besides its classical role in calcium and bone homeostasis , vitamin d is considered a potent immunomodulator that can affect the pathogenesis of several autoimmune diseases .
our aim is to evaluate the effect of vitamin d correction to a patient with new onset graves disease ( gd ) with an underlying vitamin d deficiency .
we describe the effect of vitamin d3 on untreated graves disease with vitamin d deficiency .
a healthy saudi woman in her 40s sought consultation with a three - month history of palpitation .
she denied any history of heat intolerance , weight loss , menstrual irregularity or sweating .
. physical examination revealed a mild diffusely enlarged and non - tender thyroid gland with no bruit .
the initial thyroid function test , which was done in an outside hospital , revealed a tsh , 0.01 miu / l ; ft4 , 22.5
vitamin d 25-oh level was done in our hospital and showed a result of 26.0 nmol / l with a tsh , 0.013 miu / l ; ft4 , 16.7
tc-99 m thyroid scintigraphy demonstrated an enlarged thyroid gland with increased radiotracer trapping and heterogeneous distribution .
the patient was given only oral cholecalciferol 4000 iu per day since november 2012 ( prescribed by an outside hospital ) then from may 2013 onwards she was given 50,000 iu per month .
follow - up laboratory exams revealed improved vitamin d levels as well as tsh and ft4 .
vitamin d deficiency may exacerbate the onset and/or development of gd and correction of the deficiency may be able to reverse it .
however , further prospective clinical studies will be needed to define the role of vitamin d treatment in gd .
more recently , vitamin d has been shown to be a modulator in both innate and adaptive immunity.1 there is a well - established link between vitamin d deficiency and various autoimmune diseases , including type 1 diabetes mellitus ( t1 dm ) , systemic lupus erythematosus ( sle ) , rheumatoid arthritis ( ra ) , inflammatory bowel disease ( ibd ) , and multiple sclerosis ( ms ) .
furthermore , it has been found that the supplementation of vitamin d can prevent the onset and/or development of different kinds of autoimmune disorders in human beings and animal models.2 in addition , it has been shown that the prevalence of vitamin d deficiency is common in patients with graves disease ( gd),3 and is associated with higher thyroid volume.4 in our case report , we evaluated the effect of vitamin d correction to a patient with new onset gd with an underlying vitamin d deficiency .
a healthy saudi woman in her 40s sought consultation with a 3 months history of palpitation .
she denied any history of heat intolerance , weight loss , menstrual irregularity , diarrhea , or sweating .
there was no personal or family history of thyroid disease and no specific medication history .
physical examination revealed a mild diffusely enlarged and non - tender thyroid gland with no bruit .
the initial thyroid function test , which was done in an outside hospital , revealed a tsh , 0.01 miu / l ; ft4 , 22.5
vitamin d 25-oh level was done in our hospital and showed a result of 26.0 nmol / l with a tsh , 0.013 miu / l ; ft4 , 16.7
anti - thyroid antibodies showed a tg , 17.1 iu / ml ; tpo , 0.19 iu / ml with a positive tsh receptor antibody .
tc-99 m thyroid scintigraphy demonstrated an enlarged thyroid gland with increased radiotracer trapping and heterogeneous distribution ( fig .
the patient was given only oral cholecalciferol 4000 iu per day since november 2012 ( took it from an outside hospital ) then from may 2013 onwards she was given 50,000 iu per month .
the serial thyroid function tests , vitamin d levels , and titer autoantibodies are summarized in table 1 .
follow - up laboratory exams revealed improved vitamin d levels as well as tsh and ft4 .
written informed consent was obtained from the patient for the publication of this case and accompanying images .
it has become apparent that multiple factors contribute to the etiology of gd , including genetic and environmental factors .
these activated t cells in turn increase the secretion of thyroid - specific autoantibodies from b cells .
the prevalence of vitamin d deficiency was reported to be common in patients with gd.3 whether vitamin d deficiency has a causal relationship with gd remains a controversial issue .
misharin et al.5 observed that vitamin d deficiency was found to modulate graves hyperthyroidism induced in balb / c mice by thyrotropin receptor immunization . in this study ,
balb / c mice on a vitamin d deficient diet were more likely to develop persistent hyperthyroidism than other mice receiving adequate vitamin d supply . in another study ,
combination treatment with methimazole and vitamin d3 ( 1,25 ( oh)2d ) in patients with gd has more rapid euthyroidism achievement compared with patients receiving methimazole alone.6 in addition , vitamin d supplementation has been shown to inhibit inflammatory responses in human thyroid and t cells.7 interestingly , vitamin d deficiency is found to be associated with higher thyroid volume in patients with newly onset gd.4 it has been recently discovered that vitamin d - receptor gene and vitamin d - binding protein gene polymorphisms are associated with gd.8,9
our present case supports the current literature and strongly suggests that vitamin d deficiency may exacerbate the onset and/or development of gd and correction of which may be able to reverse it .
however , further prospective clinical studies will be needed to define the role of vitamin d treatment in gd .
 objectivebesides its classical role in calcium and bone homeostasis , vitamin d is considered a potent immunomodulator that can affect the pathogenesis of several autoimmune diseases . 
 our aim is to evaluate the effect of vitamin d correction to a patient with new onset graves disease ( gd ) with an underlying vitamin d deficiency.methodwe describe the effect of vitamin d3 on untreated graves disease with vitamin d deficiency.resultsa healthy saudi woman in her 40s sought consultation with a three - month history of palpitation . 
 she denied any history of heat intolerance , weight loss , menstrual irregularity or sweating . 
 she has a history of chronic muscle aches and pains . physical examination revealed a mild diffusely enlarged and non - tender thyroid gland with no bruit . 
 she had no signs of graves ophthalmopathy . in laboratory examinations , 
 the initial thyroid function test , which was done in an outside hospital , revealed a tsh , 0.01 miu / l ; ft4 , 22.5 
 pmol / l and ft3 , 6.5 pmol / l . 
 vitamin d 25-oh level was done in our hospital and showed a result of 26.0 nmol / l with a tsh , 0.013 miu / l ; ft4 , 16.7 
 pmol / l ; and ft3 , 3.8 pmol / l . 
 tsh receptor antibody was positive . 
 tc-99 m thyroid scintigraphy demonstrated an enlarged thyroid gland with increased radiotracer trapping and heterogeneous distribution . 
 the patient was given only oral cholecalciferol 4000 iu per day since november 2012 ( prescribed by an outside hospital ) then from may 2013 onwards she was given 50,000 iu per month . 
 follow - up laboratory exams revealed improved vitamin d levels as well as tsh and ft4 . 
 she eventually improved both clinically and biochemically with a satisfactory outcome.conclusionvitamin d deficiency may exacerbate the onset and/or development of gd and correction of the deficiency may be able to reverse it . 
 however , further prospective clinical studies will be needed to define the role of vitamin d treatment in gd . 