Summary of the Report
A Prevalence Study on Rickets in Children of Chakaria
Institute of Child and Mother Health, Dhaka, 1998
Dr. ARM Luthful Kabir, Principal Investigator
Abstract
An epidemiological survey was conducted on 900 children between 1-15 years chosen randomly out of 30 villages sampled randomly from 340 villages of Chakaria thana of Bangladesh to determine the prevalence of rickets . After the recruitment of necessary staff a training of 6 days was conducted in the local SARPV office at Chakaria about the purpose and procedure of the study. Geographical reconnaissance sheets were used by the Health Assistants of selected 30 villages to identify and collect the children with the help of an identification slip to a particular place. Interview of the parents was taken and the children were examined for evidences of rickets and necessary radiological and blood examination (serum calcium and phosphorus and ALP) were done in all clinically suspected cases and in a control of every eighth child. Out of 900 children, there were 498 (55.3%) male and 402 (44.7%) female. The commonest food intake, other than rice, in last 24 hours was dry fish (49.6%) followed by fresh fish (46.6%). Only 11.9% children took milk or milk products and 16% had taken meat on the previous day. Seventy eight (8.6%) children had at least one feature suggestive of >clinical rickets=. Pectus carinatum was the most common clinical feature in 26 (33.3%) followed by genu valgum in 23 (29.4%) cases. Of them 20 (2.2%) children had raised Alkaline phosphatase (ALP) level (>biochemical rickets=) including all 8 (0.9%) having radiological features of rickets (confirmed rickets). Of 111 control children 22 (19.8%) had raised level of ALP. Further study is needed to find out the exact aetiology of >only biochemical= (1.3%) (children having clinical and biochemical features but negative radiology) and >only clinical rickets= (6.4%) (children having clinical features but negative biochemistry and radiology) and immediate intervention is to be started to treat the already affected children.
Introduction
Background
Social Assistance and Rehabilitation for the Physically Vulnerable (SARPV) has been working with the disabled people since 1991 in Chakaria. According to them they first reported large number of rickets cases in children in that area during a cyclone relief program in 1991. So far several other surveys were undertaken by different groups of people and organisations.
Memorial Christian Hospital (MCH) of Chakaria identified 93 cases of rickets. Institute of Epidemiology, Disease Control and Research (IEDCR), Dhaka reported 64 patients of rickets. DG Health conducted one survey by Dr Badrul Alam, Associate Professor of Chittagong Medical college and Dr Nazma Kabir of UNICEF and reported 28 cases of rickets out of 23 families on the basis of clinical assessment in June 1994. AEM, an organisation working for children in France, became interested as they happen to meet Mr Shahidul Haq, Executive Director of SARRPV. They investigated eight affected children out of forty referred to them by the local people. AEM also studied the nutritional and agronomic aspects to look into the causes of rickets. Biological, hormonal, radiological and chemical analysis results were suggestive of calcium deficiency rickets to be the cause in Chakaria.
Three paediatricians from ICMH visited five villages of Chakaria during 27-28th September 1996 and observed 15 cases of rickets including 8 out of 19 as registered to be cases of >rickets= by SARPV people. The other 11 cases were CP, , telepes, post-polio paresis, severe kyphosis, hydrocephalus, Down=s syndrome, short leg and probable Blount=s disease. ICMH recommended a rapid epidemiological survey in Chakaria and in its vicinity to see the prevalence of rickets over there.
In October 1997 an International group of 9 organisations (Utah University and Cornell University of USA, SARPV, ICMH, INFS , UNICEF and CYMMYT of Dhaka, AEM of France, CHM of Chakaria visited Chakaria. A case-control study of 27 children (14 rachitic cases and 13 control) was done. The conclusion were that : (1) active rickets in children in Chakaria is not usually associated with vitamin D deficiency (2) clinical presentation of rickets in Chakaria is similar to that of African children with calcium deficiency rickets and (3) subclinical calcium deficiency might be more prevalent as suggested by rachitic deformities and elevated serum 1,25(OH)2 vitamin D levels among unaffected children. ICMH submitted a project proposal to UNICEF for the epidemiological study and today=s achievement is the result of that proposal which UNICEF agreed to sponsor.
Rickets
Rickets is a skeletal disorder of growing infants and children due to inadequate or delayed mineralization of bone. For normal bone formation the cartilage must first undergo provisional mineralisation before being resorbed and replaced by osteoid, which then undergoes mineralisation to create bone. Failure of mineralisation of the of cartilaginous spicules at the metaphyseal interface is the fundamental defect 6 cartilage cells do not mature and disintegrate not invaded by capillary fibroblasts 6 resultant overgrowth of cartilage with widened epiphysis 6 osteoid matrix is produced by normally functioning osteoblasts and is unmineralised 6 this zone of disorderly osteoid matrix and cartilage is soft and become distorted under the stress of weight bearing 6 bending, compression and microfracture of soft, weakly supported osteoid and cartilaginous tissue with resultant skeletal deformities.
The implications of rickets include: short stature, swelling of metaphysis of the wrists and ankles, deformity of limbs (genu valgum, genu vara, sabre tibiae), chest deformities (rickety rosary, Harrison=s sulcus, kyphoscoliosis, pectus carinatum), head deformities (delayed closure of fontanel, frontal bossing, box headedness, craniotabes), delayed development (sitting, standing, walking), delayed dentition (hypoplastic teeth).
Rickets can be caused by several factors: vitamin D deficiency due to inadequate vitamin D intake and/or lack of sun exposure leading to inadequate biosynthesis of the vitamin; dietary deficiencies of calcium and/or phosphorus deficiency; renal disease; abnormalities in the vitamin D receptors. Rickets due to calcium deficiency has been reported in South Africa and Nigeria.
It has been recently reported that there have been clustering of rickets in a coastal area, Chakaria, of Bangladesh. In few of the studied cases, calcium deficiency has been thought to be the cause responsible for causing rickets there. The salient features of the calcium deficiency rickets are (1) clinical, radiological and biochemical evidence of rickets with normal serum concentration of 25-hydroxyvitamin D (2) the patients are resident of a particular area (3) secondary hyperparathyroidism as manifested by high urinary cyclic adenosine monophosphate excretion and generalised aminoaciduria and (4) the rickets heals with a normal hospital ward diet without supplementary vitamin D therapy. Biochemically, it is characterised by increased parathyroid hormone, increased 1,25 (OH)2 D in the face of normal levels of 25 (OH) D, an increased 1,25 (OH)2 D to 25-hydroxyvitamin D ratio, increased osteocalcin, increased alkaline phosphatase and slightly decreased serum calcium. Calcium deficiency rickets may be differentiated biochemically from vitamin D dependent rickets by the elevated level of 1,25(OH)2D and normal 25(OH)D.
Methods
The study site
The study took place in Chakaria thana of Cox=s Bazar district, which is situated in the south-eastern part of Bangladesh. Chakaria is the biggest thana of Cox=s Bazar district in respect to both area and population. Chakaria thana occupies an area of 643.46 sq. km. including 38.95 sq. km. river area and 17.77 sq. km. forest area. The thana is bounded on the east by Lama and Nakhyongchhari thana of Bandarban district, on the west by Moheshkhali and Kutubdia district, on the north by Bashkhali and Lohagara thana of Chittagong district and on the south by Cox=s Bazar Sadar and Ramu thana. The thana consists of 17 unions, 66 Mauza and 340 villages. The total population of the thana is 468,000 as estimated in 1995 and about 50% of the population are under fifteen years of age. The socio-economic condition of the people are poor. In 1991 the literacy rate is 23.4% and occupation of the majority (about 54%) of the population are cultivation. However, about 62% of the population do not have agricultural land. There are 340 villages in Chakaria. For the purpose of study we needed 30 villages which had been selected randomly using a random number table. This selection of villages was due to avoid biases and giving the opportunity of equal chance to every village considered for the study, which was conducted during the period of April to June 1998.
Study population
Children between the ages of 1 year and 15 years were studied. In survey reports it was reported that majority of the rickets cases occurred in this age group. The estimated population of under 15s in Chakaria thana were 251,1392 (assuming annual growth rate of 1.89%). A sample of children was drawn from this population.
Although there are no national statistics on the prevalence of rickets in the country, UNICEF estimates that the proportion of rickets cases among under 15 children at Chakaria could be as high as 12-14%15. However, other casual observations have indicated a much lower prevalence. For the calculation of sample size for this survey a prevalence of 1% was assumed.
Sampling : Chakaria thana
30 villages
1-15 year old children
30 X 30 = 900 children
A data sheet was completed during screening of the children who will be positive for evidence of rickets and those children will be transported on the same day for blood biochemistry (serum calcium, phosphate and ALP) and x-ray of wrists and knees in a local private health centre.
The following signs were used as clinical evidence of rickets: widening of wrists, ankle and knees; macrocephaly; frontal bossing; rachitic rosary; Harrison=s sulcus; pigeon breast deformity; genu valgum; genu vara; delayed dentition and caries tooth. If a child was found to have any one of these signs he/she was subjected to radiological examination of the wrist and knee.
Radiographs were examined for the following signs of rickets: splaying, fraying or cupping of metaphyses; increased distance between metaphysis and diaphysis; osteopenia; fracture. The radiological investigation was conducted at a private x-ray diagnostic facility in Chakaria.
Blood was collected on all positives for clinical features and every eighth child by the physician/ lab technician for serum alkaline phosphatase, calcium and inorganic phosphorus.
Ten staff were recruited including 3 physicians, 1 field co-ordinator, 4 field workers, 1 lab technician and 1 data enterer.
Before starting, parents and children were briefed about the purpose of our visit as to finding out of rickets cases among 30 children chosen by lottery and the necessary interview of the parents particularly the mothers and required physical examination and subsequent radiological and blood examination at a central location. Immediately after the briefing, a 5-7 minute session was used for feedback to ensure participant understanding of the purpose of the study and to obtain informed consent for interview, physical examination and necessary radiology and blood drawing.
Results
Nine hundred children were interviewed and examined for clinical evidences of rickets. There were 498 (55.3%) male and 402 (44.7%) female. A total of 78 (8.7%) children had at least one feature for clinical suspicion of rickets. Seventy three children could be examined radiologically and 71 biochemically. Of which 20 (2.2% of 900) had raised ALP( >300 u/L) including all of 8 (0.9% of 900) radiologically confirmed rickets cases (Table-I). Among 111 normal randomly selected children who were subjected to blood biochemistry, 22 (20% of 111) showed raised ALP. There were more or less equal distribution of children in all age groups (Table-II). The mean age of children was 77.6 mo(45.3). Most of the fathers were illiterate or minimally educated considering year of schooling (81%). They were mostly day labourers and their economic status was very poor as reflected by deficit budget in 62% families (Table-III). The children were found to take, other than rice, mostly dry fish (50%) and fresh fish (47%) but little meat and milk or milk products (Table -IV). Consanguinity between the parents were 14% and there was history of developmental delay in children in 8% cases (Table-V). Pectus carinatum (33%), genu valgum (29%), Harrison=s sulcus (27%) and wide wrist (18%) were the most common features suggestive of rickets (Table-VI). Fifty six percent children had at least one feature suggestive of clinical rickets (Table-VII) and more than 62% children had 2 or more clinical features in case of confirmed rickets (Table-VIII). The nutritional status were uniformly poor in all groups of children with more stunting in confirmed rickets cases when compared to controls (though not significant OR 4.04, CI 0.48-89.6) (Table-IX and X). The mean serum ALP level was very raised (787.87 U/L) in confirmed rickets and to some extent (375.83 U/L) in >only biochemical rickets= but the serum calcium (2.24 mmol/L) and phosphorus level (1.25 mmol/L) were lower normal in confirmed rickets but exactly normal in only biochemical and >only clinical rickets= (Table-XIV). On analysing the association of health factors between confirmed rickets and the controls, there was found strong association between developmental delay and the presence of >clinical rickets= (Table XVIII and XIX) . Similarly among the socio-economic factors, the intake of dry fish had negative association for the development of clinical rickets (Table- XIX).
Distribution of Subjects by Findings:
*Confirmed rickets 8 0.9
**Only Biochemical rickets 12 1.3
***Only clinical rickets 58 6.4
_____________________________________________________________
*Confirmed rickets : clinical + raised ALP + radiological
**Biochemical rickets : clinical + raised ALP
***Clinical rickets : having at least one feature suggestive of rickets with normal ALP
Table II : Age structure of children (n=898)
Age group, months | children | % |
12 - 35 | 193 | 21.5 |
36 - 59 | 163 | 18.2 |
60 -119 | 335 | 37.3 |
120 - 180 | 207 | 23.1 |
Total: 898 100
Distribution of age showed more or less equal distribution of children in different age groups excepting more children in the age group of 60-119 months (37.3%).
Table III : Socio-economic characteristics of the families (n=900)
Characteristics | Number | Percentage |
Father=s education | ||
No schooling | 539 | 59.9 |
Primary | 189 | 21.0 |
Secondary | 121 | 13.4 |
Above secondary | 51 | 5.7 |
Father=s main occupation | ||
Day labour | 348 | 38.7 |
Business | 181 | 20.1 |
Agriculture work | 167 | 18.6 |
Service | 88 | 9.8 |
Others | 116 | 12.8 |
Economic status | ||
*Deficit | 555 | 61.7 |
**Balance | 307 | 34.1 |
***Surplus | 37 | 4.1 |
Family members | ||
1-3 | 53 | 5.9 |
4-6 | 399 | 44.3 |
7-10 | 383 | 42.6 |
11+ | 65 | 7.2 |
*Deficit : when one has to lend to run family
**Balance : When one manages family expenditure without landing
***Surplus : When one can save after family expenditure
Most of the fathers were either illiterate (never gone to school) or having minimum education (primary education) (80%). A large number of fathers= occupation (38.7%) were day labour. The economic status was poor as reflected by the deficit budget in 61.7% families. The size of the family were 4-10 members in 86.9% cases.
Table IV : Selected food habits as reported by the parents (n=900)
Food | No. children taking food in last 24 hrs. | % |
Dry fish | 44 | 49.6 |
Fresh fish | 419 | 46.6 |
Fruits | 260 | 28.9 |
Meat | 144 | 16.0 |
Milk | 107 | 11.9 |
The children took mostly dry fish (49.6%) and fresh fish (46.6%) but little meat (16.0%) and milk or milk products (11.9%) in last 24 hours.
Table V: Selected health factors as reported by the parents (n=900)
Health characteristics | Number | Percentage |
Consanguineous parents | 130 | 14.4 |
Family history of rickets | 40 | 4.4 |
History of chronic diarrhoea | 31 | 3.5 |
History of malaria | 129 | 14.4 |
History of other illness (Wheeze) | 234 | 26.0 |
Developmental delay | 70 | 7.8 |
Consanguineous parents were in 14.4% families and there was history of ever wheeze in 26% children and developmental delay in 7.8% cases. |
Table VI: Evidences of rickets among clinically suspected cases (n=78)
Features | cases | % |
Pectus carinatum | 26 | 33.3 |
Genu vulgum | 23 | 29.4 |
Harrison sulcus | 21 | 26.9 |
Wide wrist | 14 | 17.9 |
Frontal bossing | 12 | 15.3 |
Genu vara | 10 | 12.8 |
Wide ankle | 06 | 07.6 |
Chest beads | 06 | 07.6 |
Delayed dentition | 06 | 07.6 |
Wide knee | 05 | 06.4 |
Sabre tibiae | 04 | 05.1 |
Others | 06 | 07.6 |
Multiple features were present in some cases. Pectus carinatum (33.3%), genu valgum (29.4%) and Harrison=s sulcus (26.9%) were the commonest clinical features suggestive of rickets.
Table VII : Distribution of rickets signs in children of Chakaria (n=900)
No. of signs | children | % |
No sign | 822 | 91.3 |
signs found | 78 | 08.7 |
Distribution of rickets signs in clinically positive cases (n=78) |
1 sign |
44 | 56.4 |
2 signs | 22 | 28.2 |
3 or more signs | 12 | 15.3 |
Total |
100 |
Eighty five percent of clinically suspected children presented with 1 or 2 clinical signs suggestive of rickets.
Table VIII : Distribution of rickets signs in confirmed rickets cases (n=8)
No. of signs | cases | % |
1 sign | 03 | 37.5 |
2 signs | 02 | 25 |
3 or more signs | 03 | 37.5 |
Total | 08 | 100 |
C Two patients had 8 features of rickets
More than 62% children having confirmed rickets presented with 2 or more signs of rickets
Table IX: Nutritional status of the studied children < 10 years (n= 690)
Nutritional status | Confirmed rickets (7) | Only biochemical rickets (8) | Clinical rickets (67) |
Other children (608) |
Stunted | 06 (86%) | 05 (62.5%) | 47 (70%) | 367 (60.3%) |
Wasted | 01 (14.2%) | 00 | 07 (10.4%) | 128 (21.05%) |
Table X: Nutritional status of children of 10 years or more (n= 169)
BMI | children | % |
<16 16-18.5 > 18.5 |
116 39 14 |
68.6 23.1 08.3 |
About 92% children over 10 years were found thin and only 8% children found having normal state of nutrition considering BMI.
Table XI: Unadjusted Odds Ratio (OR) and its 95% confidence interval for the association of Nutritional status (stunting) of children having clinical rickets (67) vs. other children (623) under 10 years
Total children below 10 years (690) | Cases (n=67) |
Controls (n=623) |
Odds Ratio | 95% CI | p-value |
|
No. |
% | No. | % |
|
| |
Stunting |
47 | 70 | 367 | 59 | 1.64 | 0.92-2.94 | NS |
Not stunting | 20 | 30 | 256 | 41 |
|
|
Table XII :Unadjusted Odds Ratio (OR) and its 95% confidence interval for the association of Nutritional status (wasting) of children having clinical rickets (67) Vs other children (623) under 10 years
Total children below 10 years (690) | Cases (n=67) |
Controls (n=623) |
Odds Ratio | 95% CI | p-value |
|
No. |
% | No. | % |
|
| |
Wasted |
7 | 10.4 | 128 | 20.5 | 0.45 | 0.18-1.05 | NS |
Not wasted | 60 | 89.5 | 495 | 79.5 |
|
|
Table XIII: Radiological evidence in clinically suspected cases (n=73)
Findings | cases | % |
Positive | 08 | 10.9 |
Negative | 65 | 89.0 |
Total 73 100
Clinically suspected cases were 78, and 5 children did not turn up for x-ray examination.
Table XIV: Mean levels of serum calcium, phosphorus and alkaline phosphatase in different groups of children
Groups of children | Calcium | Phosphorus | ALP |
Confirmed rickets (8) | 2.24 (0.15 ) | 1.25 (0.28 ) | 786.87 ( 334.69) |
Biochemical rickets (12) | 2.45 (0.12) | 1.61 (0.15) | 375.83 (88.41) |
Clinically suspected (51) | 2.45 (0.15) | 1.66 (0.27) | 216.98 (46.98) |
Controls (111) | 2.45 (0.12) | 1.66 (0.21) | 252.68 (88.78) |
(Normal values : serum calcium = 2.02-2.60 mmol/L,,phosphorus = 1.30-2.26 mmol/L, ALP = upto 300 U/L)
The serum ALP level were very raised (787.87 U/L) in confirmed rickets and to some extent raised (375.83 U/L) in biochemical rickets but the serum calcium and phosphorus level were lower normal (2.24 mmol/L) and (1.25 mmol/L) respectively in confirmed rickets but almost normal only biochemical and clinical rickets.
Table XV : Comparison of blood biochemistry between controls and confirmed rickets
Parameters | Controls (111) | Confirmed rickets (8) | t-value | p-value |
Calcium (mmol/L) | 2.45 (0.12) | 2.24 (0.15 ) | 4.63 | <0.0001 |
Phosphate (mmol/L) | 1.66 (0.21) | 1.25 (0.28) | 5.26 | <0.0001 |
ALP (U/L) | 252.68 (88.78) | 786.87 (334.69 ) | 12.28 | <0.0001 |
Though the serum calcium and phosphorus levels of confirmed rickets are within normal range but there are significantly different from those of the controls.
Table XVI : Comparison of blood biochemistry between controls and biochemical rickets
Parameters | Controls (111) | Only biochemical rickets (12) | t-value | p- value |
Calcium (mmol/L) | 2.45 (0.12) | 2.45 (0.12) | 0.10 | 0.91ns |
Phosphate (mmol/L) | 1.66 (0.21) | 1.61 (0.15) | 0.79 | 0.56 Ns |
ALP (U/L) | 252.68 (88.78) | 375.83 (88.41) | 4.57 | <0.001 |
The serum ALP of the >only biochemical rickets= are significantly raised than that of the controls.
Table XVII: Comparison of blood biochemistry between biochemical rickets and confirmed rickets
Parameters | Biochemical rickets (12) | Confirmed rickets (8) | t-value | p- value |
Calcium (mmol/L) | 2.45 (0.12) | 2.24 (0.15) | 3.28 | 0.004 |
Phosphate (mmol/L) | 1.61 (0.15) | 1.25 (0.28) | 3.69 | 0.002 |
ALP (U/L) | 375.83 (88.41) | 786.87(334.69 ) | 4.09 | <0.001 |
All the biochemical values (serum calcium, phosphorus and ALP) of confirmed rickets are significantly different from those of the confirmed rickets.
Table XVIII: Unadjusted Odds Ratio (OR) and its 95% confidence interval for the association between confirmed rickets cases and some selected risk factors
Factors | Cases (n=8) |
Controls (n=892) |
Odds Ratio | 95% CI |
|
No. |
% | No. | % |
| |
Consanguineous parents |
3 | 37.5 | 127 | 14.2 | 3.60 | 0.85-15.27 |
Developmental delay | 4 | 50 | 66 | 7.4 | 12.48 | 2.56-60.97 |
Family history of rickets | 0 | 0 | 40 | -- | -- | -- |
History of major illness | 3 | 37.5 | 137 | 15.3 | 3.29 | 0.77-13.95 |
History of malaria | 1 | 12.5 | 128 | 14.3 | 0.850 | 0.10-6.97 |
Low economic condition | 6 | 75 | 549 | 61.5 | .99 | 0.98-.99 |
Illiterate father | 7 | 87.5 | 532 | 59.4 | 4.73 | 0.58-38.66 |
Intake of dry fish | 4 | 50 | 442 | 49.5 | 1.01 | 0.25-4.08 |
Intake of fresh fish | 3 | 37.5 | 416 | 46.6 | 0.68 | 0.16-2.88 |
Intake of fruits | 3 | 37.5 | 257 | 28.8 | 1.48 | 0.35-6.23 |
Intake of milk | 0 | 0 | 107 | 20 | -- | -- |
Intake of meat | 1 | 12.5 | 143 | 16 | 0.74 | 0.09-6.12 |
Sex (male) | 4 | 50 | 494 | 53.4 | 0.80 | 0.20-3.24 |
There is a strong association between developmental delay and confirmed rickets.
Table XIX : Unadjusted Odds Ratio (OR) and its 95% confidence interval for the association of different factors (age, socio-economic, food, health and clinical) between clinically suspected (78) and the controls(820)
Factors |
Case | Controls | OR | 95% CI |
Age < 5 years > 5 years |
48 (61.5%) 30 (38.4%) |
344 (41.9%) 476 ((58.0%) |
2.21 | 1.37-3.56 |
Father=s education No schooling Literate |
46 (58.9%) 32 (41.0%) |
393 (47.9%) 329 (40.1%) |
0.959 |
0.598-1.53 |
Family size <5 >5 |
27 (34.6%) 51 (65.3%) |
252 (30.7%) 570 (69.5%) |
1.19 | 0.734-1.954 |
Hist. chron. diarrhoea yes no |
3 (3.8%) 75 (96.0%) |
28 (3.4%) 792 (96.5%) |
1.13 |
0.336-3.809 |
Consang. parents yes no |
16 (20.0%) 62 (79.4%) |
114 (13.9%) 706 (86.0%) |
1.59 |
0.891-2.866 |
Delayed developmnt. Yes no |
54 (69.2%) 24 (30.7%) |
46 (5.6%) 774 (94.3%) |
7.48 |
4.09-13.65 |
Exposure to sun : yes no |
77 (98.7) 01 (1.2%) |
809 (98.6%) 11 (1.3%) |
1.04 |
0.133-8.218 |
Intake of fresh fish yes no |
38 (48.7%) 40 (51.2%) |
381 (46.4%) 440 (53.6%) |
1.09 |
0.689-1.746 |
Fruits in last 24 hours yes no |
27 (34.6%) 51 (65.3%) |
233 (28.4%) 588 (71.7%) |
1.336 |
0.818-2.182 |
Hist. major illness yes no |
17 (21.7%) 61 (78.2%) |
123 (15.0%) 697 (85.0%) |
1.59 |
0.892-2.794 |
Intake of meat yes no |
12 (15.3%) 66 (84.6%) |
132 (16.0%) 689 (84.0%) |
0.949 |
0.499-1.805 |
Intake of milk : yes no |
7 (8.9%) 71 (91.0%) |
100 (12.1%) 721 (87.9%) |
0.71 |
3.18-1.589 |
Sex : male female |
49 (62.8%) 29 (37.1%) |
449 (54.7%) 373 (45.4%) |
1.40 |
0.869-2.262 |
Intake of dry fish yes no |
29 (37.1%) 49 (62.8%) |
417 (50.8%) 404 (49.2%) |
0.573 |
0.355-0.926 |
Family hist.rickets yes no |
8 (10.2%) 70 (89.7%) |
32 (3.9%) 788 (96.0%) |
2.81 |
1.249-6.341 |
It is interesting to note that intake of dry fish appears to be a protective factor for the development of rickets. All other factors do not show any positive association with the development of rickets.
Table XX : Clinical features in number in different groups of rickets
Features | Confirmed rickets (8) | Biochemical rickets (12) | Clinical rickets where blood biochemistry not done (7) |
Pcetus carinatum | |||
Genu valgum | |||
Harrison=s sulcus | |||
Wide wrist | |||
Frontal bossing | |||
Genu vara | |||
Wide ankle | |||
Chest beads | |||
Delayed dentition | |||
Wide knee | |||
Sabre tibiae | |||
Delayed fontal closure | |||
Box head | |||
Mean age (mo) |
Discussion
The study showed that the prevalence of confirmed rickets was 0.9%, >only biochemical rickets= 1.3% and that of >only clinical rickets= 6.4% (Table-1). Traditionally, the clinical impression of active rickets is confirmed by roengenographic evidences of changes at the epiphysis and metaphyseal plates combined with biochemical analysis revealing alterations in serum calcium, ALP, phosphorus and vitamin D concentrations. In some studies rickets have been diagnosed only clinically15 in a community study or clinically and biochemically16. Pectus carinatum (33%), genu valgum (29%), Harrison=s sulcus (27%) and wide wrist (18%) were the most common features suggestive of rickets (Table-VI). Fifty six percent children had at least one feature suggestive of clinical rickets (Table-VII) and more than 62% children had 2 or more clinical features in case of confirmed rickets (Table-VIII).
We have confirmed some cases radiologically and with limited biochemical analysis. The serum ALP level were very raised (mean 87.87 U/L) in confirmed rickets and to some extent raised (mean 375.83 U/L) in >only biochemical rickets= but the serum calcium and phosphorus level were lower normal (2.24 mmol/L) and (1.25 mmol/L) respectively in confirmed rickets but exactly normal in >only biochemical= and >only clinical rickets=. All the mean biochemical parameters of confirmed rickets were significantly different than those of controls (Table- XV) and biochemical rickets (Table-XVII). The mean serum ALP of >only biochemical rickets= is also significantly higher than that of controls. Sometimes it needs extensive laboratory approach to find out the exact aetiology of the conditions the children are suspected to have disorders of calcium and bone metabolism17. Bony deformity can also result from fluorosis which can make bones weaker resulting in deformities as reported in endemic form in parts of Andhra Pradesh and Panjab because of high fluoride content in water and soil18. It is interesting to note that the mean serum ALP level was raised (387.9 U/L) in 22 controls. Normal level of ALP varies considerably throughout life, and absolute upper and lower values are not clearly defined. Elevated values derived from osteoblasts occur in any condition with increased bone turn over, such as all forms of rickets, fractures, osteogenic sarcoma, osteomalignancies or Juvenile Paget=s disease and also whenever bile duct epithelium is damaged, as in obstructive jaundice19.
Clinically, all the control children appeared to be otherwise healthy.
We found mostly illiterate (60%) and poor socio-economic background (62%) of the families of the children of Chakaria. The significant number of children were used to taking dry fish and it is interesting to note that this dry fish intake has proved to be having a negative association for the development of rickets in children (OR 0.573, 95% CI 0.355-0.926, Table-XIX). History of developmental delay was strongly associated with the presence of rickets in children (OR 10.96 95% CI4.00-29.84,).
The nutritional status of children showed that the children have severe stunting (60%) like other rural area (61%) of Bangladesh20. The children who had rickets were less wasted than the controls (Table-IX) which is comparable to other study16.
Recommendations
The Chakaria rickets study has confirmed the existence of rickets in whole area of Chakaria. The study showed the prevalence of confirmed rickets to be 0.9%, >only biochemical rickets= 1.3% and >only clinical rickets= 6.4%. There is no doubt that 8.7% children are having some >bony disorders= mimicking rickets at least clinically. That means about 40,000 children up to 15 years of age are suffering from >rickets like conditions= only in Chakaria thana. Keeping in the backdrop of mind all the previous sporadic studies conducted so far at Chakaria the following recommendations are being put forward for future considerations :
1. The children who are suffering from confirmed rickets need to be treated and rehabilitated immediately.
2. An exhaustive laboratory approach could be considered with some of the available blood of the Chakaria children to find out the cause of rickets or some other >bony disorders= that might inflict these children.
3. A case-control study could be designed to ascertain the risk factors or the protective factors for the >rickets like condition= of children in this region
4.The Pettifor=s criteria21, 22 of calcium supplementation could be intervened to a group of children having >biochemical rickets= to make the diagnosis supporting the hypothesis of calcium deficiency rickets.
5. A nation wide prevalence study on rickets in children could be conducted to see the extent of problem in other regions of Bangladesh.
References
10 Cimma JP, Cremodes R, Gaudin JC, Idelman S. Unpublished observations, 1994,
20 Fischer PR, Rahman A, Cimma J, Kyaw-Mint TO, Kabir ARML, Talukder K et al. Nutritional rickets without vitamin D Deficiency in the Chakaria region of Bangladesh. 7th Annual Scientific Conference (ASCON) 14-15 February 1998.
30 Second Annual Report. Institute of Child and Mother Health, 1993-94
40 Pettifor JM, Ross P, Wang J et al. Rickets in children of rural origin in South Africa. Is low dietary calcium a factor ? J of Paediatrics 1978; 92(2): 320-324
50 Oginni LM, Worsfold M, Oyelami OA et al. Etilogy of rickets in Nigerian children. J Paediatrics 1996 May; 128: 692-4
60 Quasem MF. Rickets : a potential cause of child disability at Chakaria. In Touch 1992Jun; 11(106): 8
70 The Statistical Year Book of Bangladesg. Bangladesh Bureau of Statistics, Statistics Division. Ministry of Planning, Government of Bangladesh, 1996.
80 UNICEF report by Dr. T O Kyaw-Myint, Officer in Charge, Health and Nutrition Section, January 1997
90 et-Hag-Al, Karrar ZA. Nutritional deficiency rickets in Sudanese children. Ann Trop Paediatr 1995; 15(1): 69-76.
100 Baser E, Cakmakci T. Factors affecting the morbidity of vitamin D deficiency rickets and primary protection. East Afr Med J 1994Jun; 71(6): 358-62.
110 Glorieux FH, Marie PJ, Pettifor JH et al. Bone response to phosphate salts, ergocalciferol and calcitriol in hypophosphatemic vitamin D resistant rickets. New Eng J Med 1980; 303: 1023
120 Malluche H, Faugere M. Renal osteodystrophy. N Eng J Med 1989; 321: 317
130 Chesney RW, Kaplan BS, Phelps M et al. Renal tubuilar acidosis does not alter the circulation values of calcitriol (1, 25 (OH)2 vitamin D) J Paediatr 1984; 104: 51
140 Norman ME. Metabolic bone disease. In. Richard E Behrman, Robert M Kliegman et al. eds 14. Nelson Text book of Paediatrics. Philadelphia. WB Saunders Company 1992; 1748-1757
150 Eil C, Lieberman UA, Rosen JF et al. Cellular defects in hereditary vitamin D -dependent rickets type-II : Defective nuclear uptake of 1,25(OH)2 vitamin D in cultured skin fibroblasts. N Eng J Med 1981; 304: 1588
160 Salimpour R. Rickets in Tehran. Study of 200 cases. Arch Dis Child 1975; 50:63-66.
170 Edidin DV, Levitsky LL, Schey W et al. Resurgence of nutritional rickets associated with breastfeeding and special dietary practices. Paediatrics 1980; 65: 232-235.
180 Ozur S, Sumer H, Kocoglu G. Rickets and soil strontium. Archives of Disease in Childhood. December 1996; 75 (6) : 524-526.
190 Walter EA, Scariano JK, Easington CR et al. Rickets and Protein Malnutrition in Northern Nigeria. Journal of Tropical Paediatrics April 1997; 43 (2): 98-102.
200 Kruse K. Laboratory approach to the child with suspected disorders of calcium and bone metabolism. In: Book CGD (ed) 1989. Clinical Paediatric Endocrinology. 2nd edn. Blackwell Scientific Publications, Oxford, pp 550-552.
210 Ghosh Santi. In Nutrition needs of children. Nutrition and child care: A practical guide 1997. Jaypee Brothers, New Delhi, India, pp 2-12.
220 Buist NR. Inborn errors of metabolism. In: Book Inborn error of metabolism. Forfar and Arneil=s Textbook of Paediatrics. 4th edn. Churchill Livingstone, UK, pp 1250-1252.
230 Kiess L . Comparison of nutritional status among Pre-school children living in rural, slum and urban area. An abstract for 7th Annual Scientific Conference (ASCON), 14-15 February 1998, Dhaka.
240 Marie PJ, Pettifor JM, Ross PP, Glorieux FH. Histological osteomalacia due to dietary calcium deficiency in children. N Engl J Med 1982; 307 : 584-8.
250 Pettifor JM, Ross P, Moodley G, Shuenyane E. The effect of dietary calcium supplementation on serum calcium, phosphorus and alkaline phosphatase concentrations in a rural black pipolation. Am J Clin Nutr 1981; 34: 2187-91