Serious lead poisoning in childhood: still a problem after a century

OBJECTIVE: To describe a series of patients with clinically significant lead poisoning. METHODOLOGY: A case series of nine patients with lead poisoning who required inpatient management, identified through a Clinical Toxicology Service. RESULTS: Nine children presented with clinically significant lead poisoning. The median serum lead was 2.5 micro mol/L (range 1.38-4.83). Eight of the children were exposed to lead-based paint, with seven due to dust from sanded lead paint during house renovations. Serial blood determinations suggested re-exposure in four of the patients, and in one of these patients the re-exposure was from a different source of lead. Eight of the patients required chelation therapy. CONCLUSIONS: Serious lead poisoning continues to occur and there appears to be complacency regarding the hazard posed by lead paint in old houses.     

Using unstimulated urinary lead excretion to assess the need for chelation in the treatment of lead poisoning

To determine whether unstimulated urine samples could be used to identify children needing chelation therapy for lead poisoning, we compared urinary lead excretion with and without chelation. A convenience sample of 39 children was admitted to a pediatric clinical research center for therapeutic chelation. Urine was collected for 24 hours on 2 consecutive days. Edetate disodium calcium, 1000 mg/m2, was given intramuscularly in two divided doses on the second day. Significant correlations existed between urinary lead excretion (PbU) on the control day at 12- and 24-hour collection intervals and on the first day of chelation (p less than 0.0001). Published criteria for positive edetate disodium calcium provocative tests were used to calculate corresponding cutoff points for unstimulated 24-hour PbU. Resultant PbU values ranged from 10.4 to 35.6 micrograms (0.05 to 0.17 mumol). When PbU was expressed in terms of creatinine excretion, cutoff points of 0.06 and 0.19 microgram PbU/mg creatinine were determined, making possible the use of random unstimulated samples to assist in the identification of children in need of chelation.     

Effects of iron deficiency on lead excretion in children with moderate lead intoxication

The effect of iron status on calcium disodium edetate (CaNa2EDTA)-induced lead diuresis was examined in 112 children with moderate lead intoxication. Patients whose blood lead levels were between 25 and 55 micrograms/dl and who had erythrocyte protoporphyrin concentrations greater than or equal to 35 micrograms/dl underwent provocative testing to determine the need for a full course of chelation therapy. A blood sample for lead, erythrocyte protoporphyrin, and serum ferritin determinations was obtained immediately before the intramuscular administration of CaNa2EDTA, 500 mg/m2. Determination of urinary lead level was based on an 8-hour urine collection. Blood lead and ferritin levels were significantly correlated with urinary lead excretion: r = 0.542 and 0.298, respectively, p less than 0.01 for both. Multiple regression models were tested to assess the independent effects of the variables. With blood lead level controlled, ferritin remained significantly associated with urinary lead excretion; for every 1 ng/ml increase in ferritin, urinary lead increased by 2.4 micrograms. This small effect of ferritin on urinary lead was illustrated in a discriminant analysis. Using blood lead level by itself as the independent variable resulted in a 76% correct assignment of provocative test outcomes. Knowing the ferritin level improved this assignment accuracy by only 3%. We conclude that the iron status, as measured by serum ferritin, of children with moderate lead intoxication, has a small but significant effect on CaNa2EDTA-induced lead diuresis. This effect may influence the interpretation of borderline provocative test outcomes. Although chelation therapy should not be withheld pending treatment of iron deficiency, lead stores should be reassessed after iron repletion.     

Hazards of 'deleading' homes of children with lead poisoning

"Deleading" the homes of children with lead poisoning is a necessary step to terminate the child's exposure to lead. Lead poisoning as a result of lead exposure during the process of deleading has occurred in deleading workers but has not been well documented among children whose homes are deleaded. We treated four children with classes I through III lead poisoning (range of blood lead [Pb-B] level, 1.6 to 2.75 mumol/L [33 to 57 micrograms/dL]) who had significant elevation of their Pb-B levels (range, peak 4.34 to 6.27 mumol/L [90 to 130 micrograms/dL]) following deleading of their homes. The methods used for deleading included scraping, sanding, and burning of the paint. Symptoms included irritability (n = 3) and vomiting (n = 1). The elevation of the Pb-B levels was detected early, allowing prompt chelation therapy. Because exacerbation of lead poisoning may occur in children following deleading of their homes, safer approaches of deleading should be determined.     

Childhood lead poisoning in 2 families associated with spices used in food preparation

Although most cases of childhood lead poisoning are caused by contaminated paint and dust in older homes, a variety of unusual sources of lead exposure are occasionally found. We report here 2 families whose children were poisoned by lead-contaminated spices that were purchased in foreign countries, brought to the United States, and then used in the preparation of the family's food. Six children (2-17 years old) in a family from the Republic of Georgia were poisoned by swanuri marili (lead content: 100 and 2040 mg/kg in separately sampled products) and kharchos suneli (zafron) lead content: 23,100 mg/kg) purchased from a street vendor in Tbilisi, Georgia. The second family had purchased a mixture of spices called kozhambu (lead content: 310 mg/kg) while traveling in India. Both the parents and their 2-year-old child subsequently suffered lead poisoning. The young children in both families required short-term chelation to bring their blood lead levels down to a safer range. Clinicians should be vigilant for all sources of lead contamination, including spices, when whole families are found to have elevated blood lead levels despite a confirmed lead-safe home environment. Families traveling abroad should be aware of the potential health risks associated with the purchase and use of spices that have not been tested for purity.     

Residential deleading: effects on the blood lead levels of lead-poisoned children

Acute elevations of venous blood lead levels (PbB) are periodically reported in children with chronic lead poisoning, during deleading of their houses. To evaluate this phenomenon 114 preschool children who entered the Massachusetts Childhood Lead Poisoning Prevention Program case management system during 1984 and 1985 were retrospectively studied. PbB increased from a mean (+/- SE) of 1.76 +/- 0.03 mumol/L (36.4 +/- 0.6 micrograms/dL) prior to deleading to 2.03 +/- 0.07 mumol/L (42.1 +/- 1.5 micrograms/dL) during deleading (P less than .001). Among 41 subjects for whom deleading was done by dry scraping and sanding, the mean mid-deleading PbB was higher than the pre-deleading PbB by 0.44 +/- 0.12 mumol/L (9.1 +/- 2.4 micrograms/dL). However, when deleading was done by covering or replacement of painted surfaces in the residences of 12 subjects, mid-deleading PbB decreased 0.11 +/- 0.12 mumol/L (2.25 +/- 2.4 micrograms/dL) (P less than .005). In a subset of 59 subjects who had no chelation therapy and were available for follow-up 250 +/- 14 days after completion of deleading, PbB had decreased from 1.72 +/- 0.04 mumol/L (35.7 +/- 0.9 micrograms/dL) to 1.24 +/- 0.04 mumol/L (25.5 +/- 0.9 micrograms/dL) (P less than .001). The long-term effect of deleading is a significant reduction in PbB. However, deleading resulted in a significant, albeit transient, increase in PbB.     

Severe lead poisoning in pregnancy.

BACKGROUND: Lead freely crosses the placenta. Consequently, gestational lead poisoning is not only harmful to the woman but also to the developing fetus, invariably producing congenital lead poisoning. The scope and consequences of severe lead poisoning in pregnancy (blood lead level > or =45 microg/dL) have not been well characterized. METHODS: We reviewed our experience in the management of women with severe gestational lead poisoning. Additionally, we reviewed the literature on this disorder in an effort to identify patterns in etiology and outcome. RESULTS: Over a 3-year period treatment was provided to 7 severely lead-poisoned women. A 25-year review of the medical literature identified an additional 8 cases. Among these 15 women, 70% were Hispanic, all of whom developed lead poisoning from the ingestion of soil, clay, or pottery ("tierra"). Other sources of lead poisoning were paint chip ingestion (n = 2), household renovation, and use of a complementary-alternative medication (bone meal). Lead poisoning was discovered in the third trimester in 12 (86%) subjects after the women presented with subtle but characteristic findings of severe lead poisoning, including malaise, anemia, or basophilic stippling on blood smear; one woman was identified when she presented after a generalized seizure, having a blood lead level of 104 microg/dL. Five women received chelation therapy during pregnancy with CaNa(2) EDTA, dimercaprol, or succimer. At delivery mean maternal blood lead level was 55 microg/dL, whereas mean neonatal lead level was 74 microg/dL (P =.009). Thirteen neonates underwent chelation, all within the first 28 days of life. No infant in the current series had an identifiable birth defect. CONCLUSIONS: On the basis of this experience we conclude that severe lead poisoning in pregnant women has the following characteristics: 1) it most often occurs because of intentional pica, 2) its presenting features are subtle, often consisting only of malaise and anemia, and 3) blood lead levels in the neonate are higher than simultaneous maternal lead levels.     

MRI follow-up and natural history of avascular necrosis of the femoral head in Kuwaiti children with sickle cell disease

PURPOSE:: To document the MRI progression and the natural history of avascular necrosis of the femoral head (AVNFH) in Arab children with sickle cell disease. PATIENTS AND METHODS: Twenty-three SS and 7 SbetaThal patients (aged 6-17 years) were screened for AVNFH between 1998 and 1999. Eight (26.7%) were identified with varying degrees of AVNFH. Seventeen of the original 30 patients have now been followed for 1 to 4 (mean 2.0 +/- 1.2) years, with repeat MRI of the hips. Spin-echo T1-and T2-weighted images and T2 fat-saturation sequences were obtained using a 1.5-Tesla GE unit with superconductors. AVNFH was graded I (mild), II (moderate), or III (severe). RESULTS: Eleven (64.7%) of the 17 patients had significant progression of their lesions; at the initial study, 9 were normal, 7 were grade I, 1 was grade II, and none was grade III. At the end of the follow-up period, two were normal, seven were grade I, one was grade II, and seven were grade III. Of the nine who were initially normal, two still had no lesions, while four were grade I and three were grade III on follow-up. Of the seven who were classified as grade I initially, four remained at grade I, one moved to grade II, and two became grade III. The one patient who was initially grade II progressed to III. CONCLUSIONS: AVNFH is a common, chronic, and unrelenting complication in children with sickle cell disease, and it is usually progressive.     

儿童症状性癫癎手术疗效及影响因素的分析

目的：了解儿童症状性癫癎手术疗效的影响因素。方法：对从2004年10月至2008年9月经手术治疗的儿童症状性癫癎48例随访结果进行回顾性分析。结果：48例患儿中,43例获得随访,随访时间12～51个月,平均27.3月。患儿术后癫癎结果评价采用Engel标准,其中I级32例（74％）,II级4例（9％）,III级4例（9％）,IV级3例（7％）。术前癫癎发作频率是癫癎手术预后的独立因素(P<0.05)。结论：儿童症状性癫癎手术疗效良好,术前癫癎发作频次是影响手术预后的因素。［中国当代儿科杂志,2010,12（9）：709-711］     

Results of neuroblastoma treatment in Austria (1979-1984)

During the period from 1979 until 1984 55 children were registered: 4 in Evan-stage I, 13 in stage II, 16 in stage III, 18 in stage IV and 4 in stage IV-S. 39 of these 55 patients have been followed for a minimum of two years. The current two year survival rate is 10/10 in stages I and II, 6/13 in stage III, 3/14 in stage IV and 2/2 in stage IV-S. These results demonstrate but a slight improvement in patients with stage II since the last Austrian statistic 1974. Despite modern chemotherapy the chance for survival of children with stage III or IV neuroblastoma is poor and better treatment modalities should be searched for.     

Results of Treatment of 18 Children With Hodgkin Disease With MOPP Chemotherapy as the Only Treatment Modality

Eighteen children with Hodgkin disease (16 previously untreated; two relapsed) were treated with MOPP chemotherapy (nitrogen mustard, vincristine, prednisone, procarbazine) only. Ten had clinical stage I and II disease, four had stage III, and four had stage IV. In ten patients, the clinical stage was confirmed by staging laparotomy. Six courses of MOPP were given to eight stage I and II patients and two stage IV patients. Between 7 and 12 courses were given to two stage I and II, and six stage III and IV patients. Dose reduction of 75-50% was required in 13% and delay of treatment in 22% of the first six courses of MOPP. Hematologic toxicity, minor and major viral infections, and nausea and vomiting were the major complications. Complete remission (CR) was obtained in 17 patients. Of these 17, there has been one death in CR, and one relapse. Sixteen patients have discontinued treatment and have been observed off treatment for 8 months to 7.5 years. The actuarial disease-free survival with a median follow-up of 28 months is 80% and overall survival is 92%.     

Head circumference, height, bone age and weight in 103 children with congenital hypothyroidism before and during thyroid hormone replacement

Head circumference, height, bone age and weight were studied in 103 children with congenital hypothyroidism before and up to 8 years of thyroid replacement therapy. The patients were divided into 4 groups according to the age at start of treatment: group I (diagnosed by neonatal screening): less than 2 weeks (n = 55); group II: 1-3 months (n = 7); group III: 4-12 months (n = 15); group IV: greater than 1 year of age (n = 26). Before treatment, group I showed a head circumference significantly larger than normal and a delay in bone maturation in the presence of normal length and weight. In the other groups length as well as bone age were significantly lower than normal, head circumference, in contrast, was normal (groups II and III) or even increased (group IV). During therapy, head circumference and bone age of group I became normal as were length and weight from the beginning. In the other groups, therapy led to a further increase of head size resulting in a mean head circumference significantly larger than normal during 8 years of observation in group IV. There was a catch-up of height, bone age and weight in groups II, III and IV; mean height of late treated children (group IV), however, remained significantly lower than normal even after 8 years of therapy. - Our study shows that congenital hypothyroidism is associated with increased head circumference, either absolutely or in relation to stature. Thyroid hormone therapy resulted in a normalization of head growth when treatment was initiated early, and in a further increase when treatment was started late. There was a catch-up of height, bone age and weight; complete normalization, however, occurred only in those children treated before one year of age.     

The relation between the secretion of growth hormone (GH), somatomedin C/IGF I (IGF I) and steroids before and after the onset of puberty in patients of small stature

Somatomedin C/IGF I, dehydroepiandrosterone sulfate (DHAS), testosterone (T) or estradiol (E2) have been measured in 154 patients of a previous study in which growth hormone (GH) responses to classical pharmacologic stimuli and spontaneous growth hormone secretion during sleep were compared in short children before and at the beginning of puberty. Five groups were identified: Group I, normal growth hormone secreting children; group II, completely growth hormone deficient; group III, partially growth hormone deficient; group IV, with normal sleep secretion and low responses to stimuli; group V, with the reverse situation. The somatomedin C/IGF I levels were widely dispersed. In group I, the mean +/- SEM levels of somatomedin C/IGF I were 0.77 +/- 0.047 U/ml before puberty and 1.36 +/- 0.142 U/ml in early pubertal patients, with a relation to age (r = 0.52, p less than 0.001). The difference between prepubertal and pubertal patients was significant. In groups II to V, there was no pubertal rise of somatomedin C/IGF I. In group II, the mean IGF I level was 0.48 +/- 0.05 U/ml, significantly lower than in prepubertal patients of group I. In groups III, IV and V, it was 0.7 +/- 0.069 U/ml, 0.8 +/- 0.059 U/ml, and 0.73 +/- 0.059 U/ml respectively, not different from prepubertal patients of group I, but significantly lower than in early pubertal patients of the same group. In prepubertal patients, somatomedin C/IGF I was slightly but highly significantly correlated to growth hormone sleep secretion (r = 0.27, p less than 0.001) and to dehydroepiandrosterone sulfate (r = 0.36, p less than 0.001), but growth hormone and dehydroepiandrosterone sulfate were not correlated with each other.(ABSTRACT TRUNCATED AT 250 WORDS)     

Functional megacolon in children

During 1980-1985, 304 children with functional megacolon were examined. Group I was made up of 95 patients with chronic constipation; group II of 130 patients with associated megacolon and encopresis; group III of 54 patients who mainly complained of abdominal pain (the mean age was 5.2, 7.5 and 8.8 years, respectively); group IV included 25 children (19.6%) with megacolon recognized from the group of 127 patients in whom acute appendicitis was excluded according to irrigoscopy. In the children of the first 3 groups, the x-ray signs of colitis or irritated colon were identified in 54, 72 and 87%, respectively. These groups may in fact illustrate the natural time-course of changes in the disease development. It has been demonstrated that with age functional megacolon may be aggravated by colitis. A pathogenetic diagram of the development of functional megacolon is provided.     

Prevention of childhood lead poisoning

Although past national public health efforts have reduced lead exposure significantly, lead poisoning remains the most common environmental health problem affecting American children. Currently, lead exposure occurs predominantly through ingestion of lead-contaminated household dust and soil in older housing containing lead-based paint; exposure can be increased with housing deterioration or renovation. Environmental prevention efforts focus on improvement in risk assessment, development of housing-based standards for lead-based paint hazards, and safe and cost-effective lead hazard remediation techniques. Educational efforts address parental awareness of lead exposure pathways, hygiene, and housekeeping measures to prevent ingestion of dust and soil. Blood lead screening is recommended either universally at ages 1 and 2 years or in a targeted manner where local health departments can document a low prevalence of elevated blood lead levels. Nutritional interventions involve provision of regular meals containing adequate amounts of calcium and iron and supplementation for iron deficiency. Lead chelation should complement environmental, nutritional, and educational interventions, when indicated. Collaboration of multiple federal agencies in a new strategy to eliminate childhood lead poisoning should further prevention efforts.     

Comparison of dimercaptosuccinic acid and calcium disodium ethylenediaminetetraacetic acid versus dimercaptopropanol and ethylenediaminetetraacetic acid in children with lead poisoning

Objectives: To compare the response to dimercaptopropanol (BAL) and calcium disodium ethylenediaminetetraacetic acid (EDTA) versus orally administered meso-2,3-dimercaptosuccinic acid (DMSA) and EDTA in children with lead poisoning.Methods: Retrospective review of medical records of children admitted to MetroHealth Medical Center with a whole blood lead (BPb) concentration of 2.17 μmol/L (45 μg/dl) or more (or less than 2.17 μmol/L and not a candidate for outpatient oral chelation) and treated with BAL + EDTA or DMSA + EDTA. In each group, the mean BPb values at the end of therapy and at 14 and 33 days after chelation were compared with pretreatment BPb by the Wilcoxon signed-rank test, whereas the Mann-Whitney U test was used to compare percentage change from pretreatment at each follow-up day between the two groups.Results: Twenty-three children received BAL + EDTA and 22 received DMSA + EDTA.The BPb values (mean ± SD) at the end of therapy and at 14 and 33 days after chelation were significantly lower than pretreatment in both groups (BAL + EDTA: 17 ± 10, 34 ± 7, 36 ± 11 vs 58 ± 14 μg/dl, p <0.02, 0.01, 0.001, respectively; DMSA + EDTA: 10 ± 4, 30 ± 10, 30 ± 14 vs 50 ± 10 μg/dl, p <0.01, 0.001, 0.01, respectively). The percentage reduction (mean ± SD) in BPb from pretreatment at the end of therapy and on days 14 and 33 after chelation did not differ between the groups (BAL + EDTA: −71.2% ± 19.8%, −40.2% ± 13.8%, −37.1% ± 17%; DMSA + EDTA: −79.9% ± 8.7%, −38.3% ± 21.6%, −37% ± 32%; p >0.20). Elevation of alanine aminotransferase and vomiting during therapy were observed more frequently in the BAL + EDTA group compared with the DMSA + EDTA group.Conclusions: Treatment with DMSA or BAL combined with EDTA results in a comparable reduction in BPb. (J Ppediatr 1997;130:966-71)     

Early tubular involvements in lead poisoning in children]

One of the main targets of lead poisoning is the kidney. Chronic poisoning can lead to kidney failure, and acute poisoning to tubulopathy with Toni-Debré-Fanconi syndrome. The primum movens of this tubulopathy is a distortion of mitochondrial energetic metabolism. We studied 27 children presenting with non symptomatic poisoning. Serum creatinine levels were normal. There was neither proteinuria nor glycosuria and only one child presented with hyperaminoaciduria. One third already presented with signs of tubulopathy, as shown by an increase in beta 2 microglobinuria in 36.5% of the cases studied (8 times in 22 samples) and enzymuria in 30.4% of the cases (23.5% if one excludes the children having had a chelation before the study). Kidney is therefore involved early in lead poisoning in children.     

血液灌流抢救儿童急性中毒35例报告

目的本研究观察血液灌流（Hemoperfusion,HP）治疗中毒的效果,组织毒物再释放时间,HP和非lip期的毒代动力学,HP对血细胞和血生化的影响,儿童HP中应用肝素剂量和血流量等。方法35例中毒儿童[男26例,女9例,年龄10个月～13岁,平均年龄（3．35±2．50）岁]接受HP治疗1～3次,其中12例2次,4例3次。收集氟乙酰胺（FAM）中毒6例和毒鼠强（TET）中毒10例病人血2ml,用气相色谱法（GC法）检测毒物浓度。结果HP后所有病例中毒症状缓解或明显减轻,27例（77％）中毒儿童治愈,6例（17％）好转,2例（6％）死因多脏器衰竭。4例已缓解的病例在HP后6-24h症状反复,其中FAM 1例,TET 3例。HP后血小板、红细胞和血红蛋白降低,P〈0．05;HP前后WBC、血清丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）、尿素氮（BUN）、肌酐（CRE）和总白（TP）、总白（ALB）、球蛋白（GLO）等值比较无显著差异性,P〉0．05。检测FAM和TET中毒儿童在HP前,HP治疗60、120min FAM量（ng／ml）分别是309．00±114．75,254．67±128．15和230．00±107．53,χ^2=7．000,df=2,P〈0．030;TET量（ns／ml）分别是216．10±59．07,176．20±47．30和161．00±31．49,χ^2=13．400,df=2,P=0．001。HP1h较HP前下降值FAM是54．33（17．58％）,TET是39．9（18．46％）,HP2h较HP1h下降FAM是24．67（7．98％）,TET是15．2（7．03％）,HP2h使FAM和TET浓度下降25．57％和25．50％,HP第1小时下降速度快于第2小时;HP后2～6h,4例（FAM1例,TET3例）已降低的毒物血浓度回升,但低于HP前水平;FAM和TET的t1/2在HP期和非HP期分别为（2．40±0．66）h,（15．60±8．22）h和（4．10±1．66）h,（67．01±48．42）h。HP首次肝素平均剂量（0．54±0．15）mg／kg;每30min追加（0．20±0．06）mg／kg;血流量（4．39±0．99）ml／min。结论HP使毒物代谢消除t1/2明显缩短,能安全、有效地治疗中毒患者;HP后2～6h部分患者血浓度可能有短暂性回升;活性炭HP不能吸附与血浆白蛋白和球蛋白结合的毒物;活性炭HP可造成一过性血小板、红细胞不同程度的破坏。肝素用量应小于成人。     

血清透明质酸等四项指标在重型β地中海贫血肝纤维化诊断中的价值

目的探讨血清肝纤维化指标透明质酸(HA)、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(CⅣ)和层粘蛋白(LN)在重型β地中海贫血(简称β地贫)肝纤维化诊断中的价值.方法检测49例重型β地贫患儿和41例正常小儿血清HA、PCⅢ、CⅣ、LN水平,其中45例地贫患儿行肝组织学检查,进行肝纤维化的对比研究.结果β地贫组血清HA、PCⅢ、CⅣ、LN四项指标水平均显著高于正常小儿组(P＜0.01),HA、PCⅢ水平与纤维化分期呈低度正相关(r＝0.379、0.455,P均＜0.05),CⅣ及LN水平与纤维化分期无显著性相关(r＝0.312、0.310,P均＞0.05).四项指标联合诊断肝纤维化的判别函数为0.002 HA+0.003 PCⅢ+0.002 CⅣ+0.006 LN-1.859.判断的准确率为82.16%, 诊断的灵敏度、特异度、阳性预测价值和阴性预测价值分别为93.88%、68.29%、77.97%和90.32%.HA、PCⅢ水平的升高与肝脏铁含量有一定的相关性(r＝0.342、0.305,P均＜0.05).结论血清HA 、PCⅢ在重型β地贫肝纤维化诊断中的价值高于CⅣ及LN,四项指标联合检测可提高临床诊断的准确性和可靠性.     

Positive skin test and age

OBJECTIVE: To evaluate positive responses to skin tests for immediate hypersensitivity to allergens in children with asthma and rhinitis at different ages. METHOD: We observed positive skin test reactivity in prick tests using fifteen allergens of same origin (total dust and Dermatophagoides sp.; Dermatophagoides pteronyssinus; Dermatophagoides farinae; Blomia tropicalis; Penicillium sp; Alternaria alternata; Cladosporium herbarium; Aspergillus fumigatus; Bermuda grass; forage grass; dog and cat epithelia; feathers; Blatella germanica and wool). We placed 713 selected patients into different age groups - Group I: 6 to 11 months; Group II: 1 to 3 years and 11 months; Group III: 4 to 8 years and 11 months; and Group IV: 9 to 15 years. We used the chi-square test for statistical analysis. RESULTS: The total significant differences between these groups were: I to II = 5; II to III = 5; II to IV = 5; III to IV = 6; I to III = 10; and I to IV = 10. CONCLUSION: Skin test reactivity is acquired progressively with age, and can be observed as early as at 12 months. Reactivity is significantly more positive from the age of 4 on.