is difficult to sever this tangible and emotive link that she forges with her baby. Equally, the evidence is accumulating that growth may be improved with low birthweight formulas and the time an infant spends on a neonatal unit may be significantly reduced with optimum artificial feeding.22 Blending the mother’s own milk with low birthweight formula may provide the best food for premature babies, but there are few reports of such a manoeuvre.14 The results of a British multicentre study investigating the longer-term advantages of breast and formula feeds for premature infants are awaited. If it is shown that infants fed low birthweight formulas have an advantage in terms of subsequent neurodevelopmental outcome as well as growth, then for at least some premature infants breast will not be best.

growth19

SA, Bryan HM, Anderson GH. Human milk feeding in premature infants: protein, fat and carbohydrate balances in the first two weeks of life. J Pediatr 1981; 99: 617-24. 18. Williamson S, Finucane E, Ellis H, Gamsu HR Effect of heat treatment of human milk on absorption of nitrogen, fat, sodium, calcium and phosphorus by preterm infants Arch Dis Child 1978, 53: 555-63. 19. Stem H, Cohen D, Herman AAB, et al. Pooled pasteurized breast milk and untreated own mother’s milk in the feeding of very low birth weight babies: a randomized controlled trial. J Pediatr Gastroenterol Nutr 1986, 5: 242-47. 20. Kashyap S, Forsyth M, Zuker C, et al. Effects of varying protein and energy intakes on growth and metabolic response m low birth weight infants. J Pediatr 1986; 108: 955-63 21. Report of the RCOG sub-committee on problems associated with AIDS in relation to obstetrics and gynaecology. London: Royal College of Obstetricians and Gynaecologists, 1987 22. Lucas A, Gore SM, Cole TJ, et al. Multicentre trial on feeding low birthweight infants: effects of diet on early growth. Arch Dis Child 1984, 59: 722-30. 17. Atkinson

MUCH MORE LIGHT ON PORT-WINE STAINS CONSIDERABLE progress has been made on the treatment and the pathogenesis of port-wine stains (PWS) since the subject was last reviewed in these columns in 1981.1 PWS is a congenital vascular abnormality of the skin characterised by the presence of numerous ectatic blood vessels confined mostly to a 0-6 mm subepidermal zone of the dermis.2 The pathogenesis of PWS was largely conjectural until last year, when Rosen and Smoller showed a significant decrease in the innervation of the ectatic vessels. These results suggest that PWS is due primarily to localised autonomic nerve loss and that a subsequent inability to regulate dermal blood flow leads to progressive vascular ectasia. Until lately, there was no effective treatment for PWS, but the picture has changed dramatically with the introduction of laser therapy. A bewildering array of lasers have now been used in patients with PWS and most workers agree that the continuous wave (CW) argon laser, emitting at wavelengths of 488 and 515 .4 nm, produces satisfactory results in about 70% of cases There are fewer published data on other lasers that have been used in this condition--eg, a CW dye laser emitting at 540 nm,and at 577 nm;6 a millisecond pulsed ruby laser at 694 nm;7 a pulsed dye laser at 577 nm ;8 a CW neodymium-YAG laser at 1060 nm;9 and a CW carbon dioxide laser at 10 600 nm.10 The difficulties encountered with most of these lasers are similar, in that not all patients respond satisfactorily and in some cases scarring follows laser therapy. Lesser problems include persisting posttreatment hypopigmentation and occasionally reactive hyperpigmentation. The incidence of hypertrophic scarring varies in different series and is influenced not only by the treatment site but also by the type of laser. With argon laser therapy, the incidence of hypertrophic scarring may be as high as 10%,11 and there have been many attempts to improve treatment techniques-eg, alteration of the optical properties of the PWS by pre-chilling the lesion.12 Children with pink and easily compressible PWS are especially difficult to treat. These lesions contain relatively less target haemoglobin than more mature and purple ectatic lesions, which are much more successfully treated in adults.13 The pink lesions in children either show little or no response to argon laser therapy, or scar readily, particularly if they are on the upper lip and around the eyes or on sites off

1. Editorial. New ray of hope for port wine-stains. Lancet 1981, i: 480. 2. Finley JL, Barsky SH, Geer D, et al. Healing of port-wine stains after argon laser therapy. Arch Dermatol 1981; 117: 486-89 3. Rosen S, Smoller BR. Port-wine stains: anew hypothesis Am Acad Dermatol 1987; J

17: 164-66 4. Carruth

JAS. The argon laser in the treatment of vascular naevi. Br J Dermatol 1982, 107: 365-68 5. Hulsbergen Henning JP, Van Gemert MJC. Port-wine stain coagulation expenments with a 540 nm continuous wave dye laser. Lasers Surg Med 1983, 2: 205-10. 6. Cotterill JA. Preliminary results following treatment of vascular lesions of the skin using a continuous wave tunable dye laser which emits at 577nm. Clin Exp Dermatol 1986; 11: 628-35. 7. Oshiro T, Maruyama Y. The ruby and argon lasers m the treatment of nevi. Ann Acad Med 1983; 12: 388-95 8. Tan OT, Tang S, Garden J, et al. Pilot study. treatment of port-wine stains using a 577 nm pulsed dye laser. Lasers Surg Med 1985; 5: 178-79. 9. Landthaler M, Brunner R, Haina D, et al. First experiences with the neodymiumYAG laser in dermatology. In: Joffe SN, ed. Neodymium-YAG laser in medicine and surgery. New York. Elsevier, 1983: 175-83. 10. Ratz JL, Bailin PL. The case for the use of the CO2 laser in the treatment of port-wine stains. Arch Dermatol 1987; 123: 74-75. 11. Cosman B. Experience m argon laser therapy of port-wine stains Plast Reconstr Surg 1980; 65: 119-29. 12. Gilchrest BA, Rosen S, Noe JM. Chilling port wine stains improves the response to argon laser therapy. Plast Reconstr Surg 1982; 69: 278-83. 13. Noe JM, Barsky SH, Geer D, et al. Port wine stains and the response to argon laser therapy. successful treatment and the predictive role of color, age and biopsy Plast Reconstr Surg 1980; 65: 130-36.

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the face. One attempt to overcome this difficulty was the introduction of the pulsed tunable dye laser emitting at 577 nm, one of the absorption peaks of haemoglobin, and early results are promising.8,14 However, this type of equipment is expensive and it is technically difficult to produce an even therapeutic effect, so the CW tunable dye laser emitting at 577 nm was investigated .6,15,16 This laser is as effective as the argon laser in the treatment of PWS in general, with a lower incidence of scarring and hypopigmentary change, but is no more effective in pink lesions in children than the argon laser; overall it appears to offer few advantages. On the basis of costs and ease of use, the argon laser may be preferred by most therapists. The CW carbon dioxide laser has also been used to treat PWS in children and the incidence of scarring following treatment of PWS of the face has been claimed to be as low as 2-7%, a figure that compares very favourably with the reported incidence of scarring with the argon laser, which may be as high as 10% on the faceY Adams and colleagues have lately investigated the effect of wavelength, power, and treatment patterns on outcome of laser treatment in PWSY An argon laser was used to treat over 200 patients and these workers report that perfect cosmetic results were seldom achieved. Nevertheless, treatment results were acceptable to most patients and severe scarring occurred in less than 2% in this large group. 50 additional patients were treated to try to improve the results and a randomised control study was conducted with different treatment variables. The treatment pattern was found to be important in that results with contiguous or overlapping laser spots were significantly better than those with spot separation of one or two millimetres. Increasing the power to twice the minimum blanching power did not improve the results, nor was there an increase in the frequency of scarring. This group of workers also studied the neodymium-YAG laser and, like previous investigators, found a high incidence of scarring, so much so that they felt that this laser had only very limited indications for facial use. However, the neodymium-YAG laser does have a place in the treatment of patients with very deep cavernous lesions, particularly of the lips.l$ Thus, spot separation needs to be carefully controlled, whereas wavelength and power level appear to be less important than previously thought. Development of an automated arm system is therefore likely to benefit future laser therapy. Interestingly, a non-laser source of infrared light has given comparable results in patients with PWS.19 The capital cost of this equipment is very much less than that of a conventional laser but, properly used, the instrument will produce a controlled dermal fibrosis similar to the end-result in patients treated with argon or carbon dioxide lasers.

14. Morelli

JG, Tan OT, Garden J, et al Tunable dye laser (577nm) treatment of port Lasers Surg Med 1986, 6: 94. 15. Cartwright P, Cotterill JA. Tunable dye laser therapy of port-wine stains. Br J Dermatol (in press) 16. Lanigan SW, Cotterill JA The treatment of port-wine stains with the continuous wave dye laser at 577nm Laser surgery characterisation and therapeutics. Proceedings of the International Society for Optical Engineering, Los Angeles, Jan, 1988 17 Adams SJ, Swain CP, Mills TN, et al The effect of wavelength, power, and treatment pattern on the outcome of laser treatment for port-wine stains Br J Dermatol 1987; wine stains.

117: 487-94. 18. Landthaler M, Hainer D, Brunner R, et al Neodymium-YAG laser therapy for vascular lesions J Am Acad Dermatol 1986, 14: 107-17 19. Colver GB, Cherry GW, Dawber RPR, et al. The treatment of cutaneous vascular lesions with the infra-red coagulator: a preliminary report Br J Plast Surg 1986, 39: 131-35

ACUTE TROPICAL POLYARTHROPATHY: HOMOGENEOUS ENTITY OR DIAGNOSTIC SCRAP-HEAP? POLYARTHROPATHY is a major affliction in many tropical

countries; it may be acute or chronic. Although many cases have a discernible cause, physicians working in the tropics are well aware of a self-limiting but severely debilitating form of arthritis-acute tropical (or non-specific) polyarthritis-which, when all known causes in the local environment are excluded, does not have a recognisable aetiology. In Africa, this disease has been reported from Malawi,! Uganda,2 Kenya,3Zimbabwe,4,s and Nigeriait has also been documented in Sri Lanka8 and Papua New Guinea.9 Young adults of both sexes are affected,1,1,4although the disorder has been described in older people.’ Some workers6 but not otherss have noted an increased frequency in the dry season. Patients present with fever1,4-{,,8,9 and painful swollen joints;1.4,S,9 large joints, especially the knees, are predominantly involved, whereas small joints in the hands are seldom affected. Occasionally there are systemic symptoms,S but migratory arthropathy and morning stiffness6 are not features of the condition. Response to salicylates4 and penicillin4 is apparently rapid, but in any case the disease clears spontaneously and abnormalities seldom persist after three months.5 The sedimentation rate is usually raised, and the increase is often striking,4-7.9 but the peripheral blood count and joint radiographs are notmal. 4.6,7,9 Synovial fluid is sterile,4°6 and biopsy specimens merely show an inflammatory exudate of lymphocytes and plasma cells.69 Acute rheumatic fever, without cardiac manifestations, may account for a few cases;2,1O although the clinical manifestations superficially resemble rheumatoid arthritis, there are no other rheumatoid features. There are none of the associated features of reactive arthritis (Reiter’s syndrome).9.11,12 Gonococcal disease (with and without genitourinary symptoms) has also been excluded.13,14 Some arbovirus diseases, for example, O’nyong nyong and Chikungunya fevers, cause arthralgias, but arthropathies are unusual.’ Many other viruses, bacteria, fungi, and even parasites (including filariae, strongyloides,ls and schistosomes) have been considered, and in most cases excluded.7,16 The possibility that tropical polyarthropathy represents a rheumatological disorder whose presentation is 1.

Goodall JWD Joint swellings in Africans (a review of 90 cases). Cent Afr J Med 1956; 2: 220-23.

Shaper AG, Shaper L Analysis of medical admissions to Mulago hospital, 1957. E Afr Med J 1958; 35: 647-78. 3 Hall L. Polyarthritis m Nairobi Africans E Afr Med J 1963; 40: 354-58. 4. Gelfand M Acute non-specific arthritis m the African. Cent Afr J Med 1963, 9: 2

276-78. 5. Riley MJ Acute non-specific polyarthritis. Cent Afr J Med 1976, 22: 1-4 6. Greenwood BM. Acute tropical polyarthritis. Quart J Med 1969; 38: 295-306. 7. Greenwood BM. Polyarthritis in western Nigeria Ann Rheum Dis 1970; 29: 56-63 8. Nagaratnam N, Alagaramam K, Thambapillai AJ, Femando DCR. Acute tropical polyarthritis in Sri Lanka patients. J Trop Med Hyg 1975; 78: 34-37. 9. Jeremy R, Rhodes FA, Sharp JT, Rawls WE. Clinical and laboratory studies of a distinctive type of arthritis observed in New Guinea. Med J Aust 1969; 140: 1273-79 10. McDanald EC, Weisman MH. Articular manifestations of rheumatic fever in adults. Ann Intern Med 1978; 89: 917-20. 11. Keat A. Reiter’s syndrome and reactive arthritis m perspective N EnglJ Med 1983,

309: 1606-15. 12 Editorial. Treating Reiter’s syndrome Lancet 1987; ii. 1125-26 13 Seifert MH, Warm AP, Miller A Articular and cutaneous manifestations of

gonorrhoea: review of sixteen cases Ann Rheum Dis 1974, 33: 140-46 Goldenberg DL. "Postinfectious" arthritis: new look at an old concept with particular attention to disseminated gonococcal infection Am J Med 1983; 74: 925-28. 15. Jonge-Bok JM de, Overbosch D, MacFarlane JD. Parasitic rheumatism presenting as oligoarthritis: a case report Trop Geogr Med 1985, 37: 367-68. 16. Ward JR, Atcheson SG. Infectious arthritis. Med Clin North Am 1977, 61: 313-29

14.