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Volume 99, Number 8 >
Pp. 396-401
Review |
Clinical Research Fellow, Centre for Endocrine and Diabetes Science, School of Medicine, Cardiff University, Cardiff, UK
E-mail: okosiemeoe{at}cf.ac.uk
INTRODUCTION
Thyroid disorders are common worldwide.1 In Africa, dietary iodine deficiency is the major determinant of thyroid pathology, resulting in a spectrum of iodine deficiency disorders, including goitres, hypothyroidism and mental retardation.2 Of these, mental retardation poses the most severe threat to socioeconomic wellbeing; thus, its prevention has been the focus of current global efforts towards sustainable iodine sufficiency.3 At least 350 million Africans are at risk of iodine deficiency.4 According to World Health Organization (WHO) estimates, goitres are present in 28.3% of the African population,4 and approximately 25% of the global burden of iodine deficiency as measured by disability-adjusted life years (DALYs) occurs in Africa.5 The demands of communicable diseases, coupled with the challenges of poverty, civil conflicts and fragile political structures, have in the past frustrated efforts at eliminating iodine deficiency in Africa.6 However, recent decades have seen remarkable improvements in iodine nutrition through salt iodination in the continent.7 The effect of these developments on the pattern of thyroid gland disease are beginning to unravel and will be relevant to the strategies for extending the present gains. In this article, I examine the impact of recent progress in iodine nutrition on the epidemiology of thyroid gland pathology in Africa.
METHODS
I searched Medline references using the term ‘Africa’ in combination with various search phrases related to thyroid disease: thyroid, goitre, hyperthyroidism, hypothyroidism, thyroid autoimmunity, thyroiditis, thyroid cancer and iodine. A further query was performed using the individual names of different countries in Africa. In addition, I consulted websites of the International Council for the Control of Iodine Deficiency Disorder (ICCIDD), WHO, and the United Nations Children's Fund (UNICEF).
HISTORICAL ASPECTS
Thyroid disorders have been recognized in Africa since olden times. Indigenous terms for thyroid swellings exist locally and goitres have featured in sculptures dating back centuries.8 The historian, Leo Africanus, observed tribes with goitres around Timbuktu in 1550.9 Centuries later, the Scottish surgeon Mungo Park would comment on the occurrence of goitres in his West African expeditions.9 By the mid-20th century, goitres were clearly endemic in virtually every part of the continent and it had become apparent that iodine deficiency was a significant public health problem in the region.9 By this period, the detrimental effects of iodine deficiency on fetal development had been established in other parts of the world. Studies in Papua New Guinea, in the 1960s had clearly shown that iodine supplementation was effective in preventing brain damage.10 In 1983, Hetzel introduced the term iodine deficiency disorders, thus shifting the emphasis away from the benign neck swelling to encompass the more serious and wide-ranging effects of iodine deficiency on growth and development.2 The ICCIDD was founded soon afterwards in 1985, as an expert consultative group to oversee the control and monitoring of iodine deficiency disorders at regional and international levels.11
DEVELOPMENTS IN IODINE NUTRITION
For most of the period before the 1990s, progress in Africa remained slow; prevention of iodine deficiency was low on the priorities of regional governments, structured programmes were lacking, and iodine supplementation was often approached erratically. As a result, this era saw only modest improvements in iodine intake. The introduction of formal iodine deficiency prevention programmes in the 1990s marked a turning point in the drive towards sustainable iodine sufficiency in Africa. In 1990, the World Summit for Children endorsed a resolution aimed at the virtual elimination of iodine deficiency worldwide.12 Through joint efforts by ICCIDD, WHO, UNICEF, and individual regional authorities, a strategy of universal salt iodination was promoted within the region. Iodized salt has since been made available to 62% of households7 and iodine sufficiency has thus been attained in at least 20 African countries, representing more than half the entire continent's population (Figure 1, Table 1). 4 Despite these gains, however, at least 350 million of the population remain at risk of iodine deficiency disorders.4 Within iodine sufficient African countries, pockets of severe deficiency persist and vulnerable population sub-groups like neonates, toddlers and pregnant women continue to be in danger of iodine deficiency disorders.13,14 Nonetheless, the progress in recent years clearly indicates that iodine sufficiency is truly within reach in Africa.
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EVOLVING DISEASE PATTERNS
There is compelling evidence that the pattern of thyroid disorders in a population is dependent on environmental iodine intake.15 Iodine deficiency disorders abound in areas with inadequate iodine intake while autoimmune thyroid disorders are rare in iodine deficiency but become prevalent with transition to iodine sufficiency.16 Monitoring disease patterns in Africa has proved challenging in the absence of comprehensive biomedical information. Goitre surveys in children are frequently conducted in schools within accessible locations. The occurrence of other thyroid disorders is extrapolated from hospital case records and histopathology reviews. While providing useful information, these methods exclude large rural populations who lack access to health and educational facilities. These limitations notwithstanding, several trends in disease pattern have become apparent in recent decades.
Endemic goitre
Goitre due to dietary iodine deficiency is by far the most commonly
observed thyroid disorder in
Africa.17-19
The majority of affected people live within subsistence agricultural systems,
commonly in mountainous regions which have been deprived of iodine by leaching
of the soil. Goitrogens in local foods like cassava and millet accentuate the
effects of iodine
deficiency20 and
other micronutrient deficiencies such as selenium also play a role in the
development of
goitres.21 The
prevalence of goitres varies widely but may be as high as 85% in children in
some areas.22
Recent improvements in iodine intake have led to reductions in goitre
prevalence (Table 2) but
goitres prevail in communities who continue to rely exclusively on home grown
crops for nutrition. Children, females and pregnant women remain
disproportionately affected. Recent studies have shown total goitre rates of
close to a 100% in pregnant women, even in areas within countries with iodine
sufficiency
status.13,14
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Endemic cretinism
The extreme form of iodine deficiency, endemic cretinism has been well
characterized in Central Africa, where up to 2-6% of the overall population
may be affected.31
The myxoedematous form of cretinism is highly prevalent in this population and
hypothyroidism is seen in as much as a quarter of children in endemic
areas.32 This
pattern contrasts with other parts of the world where the neurological
variety, characterized by mental deficiency, deaf mutism and spastic diplegia
prevails.33
However, gross neurological defects are also seen in African populations and
were described in 10% of patients with cretinism in the Kivu area of
Democratic Republic of
Congo.33 Less
obvious disorders of cognition and intellect in infancy and childhood are
likely to be even more widespread and to potentially constitute a greater
burden on the economic output of affected communities. An analysis in Sierra
Leone estimates that the future five-year productivity losses in the country,
resulting from intellectual impairment associated with iodine deficiency would
be in excess of US$42.5
million.34
Iodine-induced thyrotoxicosis
Thyrotoxicosis may occur in chronically iodine deficient individuals who
are exposed to sharp increases in iodine
intake.35 It is
more likely in older patients with longstanding thyroid nodules. Toxic change
in such nodules may be accompanied by biochemical or clinically overt
thyrotoxicosis. Death from cardiac failure and arrhythmias may
occur.35 Between
1991 and 1995, a sudden rise in the incidence of thyrotoxicosis was noted by
physicians in Harare, Zimbabwe. The majority of these patients had toxic
nodular goitres and 14 deaths were
recorded.36
Likewise, biochemical thyrotoxicosis was diagnosed in 14 of 191 patients with
goitres in Kivu, a previously iodine deficient area of Northern
Zaire.37 These
incidents followed the introduction of iodized salt to both countries. A
multicentre study subsequently conducted by a team of seasoned international
researchers established that the problem was likely transient and not
widespread on the
continent.38
Accordingly, recommended levels of salt iodization in the region have been
reduced to 20-40
ppm.38
Graves' disease
Graves' disease is the commonest cause of hyperthyroidism in iodine-replete
parts of world.1 The
average annual incidence of Graves' disease in Whickham, UK, is approximately
80/100 000 for
females.39 In
Johannesburg, the incidence is about 10 times less (8.75/100 000 per
year).40 Graves'
disease was believed to be rare in Africa, based on the early experience of
physicians in the
region.41 However,
it is now more frequently reported across the continent. In South Africa, a
60% rise in its incidence was observed over an 11-year
period.40 This was
most apparent in iodine sufficient urban dwellers, a significant proportion of
who were recent migrants from iodine deficient
areas.40 The
clinical presentation of Graves' disease appears no different from elsewhere;
females are more commonly
affected,40
ophthalmopathy is
common,42 and
thyroid-stimulating hormone-receptor antibodies are present in over 80% of
patients.43
However, as a result of late presentations, a disproportionate amount of
cardiac complications are
seen.44 The
approach to management is dictated by existing local facilities. Radioiodine
is not widely available so the options vary between medical and surgical
treatments. Surgery is sometimes the more practical alternative due to the
unaffordable cost and lengthy hospital follow up of medical treatment.
Autoimmune hypothyroidism
The spectrum of autoimmune hypothyroidism includes Hashimoto's thyroiditis,
primary myxoedema and postpartum thyroiditis. These conditions form the bulk
of the thyroid physician's workload in iodine sufficient
countries.1 The
reverse is seen in Africa where autoimmune hypothyroidism is rarely
encountered, either by
clinicians18,19
or
histopathologists.17
In striking contrast to Graves' disease, the incidence of autoimmune
hypothyroidism in African blacks does not appear to have been amplified by
improvements in iodine intake. One possible explanation for this discrepancy
may lie with recognition. Unlike Graves' disease, autoimmune hypothyroidism is
particularly difficult to diagnose on clinical grounds alone and, in the
absence of sensitive laboratory facilities, it is not improbable that cases
will be missed. However, it is likely that genetic factors also contribute to
the relative rarity of thyroid autoimmunity in Africans. Black Africans have
lower levels of thyroid antibodies than Africans of European or Asian
descent.40
Interestingly, induction of thyroid antibodies following iodine
supplementation has been reported in
Europe45 and
Asia,46 but this
has not been the case in
Africa.47
Prospective population-based studies are needed to determine the true
occurrence of autoimmune hypothyroidism in Africans.
Thyroid malignancy
The histology of thyroid cancers in a population is dependent on the
ambient iodine intake. A high proportion of aggressive follicular and
anaplastic tumours are seen in iodine deficiency while the more benign
papillary type is common in iodine-rich
populations.48
Follicular carcinoma is the predominant histological variety in Africa
(Table 3). This pattern has
prevailed over the decades, suggesting persisting iodine deficiency. However,
the incidence of anaplastic carcinoma appears to be falling and other reports
suggest a relative rise in papillary tumours, implying improved iodination on
the other hand (Table 3). This
mixed picture may thus reflect a transitory period in iodine nutrition coupled
with regional variations in iodine status. Nonetheless, it is doubtful if
reversals in cancer histology will necessarily translate to improvements in
prognosis in Africa. Advanced disease at presentation and poor follow up are
common in Africans with limited access to health
services.52,55
A study in Algeria showed that survival rates in patients with differentiated
thyroid carcinoma were related to the level of health service provision rather
than the effects of iodine status on cancer
histology.51
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FUTURE CHALLENGES
If the present momentum is anything to go by, then iodine sufficiency could be attained in most parts of the continent within the next decade. However, maintenance of these gains will prove challenging in an African climate marred by wars, famine and political instability. Experience from iodine sufficient countries has shown that interruption of iodine replacement is rapidly followed by relapse of iodine deficiency.56 Sustained political will and robust legislative structures will be required to ensure the continued availability of iodized salt. With improvements in iodine nutrition, the pattern of thyroid disorders is expected to continue evolving. It remains to be established if autoimmune hypothyroidism will emerge in the stead of endemic goitres as has happened in parts of Europe. However, the primary goal of salt iodination remains the prevention of brain damage due to iodine deficiency; therefore the risks associated with iodine replacement in the African population are clearly outweighed by its benefits and should not deter continued iodine prophylaxis. Nonetheless, the possibility of side effects calls for increased vigilance in monitoring the effects of iodination.
CONCLUSION
Despite incomplete biomedical information, it is apparent that the pattern of thyroid disorders in Africa is evolving with increasing iodine sufficiency. Total goitre prevalence has fallen in populations with salt iodination programmes. However, pockets of goitres persist, and more subtle effects of iodine deficiency on cognition and intellect in childhood are likely to be still widespread. The incidence of Graves' disease is rising, particularly in African populations exposed to sharp increases in iodine consumption. In addition, transient iodide-induced thyrotoxicosis was potentially fatal in two African countries. While consolidating the present gains, salt iodination programmes must now target poor rural populations, and vulnerable sub-groups including pregnant women and children who remain at significant risk of iodine deficiency. On the other hand, researchers and clinicians in the region will need to be adequately resourced to identify and manage emerging thyroid disorders.
Footnotes
Competing interests None declared.
REFERENCES
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  M. B. Zimmermann Iodine Deficiency Endocr. Rev., June 1, 2009; 30(4): 376 - 408. [Abstract] [Full Text] [PDF]
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Moderate deficiency: 20-49;
mild deficiency 50-99;
optimal: 100-199;
more than adequate:
200-299; 
excess: >299;
status uncertain