HIGH THYROID STIMULATING HORMONE LEVEL IN DOWN’S SYNDROME A MERE RESETTING OF HYPOTHALAMOPITUITARY AXIS?: A CASE-CONTROL STUDY
AACE ePoster Library. Sanyal D. 05/15/15; 97746; 1088
Dr. Debmalya Sanyal
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Abstract
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Objective: Reduced thyroid function in Down’s syndrome (DS) has been variously attributed to causes ranging from glandular dysgenesis to altered hypothalamopituitary axis, precise etiology remaining elusive. In present study, we have compared hypothyroid Indian children with and without DS, with specific references to phenotypic presentations.
Methods: DS patients (≤18 years) with elevated thyroid stimulating hormone (TSH, ≥5 mIU/L) were consecutively recruited in a prospective manner in a secondary care hospital in India. In the control arm, patients (≤18 years) with hypothyroidism without DS were recruited. Congenital hypothyroidism was excluded in both arms. Free thyroxine (FT4), anti-thyroid peroxidase (TPO) antibody, anti-thyroglubulin (TG) antibodies were measured in the cases and controls.
Results: Forty six cases [median age 9 years (IQR: 4-16.25), M:F=18:28] and 41 controls [median age 12 years (IQR: 8-14.50),M:F=15:26] were comparable in terms of age and sex. Median age of presentation with elevated TSH levels was significantly earlier in case of DS cases [7.50 years vs. 11 years, P=0.015]. Significantly greater number of positive family history was present the cases without DS [P=0.048]. Although the rates of positivity of anti-TPO antibody [34.78% of DS vs 43.90% of non DS cases, P=0.509] and anti-TG antibody [15.21% of DS vs 12.19% of non DS cases, P=0.763] are comparable between the groups, the median titer of anti-TPO antibodies was significantly lower in the cases with DS [31.00 U/ml vs 91.00 U/ml, P=0.008]. Rates of goiter were comparable [36.95% of DS vs 34.14% of non DS cases, P=0.826].
Discussion: Important differences emerge in Indian children with hypothyroidism with or without DS. While earlier presentation, a greater incidence of traceable family history and lower antibody titers might support a possible resetting of hypothalamopituitary axis, the incidences of antibody positivity and goiter are comparable. Also, an autoimmune etiology of the thyroid disorders cannot be ruled out, given the links between chromosome 21 anomaly and other immune dysfunctions.
Conclusion: Phenotypic differences exist in Indian pediatric hypothyroid patients with and without DS. A causal association of elevation of TSH levels in DS and resetting of hypothalamopituitary axis cannot be concluded.
Methods: DS patients (≤18 years) with elevated thyroid stimulating hormone (TSH, ≥5 mIU/L) were consecutively recruited in a prospective manner in a secondary care hospital in India. In the control arm, patients (≤18 years) with hypothyroidism without DS were recruited. Congenital hypothyroidism was excluded in both arms. Free thyroxine (FT4), anti-thyroid peroxidase (TPO) antibody, anti-thyroglubulin (TG) antibodies were measured in the cases and controls.
Results: Forty six cases [median age 9 years (IQR: 4-16.25), M:F=18:28] and 41 controls [median age 12 years (IQR: 8-14.50),M:F=15:26] were comparable in terms of age and sex. Median age of presentation with elevated TSH levels was significantly earlier in case of DS cases [7.50 years vs. 11 years, P=0.015]. Significantly greater number of positive family history was present the cases without DS [P=0.048]. Although the rates of positivity of anti-TPO antibody [34.78% of DS vs 43.90% of non DS cases, P=0.509] and anti-TG antibody [15.21% of DS vs 12.19% of non DS cases, P=0.763] are comparable between the groups, the median titer of anti-TPO antibodies was significantly lower in the cases with DS [31.00 U/ml vs 91.00 U/ml, P=0.008]. Rates of goiter were comparable [36.95% of DS vs 34.14% of non DS cases, P=0.826].
Discussion: Important differences emerge in Indian children with hypothyroidism with or without DS. While earlier presentation, a greater incidence of traceable family history and lower antibody titers might support a possible resetting of hypothalamopituitary axis, the incidences of antibody positivity and goiter are comparable. Also, an autoimmune etiology of the thyroid disorders cannot be ruled out, given the links between chromosome 21 anomaly and other immune dysfunctions.
Conclusion: Phenotypic differences exist in Indian pediatric hypothyroid patients with and without DS. A causal association of elevation of TSH levels in DS and resetting of hypothalamopituitary axis cannot be concluded.
Objective: Reduced thyroid function in Down’s syndrome (DS) has been variously attributed to causes ranging from glandular dysgenesis to altered hypothalamopituitary axis, precise etiology remaining elusive. In present study, we have compared hypothyroid Indian children with and without DS, with specific references to phenotypic presentations.
Methods: DS patients (≤18 years) with elevated thyroid stimulating hormone (TSH, ≥5 mIU/L) were consecutively recruited in a prospective manner in a secondary care hospital in India. In the control arm, patients (≤18 years) with hypothyroidism without DS were recruited. Congenital hypothyroidism was excluded in both arms. Free thyroxine (FT4), anti-thyroid peroxidase (TPO) antibody, anti-thyroglubulin (TG) antibodies were measured in the cases and controls.
Results: Forty six cases [median age 9 years (IQR: 4-16.25), M:F=18:28] and 41 controls [median age 12 years (IQR: 8-14.50),M:F=15:26] were comparable in terms of age and sex. Median age of presentation with elevated TSH levels was significantly earlier in case of DS cases [7.50 years vs. 11 years, P=0.015]. Significantly greater number of positive family history was present the cases without DS [P=0.048]. Although the rates of positivity of anti-TPO antibody [34.78% of DS vs 43.90% of non DS cases, P=0.509] and anti-TG antibody [15.21% of DS vs 12.19% of non DS cases, P=0.763] are comparable between the groups, the median titer of anti-TPO antibodies was significantly lower in the cases with DS [31.00 U/ml vs 91.00 U/ml, P=0.008]. Rates of goiter were comparable [36.95% of DS vs 34.14% of non DS cases, P=0.826].
Discussion: Important differences emerge in Indian children with hypothyroidism with or without DS. While earlier presentation, a greater incidence of traceable family history and lower antibody titers might support a possible resetting of hypothalamopituitary axis, the incidences of antibody positivity and goiter are comparable. Also, an autoimmune etiology of the thyroid disorders cannot be ruled out, given the links between chromosome 21 anomaly and other immune dysfunctions.
Conclusion: Phenotypic differences exist in Indian pediatric hypothyroid patients with and without DS. A causal association of elevation of TSH levels in DS and resetting of hypothalamopituitary axis cannot be concluded.
Methods: DS patients (≤18 years) with elevated thyroid stimulating hormone (TSH, ≥5 mIU/L) were consecutively recruited in a prospective manner in a secondary care hospital in India. In the control arm, patients (≤18 years) with hypothyroidism without DS were recruited. Congenital hypothyroidism was excluded in both arms. Free thyroxine (FT4), anti-thyroid peroxidase (TPO) antibody, anti-thyroglubulin (TG) antibodies were measured in the cases and controls.
Results: Forty six cases [median age 9 years (IQR: 4-16.25), M:F=18:28] and 41 controls [median age 12 years (IQR: 8-14.50),M:F=15:26] were comparable in terms of age and sex. Median age of presentation with elevated TSH levels was significantly earlier in case of DS cases [7.50 years vs. 11 years, P=0.015]. Significantly greater number of positive family history was present the cases without DS [P=0.048]. Although the rates of positivity of anti-TPO antibody [34.78% of DS vs 43.90% of non DS cases, P=0.509] and anti-TG antibody [15.21% of DS vs 12.19% of non DS cases, P=0.763] are comparable between the groups, the median titer of anti-TPO antibodies was significantly lower in the cases with DS [31.00 U/ml vs 91.00 U/ml, P=0.008]. Rates of goiter were comparable [36.95% of DS vs 34.14% of non DS cases, P=0.826].
Discussion: Important differences emerge in Indian children with hypothyroidism with or without DS. While earlier presentation, a greater incidence of traceable family history and lower antibody titers might support a possible resetting of hypothalamopituitary axis, the incidences of antibody positivity and goiter are comparable. Also, an autoimmune etiology of the thyroid disorders cannot be ruled out, given the links between chromosome 21 anomaly and other immune dysfunctions.
Conclusion: Phenotypic differences exist in Indian pediatric hypothyroid patients with and without DS. A causal association of elevation of TSH levels in DS and resetting of hypothalamopituitary axis cannot be concluded.
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