Article, Endocrinology

Epigastric pain as presentation of an addisonian crisis in a patient with Schmidt syndrome

Case Report

Epigastric pain as presentation of an Addisonian crisis in a patient with Schmidt syndrome

Abstract

A 39-year-old woman presented with a 10-day history of epigastric pain accompanied by persistent fatigue and Loss of appetite for 3 months. She had presented several weeks earlier with adhesive capsulitis, treated by local infiltration of corticosteroids. She was not taking any other medications. Results of heart, lung, and Abdominal examinations were unremarkable, except for mild epigastric tenderness. Purple stretch marks were observed on examination of the skin. The only blood chemistry abnormalities were hyponatremia (125 mEq/L) and hyperkalemia (6.8 mEq/L). Based on the clinical and biologic picture, Adrenal insufficiency was suspected. The patient was transferred to the intensive care unit and received hydrocortisone intravenously for 3 days. She was then given oral hydrocortisone and fludrocortisone. Biologic abnormalities reversed entirely; the final diagnosis was primary autoimmune adrenal insufficiency (Addison’s dis- ease) associated with Autoimmune hypothyroidism (Schmidt syndrome). Adrenal insufficiency should be considered in patients with abdominal pain, especially when associated with electrolyte abnormalities.

A 39-year-old woman native to Eastern Europe presented to the emergency department with a 10-day history of epigastric pain. Other symptoms consisted of persistent fatigue and loss of appetite for 3 months; asthenia had increased markedly over the days before presentation. The epigastric pain had also increased after using nonsteroidal antiinflammatory drugs for pain in her left shoulder. The patient had no history of melena or vomiting, and her weight was stable. Medical history was unremarkable, except for an episode of epigastric pain and adhesive capsulitis several weeks earlier. A gastroscopy had not disclosed any lesion of the upper gastrointestinal tract. The frozen shoulder had been treated by local infiltration of corticosteroids. She was not taking any other medications.

On admission, her temperature was 36.9?C, pulse rate 65 beats per minute, blood pressure 106/54 mm Hg, and

respiratory rate 16 breaths per minute. Oxygen saturation was 99% while breathing ambient air. Purple stretch marks were observed on examination of the skin. Results of heart, lung, and abdominal examinations were unremarkable, except for mild epigastric tenderness.

The only blood chemistry abnormalities were hypo- natremia (125 mEq/L) and hyperkalemia (6.8 mEq/L). arterial pH was initially 7.36. The electrocardiogram result was normal.

Based on the clinical and biologic picture, adrenal insufficiency was suspected. After treatment of the hyperka- lemia, a blood sample was taken to determine the plasma adrenocorticotropic hormone and cortisol levels. The patient was then given 100 mg hydrocortisone intravenously, and a saline infusion was started; she was transferred to the intensive care unit for Close monitoring of electrolyte changes and for Fluid loading. She received 300 mg hydrocortisone intravenously on day 1, 150 mg on day 2, and 75 mg on day 3. She was then transferred to the general ward, where oral hydrocortisone (20 mg in the morning, 10 mg in the afternoon) along with fludrocortisone 0.1 mg were started. Under this regimen, the biologic abnormalities

Value

Reference range

Androstenedione

0.49 ng/mL

0.20-3.1 ng/mL

DHEA-S

b100 ng/mL

900-3500 ng/mL

Cortisol

15 ng/mL

-

Aldosterone

b25 pg/mL

40-310 pg/mL

Renin

N1000 ng/L

3.0-33 ng/L

ACTH

930 pg/mL

6-60 pg/mL

IGF-1

187 ng/mL

100-350 ng/mL

TSH

10 uUI/mL

0.4-4 uU/mL

Free T3

3.0 pg/mL

1.8-4.6 pg/mL

Free T4

1.1 ng/dL

0.8-1.7 ng/dL

Anti-TPO

106 U/mL

b34 U/mL

Anti-TGN

72 U/mL

b115 U/mL

Anti-adrenal gland

1:160

Anti-GAD

0.2%

b2.6%

DHEA-S, dehydroepiandrosterone-sulfate; ACTH, adrenocorticotropic hormone; IGF-1, insulin-like growth factor; TSH, thyrotropin; T3, triiodothyronine; T4, tetraiodothyronine (Thyroxine); Anti-TPO, anti- thyroid peroxydase antibody; Anti-TGN, anti-thyroglobulin antibody;

Anti-GAD, anti-Glutamic acid decarboxylase.

0735-6757/$ - see front matter (C) 2008

Table 1 Main laboratory findings

251.e4 Case Report

reversed entirely. The main laboratory findings are shown in Table 1. The final diagnosis was primary autoimmune adrenal insufficiency (Addison’s disease) [1,2] associated with autoimmune hypothyroidism (Schmidt syndrome) [3]. Adrenal insufficiency should be considered in patients with abdominal pain, especially when associated with electrolyte abnormalities, such as hyponatremia with or without hyperkalemia. Although probably harmless in a healthy patient, the possible trigger role of a transient depression of adrenal function due to the intra-articular administration of glucocorticosteroid in the genesis of the

addisonian crisis cannot be excluded in this patient [4].

Christophe Lelubre MD Philippe E.R. Lheureux MD, PhD Department of Emergency Medicine Erasme University Hospital Universite Libre de Bruxelles

B-1070 Brussels, Belgium E-mail address: [email protected]

doi:10.1016/j.ajem.2007.04.016

References

  1. Arlt W, Allolio B. Adrenal insufficiency. Lancet 2003;361(9372): 1881-93.
  2. Bouillon R. Acute adrenal insufficiency. Endocrinol Metab Clin North Am 2006;35(4):767-75, ix.
  3. Schatz DA, Winter WE. Autoimmune polyglandular syndrome. II: clinical syndrome and treatment. Endocrinol Metab Clin North Am 2002;31(2):339-52.
  4. Furst DE, Saag KG. Glucocorticoid withdrawal. In: Rose BD, editor. Waltham (Mass): UpToDate, 2006.