IgE, parasites and asthma in Tanzanian children

Carswell, F.; Merrett, J.; Merrett, T. G.; Meakins, R. H.; Harland, P. S. E. G.

doi:10.1111/j.1365-2222.1977.tb01475.x

Cited by 42 publications

(23 citation statements)

References 30 publications

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“…In Africa, a school survey in Nigeria showed a rate of 2.4 % (Sofowora and Clarke, 1969), and Carswell et al (1977) reported a rate of 7.8% in a group of Tanzanian children. These estimates, and those of the present series, suggest that bronchial asthma is as common a condition in Ibadan children as it is in European or Australian children.…”

Section: Discussionmentioning

confidence: 99%

Bronchial asthma in Nigerian children.

Adérele¹

1979

Archives of Disease in Childhood

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SUMMARY Clinical and laboratory studies on bronchial asthma in 200 Nigerian children who were seen during a 2k-year period in Ibadan are described. Contrary to reports that the condition is rare in African children, after pulmonary tuberculosis, asthma is the next most common chronic chest disease in Ibadan. While many features of the disease are similar to those seen elsewhere, skin tests indicate that ascaris is the most common antigen associated with asthma, followed by Dermatophagoides pteronyssinus.Bronchial asthma, a common childhood chronic respiratory problem in the West (Godfrey, 1974), is reported to be rare among African children (Wesley et al., 1969;Godfrey, 1975;Warrell et al., 1975).While studies by Mitchell (1970), Sofowora (1970), Anim and Edoo (1972), and Buchanan and Jones (1972) showed that the condition is common in African adults, Wesley et al. (1969) reported that bronchial asthma is extremely rare among Bantu children in South Africa. In Nigeria, Warrell et al. (1975) reported that asthma is rarely seen in children living in the savanna region of the country. Our experience at this hospital in Ibadan during the last few years indicates that the condition is far more common in children here than these reports suggest. This paper gives the results of studies on 200 asthmatic children seen at this hospital during a 2j-year period (June 1974 to December 1976). Materials and methodsThe patients in this study were referred to the chest clinic mainly from the general outpatient department of the hospital but some came from private clinics and hospitals in Ibadan and nearby. Diagnosis of asthma was based on a history of at least three attacks of breathlessness and wheezing (Blair, 1969), often associated with cough, and usually supported at the time of initial examination or during subsequent follow-up, by the auscultatory finding of widespread respiratory rhonchi. In some patients who presented in acute attacks, the diagnosis was further supported by the demonstration of at least Laboratory investigations carried out on the patients included packed cell volume, white blood count-total and differential-stool microscopical examination, chest x-rays, and in a few children, the radiology of the paranasal sinuses. Skin sensitivity tests were done by the prick method, using a selected range of commercially prepared allergen extracts (Bencard). The weal diameter of the reaction recorded was the difference in mm between it and the control. Weals of at least 2 mm in diameter were regarded as positive (Pearson, 1973).The children were classified into three groups according to the severity of the disease. This grading system was modified from one described by Dawson et al. (1969). The severe group consisted of patients with more than 10 acute attacks a year with or without complete clinical recovery between attacks. The moderate group had 5 to 10 attacks a year and usually showed complete or partial freedom from wheezing between attacks, while the mild group had I to 5 attacks a year with complete clini...

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Section: Discussionmentioning

confidence: 99%

Bronchial asthma in Nigerian children.

Adérele¹

1979

Archives of Disease in Childhood

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“…There is conflicting evidence on whether an individual's parasite burden plays a role in the pathogenesis of atopy (hygiene hypothesis), 12,13,[31][32][33] and if so, whether this is protective 14,15,[34][35][36][37][38][39] or promotes allergy. 16,[40][41][42] A role for parasites in the pathogenesis of VKC was suggested by the observed beneficial effect of anti-parasitic medication on the course of the disease, and the larger gastrointestinal parasite burden found in stools of VKC patients in Nigeria.…”

Section: Discussionmentioning

confidence: 99%

“…3,9 Many studies of allergic diseases show a rural environment to be protective but the mechanism of this effect is unknown. 10,11 There are conflicting reports on the effect of parasitic intestinal load in the pathogenesis of atopy, 12,13 and whether helminthiasis is protective 14,15 or a risk factor for allergy. 16 Anti-parasitic treatment was reported to improve the course of VKC in two case series, 8,17 and a hospital-based study in Nigeria showed that patients with VKC had a larger intestinal parasite load in their stools than unaffected controls.…”

Section: Introductionmentioning

confidence: 99%

Vernal Keratoconjunctivitis in School Children in Rwanda and Its Association with Socio-Economic Status: A Population-Based Survey

Smedt¹,

Nkurikiye²,

Fonteyne³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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Vernal keratoconjunctivitis (VKC) is an allergic eye disease and an important cause of hospital referral among children in Africa and Asia. Hospital-based studies have suggested a role for parasites in its pathogenesis. To determine the prevalence and risk factors for VKC in Central Africa, we conducted a nested population-based case control study in Rwanda, involving randomly selected primary schools from different environments (rural/urban) and climate. A prevalence of VKC of 4.0% (95% confidence interval 3.3–4.7%) was found among 3,041 children studied (participation rate 94.7%). The intestinal parasitic burden was not related to VKC. Besides hot dry climate (odds ratio [OR] = 1.5, P = 0.05) and male gender (OR = 1.7, P = 0.005), multivariate analysis identified higher economic status as a risk for VKC (OR = 1.4, P = 0.005). The effect on VKC of higher economic status appears not to act through differences in parasitic intestinal load.

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“…[19][20][21][22][23][24][25][26][27][28][29][30] However, generally elevated levels of IgE occur in patients with atopic diseases and individuals infected with helminth parasites. [1][2][3][4][5][6][7][8][9][10][11][12][13][14] Studies on the worm-atopy relationship have yielded conflicting results.…”

Section: Discussionmentioning

confidence: 99%

“…Other reports have suggested that parasite-induced IgE does not protect against allergic reaction because of the high turnover of IgE on mast cells, and that helminth-induced nonspecific IgE is too small to block all Fc receptor sites on mast cells. [22][23][24][25][26][27] This article assesses the prevalence of helminth-specific IgE among atopic subjects with nonhel-minthic allergen-specific IgE. In addition, serum levels of polyclonal (total) IgE were determined in atopic subjects with and without helminth-specific IgE.…”

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confidence: 99%

Helminth-Specific IgE and Extrinsic Allergen-Specific IgE in Patients with Atopic Diseases

et al. 1989

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To investigate the role of helminth-induced IgE in the worm-atopy relationship, the levels of IgE directed against helminthic antigens (Ascaris, Echinococcus, and Schistosoma)and total IgE were determined by radioimmunoassay in the sera of 106 atopic subjects, using extrinsic allergen-specific IgE. Ten patients were found to have detectable levels of helminth-specific IgE antibodies. The total IgE levels in these patients were approximately five-fold greater than those in patients with no detectable helminth-specific IgE. The differences were highly significant (P <0.005). The results indicate that atopy could develop in individuals with parasite-specific IgE antibodies and that helminthic antigens strongly potentiate IgE-secreting plasma cells. Atopic diseases and helminthic infections are associated with a similar IgE immune response, namely, an increased serum level of polyclonal (total) IgE antibodies. [1][2][3][4][5][6][7][8][9][10][11][12][13][14] This association has led to conflicting hypotheses. Many reports have suggested that IgE production induced by parasitic infection protects against atopic reactions by saturating the Fc receptor for IgE on mast cells with nonspecific (irrelevant) IgE antibodies. [15][16][17] It has been shown that most of the increased total IgE content in helminth-infected individuals is nonspecific, whereas only a small portion of the induced IgE is specific to the helminthic antigens. 4,5,12,18 The binding of the allergens to the V region of immunoglobulins and the cross-linking of IgE molecules cause degranulation of mast cells, with ultimate release of histamine and other vasoactiveamines. Helminth-induced nonspecific IgE for which no antigen is available competes with allergen-specific IgE for Fc receptor sites on mast cells, thus interfering with the binding of IgE to extrinsic allergens. 15,17,20,21 This process inhibits subsequent development of allergic reactions. Other reports have suggested that parasite-induced IgE does not protect against allergic reaction because of the high turnover of IgE on mast cells, and that helminth-induced nonspecific IgE is too small to block all Fc receptor sites on mast cells. [22][23][24][25][26][27] This article assesses the prevalence of helminth-specific IgE among atopic subjects with nonhel-minthic allergen-specific IgE. In addition, serum levels of polyclonal (total) IgE were determined in atopic subjects with and without helminth-specific IgE.

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IgE, parasites and asthma in Tanzanian children

Cited by 42 publications

References 30 publications

Bronchial asthma in Nigerian children.

Bronchial asthma in Nigerian children.

Vernal Keratoconjunctivitis in School Children in Rwanda and Its Association with Socio-Economic Status: A Population-Based Survey

Helminth-Specific IgE and Extrinsic Allergen-Specific IgE in Patients with Atopic Diseases

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