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Graves’ Thyrotoxicosis Leading to Adrenal Decompensation and Hyperandrogenemia in a Pediatric Patient with Salt-Wasting Congenital Adrenal Hyperplasia

Introduction. Thyroid hormone is known to accelerate glucocorticoid turnover. In a thyrotoxic state, individuals with adrenal insufficiency are unable to increase endogenous cortisol production to compensate for increased turnover, placing them at risk for symptoms of glucocorticoid deficiency and adrenal crisis. In patients with salt-wasting congenital adrenal hyperplasia (SW-CAH), hyperandrogenemia is a measurable reflection of relative glucocorticoid insufficiency. Case Presentation. A 12-year-old girl with SW-CAH reported 3 recent episodes of vomiting without diarrhea, and accompanying tachycardia, responsive to stress dose steroids. In the previous 9 months, she unintentionally lost 2.6 kg. She had tachycardia and new thyromegaly. Labs showed suppressed TSH, elevated free T4 and total T3, and elevated thyroid stimulating immunoglobulin (TSI) consistent with Graves’ disease. Adrenal androgens were markedly elevated. Maintenance hydrocortisone dose was 25 mg/m2/day and was not changed. Methimazole was initiated. Four weeks later, free T4 and adrenal androgens normalized. She had no further vomiting episodes. Conclusions. Thyrotoxicosis must be included in the differential diagnosis of individuals with SW-CAH who present with episodes concerning for adrenal crises, escalating hydrocortisone requirements, and/or inadequate suppression of adrenal hormones.

1. Introduction

Salt-wasting congenital adrenal hyperplasia (SW-CAH) is the most common cause of primary adrenal insufficiency in pediatric patients, and in over 95% of cases it is caused by a mutation in the CYP21A2 gene, which causes a deficiency of the enzyme 21-hydroxylase [1]. Deficiency in 21-hydroxylase causes both gluco- and mineralocorticoid deficiency as well as hyperandrogenism due to the diversion of adrenal steroid precursors to adrenal androgens. Treatment consists of mineralocorticoid supplementation, as well as supraphysiologic glucocorticoid doses to suppress ACTH and minimize formation of adrenal androgens.

Management of glucocorticoid dosing in the growing child with SW-CAH is challenging. Typical dosing of hydrocortisone ranges from 10 to 15 mg/m2 daily in 3 divided doses [1]. Cortisol clearance increases in puberty, and glucocorticoid dose requirements often increase [2]. Glucocorticoid overtreatment can compromise height and result in symptoms of glucocorticoid excess. Undertreatment can also compromise height due to accelerated epiphyseal maturation and can result in bothersome virilization and prompt adrenal crises. Close monitoring of growth and biochemical measurement of androgens are essential for the care of the pediatric patient with SW-CAH.

In this case report, we describe a 12-year-old female with previously well-controlled SW-CAH, who presented to a pediatric emergency department with multiple episodes concerning for adrenal crises, responsive to stress dose steroids. She was found to have poorly suppressed androgens on supraphysiologic glucocorticoid doses. Ultimately, she was diagnosed with Graves’ disease.

2. Case Presentation

A 12-year-old female with SW-CAH presented to the pediatric endocrinology clinic for routine follow-up. She was diagnosed with SW-CAH in the newborn period after presenting with ambiguous genitalia and was treated with supraphysiologic hydrocortisone divided three times daily throughout her life (prepubertal dosing range 10-15 mg/m2/day, pubertal dosing range 15-25 mg/m2/day), as well as fludrocortisone (0.1 mg daily). She was monitored every 3-4 months with clinical examinations, growth parameters, and serum measurements of 17-hydroxyprogesterone (17-OHP), androstenedione, and testosterone (Esoterix Laboratory, Calabasas Hills, CA), which together guided her medication dosing. She had no evidence of glucocorticoid excess and her growth velocity was normal, without evidence of acceleration or suppression. She and her parents reported continued excellent compliance with her medication regimen.

At age 12 3/12 years, she reported 3 recent emergency department visits for persistent vomiting without diarrhea, abdominal pain, inability to tolerate oral steroids, and tachycardia. One of the episodes was accompanied by fever >39°C. There was no hypotension during any of these episodes, but heart rates were elevated ranging from 124 to 154 beats per minute. Sodium and potassium were normal: Na 137-140 meq/L (reference range, 133-143 meq/L) and K 3.6-4.1 meq/L (reference range 3.4-4.7 meq/L). Each episode was treated with normal saline boluses and intravenous stress dose steroids, and treatment led to immediate improvement in symptoms. She was discharged from the emergency department with recommendations for stress dose steroids by mouth. Over the prior 9 months, she had also unintentionally lost 2.6 kg and had an accelerated annualized growth velocity of 10.6 centimeters per year. BMI was 15.4 kg/m2 (Z-score -1.38). She denied any heat intolerance, jitteriness, palpitations, sweating, diarrhea, or vision complaints. While in clinic, her resting pulse was elevated at 136 beats per minute and blood pressure was normal. She was noted to have new symmetric thyromegaly without nodules. She had no lid lag or stare. She was in mid-puberty, with tanner 3 breasts. There was no family history of autoimmune disease or thyroid disease. Labs (Table 1) showed a suppressed TSH, and an elevated free T4 and Total T3. Thyroid antibodies were consistent with Graves’ disease, with a thyroid stimulating immunoglobulin (TSI) of 652% (reference range <140%). She had no prior thyroid studies for comparison. Adrenal androgens were markedly elevated with 17-OHP 11,600 ng/dl (reference range 11-155 ng/dl, target <1000 ng/dl in SW-CAH). At a clinic visit 15 weeks prior to this evaluation, her 17-OHP on the same dose of hydrocortisone (25 mg/m2/day) was improved at 639 ng/dl. She was initiated on methimazole 0.5 mg/kg/day. Her hydrocortisone dose was not changed and remained at 25 mg/m2/day. Four weeks later, repeat labs demonstrated normal free T4 with mildly suppressed TSH and normal total T3. 17-OHP was stable at 717 ng/dl (Figure 1). She had no further vomiting episodes after initiation of methimazole, and her tachycardia resolved.


Lab Value Reference Range 15 Weeks prior Diagnosis 4 weeks 12 weeks

TSH (uIU/ml) 0.35-5.5 0.019 0.021 4.345
Total T3 (ng/dl) 82-213 331 150 99
Free T4 (ng/dl) 0.8-1.8 2.82 1.42 0.89
17-Hydroxyprogesterone (ng/dl) 11-155 639 11,600 717 33
Androstenedione (ng/dl) 50-170 28 257 74 89
Testosterone (ng/dl) 15-35 8 67 18 15

Three months after treatment began for Graves’ disease, her TSH and free T4 were in the reference range, and methimazole was decreased to 0. 3 mg/kg/day. Repeat 17-OHP was low at 33 ng/dl, indicating suppression on the unchanged hydrocortisone dose of 25 mg/m2/day. Her hydrocortisone dose was decreased to 21 mg/m2/day.

3. Discussion

Thyroid hormone is well-known to accelerate the metabolism of cortisol. In the adrenally sufficient individual, the thyrotoxic state both increases the production of cortisol, and shortens the half-life of cortisol due to an increased turnover rate, with a net effect of normal circulating cortisol levels [3]. Cortisol requirements are increased due to the stress and increased metabolic demands of thyrotoxicosis. The mechanism of increased cortisol clearance appears to be due to thyroid hormone effects on the activity of 11βHSD and 5-α reductase enzymes [4].

Patients with adrenal insufficiency are unable to mount an adrenal response by increasing cortisol levels in the setting of excess thyroid hormone, placing them at risk for adrenal crises. Recurrent adrenal crises have been reported in individuals with autoimmune primary adrenal insufficiency upon development of autoimmune thyrotoxicosis [5]. Similarly, it is well documented that hypothyroid patients initiated on thyroid hormone repletion with undiagnosed primary or secondary adrenal insufficiency can present with adrenal crisis [6, 7]. In the hypothyroid state, cortisol clearance is slowed, protecting the hypothyroid, adrenally insufficient patient from symptoms of adrenal insufficiency. With thyroid hormone initiation, cortisol clearance increases, and adrenal crisis may occur, similar to the thyrotoxic patient with adrenal insufficiency.

The literature includes only 2 cases of adult patients with congenital adrenal hyperplasia who experienced symptomatic adrenal insufficiency and/or adrenal crisis associated with thyrotoxicosis. Takasu et al. described a 75-year-old female who was admitted for treatment of Graves’ thyrotoxicosis and was found unconscious due to adrenal crisis during her hospitalization [8]. She was ultimately diagnosed with nonclassical 21-hydroxylase deficiency. Kim et al. reported the case of a 23-year-old male with Graves’ thyrotoxicosis who was diagnosed with nonclassic 11-beta hydroxylase deficiency after he presented with hypokalemia and hypertension and was found to have adrenal hyperplasia on imaging [9]. Our report is the first case describing a pediatric patient with CAH, who experienced repeated episodes concerning for adrenal crises and hyperandrogenemia secondary to the onset of Graves’ thyrotoxicosis, demonstrating the impact of thyroid hormone excess on the metabolism of glucocorticoids in vivo.

4. Conclusions

This unusual case demonstrates the unique findings of thyrotoxicosis in a pediatric patient with SW-CAH on glucocorticoid supplementation. She presented with classic signs and symptoms of Graves’ disease including thyromegaly, weight loss, and tachycardia, as well as SW-CAH specific symptoms reflecting cortisol deficiency including biochemical hyperandrogenemia and repeated episodes concerning for adrenal crises. Increased clearance of cortisol in the setting of thyrotoxicosis resulted in recurrent adrenal decompensations due to insufficient cortisol, though 1 episode was accompanied by fever and thus may have been triggered by illness. Hyperandrogenemia and episodes concerning for adrenal crises resolved with normalization of thyroid levels, without any change in glucocorticoid dose. Thyrotoxicosis must be included in the differential diagnosis of individuals with any form of adrenal insufficiency, including CAH, who present with escalating glucocorticoid requirements, or recurrent adrenal crises despite appropriate glucocorticoid adherence and dosing.

Disclosure

This case was presented as a poster at the 99th Annual Meeting of the Endocrine Society.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

Copyright

Copyright © 2018 Meghan E. Fredette and Lisa Swartz Topor. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Overactive thyroid (hyperthyroidism) – NHS

An overactive thyroid, also known as hyperthyroidism or thyrotoxicosis, is where the thyroid gland produces too much of the thyroid hormones.

The thyroid is a small butterfly-shaped gland in the neck, just in front of the windpipe (trachea). It produces hormones that affect things such as your heart rate and body temperature.

Having too much of these hormones can cause unpleasant and potentially serious problems that may need treatment.

An overactive thyroid can affect anyone, but it’s about 10 times more common in women than men, and typically happens between 20 and 40 years of age.

Symptoms of an overactive thyroid

An overactive thyroid can cause a wide range of symptoms, including:

Find out more about the symptoms of an overactive thyroid.

When to see a GP

See a GP if you have symptoms of an overactive thyroid.

They’ll ask about your symptoms and if they think you might have a thyroid problem, they can arrange for a blood test to check how well your thyroid is working.

If the blood test shows that you have an overactive thyroid, you may be referred for further tests to identify the cause.

Find out more about how an overactive thyroid is diagnosed.

Treatments for an overactive thyroid

An overactive thyroid is usually treatable.

The main treatments are:

  • medicine that stops your thyroid producing too much of the thyroid hormones
  • radioiodine treatment – where a type of radiotherapy is used to destroy cells in the thyroid, reducing its ability to produce thyroid hormones
  • surgery to remove some or all of your thyroid, so that it no longer produces thyroid hormones

Each of these treatments has benefits and drawbacks. You’ll usually see a specialist in hormonal conditions (endocrinologist) to discuss which treatment is best for you.

Find out more about how an overactive thyroid is treated.

Causes of an overactive thyroid

There are several reasons why your thyroid can become overactive.

These include:

  • Graves’ disease – a condition where your immune system mistakenly attacks and damages the thyroid (about 3 in every 4 people with an overactive thyroid have Graves’ disease)
  • lumps (nodules) on the thyroid – this extra thyroid tissue can produce thyroid hormones, causing your levels to be too high
  • some medicines such as amiodarone, which can be used to treat an irregular heartbeat (arrhythmia)

Find out more about the causes of an overactive thyroid.

Further problems

An overactive thyroid can sometimes lead to further problems, particularly if it’s not treated or well controlled.

These include:

Find out more about the complications of an overactive thyroid.

Page last reviewed: 24 September 2019
Next review due: 24 September 2022

Feeling Tired? Stress Hormones & Thyroid Lab Tests


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Thyroid and Parathyroid Disorders – Diabetes and Endocrinology

Assessing Thyroid and Parathyroid Function

An accurate evaluation of the way your thyroid or parathyroid glands are functioning is essential to determine the most appropriate therapy. We use a number of noninvasive procedures to accomplish this, including lab tests, ultrasound, thyroid scans, function stimulation tests, bone x-rays, and biopsy. You can receive any procedures you need in our hospital.

Graves’ Disease and Overactive Thyroid Care

In people with hyperthyroidism, the thyroid gland produces high levels of thyroid hormones, increasing metabolism and causing symptoms such as rapid heartbeat, nervousness, high blood pressure, and weight loss. Graves’ disease is a type of hyperthyroidism that can also cause a goiter (bulge in the neck from an enlarged thyroid gland), bulging eyes, and thickened skin. Our team tests thyroid hormone levels in the blood and performs a thyroid scan to diagnose Graves’ disease and other types of hyperthyroidism. Treatments may include one or more of these approaches:

  • Medication to block or change how the thyroid gland uses iodine. These drugs may be used as long-term treatment, or to control an overactive thyroid gland before surgery or radioiodine therapy.
  • Radioiodine therapy, in which radioactive iodine is given by mouth. It concentrates in overactive thyroid tissue and destroys it. Thyroid hormone replacement therapy is prescribed for the rest of your life after this treatment to provide the hormones that your thyroid used to make.
  • Surgery to remove the thyroid. We perform thyroidectomy using small incisions. Thyroid hormone replacement therapy is also prescribed after thyroid surgery.

Hypothyroidism Treatment

Hypothyroidism (under-active thyroid) is the most common thyroid disorder. It most often results from an autoimmune disorder or the treatment of hyperthyroidism. You may have hoarseness, weight gain, a puffy face, coarse skin and hair, and a reduced heart rate. Our doctors will treat you with thyroid hormone replacement therapy.

Care for Thyroiditis

Thyroiditis is inflammation of the thyroid gland. Hashimoto’s thyroiditis is the most common form of thyroiditis and can cause goiter, fatigue, muscle weakness, and weight gain. It is often associated with other endocrine disorders, such as diabetes, under-active parathyroid or adrenal glands, or autoimmune disorders. Hashimoto’s thyroiditis can cause under-active thyroid activity and is typically treated with thyroid hormone replacement therapy.

Thyroid Cancer

Benign thyroid tumors (adenomas) may over-produce thyroid hormone and require treatment, or become very large and cause symptoms. For patients with “indeterminate” thyroid nodules—growths for which it is hard to tell if they are benign or malignant, using standard pathology techniques—we can perform molecular testing. Thyroid cancers are frequently curable through surgery and/or hormone and radioactive iodine therapy. The endocrine cancer specialists at NewYork-Presbyterian Brooklyn Methodist Hospital treat thyroid cancer using a multidisciplinary approach. Learn more.

Genetic Endocrine Disorders

Some people have a hereditary predisposition to endocrine disorders, such as multiple endocrine neoplasia (MEN). People with MEN I have a defect in a gene that carries the code for a protein called menin. The condition causes tumors of the pancreas, parathyroid, or pituitary glands to appear in the same person, but not necessarily at the same time. People with MEN II have a defect in the RET gene and may develop overactivity or tumors in the thyroid gland as well as the adrenal or parathyroid glands. Treatment for MEN may include medication or surgery. At NewYork-Presbyterian Brooklyn Methodist, we provide genetic counseling and screening for families with MEN and other hereditary endocrine syndromes to detect problems and complications early, when they may be treated most effectively.

Parathyroid Disorders

Our doctors are experienced treating disorders of the parathyroid glands.

  • Parathyroid tumors may cause high levels of calcium in the blood, increasing the risk of osteoporosis and possibly damage to organs such as the kidneys, bones, heart, and blood vessels. They rarely affect more than one of the four glands. Typically only the affected gland needs to be surgically removed—resulting in a cure in more than 95 percent of patients
  • Hyperparathyroidism (overactive parathyroid) may result from another problem in the body, such a kidney failure, which leads to low blood levels of calcium and triggers an increase in parathyroid activity to compensate. We treat hyperparathyroidism using medication, and surgery to remove some or all four of the parathyroid glands if medication is not sufficient. Our surgeons perform minimally invasive parathyroidectomy as well as conventional surgery to remove all four glands. Your doctor will discuss the most appropriate treatment for you.
  • Hypoparathyroidism (under-active thyroid) can lead to blood low calcium levels, which can result in seizures or uncontrollable spasms of the face, hands, arms, and feet. Your doctor may prescribe calcium and vitamin D supplements to correct blood calcium levels and treat your symptoms.

Adrenal Tumors

Adrenal tumors may produce excess hormones that can adversely affect your quality of life. They are best treated through surgical removal of the affected adrenal gland, which we typically do in a minimally invasive manner (“laparoscopic adrenalectomy”).

Warning Signs of High Cortisol and Low Thyroid

 

When a person feels stressed, they may reach for comfort foods that contain carbohydrates and sugars and proclaim that they’re “eating their feelings.

Many patients have a sense that stress, metabolism, and sugar are related to one another. They often can make the connection between eating poorly and feeling sluggish. What they may not know is that changes in diet and other lifestyle behaviors that lead to alterations in coping skills can impact cortisol, insulin, and thyroid levels, which can result in fatigue and slowed metabolism.

Receptors for all three hormones are located in nearly every cell of the body, so the relationship between them and the adrenal gland, thyroid, and pancreas is critical for energy production and balanced physiology.

When this relationship is functioning normally, people tend to feel vital and well. When they aren’t functioning properly, or when their function is impacted by poor rest, diet, and exercise, patients feel unwell, gain weight, and appear in your office with issues related to adrenal fatigue and thyroid problems.