- Email: [email protected]
FAILURE TO THRIVE REVISITED
662
cycles in the body, the apparent weekly (or circaseptan) cycle of the striae of Retzius is harder to understand. It has been suggested that other physiological processes may also exhibit a circaseptan pattern, possibly resulting from an interaction between two or more systemic cycles of slightly different length-eg, a 24 hour and a 27 hour cycle would produce "beats" at 7-8 day intervals.2 The circaseptan rhythm in matrix secretion may also be influenced by systemic factors-for example, metabolic changes due to disease and dietary deficiency. Serious illness is thought to potentiate the effects of the cycle on enamel formation and cause the striae to appear darker and more prominent. Adverse physiological conditions may induce a greater suppression of ameloblast activity during the slow phase of the cycle than would occur normally and may even induce cells approaching the terminal phase of secretion to cease enamel production altogether.3 Thus, since periods of systemic stress are reflected in the structure of the dental enamel forming at the time, areas of enamel with prominent striae of Retzius may reveal valuable information about childhood disease in a long byegone age. A pilot study was carried out on 80 teeth from 35 contemporary children with known and documented medical histories in order to determine a possible correlation between disease and the occurrence of prominent striae of Retzius.4 The results showed that, for the deciduous teeth, the total number of prominent striae was significantly higher in the children with chronic disease (eg, recurrent infection and malabsorption) than in the healthy children. It remains to be established whether these findings hold true for the permanent teeth and whether these prominent striae can be linked temporally to specific disease episodes. 1. Dean MC. Growth layers and incremental markings in hard tissues: a review of the literature and some preliminary observations about enamel structure in Paranthropus boisei. J Hum Evol 1987; 16: 157-72. 2. Newman HN, Poole DFG. Observations with scanning and transmission electron microscopy of human surface enamel. Arch Oral Biol 1974; 19: 1135-43. 3. Boyde A. The surface of the enamel in human hypoplastic teeth. Arch
Oral Biol 1970; 15: 879-98. 4. Hillier RJ, Craig GT. Striae of Retzius as indicators of systemic disturbances in childhood. Presented at meeting of British Society for Dental Research, King’s College London, April, 1990.
FAILURE TO THRIVE REVISITED The term failure to thrive (FTT) evokes a pathetic image, but do all those who care for children have a similar concept of what it means? Perhaps the biggest gap is between those who dig deep for biochemical or metabolic causes ("organic" FTT) and those for whom the social history reveals all the necessary clues ("non-organic" FTT). Batchelor and Kerslake1 now suggest that this distinction is artificial, that much FTT is missed, and that the feeding process is the root cause. For a start, how should one define the condition? The word thrive is not widely used in medicine, and dictionaryproffered synonyms such as prosper, flourish, grow rich, and grow vigorously cover more than mere weight gain. However, weight is usually the criterion for defining the presence of FTT. So, we should either adopt the term failure to gain weight appropriately, or include behavioural criteria in the definition. Even weight criteria for FTT vary considerably.2-4 Weight below the 3rd centile is commonly used,s but what happens if a child started at the 90th and drops to the 25th?
Logically the definition should include the concept of deviating downwards. The measure adopted by Edwards and colleagues6 in Newcastle upon Tyne in a communitybased study is more clearcut-aweight deviation downward from the true centile (defined as the maximum centile achieved between 4-8 weeks of age) crossing two or more centile lines and persisting for more than one month. The Newcastle study also provides local data on the population prevalence of FTT, and shows that 20-9% of children in two economically disadvantaged areas of Newcastle fell within this definition. This figure contrasts with values of 9-6%’ and 1.3%8 in other studies. Batchelor and Kerslake’s main message is that one in three children with low weight gain is missed by professionals, with likely adverse consequences for later growth and development. This social work investigation was carried out in south-west England by use of health visitor data and was in two parts: the first relied on health visitor recall as the primary source of cases and the second on an analysis of children’s clinic and health visitor records. The researchers’ narrow definition of FTT as weight below the 3rd centile provided them with 39 children in the first study and 121 in the second, out of a total under-fives population of 12 600, giving a prevalence of only 1.3%. However, the records analysis and interviews with health visitors provided valuable qualitative data. Health visitors expressed dissatisfaction with weighing equipment, with the quality of communication with general practitioners (in only 48% was it good), and with the management of FTT by paediatricians ("all the paediatricians do is tell the health visitors to monitor"). The 39 FTT children were divided into 18 non-organic, 11 organic, 8 "small", and 2 unknown. The main differences between non-organic and small were in socioeconomic indices (seven of the so-called small were over the 10th centile at birth). Batchelor and Kerslake suggest that social disadvantage predicated a diagnosis of "NOFTT" (nonorganic FTT). Outcome data showed that children who improved after a stay in hospital were less likely than non-improvers to have had feeding problems identified by the health visitors. The researchers conclude that feeding difficulties are related to failure-to-thrive outcome, and their second study (review of 6000-8000 clinic records and 2000 health visitor records) was designed to address this hypothesis. Centile charts were often incomplete and inaccurate and Batchelor and Kerslake identified many previously unrecognised children with low weight gainone child whose weight had crossed three major centile lines was described as "healthy" by a clinical medical officer at an 18-month check. Hospital records were no better, with discharge weights being hard to locate and centile charts inadequate. The main finding of this study was that feeding difficulties among those who did not improve were twice as common as among "improvers". The researchers recommend that centile charts should be used more effectively, that greater efforts be made to identify FTT early, and that health visitors should use behavioural methods such as those of Iwaniec et al9 in the management of feeding problems. Although the conclusions are based on a small study, they are of considerable value because they represent a crossdisciplinary view. The emphasis on feeding problems comes from secondhand information, and the importance of socioeconomic factors revealed by other surveys seems to have been overlooked.1O Further follow-up studies and
663
intervention on a population basis are much needed. Batchelor and Kerslake’s findings run counter to the views of the Hall reportll... "we are not convinced that the advantages conferred by regular weighing justify the resources required ...". A pilot project of weight surveillance in infancy12 (weights forwarded by health visitors to a central computer on six occasions in the first 18 months) is now being conducted in Newcastle and should provide much-needed information on FTT population prevalence. Optimum child growth should top any child welfare agenda since it has long-term implications for behaviour and development. 13,14
Solar urticaria can be very trying for its victims, since venturing outdoors can produce intense discomfort, even on a day without much sun. The first part of management is to establish the spectral sensitivity of the disorder, which will determine the advice that should be offered about protection from the sun. Unfortunately most patients react to the longer ultraviolet wavelengths (UVA) in excess of 300 nm, and even to visible light (in excess of 400 nm).3 This pattern of sensitivity means that protection by sunscreens is less effective than for UVB, since most of these products are better at protecting against the shorter wavelengths. It also means that some patients will manifest their rash if they sit windows because UVA rays penetrate most types of glass. Ordinary (HI antagonist) antihistamines seldom help,4 and the addition of H2 blocking agents does not seem to confer any advantage.5 Patients obtain some relief from a programme of desensitisation, in which they are rendered tolerant to UVA by repeated exposures.6,7 How does this technique work? Leenutaphong et al8 in Dusseldorf have studied two patients with solar urticaria; one was sensitive in the spectral range 320-455 nm and the other in the range 400-495 nm. These researchers found that they could still elicit weal and flare responses, in skin made tolerant by repeated irradiation, by intracutaneous injection of histamine and codeine, which is a histamine-releasing agent. This observation indicates that neither "mast cell exhaustion" nor lack of vascular reactivity to histamine was responsible for the development of tolerance. In the pathogenesis of the disorder it has been supposed that a photoallergen is produced, and when Leenutaphong et al injected plasma irradiated in vitro (containing the putative photoallergen) into unirradiated skin, a weal was produced. However, no reaction occurred when the irradiated plasma was injected into tolerant skin, which indicates that tolerance was not due to exhaustion of the photoallergen, as had been supposed by Keahey and colleagues.6 Repeated injection of the irradiated plasma into unexposed skin produced tolerance, although intradermal codeine still caused weals. This logical and systematic approach allowed the German workers to suggest that the binding sites on the IgE adherent to mast cells in the skin remain occupied by the "photoallergen" during the state of tolerance. Somehow the repeated exposure to UVR in the process of desensitisation specifically blocks IgE-mediated release of histamine from mast cells. This new information greatly assists our understanding of this strange example of a physical urticaria. A ray of hope for ordinary chronic idiopathic urticaria? near
1. Batchelor J, Kerslake A. Failure to find failure to thrive. London: Whiting and Birch, 1990. £6.50. Pp 72. ISBN 1-871177057. 2. Hutton IW, Oates RK. Non-organic failure to thrive: a long term follow-up. Pediatrics 1977; 59: 75-77. 3. Rosenn DW, Loeb LS, Jura MB. Differentiation of organic from non-organic failure to thrive syndrome in infancy. Pediatrics 1980; 66: 698-704. 4. Berwick DM, Levy JC, Kleinerman R. Failure to thrive: diagnostic yield of hospitalisation. Arch Dis Child 1982; 57: 347-51. 5. Hannaway PJ. Failure to thrive: a study of 100 infants and children. Clin Paediatr 1970; 9: 96-99. 6. Edwards A, Halse P, Parkin M, Waterston AJR. Recognising failure to thrive in early childhood. Arch Dis Child (in press). 7. Mitchell WG, Gorrell RW, Greenberg RA. Failure to thrive: a study in a primary care setting—epidemiology and follow-up. Pediatrics 1980; 65: 971-77. 8.Dowdney L, Skuse D, Heptinstall E, Puckering C, Zur-Szpiro S. Growth retardation and developmental delay amongst inner city children. J Child Psychol Psychiatry 1987; 28: 529-41. 9. Iwaniec D, Herbert M, Sluckin A. Helping emotionally abused children who fail to thrive. In: Browne K, Davies C, Stratton P. Early prediction and prevention of child abuse. Chichester: Wiley, 1988: 229-44. 10. Frank DA, Allen D, Brown JL. Primary prevention of failure to thrive: social policy implications. In: Drotar D, ed. New directions in failure to thrive: implications for research and practice. New York: Plenum, 1985. 11. Hall D, ed. Health for all children. Oxford: Oxford University Press, 1989. 12. Wright C. A prevalence study on failure to thrive. Paper presented at Community Paediatric Research Group, Newcastle, December, 1989. 13. Galler JR, Ramsey F, Solimano G. The influence of early malnutrition on subsequent behavioral development. J Am Acad Child Psychiatry 1985; 24: 58-64 14. Glaser HH, Heagarty MC, Bullard DM, et al. Physical and psychological development of children with early failure to thrive. J Pediatr 1980; 73: 690-98.
RED WEALS UNDER THE SUN It does not take much to annoy a mast cell. In some unfortunates urticarial weals seem to develop almost at the drop of a hat. A morsel of crab, a tablet of aspirin, a minor scratch, a hot bath, or a cold wind-these are just some of the stimuli capable of eliciting urticarial lesions. Dermatologists take special pleasure in trying to work out the cause of weals in their patients with the all too common disorder of chronic urticaria, even though most recognise that despite their best efforts the precipitating cause will usually elude their investigative grasp. But there is little difficulty in pinpointing the problem in a small group of individuals who complain that an itchy rash develops on the exposed skin after a few minutes whenever they go into the sun. Once it is clear that the patient has an urticarial type of rash, with itchy raised pink or red weals lasting a few hours only, and that the rash is due to sun exposure rather than heat,1 a diagnosis of solar urticaria is established. The only disorders to simulate this odd condition are erythropoietic protoporphyria, polymorphic light eruption, and lupus erythematosus, in which urticaria-like lesions occasionally arise at exposed sites but alongside other lesions.2
.
CA. Localised heat urticaria treated by inducing tolerance to heat. Br J Dermatol 1975; 90: 191-93. 2. Black AK. The physical urticarias. In: Champion RH, Greaves MW, Black AD, Pye RJ, eds. The urticarias. Edinburgh: Churchill Livingstone, 1985: 180. 3. Czarnetzki BM. Solar urticaria. In: Urticaria. Berlin: Springer, 1986: 79-83. 4. Parrich JA, Jaenick KF, Morison WL, Momtaz K, Shea C. Solar urticaria: treatment with PUVA and mediator studies. Br J Dermatol 1982; 106: 575-80. 5. Mitchell P, Hawk JLM, Shafrir A, Corbett MF, Magnus UA. Assessing the treatment of solar urticaria: the dose-response as a quantifying approach. Dermatologica 1980: 160: 198-207. 6. Keahey TM, Lavker RM, Kaidbey KH, et al. Studies on the mechanism of clinical tolerance in solar urticaria. Br J Dermatol 1984; 110: 327-38. 7. Ramsay CA. Solar urticaria treatment by inducing tolerance to artificial radiation and natural light. Arch Dermatol 1977; 113: 1222-25. 8. Leenutaphong V, Hölzle E, Plewig G. Solar urticaria: studies on mechanisms of tolerance. Br J Dermatol 1990; 122: 601-06. 1.
Leigh IM, Ramsay
cycles in the body, the apparent weekly (or circaseptan) cycle of the striae of Retzius is harder to understand. It has been suggested that other physiological processes may also exhibit a circaseptan pattern, possibly resulting from an interaction between two or more systemic cycles of slightly different length-eg, a 24 hour and a 27 hour cycle would produce "beats" at 7-8 day intervals.2 The circaseptan rhythm in matrix secretion may also be influenced by systemic factors-for example, metabolic changes due to disease and dietary deficiency. Serious illness is thought to potentiate the effects of the cycle on enamel formation and cause the striae to appear darker and more prominent. Adverse physiological conditions may induce a greater suppression of ameloblast activity during the slow phase of the cycle than would occur normally and may even induce cells approaching the terminal phase of secretion to cease enamel production altogether.3 Thus, since periods of systemic stress are reflected in the structure of the dental enamel forming at the time, areas of enamel with prominent striae of Retzius may reveal valuable information about childhood disease in a long byegone age. A pilot study was carried out on 80 teeth from 35 contemporary children with known and documented medical histories in order to determine a possible correlation between disease and the occurrence of prominent striae of Retzius.4 The results showed that, for the deciduous teeth, the total number of prominent striae was significantly higher in the children with chronic disease (eg, recurrent infection and malabsorption) than in the healthy children. It remains to be established whether these findings hold true for the permanent teeth and whether these prominent striae can be linked temporally to specific disease episodes. 1. Dean MC. Growth layers and incremental markings in hard tissues: a review of the literature and some preliminary observations about enamel structure in Paranthropus boisei. J Hum Evol 1987; 16: 157-72. 2. Newman HN, Poole DFG. Observations with scanning and transmission electron microscopy of human surface enamel. Arch Oral Biol 1974; 19: 1135-43. 3. Boyde A. The surface of the enamel in human hypoplastic teeth. Arch
Oral Biol 1970; 15: 879-98. 4. Hillier RJ, Craig GT. Striae of Retzius as indicators of systemic disturbances in childhood. Presented at meeting of British Society for Dental Research, King’s College London, April, 1990.
FAILURE TO THRIVE REVISITED The term failure to thrive (FTT) evokes a pathetic image, but do all those who care for children have a similar concept of what it means? Perhaps the biggest gap is between those who dig deep for biochemical or metabolic causes ("organic" FTT) and those for whom the social history reveals all the necessary clues ("non-organic" FTT). Batchelor and Kerslake1 now suggest that this distinction is artificial, that much FTT is missed, and that the feeding process is the root cause. For a start, how should one define the condition? The word thrive is not widely used in medicine, and dictionaryproffered synonyms such as prosper, flourish, grow rich, and grow vigorously cover more than mere weight gain. However, weight is usually the criterion for defining the presence of FTT. So, we should either adopt the term failure to gain weight appropriately, or include behavioural criteria in the definition. Even weight criteria for FTT vary considerably.2-4 Weight below the 3rd centile is commonly used,s but what happens if a child started at the 90th and drops to the 25th?
Logically the definition should include the concept of deviating downwards. The measure adopted by Edwards and colleagues6 in Newcastle upon Tyne in a communitybased study is more clearcut-aweight deviation downward from the true centile (defined as the maximum centile achieved between 4-8 weeks of age) crossing two or more centile lines and persisting for more than one month. The Newcastle study also provides local data on the population prevalence of FTT, and shows that 20-9% of children in two economically disadvantaged areas of Newcastle fell within this definition. This figure contrasts with values of 9-6%’ and 1.3%8 in other studies. Batchelor and Kerslake’s main message is that one in three children with low weight gain is missed by professionals, with likely adverse consequences for later growth and development. This social work investigation was carried out in south-west England by use of health visitor data and was in two parts: the first relied on health visitor recall as the primary source of cases and the second on an analysis of children’s clinic and health visitor records. The researchers’ narrow definition of FTT as weight below the 3rd centile provided them with 39 children in the first study and 121 in the second, out of a total under-fives population of 12 600, giving a prevalence of only 1.3%. However, the records analysis and interviews with health visitors provided valuable qualitative data. Health visitors expressed dissatisfaction with weighing equipment, with the quality of communication with general practitioners (in only 48% was it good), and with the management of FTT by paediatricians ("all the paediatricians do is tell the health visitors to monitor"). The 39 FTT children were divided into 18 non-organic, 11 organic, 8 "small", and 2 unknown. The main differences between non-organic and small were in socioeconomic indices (seven of the so-called small were over the 10th centile at birth). Batchelor and Kerslake suggest that social disadvantage predicated a diagnosis of "NOFTT" (nonorganic FTT). Outcome data showed that children who improved after a stay in hospital were less likely than non-improvers to have had feeding problems identified by the health visitors. The researchers conclude that feeding difficulties are related to failure-to-thrive outcome, and their second study (review of 6000-8000 clinic records and 2000 health visitor records) was designed to address this hypothesis. Centile charts were often incomplete and inaccurate and Batchelor and Kerslake identified many previously unrecognised children with low weight gainone child whose weight had crossed three major centile lines was described as "healthy" by a clinical medical officer at an 18-month check. Hospital records were no better, with discharge weights being hard to locate and centile charts inadequate. The main finding of this study was that feeding difficulties among those who did not improve were twice as common as among "improvers". The researchers recommend that centile charts should be used more effectively, that greater efforts be made to identify FTT early, and that health visitors should use behavioural methods such as those of Iwaniec et al9 in the management of feeding problems. Although the conclusions are based on a small study, they are of considerable value because they represent a crossdisciplinary view. The emphasis on feeding problems comes from secondhand information, and the importance of socioeconomic factors revealed by other surveys seems to have been overlooked.1O Further follow-up studies and
663
intervention on a population basis are much needed. Batchelor and Kerslake’s findings run counter to the views of the Hall reportll... "we are not convinced that the advantages conferred by regular weighing justify the resources required ...". A pilot project of weight surveillance in infancy12 (weights forwarded by health visitors to a central computer on six occasions in the first 18 months) is now being conducted in Newcastle and should provide much-needed information on FTT population prevalence. Optimum child growth should top any child welfare agenda since it has long-term implications for behaviour and development. 13,14
Solar urticaria can be very trying for its victims, since venturing outdoors can produce intense discomfort, even on a day without much sun. The first part of management is to establish the spectral sensitivity of the disorder, which will determine the advice that should be offered about protection from the sun. Unfortunately most patients react to the longer ultraviolet wavelengths (UVA) in excess of 300 nm, and even to visible light (in excess of 400 nm).3 This pattern of sensitivity means that protection by sunscreens is less effective than for UVB, since most of these products are better at protecting against the shorter wavelengths. It also means that some patients will manifest their rash if they sit windows because UVA rays penetrate most types of glass. Ordinary (HI antagonist) antihistamines seldom help,4 and the addition of H2 blocking agents does not seem to confer any advantage.5 Patients obtain some relief from a programme of desensitisation, in which they are rendered tolerant to UVA by repeated exposures.6,7 How does this technique work? Leenutaphong et al8 in Dusseldorf have studied two patients with solar urticaria; one was sensitive in the spectral range 320-455 nm and the other in the range 400-495 nm. These researchers found that they could still elicit weal and flare responses, in skin made tolerant by repeated irradiation, by intracutaneous injection of histamine and codeine, which is a histamine-releasing agent. This observation indicates that neither "mast cell exhaustion" nor lack of vascular reactivity to histamine was responsible for the development of tolerance. In the pathogenesis of the disorder it has been supposed that a photoallergen is produced, and when Leenutaphong et al injected plasma irradiated in vitro (containing the putative photoallergen) into unirradiated skin, a weal was produced. However, no reaction occurred when the irradiated plasma was injected into tolerant skin, which indicates that tolerance was not due to exhaustion of the photoallergen, as had been supposed by Keahey and colleagues.6 Repeated injection of the irradiated plasma into unexposed skin produced tolerance, although intradermal codeine still caused weals. This logical and systematic approach allowed the German workers to suggest that the binding sites on the IgE adherent to mast cells in the skin remain occupied by the "photoallergen" during the state of tolerance. Somehow the repeated exposure to UVR in the process of desensitisation specifically blocks IgE-mediated release of histamine from mast cells. This new information greatly assists our understanding of this strange example of a physical urticaria. A ray of hope for ordinary chronic idiopathic urticaria? near
1. Batchelor J, Kerslake A. Failure to find failure to thrive. London: Whiting and Birch, 1990. £6.50. Pp 72. ISBN 1-871177057. 2. Hutton IW, Oates RK. Non-organic failure to thrive: a long term follow-up. Pediatrics 1977; 59: 75-77. 3. Rosenn DW, Loeb LS, Jura MB. Differentiation of organic from non-organic failure to thrive syndrome in infancy. Pediatrics 1980; 66: 698-704. 4. Berwick DM, Levy JC, Kleinerman R. Failure to thrive: diagnostic yield of hospitalisation. Arch Dis Child 1982; 57: 347-51. 5. Hannaway PJ. Failure to thrive: a study of 100 infants and children. Clin Paediatr 1970; 9: 96-99. 6. Edwards A, Halse P, Parkin M, Waterston AJR. Recognising failure to thrive in early childhood. Arch Dis Child (in press). 7. Mitchell WG, Gorrell RW, Greenberg RA. Failure to thrive: a study in a primary care setting—epidemiology and follow-up. Pediatrics 1980; 65: 971-77. 8.Dowdney L, Skuse D, Heptinstall E, Puckering C, Zur-Szpiro S. Growth retardation and developmental delay amongst inner city children. J Child Psychol Psychiatry 1987; 28: 529-41. 9. Iwaniec D, Herbert M, Sluckin A. Helping emotionally abused children who fail to thrive. In: Browne K, Davies C, Stratton P. Early prediction and prevention of child abuse. Chichester: Wiley, 1988: 229-44. 10. Frank DA, Allen D, Brown JL. Primary prevention of failure to thrive: social policy implications. In: Drotar D, ed. New directions in failure to thrive: implications for research and practice. New York: Plenum, 1985. 11. Hall D, ed. Health for all children. Oxford: Oxford University Press, 1989. 12. Wright C. A prevalence study on failure to thrive. Paper presented at Community Paediatric Research Group, Newcastle, December, 1989. 13. Galler JR, Ramsey F, Solimano G. The influence of early malnutrition on subsequent behavioral development. J Am Acad Child Psychiatry 1985; 24: 58-64 14. Glaser HH, Heagarty MC, Bullard DM, et al. Physical and psychological development of children with early failure to thrive. J Pediatr 1980; 73: 690-98.
RED WEALS UNDER THE SUN It does not take much to annoy a mast cell. In some unfortunates urticarial weals seem to develop almost at the drop of a hat. A morsel of crab, a tablet of aspirin, a minor scratch, a hot bath, or a cold wind-these are just some of the stimuli capable of eliciting urticarial lesions. Dermatologists take special pleasure in trying to work out the cause of weals in their patients with the all too common disorder of chronic urticaria, even though most recognise that despite their best efforts the precipitating cause will usually elude their investigative grasp. But there is little difficulty in pinpointing the problem in a small group of individuals who complain that an itchy rash develops on the exposed skin after a few minutes whenever they go into the sun. Once it is clear that the patient has an urticarial type of rash, with itchy raised pink or red weals lasting a few hours only, and that the rash is due to sun exposure rather than heat,1 a diagnosis of solar urticaria is established. The only disorders to simulate this odd condition are erythropoietic protoporphyria, polymorphic light eruption, and lupus erythematosus, in which urticaria-like lesions occasionally arise at exposed sites but alongside other lesions.2
.
CA. Localised heat urticaria treated by inducing tolerance to heat. Br J Dermatol 1975; 90: 191-93. 2. Black AK. The physical urticarias. In: Champion RH, Greaves MW, Black AD, Pye RJ, eds. The urticarias. Edinburgh: Churchill Livingstone, 1985: 180. 3. Czarnetzki BM. Solar urticaria. In: Urticaria. Berlin: Springer, 1986: 79-83. 4. Parrich JA, Jaenick KF, Morison WL, Momtaz K, Shea C. Solar urticaria: treatment with PUVA and mediator studies. Br J Dermatol 1982; 106: 575-80. 5. Mitchell P, Hawk JLM, Shafrir A, Corbett MF, Magnus UA. Assessing the treatment of solar urticaria: the dose-response as a quantifying approach. Dermatologica 1980: 160: 198-207. 6. Keahey TM, Lavker RM, Kaidbey KH, et al. Studies on the mechanism of clinical tolerance in solar urticaria. Br J Dermatol 1984; 110: 327-38. 7. Ramsay CA. Solar urticaria treatment by inducing tolerance to artificial radiation and natural light. Arch Dermatol 1977; 113: 1222-25. 8. Leenutaphong V, Hölzle E, Plewig G. Solar urticaria: studies on mechanisms of tolerance. Br J Dermatol 1990; 122: 601-06. 1.
Leigh IM, Ramsay