Delayed Diagnosis of Graves’ Thyrotoxicoisis Presenting as Recurrent Adrenal Crisis in Primary Adrenal Insufficiency

Abstract

A 42-year-old female diagnosed with primary adrenal insufficiency, 2 years prior in another institution, was referred to the department of Endocrinology for the persistence of tiredness, weakness, giddiness and progressive weight loss. She was being previously evaluated for symptoms of vomiting, abdominal pain and refractory hypotension. Her blood investigations then had showed a random serum cortisol of 2 µg/dl dl, (Normal 5-27µg/dl ), serum sodium of 123 mEq/L(135-145), potassium of 5.6mEq/L (3.5-5) and plasma ACTH of 345 pg/ml (0-45 ),all were suggestive of primary adrenal insufficiency. Her Chest X ray, CT abdomen with contrast and thyroid function were all within normal limits during the time of initial admission. Thus final diagnosis of primary adrenal insufficiency with adrenal crisis was considered and was initially treated with intravenous hydrocortisone followed by twice daily dose of 5mg oral prednisolone. She was apparently asymptomatic for 1 and ½ years from the time of her initial diagnosis of primary adrenal insufficiency. Six months prior to an episode of of an adrenal crisis the patient noticed symptoms of fatigue, weakness, weight loss, giddiness and increasing hyper pigmentation. She was admitted twice to hospital with features suggestive of adrenal crisis requiring intravenous hydrocortisone and Intravenous fluids for improvement. The time interval between the first and second episode of adrenal crisis was 4 months. ACTH or CRH stimulation tests were not done during the follow-ups. During both these episodes of adrenal crisis she had no other precipitating factors such as fever, diarrhea or any infection.The diagnosis of adrenal crisis was considered based on the clinical features (vomiting, abdominal pain hypotension, weight loss) in the setting of underlying primary adrenal insufficiency. Details of previous biochemical investigations (sodium, potassium, plasma glucose or arterial blood gas analysis) reports during the admission for adrenal crisis were not available with the patient and hence could not be evaluated.Due to recurrent episodes of crisis the dose of prednisolone was increased to 10mg in the morning and 5mg in the evening. Even then she continued to have persistence of symptoms with progressive weight loss, for which she was referred for further evaluation. However, she was not evaluated for malabsoption or any gastro intestinal related other disorders to rule out possibility of poor intestinal absorption of prednisolone. On the other hand she did not have symptoms of alerted bowel habits (on and off diarrhea or constipation).During evaluation at the time of present admission, she was a thin build lady with hyper-pigmentation of the oral mucosa, palmar creases of both hands and extensor aspects of both arms with no vitiligo. Her supine neck examination showed a WHO grade -II diffuse thyromegaly and there were no obvious signs of thyrotoxicosis (fine tremor, prominence of eye balls) and there was no thyroid bruit. Her supine blood pressure was 100/70 mmHg and on standing, the blo...

Adrenal insufficiency – recognition and management

“…Phrenic nerve palsy, both unilateral and bilateral is well described in neuralgic amyotrophy and maybe the presenting and only feature. [3][4][5][6][7] ■…”

“…After she became euthyroid, she remained symptom free and gained 8 kg in weight while taking prednisolone 5 mg/day and fludrocortisone 50 µg/day . 3 Although the association of Addison's disease and thyrotoxicosis is rare, 2-5 there should be a heightened index of suspicion for coexisting thyrotoxicosis when symptoms and signs of hypoadrenalism persist despite progressively increasing doses of replacement therapy 4 or when a previously well managed patient experiences Addisonian crisis without an obvious precipitating cause. ■…”

Relative Adrenocortical Insufficiency Following Radioactive Iodine Therapy for Graves’ Disease: A Report of Two Cases

“…In clinical practice, adrenocortical insufficiency, a potentially life-threatening syndrome may occur when thyrotoxicosis is exacerbated. It has been reported in situations such as misuse of thyroid hormone in a background of latent adrenal insufficiency, 10 , 11 new onset thyrotoxicosis in a patient with congenital adrenal hyperplasia, 6 or secondary adrenal insufficiency, 8 and simultaneous presentation of Graves’ disease and Addison’s disease. 7 …”

“…In clinical practice, adrenocortical insufficiency, a potentially life-threatening syndrome may occur when thyrotoxicosis is exacerbated. It has been reported in situations such as misuse of thyroid hormone in a background of latent adrenal insufficiency, 10,11 new onset thyrotoxicosis in a patient with congenital adrenal hyperplasia, 6 or secondary adrenal insufficiency, 8 and simultaneous presentation of Graves' disease and Addison's disease. 7 Previous research demonstrated the association between long-standing thyrotoxicosis and deficient adrenocortical reserves, [12][13][14][15][16] despite the lasting hyperactivity of the hypothalamic-pituitary-adrenal axis.…”

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

“…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].…”