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Biomedical subjects

N Kochupillai

Publications and source records attributed to N Kochupillai.

At least 19 recordsLinked to original sources
PubMed2006

Fluorotoxic metabolic bone disease: an osteo-renal syndrome caused by excess fluoride ingestion in the tropics.

BACKGROUND: There is scant data available on the pathogenetic mechanisms of varied clinical presentation of bone disease in patients with excess fluoride ingestion in the Indian subcontinent. The present study is comprehensive and state of the art, incorporating all essential elements of bone mineral metabolism in patients with excess fluoride ingestion. METHODS: We studied 24 patients (age 31 +/- 16 years) with fluorotoxic metabolic bone disease (FMBD) for their clinical, radiological and biochemical parameters like serum calcium, phosphorous, alkaline phosphatase (SAP), 25-hydroxyvitamin D, 1,25 dihydroxyvitamin D, and parathyroid hormone levels, nephrologic parameters that assess renal handling of calcium and phosphorous and skeletal dynamics as revealed by bone histomorphometry. FINDINGS: Major clinical manifestations were bone pain (79%), Tetany (12.5%) and dental mottling (38%). Radiological findings included osteosclerosis (96%), pseudofracture and ligamentous calcification (50%). These patients manifested hypocalcemia and raised SAP with normal serum phosphorus. There was a positive correlation between serum creatinine and phosphorous excretion index (PEI) and a negative correlation between declining endogenous creatinine clearance (Cr.Cl) and increasing renal loss of calcium and phosphorus as indicated by increased calcium to creatinine ratio and PEI. Bone histomorphometry revealed impairment of primary mineralization with hypomineralized lacunae, interstitial mineralization defects and very thick and extended osteoid seams. Autopsy findings in a patient who died of azotemia showed tubular atrophy with secondary glomerular changes. INTERPRETATION: Fluoride intoxication plays an important role in the pathogenesis of the unique osteo-renal syndrome.

Adolescent↗
PubMed2006

Endocrine regulation in asymmetric intrauterine fetal growth retardation.

OBJECTIVE: The ponderal index (PI) is a widely accepted measure of disproportionate growth or asymmetrical growth retardation by pediatricians worldwide. Identification of disproportionately grown small for gestational age (SGA) neonates by using the ponderal index as a measure of the nutritional status at birth, is important because they constitute a high-risk group among SGA neonates. Poor nutritional status of the mother could have a direct effect on the organs of the developing fetus and/or affect the endocrine milieu in the maternal feto-placental unit resulting in an increased incidence of intrauterine growth-retarded (IUGR)/SGA births. IUGR is a significant risk factor for adult disease. In this study, we have investigated the endocrine adaptation by the fetus to overcome the growth disadvantage caused due to poor nutritional status of the mother. MATERIALS AND METHODS: We examined the quantitative variations in hormonal and growth factor profiles in paired maternal and cord blood samples obtained from mothers and their neonates who were classified based on their growth status into SGA and appropriate for gestational age (AGA). RESULTS: (1) A total of 24.7% neonates had a PI < 2, indicating a high incidence of asymmetric IUGR in the population studied. (2) Anthropometric parameters measured in the mothers indicate that the mothers giving birth to neonates with a PI < 2 had poor nutritional status, both prior to and during pregnancy. (3) We observed increased levels of placental lactogen and prolactin and decreased levels of insulin in the cord blood of neonates with PI < 2, while lower levels of insulin-like growth factor 1 (IGF-1) and higher levels of epidermal growth factor (EGF) were observed in their mothers. CONCLUSION: Poor maternal nutritional status results in fetal adaptation to a growth restricted environment via the modulation of the pituitary-thyroid axis thereby altering the endocrine milieu, thus affecting fetal growth.

Adult↗
PubMed2005

Thyroid hormone dysregulation in intrauterine growth retardation associated with maternal malnutrition and/or anemia.

Data on the effect of maternal malnutrition and/or anemia on thyroid hormone regulation in human fetuses are scarce, and would be of great importance in examining the relevance of Barker's hypothesis, which proposes adaptation of fetuses to undernutrition leading to permanent metabolic and endocrine changes that form the basis of adult diseases. To examine the quantitative variations in thyroid hormone profile of neonates born to malnourished and/or anemic mothers, we quantitated the T3, T4, rT3 and TSH levels in cord blood of neonates and maternal blood of their corresponding mothers that are malnourished and/or anemic. Further, we classified neonates born to each of these groups of mothers into Small for Gestational Age (SGA) or Appropriate for Gestational Age (AGA) based on the intrauterine growth curve for our population, and examined the thyroid hormone profile in these neonates. Our results show that firstly, the effects of malnutrition or anemia on thyroid hormone profile are distinct, secondly, significantly higher levels of cord blood T4 and correspondingly lower levels of T3 and rT3 are observed in the neonates born to anemic and malnourished mothers and thirdly, decreases in cord blood T3 levels were observed in Small for Gestational Age neonates born to anemic mothers. These observations lead us to speculate that alterations in the pituitary-thyroid function result in beneficial adaptations to the hostile intrauterine environment in malnutrition related growth retardation and anemia.

Anemia↗
PubMed2005

Reversal of subclinical adrenal insufficiency through antituberculosis treatment in TB patients: a longitudinal follow up.

BACKGROUND & OBJECTIVE: Subclinical adrenal insufficiency has been shown to occur in patients with tuberculosis. Whether this insufficiency can be reversed with therapy and on long-term follow up, is not known. We studied the effect of antituberculosis treatment (ATT) with respect to reversal of the adrenal insufficiency, as assessed by response to standard dose adrenocorticotropin (ACTH) stimulation test in TB patients. METHODS: One hundred and five HIV-negative tuberculosis patients were studied. Of these, 72 patients had pulmonary and 33 had extrapulmonary forms of the disease. Baseline (pre-treatment) standard-dose ACTH stimulation test was done on all the subjects, following which, they were put on standard antituberculosis therapy, depending on the type of disease and were followed up for a period of 30 months. ACTH stimulation tests were performed at follow up, every 6 months. RESULTS: Baseline (pre-treatment) standard-dose ACTH stimulation test revealed an impaired response in 52 of 105 patients (49.5%). At 6 months, the percentage of responders had increased to 71 per cent with a gradual increasing trend noted thereafter. At 24 months, 31 of the 32 patients (97%) who were followed up demonstrated a normal response to ACTH stimulation. The percentage of responders was comparable in both pulmonary [21 of 22 patients (95%)] and extrapulmonary TB [10 of 10 patients (100%)] groups at follow up. INTERPRETATION & CONCLUSION: Our study shows that nearly half of patients with active tuberculosis had a subclinical adrenal insufficiency indicated by an impaired response to ACTH stimulation test. This insufficiency reverse with therapy in most patients on long-term follow up.

Adrenal Insufficiency↗
PubMed2004

Effect of maternal malnutrition and anemia on the endocrine regulation of fetal growth.

Fetal growth retardation is a result of a complex pathology caused by multiple factors of fetal, placental, and maternal origin. Hormones and growth factors released as a result of maternal-fetal physiological interactions play an importance role in fetal well being and fetal outcome. Intrauterine Growth Retardation (IUGR) is associated with significant perinatal and childhood morbidity. It is estimated that 13.7 million infants are born annually with IUGR, comprising 11% of all births in developing countries. Both maternal malnutrition and anemia are associated with various degrees of fetal growth retardation. The relationship between decreasing birth weight percentiles and increasing fetal morbidity and mortality has been demonstrated by several investigators and epidemiological studies suggest that IUGR is a significant risk factor for the subsequent development of chronic hypertension, ischemic heart disease, diabetes, and obstructive lung disease in adult life (Barker's Hypothesis). Maternal anemia and/or malnutrition are recognized to be the most frequent cause of IUGR and SGA birth in developing countries like India. In order to investigate adaptive mechanisms by the fetus to overcome the growth disadvantage caused due to maternal nutritional limitations, we examined the quantitative variations in hormonal and growth factor profiles in paired cord blood and maternal samples obtained from neonates born to malnourished and/or anemic mothers. The results of our study show that: 1) The percentage of small for gestational age (SGA) neonates born to malnourished and anemic mothers was significantly higher than those born to mothers who were either malnourished or anemic; 2) Significantly higher levels of GH, PRL, HPL and IGF-1 were observed in the cord blood of neonates born to malnourished and anemic mothers indicative of an adaptive response on part of the fetus to over come an in-utero growth disadvantage; 3) The anoxemia-related fetal perturbations may have unique features that make them distinct from nutrient deficiency-related IUGR. Thus, these novel observations are relevant to the context of the ongoing scientific debate on Barker's hypothesis.

Adult↗
PubMed2003

Residual goitre in the postiodization phase: iodine status, thiocyanate exposure and autoimmunity.

OBJECTIVE: This study was done to assess goitre prevalence, thyroid functional status and cause of residual goitre among school children in the postsalt iodization phase in India. DESIGN: A cross-sectional study in which, 14762 school children in the age group of 6-18 years, from different States and Union territories of India, were evaluated for goitre prevalence, urinary iodine and thiocyanate excretion, functional status of the thyroid as well as serological and cytopathological markers for thyroid autoimmunity. MEASUREMENTS: Urinary iodine (wet ashing method), urinary thiocyanate (colourimetric method), serum thyroxine [in-house radioimmunoassay (RIA)], serum TSH (IRMA), antithyroid microsomal and antithyroglobulin antibodies (haemagglutination method) were estimated. Fine-needle aspiration cytology was performed in all goitrous subjects giving consent. RESULTS: The overall goitre prevalence was 23% (27.1% girls; 17.8% boys, P < 0.001). Subjects belonging to poor socio-economic strata had significantly higher goitre prevalence. Median urinary iodine excretion (UIE) in goitrous subjects (2-53 micromol/l) was significantly higher than in controls (2-24 micromol/l; P < 0.001). Levels of UIE observed among goitrous subjects showed no relationship with the presence or absence of thyroid dysfunction or with thyroid antibody status. High titres (> or = 1:1600) of TMA were present more often in goitrous subjects (6.08%) than nongoitrous controls (0.34%; P < 0.001) and in girls (7.3%) than boys (2.35%; P < 0.001). TMA positivity were significantly more among goitrous subjects with thyroid dysfunction than in euthyroid subjects. Significantly higher median urinary thiocyanate (USCN) excretion was observed in goitrous subjects (0.75 mg/dl) compared to controls (0.64 mg/dl; P < 0.001) and goitrous girls compared to goitrous boys. USCN excretion of goitrous subjects and controls showed no relationship with functional or thyroid antibody status in various groups. CONCLUSIONS: Persistent, albeit reduced prevalence of goitre, despite adequate iodine prophylaxis, suggests existence of additional factors in goitrogenesis in India. Thyroid autoimmunity can explain only a part of the goitre prevalence. The role of goitrogens in residual goitre prevalence is brought forth.

Adolescent↗
PubMed2002

Reversible peripheral neuropathy in idiopathic hypoparathyroidism.

We describe a 40-year-old male with idiopathic hypoparathyroidism presenting with tetany, proximal weakness, signs of hypocalcaemia including Chvostek and Trousseau's and diminished tendon reflexes in the upper and lower limbs. Electrophysiological studies revealed a sensory-motor neuropathy, predominantly axonal as evidenced by decreased CMAP amplitudes, with normal distal latencies-velocites, except for median nerve where a prolonged distal latency was observed. Serial nerve conduction studies were performed at repeated intervals for 2 years, while he received treatment for hypoparathyroidism (calcium and vitamin D supplementation). A progressive improvement in neuropathy both clinical and on electrophysiological studies was observed. Occurrence of peripheral neuropathy in hypocalcaemic states such as hypoparathyroidism and its reversibility after normalization of calcium homeostasis lend proof to the role of critical Ca2+ ion concentration in the normal functioning of the peripheral axons.

Adult↗
PubMed2001

Islet cell autoimmunity in youth onset diabetes mellitus in Northern India.

We characterised a consecutive cohort of 132 youth onset diabetic individuals (age at onset<30 years, mean duration of disease 5.5+/-6.0 years) from North India, by serological determination of the determination of the islet cell autoantibodies, GAD(65) and IA2, and clinically for coexisting autoimmune thyroid disease, malnutrition and pancreatic calcification. Five types of diabetes were delineated: Type 1 (37%), ketosis resistant (32%), Type 2 (13%), fibrocalculous pancreatopathy (11%) and autoimmune polyglandular syndrome (7%). C-peptide response to glucagon was assessed in a representative subset of 50 patients with Type 1, ketosis resistant, and autoimmune polyglandular syndrome. A total of 22.4% of Type 1 and 30% of autoimmune polyglandular syndrome subjects showed both GAD(65) plus IA-2 autoantibody positivity, significantly more than the 4.7% positivity shown by the ketosis resistant type. However, GAD(65) antibody positivity alone was seen in 38% of ketosis resistant subjects which was significantly more than the 14.2 and 10% positivity seen in Type 1 and autoimmune polyglandular groups, respectively. The fibrocalculous pancreatopathy group showed GAD(65) plus IA-2 autoantibody positivity in 14.2% and GAD(65) autoantibody alone positivity in 7.1%. 26 and 60%, respectively, of the Type 1 and autoimmune polyglandular syndrome groups had thyroid microsomal autoantibody positivity. Type 1 showed significantly less C-peptide response to glucagon when compared to the ketosis resistant and autoimmune polyglandular syndrome groups. The controls and Type 2 diabetic individuals tested negative for islet cell autoimmunity markers. These findings demonstrate a role of islet cell autoimmunity in the pathogenesis of four out of the five clinical types of youth onset diabetes seen in North India.

Adolescent↗
PubMed2001

Prevalence of urinary tract infection and renal scars in patients with diabetes mellitus.

In a case control study, we assessed the prevalence of bacterial urinary tract infections (UTI) and renal scarring in 155 consecutive type 1 (n=102) and type 2 (n=53) diabetic individuals and 128 healthy controls. Subjects who received antibiotics during the past 6 months, pregnant women and those with overt renal failure were excluded. In all subjects, urine culture and 99m Technetium (Tc) dimercapto-succinic acid renal scan was performed. UTI was diagnosed if two consecutive urine cultures grew the same organism with at least 10(5) colony forming unit (cfu)/ml in asymptomatic and at least 10(4) cfu/ml in symptomatic subjects, respectively. Renal scan was considered abnormal if focal or multiple tracer uptake defects and/or break in cortical outline were observed. The prevalence of UTI in diabetes mellitus was higher, when compared to that in controls (9% vs. 0.78%, P=0.005). Escherichia coli was the most commonly grown organism (64.3%), followed by Staphyloccocus aureus (21.4%) and Klebsiella pneumoniae (14.3%). Prevalence of renal scarring was higher in patients with diabetes (28/155, 18.0%), when compared to that of controls (7/128, 5.4%, P=0.002). Fifty percent of patients with diabetes and UTI had renal scarring. The prevalence in diabetics with no UTI was also higher, when compared to controls (14.8 vs. 5.5%, P<0.01). The prevalence of UTI as well as renal scarring was significantly higher in females, when compared to male diabetics. No significant difference in vascular events, hypertension, proteinuria, renal function tests and HbA1 was observed in patients with and without renal scar. Thus, patients with diabetes mellitus have 10- and 3-folds increased risk of UTI and renal scarring, respectively. The results could help prioritize protocols for management of UTI among patients with diabetes mellitus.

Adult↗
PubMed2000

Prevalence and significance of low 25-hydroxyvitamin D concentrations in healthy subjects in Delhi.

BACKGROUND: Despite abundant sunlight, rickets and osteomalacia are prevalent in South Asian countries. The cause of this paradox is not clear. OBJECTIVE: The objective was to assess 25-hydroxyvitamin D [25(OH)D] status and its functional significance in apparently healthy subjects residing in Delhi, a city in the northern part of India. DESIGN: Serum 25(OH)D, total calcium, inorganic phosphate, alkaline phosphatase, intact parathyroid hormone, and 1, 25-dihydroxyvitamin D [1,25(OH)(2)D] were measured in groups of healthy subjects who differed with respect to variables relevant to vitamin D and bone mineral metabolic status, such as direct sunlight exposure, season of measurement, skin pigmentation, dietary calcium and phytate contents, and altered physiologic states such as pregnancy and neonatal age. RESULTS: All groups except one with maximum direct sunlight exposure had subnormal concentrations of 25(OH)D. The 25(OH)D-deficient groups tended to have an imbalance in bone mineral metabolic homeostasis when exposed to winter weather and low dietary calcium and high dietary phytate, with significantly low calcium and elevated intact parathyroid hormone concentrations, chemical osteomalacia, or both. Increased values of 1,25(OH)(2)D during pregnancy did not help correct the imbalance in bone mineral metabolic homeostasis. CONCLUSION: Healthy subjects with low 25(OH)D concentrations are at risk of bone mineral metabolic imbalance when exposed to factors that strain bone mineral homeostasis.

Adult↗
PubMed2000

Hashimoto's thyroiditis: countrywide screening of goitrous healthy young girls in postiodization phase in India.

Countrywide salt iodization, to prevent nutritional iodine deficiency, has been achieved in India recently. The current study was planned to evaluate the prevalence of goiter and thyroid autoimmunity and assess thyroid functional status in a cohort of 6283 healthy schoolgirls from different parts of the country in the postiodization phase. Goitrous girls (n = 1810; 28% of subjects) were investigated for serum T4 and TSH, antithyroid microsomal antibody (TMA) and antithyroglobulin antibody (TGA), urinary iodine excretion, and cytomorphology by fine-needle aspiration cytology (FNAC). FNAC carried out successfully in 764 goitrous girls revealed juvenile autoimmune thyroiditis (JAT) in 58 (7.5%), which included Hashimoto's thyroiditis in 43 (5.6%) and focal lymphocytic thyroiditis in 15 (1.9%). TMA and TGA estimated in 722 goitrous girls detected significantly positive titers of TMA (> or =1:1600) and TGA (> or =1:160) in 52 (7.2%) and 4 (0.55%) girls, respectively. Only 29 (67.4%) girls with Hashimoto's thyroiditis were TMA positive. In patients with FNAC-proven JAT, overt clinical and biochemical hypothyroidism was seen in three (6.5%) and subclinical hypothyroidism in seven (15%). Subclinical hyperthyroidism was detected in 5.1% cases of JAT, and none had overt hyperthyroidism. No definite correlation was seen between urinary iodine excretion and thyroid autoimmunity.

Adolescent↗
PubMed1999

Residual pituitary enlargement in primary hypothyroidism despite 1 1/2 years of L-thyroxine therapy.

Pituitary hyperplasia consequent to untreated primary hypothyroidism undergoes impressive regression following thyroxine therapy. We describe a young man with primary hypothyroidism and pituitary hyperplasia, who showed significant but incomplete regression of pituitary enlargement despite 18 months of L-thyroxine therapy (1 year in replacement dose (150 micrograms/day) and an additional 6 months in suppressive dose (300 micrograms/day)).

Adult↗
PubMed1998

Reversal of abnormalities of myelination by thyroxine therapy in congenital hypothyroidism: localized in vivo proton magnetic resonance spectroscopy (MRS) study.

Deficiency of thyroid hormone during central nervous system ontogeny results in a variety of clinical, anatomical and biochemical defects. Delay in thyroxine therapy in newborns with congenital hypothyroidism leads to irreversible brain damage. We have used localized in vivo proton magnetic resonance spectroscopy (MRS) to assess biochemical changes in different regions of brain in three patients with congenital hypothyroidism before and after thyroxine therapy. An abnormal lipid peak which disappeared with thyroxine therapy was observed in cerebellum and frontal lobe in one patient. Statistically significant reduction of NAA/(Cr+PCr) [P<0.009] and elevation of Cho/(Cr+PCr) [P<0.008] ratios in comparison to controls were documented in all three patients which tended to normalise with thyroxine therapy. A variety of biochemical abnormalities relatable to myelin maturation were documented and these were found to be reversible on thyroxine therapy. Reversibility was documented even though thyroxine therapy was initiated at ages beyond which abnormalities in myelinogenesis are considered irreversible. Also, proton MRS revealed biochemical heterogeneity between patients with congenital hypothyroidism.

Adolescent↗
PubMed1998

Insulin autoantibodies before and after carbimazole therapy in Asian Indian patients with Graves' disease.

Carbimazole therapy can induce insulin autoantibodies (IAA) in Japanese Graves' disease patients, a phenomenon possibly linked to their immunogenetic profile. This phenomenon is not observed in Caucasians. We assessed IAA levels in 114 North Indian Graves' disease patients before and after carbimazole therapy (mean duration 6.2 +/- 3.9 months). The functional significance of IAA was assessed in 46 of them by first phase (sum of +1 and +3 min) insulin response to intravenous glucose (IVGTT) and an oral glucose tolerance test (OGTT) undertaken before commencement of the carbimazole therapy. IAA were measured using a radiobinding assay and expressed as the assay precision unit, S.D. scores (S.D.S), over healthy controls. Before treatment 22 of 114 (19.3%) patients were IAA positive (mean +/- S.D., 5.9 +/- 3.2 S.D.S). After carbimazole therapy a further 11 (9.6%) showed positive for IAA (mean +/- S.D., 3.5 +/- 1 S.D.S). Of the 22 patients who were IAA positive before treatment, 12 became negative after carbimazole therapy. The fasting insulin and first phase insulin responses were similar in IAA positive and IAA negative Graves' disease patients (mean +/- S.D., 61.7 +/- 35.9 versus 88.3 +/- 46.6 pmol/l, P = 0.123 and 1127 +/- 696 versus 1033 +/- 430 pmol/l, P = 0.716, respectively). The OGTT results were comparable in the IAA positive and the IAA negative groups. Thus, North Indian Graves' disease patients, who resemble Caucasians in their HLA haplotypes, behave like Japanese in their tendency to become IAA positive with carbimazole therapy. A subset of the patients who were IAA positive before treatment also demonstrated negative IAA (12/22) after carbimazole therapy.

Adult↗
PubMed1998

Prevalence and significance of steatorrhea in patients with active Graves' disease.

OBJECTIVE: The aim of this study was to determine the prevalence of steatorrhea in patients with Graves' disease and to assess its significance and correlation with changes in body mass index (BMI), coefficient of fat absorption (COFA), and pancreatic exocrine function in these patients. METHODS: Daily dietary fat intake, 24 h fecal fat, COFA, fecal chymotrypsin activity (as an index of pancreatic exocrine function), and total T3, T4, and TSH levels were assessed in 28 patients with active Graves' disease. In 24 patients, reassessment was done after attaining a euthyroid state with carbimazole therapy. RESULTS: In the thyrotoxic state, 13 of 28 patients had steatorrhea, whereas 15 had normal (<6 g/day) fat excretion (11.4 +/- 6.7 g vs 2.9 +/- 0.8 g, p = 0.0007). Daily fat intake, basal BMI, and serum T3 and T4 levels were similar in the steatorrheic and nonsteatorrheic groups. The mean COFA of the steatorrheic group was significantly lower than that of nonsteatorrheic group (91.6% +/- 4.8% vs 97.7% +/- 0.9%, respectively; p = 0.0006). In the steatorrheic group, fat excretion and COFA normalized after attainment of euthyroidism (changes in fat excretion and COFA = 7.3% +/- 6.3 g/day and 7.7% +/- 5.4%, respectively). Fecal chymotrypsin levels were similar in the steatorrheic and nonsteatorrheic thyrotoxics and in 16 healthy control subjects. The levels did not show any significant changes following attainment of euthyroid status. CONCLUSION: Steatorrhea associated with a decrease in COFA can occur in a reversible manner in 46% of patients with Graves' disease. However, steatorrhea in these patients is not linked with weight loss or with pancreatic exocrine dysfunction.

Absorption↗
PubMed1997

Prevalence of enuresis and other bladder symptoms in patients with active Graves' disease.

OBJECTIVE: To determine the prevalence of bladder symptoms in patients with Graves' disease and assess their abnormalities on urodynamic studies. PATIENTS AND METHODS: The study comprised 30 consecutive patients (13 female, 17 male, mean age 31 years, SD 10) with active Graves' disease. Before and after attaining euthyroidism with carbimazole, their bladder symptoms were assessed using a questionnaire adapted from the American Urologic Association voiding symptom score, the serum levels of total triiodo-L-thyronine (T3), serum thyroxine (T4) and thyroid-stimulating hormone (TSH) were measured by radioimmunoassay, and uroflowmetry, cystometry and perineal muscle electromyography were performed. RESULTS: Twelve of the 30 patients (40%) had the onset of bladder symptoms 1-6 months after the onset of symptoms of Graves' disease; four of the 12 patients had enuresis. Urodynamic studies were possible in five patients and showed reduced flow rates in all, a significant post-void residual volume in four, and enlarged bladder capacity and increased perineal muscle electromyographic activity during the voiding phase in three. Voiding disturbances and urodynamic abnormalities resolved after attaining euthyroidism. CONCLUSION: Significant bladder symptoms can occur in about 40% of patients with active Graves' disease but resolve on euthyroidism; in some patients, urodynamic studies show significant abnormalities which are also reversible.

Adolescent↗