diabetes control in thyroid disease

148Diabetes Spectrum Volume 19, Number 3, 2006

In Brief

Diabetes Control in Thyroid Disease

Thyroid disease is a pathological statethat can adversely affect diabetes con-trol and has the potential to negative-ly affect patient outcomes. Thyroiddisease is found commonly in mostforms of diabetes and is associatedwith advanced age, particularly intype 2 diabetes and underlyingautoimmune disease in type 1 dia-betes. This article defines the preva-lence of thyroid disease in diabetes,discusses normal physiology andscreening recommendations for thy-roid disease, and elucidates throughcase studies the assessment, diagnosis,and clinical management of thyroiddisease and its impact on diabetes.

Thyroid Disease PrevalenceThe prevalence of thyroid disease inthe general population is estimated tobe 6.6%, with hypothyroidism themost common malady.1 Participantsattending a health fair in Colorado (n= 25,862) were screened for thyroiddisease, using thyroid-stimulating hor-mone (TSH) and thyroxine (T4) mea-surements. Of the participants, 9.5%were found to have an elevated TSHlevel. Also, 6% of study participantswere diagnosed with thyroid diseasebefore the screening. However, 40%of those already diagnosed had elevat-ed TSH levels, indicating inadequatetreatment. In the undiagnosed popula-tion with TSH elevations, 9.9% werefound to have an unrecognized thyroid

abnormality. Several studies, includingthe Colorado study, have documenteda higher prevalence of thyroid diseasein women, with prevalence rates rang-ing from 4 to 21%, whereas the rate inmen ranges from 2.8 to 16%.1

Thyroid disease increases with age. Inthe Colorado study, the 18-year-oldshad a prevalence rate of 3.5% com-pared with a rate of 18.5% for those ≥ 65 years of age.

The prevalence of thyroid disease indiabetes has been estimated at 10.8%,2

with the majority of cases occurring ashypothyroidism (~ 30%) and subclini-cal hypothyroidism (~ 50%).2 Hyper-thyroidism accounts for 12%, andpostpartum thyroiditis accounts for11%.2 Of the female patients withtype 1 diabetes, 30% have thyroid dis-ease, with a rate of postpartum thy-roid disease three times that of thenormal population. Ostensibly, this isbecause of the higher prevalence ofthyroid disease in women, as well asthe link to autoimmune disease. Onceone autoimmune disease occurs, it isnot uncommon for a different autoim-mune disease to be present.

There are also reports that theprevalence of thyroid disease in type 2diabetes is higher than in the generalpopulation.3 Whereas the FremantleDiabetes Study found a 8.6% preva-lence of subclinical hypothyroidism inwomen with type 2 diabetes inAustralia,4 a study of the prevalence

Jennal L. Johnson, MS, RNC, FNP,BC-ADM, CDE

Thyroid disease is commonly found in most types of diabetes. This articledefines the prevalence of thyroid disease in diabetes and elucidates throughcase studies the assessment, diagnosis, and clinical management of thyroiddisease in diabetes.


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of autoimmune thyroid disease in type2 diabetes in Jordan reported an over-all prevalence rate of 12.5%, withsubclinical hypothyroidism at 5%.5

Thyroid Anatomy and Physiology A thorough understanding of theanatomy and physiology of the thy-roid gland allows diabetes cliniciansto understand the rationale for specif-ic assessments and to rapidly identifythyroid abnormalities. The thyroid isthe largest endocrine gland, weighing~ 20 g. It is shaped like a butterfly orshield and is derived from the base ofthe tongue.6 The thyroid gland hassignificant blood flow; when com-pared by tissue weight, it has moreblood flow than the kidney.7

Understanding the Role of theThyroidThyroid physiology is based on a reg-ulatory feedback system typicallyfound in endocrine systems.7 Thehypothalamus secretes thyrotropin-releasing hormone (TRH), whichstimulates the anterior pituitary glandto secrete thyrotropin or TSH. TSHincreases iodide uptake and oxidationthat leads to organification and cou-pling, which are necessary steps toproduce the thyroid hormones T4 andtriiodothyronine (T3). TSH also stim-ulates growth and vasculature of thethyroid that could potentially lead toa goiter if excessive. Of the thyroidhormone secreted, 90% is T4, and9% is T3.7 T3 derives from deiodina-tion of T4; therefore, 80% of circulat-ing T3 is from T4.7 During seriousdebilitating illness or starvation, T3production is reduced, possibly as acontrol mechanism to reduce themetabolic rate, which may be usefulduring recovery.

Thyroid hormones enter cells bydiffusion and carrier-mediated trans-port and bind to nuclear TSH recep-tors. TSH receptors are found on thesurface of the follicular cells withinthe thyroid as well as on adipocytes,lymphocytes, fibroblasts, and gonads.This is important because TSH stimu-lates adipocyte lipolysis. T4, and to asmall degree T3, circulating in theserum inhibits secretion of TSH andTRH, thereby completing the feed-back cycle. Transport and binding ofthyroid hormone is carried out by thy-roxine-binding globulin (TBG).Normal thyroid hormone synthesisrequires an adequate iodine intake of150 �g in adolescents and adults, 200in pregnancy, and 90–120 in

children.8 Iodine deficiency leads todecreased thyroid hormone synthesis,which in turn leads to increased TSHsecretion and increased gland growthor goiter. Gland size, however, doesnot indicate thyroid function.Therefore, a goiter can be present inhypothyroidism, hyperthyroidism, oreuthyroidism.

The thyroid gland is divided intolobules that have a distinct vascularsupply. Each lobule has 20–40 follicles,and follicles are the basic functioningunit of the thyroid gland. The lumen ofeach follicle is filled with viscous col-loid identified as the glycoprotein thy-roglobulin. Thyroglobulin contains themolecular structure of thyroid hor-mones and is the precursor of all thy-roid hormones.9 Thyroperoxidase(TPO) is a membrane-bound enzymefound on the surface of the follicularcell. It is necessary to catalyze iodideinto an active intermediate, an impor-tant step in thyroid hormonesynthesis.7 Thyroglobulin and TPOantibodies are useful thyroid laborato-ry test evaluations that can identifypotential harm to the synthesis of thy-roid hormone from an autoimmuneprocess.

The follicle is surrounded by a sin-gle layer of epithelial cells andenclosed by a basement membrane.The basement membrane has parofol-licular cells that have contact withfollicle cells and produce calcitonin.7

Iodine is taken up as inorganic iodidevia the “iodide trap” in the follicularcell. This aspect of thyroid physiologyis important because the thyroid isthe only gland that takes up iodine,which allows for scanning and treat-ment of the thyroid gland usingradioiodine.

After thyroid hormones are synthe-sized and secreted into the serum, theyare bound to serum carrier proteinsTBG, thyroxine-binding prealbumin,and albumin. The affinity of the T3receptor is much higher (~ 10 times)than that of T4.7 The majority of T4(99.96%) and T3 (99.6%) are bound,and binding is affected by certainphysiological or pathological statesthat increase or decrease TBG.Estrogen increases found in pregnan-cy, estrogen replacement, and birthcontrol pills increase TBG, whereasandrogens, glucocorticoids, and mal-nutrition decrease TBG.7

Free or unbound thyroid hormoneenters cells and exerts a biologicaleffect. The bound hormone serves as areservoir that buffers short-term alter-

ations in thyroid hormone secretionrates, facilitating a more steady state.Standard laboratory assays measurethe total free and bound thyroid hor-mone levels of T4 and T3 unless freehormone levels are specificallyrequested. Free hormone levels arehelpful in evaluating thyroid functionin states of decreased or increasedTBG.

Thyroid hormone exerts influenceson numerous body systems, includinggrowth and development, muscularfunction, sympathetic nervous systemfunction, cardiovascular system, andcarbohydrate metabolism. For exam-ple, thyroid hormone is necessary formaturation and differentiation duringdevelopment. Children with hypothy-roidism show bone maturation delaysas well as delayed or absent puberty.Children with thyroid deficiency havestunted growth because inadequatethyroid hormone secretion lowersgrowth hormone. Thyroid hormonealso plays an important role in lungmaturation.7

Thyroid hormones are necessaryfor normal fetal and neonatal braindevelopment by regulating neuronalproliferation and differentiation,myelinogenesis, neuronal outgrowth,and synapse formation. The criticaltime for brain development starts inutero and continues to age 2.Deficiency of thyroid hormone duringthis important time can lead to struc-tural and physiological impairmentresulting in brain damage or severeneurological impairment.7 Thisprocess cannot be reversed once com-pleted, which is the reasoning behinduniversal screening for congenitalhypothyroidism.

Hypothyroidism in adults can leadto dullness, decreased reflexes, lethar-gy, delayed cognitive function, andexcessive sleep, as well as psychologi-cal disturbances. Correcting theunderlying thyroid abnormality canreverse impaired neurological func-tioning in adults. Hyperthyroidism inadults can also result in insomnia,decreased reflex time or hypereflexia,restlessness, excitability, and lack offocus and concentration.7

Thyroid hormones have metabolicfunctions that serve to control thebasic hormone metabolic rate. Basichormone metabolic rate is decreasedin hypothyroidism and increased inhyperthyroidism. Thyroid hormonesstimulate most metabolic pathwaysand are either anabolic and catabolic.In hypothyroidism, protein synthesis


is decreased, as is protein degradation,which results in decreased percentageof protein body weight. Alternatively,hyperthyroidism increases proteinsynthesis and degradation, resulting inwasting.7 Thyroid hormones arelipolytic as well as lipogenic.However, there is usually more degra-dation compared to synthesis. Inhypothyroidism, there is decreased fatsynthesis and degradation, leading toincreased body fat and elevated lipids.In hyperthyroidism there is increasedfat synthesis and degradation, result-ing in decreased lipids.

Thyroid hormones exert a directeffect on muscles. In hypothyroidism,this can lead to myopathies, musclestiffness with associated discomfortand slowness of movements,increased muscle mass (mechanismunknown), and impaired muscleglycogenolysis, leading to glycogenaccumulation.7 In hyperthyroidism,myalgias can also occur as well asmuscle weakness, muscle wasting,and muscle fatigue, particularly in theproximal muscles in the legs, makingit difficult to climb.

Within the cardiovascular system,thyroid hormones increase heart rate,myocardial contractility, and cardiacoutput by increased sinus node stimu-lation and direct effects on themyocardium.7 In hyperthyroidism,excess thyroid hormone producesmyocardial hypertrophy. Thyroid hor-mones act as positive inotropes aswell as positive chronotropes indepen-dent of circulating catecholamines.Resultant electrocardiogram changesshow left ventricular hypertrophy.Stoke volume, heart rate, and meansystolic ejection velocity increase withdecreased peripheral resistancebecause of increased production ofvasodilators, with evidence of warm,moist skin and increased pulse pres-sure.

The opposite occurs in hypothy-roidism. Peripheral resistance is nor-mal or slightly increased by decreasedsecretion of vasodilators, resulting incutaneous vasoconstriction evidencedby cold, dry skin. The ECG inhypothyroidism shows inverted Twaves and low P, QRS, and T waveamplitudes. Excess thyroid hormoneresembles increased sympathetic ner-vous system activity by increasedbeta-adrenergic stimulation, leadingto increased heart rate, tremors, andexcessive sweating.7 This stimulationcould interfere with diabetic patients’ability to recognize hypoglycemia.

Thyroid Hormone Effects on DiabetesThe effect on carbohydrate metabo-lism can potentially lead to disruptionsin diabetes control. Although the glu-cose level does not always change,there can be an abnormal response toglucose tolerance testing in hyperthy-roidism because glucose rises fasterthan normal.7 Additionally, excessivethyroid hormones increase the rate ofdigestive tract absorption and thyroidhormone levels and therefore increaseinsulin resistance and insulin degrada-tion.

In hyperthyroidism, glycogen syn-thesis and degradation increase, lead-ing to decreased glycogen levels.3

Glucose absorption is increased, aswell as utilization and production.Peripheral tissues have increasedrates of glucose uptake that can leadto the aforementioned exaggeratedglucose peak during a timed glucosetest. Insulin requirements areincreased, and, if not addressed ade-quately, control can decompensate,leading to diabetic ketoacidosis.Additionally, in patients with unde-tected diabetes, hyperthyroidism canunmask diabetes because glucose lev-els can be abnormally elevatedbecause of increased insulin resis-tance.3 Increased dosages of diabetesmedications may be necessary inthose already treated, until thyroidfunction is stabilized and resultantglucose stabilization occurs.

In hypothyroidism, liver secretionof glycogen decreases, but so doesdegradation, leading to increased lev-els of glycogen. Absorption of glucosefrom the gastrointestinal tract isslowed, and glucose utilization isslowed in the peripheral tissues. Theavailability of gluconeogenic substrateis decreased. Additionally, the insulinhalf-life is prolonged, insulin levels arelower, and insulin secretion isreduced, which may lead to reducedinsulin requirements. If exogenousinsulin is not decreased, hypoglycemiamay occur. It is likely that glucose lev-els will stabilize during hypothy-roidism treatment. But when thyroidfunction is normalized, this may leadto higher blood glucose levels andadverse effects on glycemic control.

Screening RecommendationsThe American Thyroid Association(ATA) recommends testing thyroidfunction in all adults beginning at age35 and reassessing thyroid functionevery 5 years. More frequent testing isindicated in high-risk or symptomatic

individuals. The American Assoc-iation of Clinical Endocrino-logists(AACE) recommends a screening TSHin women of childbearing age beforepregnancy or during the firsttrimester.10

In 2005 AACE, ATA, and theEndocrine Society (TES) published aconsensus statement regarding screen-ing for subclinical thyroid dysfunc-tion.11 The authors of the consensusstatement recommended the measure-ment of anti-TPO antibodies in evalu-ating patients with subclinicalhypothyroidism because those whoare antibody positive have a higherrisk of developing overt thyroid dis-ease.11 For patients with type 1 dia-betes, it is recommended to test foranti-TPO antibodies at diagnosis. Ifanti-TPO antibodies are present, it isrecommended that clinicians performannual TSH screening. In type 2 dia-betes, it is recommended that clini-cians measure TSH at diagnosis ofdiabetes and every 5 years thereafter.2

Case Studies

Case Presentation 1M.J. is a 70-year-old woman withtype 2 diabetes. She is evaluated in anoutpatient endocrine clinic. She wasdiagnosed with diabetes recently andhas not completed a comprehensivediabetes education program. Her fast-ing blood glucose levels are 110–115mg/dl, and she does not check 2-hourpostmeal blood glucose readings. Shehas no known macrovascular ormicrovascular complications.

She comes to clinic with complaintsof fatigue and weight gain. She is tak-ing glimiperide, 4-mg tablet twicedaily. It is interesting to note that theinitial signs and symptoms presentedand the routine screening results areconsistent with the metabolic syn-drome or diabetes. Unless the clinicianscreened for thyroid disease, theabnormalities could be attributed tothe usual course of type 2 diabetes.

M.J.’s physical exam is normalexcept that she has a 45-g goiter. Herlaboratory results are:• TSH: 5.6 IU/ml (normal 0.29–3.0)• T4: 5.5 ug/dl (normal: 4.5–12.5)• Positive for anti-TPO antibodies

(normal: negative)• Total cholesterol: 220 mg/dl (nor-

mal 130–200)• HDL cholesterol: 34 mg/dl (normal

30–80)• Triglycerides: 158 mg/dl (normal

35–160)


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• LDL cholesterol: 140 mg/dl (nor-mal ≤ 70)

• Hemoglobin A1c (A1C): 6.8% (nor-mal 4.0–6.3)M.J. has dyslipidemia and an ele-

vated glucose average, as evidenced byher A1C elevation. She has a goiter,TSH elevation with a normal T4, andshe tested positive for anti-TPO anti-bodies, indicating subclinical hypothy-roidism.

Treatment goals include initiatinglevothyroxine therapy, completingdiabetes education, and improvingglycemic control. The lipid levels willlikely decrease with levothyroxinetherapy. However, because diabetes isa risk equivalent for cardiovasculardisease (CVD), a cholesterol-loweringagent such as a statin is also indicated.The statin can be initiated beforedetermining the effect of thyroid hor-mone replacement on her lipid levelsbecause the purpose of the statin iscardiovascular prevention.

DiscussionThe Rotterdam Study (n = 1,149)showed that subclinical hypothy-roidism may be a risk factor forCVD.12 Participants were female and > 55 years of age. Subclinical hypothy-roidism was defined as a TSH > 4.0mU/L with a normal free T4 level.Subclinical hypothyroidism was astrong risk factor for atherosclerosisand myocardial infarction (MI) inelderly women.12 Subclinical hypothy-roidism was found to be a greater riskfor MI in postmenopausal womenthan hyperlipidemia, diabetes, previ-ous smoking, or hypertension.Additional studies have looked at thebenefits of treating subclinicalhypothyroidism, and the resultsshowed that treatment to lower TSHresulted in lower total and LDL cho-lesterol levels.13 Alternatively, long-term data from the Whickham cohortpublished in 1996 found no higherrate of death from CVD in subjectswith subclinical hypothyroidism com-pared with euthyroid subjects, con-tributing to the controversy surround-ing treatment of subclinical hypothy-roidism.14

The National Health and NutritionExamination Survey evaluated men,women, and children from 1988 to1994 and measured TSH and antithy-roid antibody levels to evaluate thestatus of thyroid functioning, usingpopulation data.15 The study foundthat the prevalence of antithyroidantibodies increases with age, is high-

er for female subjects, and is higher inwhites and Mexican Americans thanin African Americans.15 Anti-TPOantibodies may be positive before clin-ical disease occurs and therefore maybe an indicator of early thyroid dis-ease. Although still controversial,treatment of subclinical hypothy-roidism is indicated in patients whoare elderly, have elevated cholesterol,have TSH > 10 mU/l, and have othersymptoms of hypothyroidism.16

The goal of thyroid replacementtherapy is to render the patienteuthyroid without over- or underre-placement, with a TSH goal between0.3 and 3.0 IU/ml unless thyroid can-cer is present.17 Levothyroxine is anarrow therapeutic index drug,which means that there is a “narrowtoxic to theurapeutic ratio with sig-nificant clinical consequences ofexcessive or inadequate treatment”that could impact bone, pregnancy,or heart.18 Within the past severalyears, several generic levothyroxineproducts have come to the market,and the U.S. Food and DrugAdministration (FDA) has deemedthem to be bioequivalent to somebranded preparations. The majorthyroid organizations (AACE, TES,and the ATA), have voiced concernabout the methodology the FDA usedto determine bioequivalence and rec-ommended that levothyroxine not besubstituted for other preparations.19

The organizations’ joint positionstatement recommends that patientsbe maintained on the same brand oflevothyroxine that they have been tak-ing and, in the event they are switchedto another brand or generic product,measure a serum TSH in 6 weeks andmake adjustments as indicated.Patients should be educated aboutusing the same brand of medicationduring treatment and, when pickingup medications at the pharmacy, betold to indicate that the brand of thy-roid medication should not bechanged without first checking withtheir provider.

The initial dose of levothyroxinetherapy is determined by the underly-ing cause of the disease, severity ofdysfunction, and health and age of theperson being treated. This is highlyindividualized; however, the adage inthe elderly or those with underlyingCVD is to start low (typically 25 �gdaily) and go slow with drugtitration.2

The woman in this case study islikely to see improvement in her

symptoms within 6–8 weeks after ini-tiating levothyroxine therapy. It isimportant that she closely monitor herblood glucose levels because improvedthyroid function may increase her glu-cose, leading to more hyperglycemia.She may need additional diabetesmedication intervention.

Case Presentation 2L.M. is a 38-year-old man with type 1diabetes who uses an insulin pump.He presents with tachycardia, short-ness of breath, decreased exercise tol-erance, fatigue, muscle weakness,double vision, blisters on lower legs,weight loss, hyperglycemia, moodswings, anxiety/nervousness, heatintolerance, and increased frequencyof bowel movements. Physical exami-nation reveals:• Skin: moist and warm, blisters with

an orange peel appearance on bothlower legs

• Head/eyes/ears/nose/throat: bilater-al proptosis, stare, lid lag, scleralinjection, double vision with eyemotility, thyroid 60+ g and firm

• Heart: tachycardia, heart rate 106bpm, regular rhythm without mur-mur

• Lungs: clear to ausculatation andpercussion

• Lower extremities: pretibial myx-emdema in lower legs

• Neurological exam: hyperreflexia

Laboratory results included:• T4: 22.0 ug/dl (normal 4.5–12.5)• TSH: < 0.01 IU/ml (normal 0.29–

3.0)• Thyroid-stimulating immunglobu-

lin: 300% (normal < 130%)• Blood glucose: 345 mg/dl (normal

< 100)• A1C: 9.2% (normal 4.0–6.3)Imaging revealed a 77% uptake in 4hours (normal 4–12%) and bone den-sity T scores of �1.1 for spine and�2.1 for hip.

Treatment strategies include �-blocker therapy, an increase ininsulin, and oral steroids for the eyes,as well as discussion of options—including radioiodine therapy,surgery, or anti-thyroid therapy—andprovision of education.

DiscussionThere is an autoimmune link (HLAmarkers) between type 1 diabetes andGraves’ disease. The prevalence ofGraves’ disease with type 1 diabeteshas been reported to be 2.7% in menand 2–19% in women.20 Patients


should be monitored closely to evalu-ate their response to thyroid therapyas well as their diabetes control. AsGraves’ disease stabilizes, insulinrequirements may decrease. It may bebeneficial to place the patient in thiscase study on a glucose sensor becausethe glucose levels will be elevated ini-tially, and higher doses of insulin willbe needed. Once successful treatmentis completed, close monitoring willalso be necessary to avoid hypo-glycemia when insulin requirementsdecrease.

Case Presentation 3R.D. is an 18-year-old woman withtype 2 diabetes diagnosed 5 years ago.Since her diagnosis, she has lost 50 lbthrough a diet and exercise program.She is normoglycemic. Coexistinghealth problems include polycysticovarian disease and vitiligo. Familyhistory is significant for thyroid dis-ease. She was taking metformin untila recent positive pregnancy test.

The patient complains of fatigue,nausea, constipation, and feeling cold.Her weight loss plateaued severalmonths ago, and now her weight isslowly increasing.

Physical examination is unremark-able except a 30-g thyroid.Laboratory results include:• A1C: 6.2% (normal <4.0-6.3)• Free T4: 0.6 ug/dl (normal 0.9–1.9)• TSH: 13.4 IU/ml (normal 0.29–3.0)• Positive for anti-TPO antibody

(normal: negative)

A referral to a dietitian is recom-mended to evaluate adequate calorieintake for diabetes, pregnancy, andappropriate weight gain. Swift initia-tion of levothyroxine therapy is indi-cated because the patient is hypothy-roid and pregnant. Initial symptomsshould improve within 4–6 weeksunless they are secondary to the preg-nancy rather than hypothyroidism.

The 1990 Haddow PregnancyStudy (n = 92) showed that euthyroidchildren of hypothyroid mothers hadadverse results and hypothyroid chil-dren from hypothyroid mothers hadfetal brain and IQ abnormalities.21

Euthyroid women with positiveantithyroid antibodies had higherrates of miscarriage, women withhigher TSH levels had a more thanthreefold increase in risk of very pre-term delivery, and those with positiveantithyroid antibodies had a twofoldincrease in preterm delivery. The rateof fetal death was 3.8% in women

with TSH ≥ 6 mU/l and 8.1% inwomen with TSH ≥ 10 mU/l com-pared with 0.9% in women with TSH < 6 mU/l.21 In the first trimester, preg-nant women are the sole source ofthyroid hormones for their developingfetuses.

It is important to screen women ofchildbearing age and those in the firsttrimester of pregnancy for hypothy-roidism to optimize thyroid function.History of another autoimmune disor-der or a family history of thyroid dis-ease increases the possibility ofhypothyroidism, which underlines theneed for screening. For patients newlydiagnosed with thyroid disease,levothyroxine therapy should be initiat-ed as soon as possible and at a dose asclose as possible to the anticipatedrequirement. Dosage increases may beseen as high as 50% because of increas-es in thyroid hormone binding globulinin women already diagnosed with thy-roid disease before pregnancy.22

Additional considerations includethe effects of diabetes on pregnancy.In early pregnancy, patients with dia-betes can be affected by pregnancy-related hormones that cause increasedinsulin secretion, decreased insulinrequirements, and decreased glucoseproduced by the liver, which can leadto hypoglycemia.23 During the thirdtrimester, the opposite occurs.Estrogen and cortisol can cause signif-icant insulin resistance, thereforepotentially causing hyperglycemia.Close monitoring of blood glucoseduring pregnancy allows for medica-tion, diet, and exercise alterations tooptimize diabetes control while nor-malizing thyroid function.

SummaryThe prevalence of thyroid disease ishigher in diabetes because of theincreased age of diabetic patients aswell as an autoimmune link. Untreat-ed or inadequately treated thyroiddisease can negatively impact dia-betes control. Pregnancy is a chal-lenging state associated with diabetesand can be complicated by the effectsof untreated or undertreated thyroiddisease.

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Williams JR, Knight GJ, Gagnon J, O’Heir CE,Mitchell ML, Hermos RJ, Waisbren SE, Faix JD,Klein RZ: Maternal thyroid deficiency duringpregnancy and subsequent neuropsychologicaldevelopment of the child. N Engl J Med341:549–555:1999

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requirement in the late first trimester of diabeticpregnancy. Diabetes Care 24:1130–1136:2001

Jennal L. Johnson, MS, RNC, FNP,BC-ADM, CDE, is an endocrinologynurse practitioner at EndocrinologyAssociates in Phoenix, Ariz.

Note of disclosure: Ms. Johnson hasreceived honoraria for speakingengagements from AbbottLaboratories, which manufacturesproducts for the treatment of thyroiddisease.

diabetes control in thyroid disease

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