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Iodine Excess is a Risk Factor for Goiter Formation

Washington L1, Makumbi T2, Fualal OJ1, Galukande M2

  1. Department of Surgery, Mulago National Referral Hospital, Kampala, Uganda

  2. College of Health Sciences, Makerere University, Kampala, Uganda

Correspondence to: Dr. Leonard Washington. P.O Box 7072 Kampala, Uganda. Email: drlwashington@yahoo. co.uk

 

Abstract

Background: Goiters have been associated with iodine deficiency. Although universal salt iodization in Uganda achieved a household coverage of 95% by 2005, goiter rates are still high. This study investigated the association between iodine excess and goiter. Methods: In a case control study, urinary iodine levels, complete blood count, T3, T4 and TSH levels were determined. Results: We recruited, 60 goiter and 63 non goiter patients. The median urine iodine level for goiter patients was significantly higher than in non-goiter controls. Urinary iodine excretion was sufficient in 43%, more than sufficient in 31% and excess in 10% of cases. There was an association between excess urinary iodine levels and goiter. Conclusion: Urinary iodine excess was significantly associated with occurrence of goiter.

 

Key Words: Iodine excess, Goiter, Sub Saharan Africa

Introduction

Goiter refers to an enlarged thyroid gland. Biosynthesis defects and iodine deficiency are associated with reduced efficiency of thyroid hormone synthesis leading to increased thyroid stimulating hormone (TSH) which stimulates thyroid growth and enlargement as a compensatory mechanism to overcome a block in hormone synthesis (1). Goiters are still common in Uganda despite majority (>90%) of people having excess iodine in urine. After mandatory iodine fortification of salt, goiter rates reduced to 14% from 74% in 1991, even though, it was expected according to WHO that fortifying salt would reduce this to less than 5% (2–4). It is unclear why the goiter rate is indeed still high despite the successful iodine fortification program and a 95% households’ coverage (5). Some reasons advanced for this include pockets of iodine deficiency, other causes of goiter such as cancer or goitrogens ingestion, selenium deficiency and vitamin A deficiency. Some studies have suggested that excess iodine may be the cause of reactive goiters (5–15). Thus, the aim of this study was to explore the association between goiter and iodine excess at a surgical endocrine unit in Uganda.

Methods

This case control study took place at Mulago, a 1500 bed national referral teaching hospital for Makerere University, Kampala, Uganda. The surgical endocrine unit conducts an outpatient clinic weekly where an average of 10 new thyroid patients are seen. Patients with goiter attending this endocrine clinic were recruited as cases. The controls were recruited from other outpatient surgical units.Cases were matched with controls for age and sex. Exclusion criteria included pregnancy, lactating mothers, chronic renal failure, those receiving radioiodine therapy, presence of goiter for >15 years, and those who had received intravenous contrast or were using drugs that alter thyroid function.

 

Study variables collected included urinary iodine levels, dietary goitrogens, serum creatinine, age, sex, address (district/regions), occupation, place of residency, duration of symptoms, use of iodized salt, thyroid size and thyroid hormonal levels. A standardized pretested questionnaire was administered. Patients were interviewed and underwent a thorough physical examination to establish the presence of goiter and its size according to WHO grading (16,17). Urine specimens were collected in sterile containers (Falcon tubes), acidified, labeled and wrapped with aluminum foil and kept in a cool, dark container whilst awaiting analysis. All urine samples were taken for analysis using the wet digestion method. In this method, the change in color of cerric ammonium sulfate by arsenious acid accelerated by iodine, which acts as a catalyst. The rate of this colour change, which depends upon the amount of iodine present, was measured by a colorimeter. The amount of iodine in the urine was calculated by a comparison with standard solutions of known iodine content, and expressed as mcg iodine per 100ml urine. Blood samples were taken for thyroid function tests, complete blood count and renal function tests. The renal functions tests were done by measuring the serum creatinine levels.

 

 

Data captured was entered to SPPS version 16 for analysis. Conditional logistic regression analysis was performed to assess the relationship between excess urinary iodine levels and the presence of goiter. P values of <0.05 were considered significant. Adjusting for confounding and interaction (goitrogens, age and sex, renal functions, district of residence etc): Variables found to have p-values <0.2 were entered into a multivariate logistic for analysis. Confounding was reported by the percentage difference when a given variable was in or out of the model as less than 10%. Permission was obtained from the College of Health Sciences, School of Medicine Research and Ethics Committee (SOMREC) at Makerere University. A voluntary informed written consent was obtained from all study participants.

 

Results