Endocrine Abstracts

Sheehan’s syndrome (SS) may be defined as development of anterior pituitary ischemic necrosis, first of which is caused by failure to meet the blood build-up required due to pituitary expansion secondary to lactotroph cell proliferation during pregnancy. Vasospasm, thrombosis and vascular compression of hypophyseal arteries have been described among the possible causes of SS. Additionally, expansion of pituitary gland, small sella, disseminated intravascular coagulation (DIC) and autoimmunity may as well play a role in pathogenesis of SS. SS is characterized by the loss, to varying degrees of anterior pituitary functions. We aimed to present a case with bicytopenia who was treated being diagnosed in our clinic with colonic pseudo-obstruction, acute renal failure, and SS as well, and discharged with full remission after treatment.

Case presentation: A 67-year-old female patient was admitted to our emergency department with the complaint of constipation, reduction of amount of her urine, and deterioration of general health. In medical history, she had been unable to pass gas and defecate for the last three days. She had ten children. She had given birth her last child when she was 38 years old. Her last child lived for ten days and never been breastfed. After she born her last child her menstrual cycle ceased. In the systemic examination, we detected cachectic appearance, extensively decreased skin turgor (tone), absent axillary hair, pale skin and conjunctivae in her physical examination. A 7 cm subcostal incision scar secondary to abdominal cholecystectomy was found and hypoactive bowel sounds were heard (1/min). The first laboratory tests in the Emergency Clinic were below: Glucose: 72 mg/dl, Urea: 65 mg/dl, Crea: 2.4 mg/dl, Na: 126 mmol/l, K:6.7 mmol/l, Calcium: 7.9 mg/dl, Alb: 4 gr/dl, AST: 78 U/l, ALT: 13 U/l, LDH: 669 U/l (220–480), amylase:160 U/L (28–100), Mg: 1.63 mg/dl (1.58–2.55), Total protein: 7.5 gr/dl, CK: 2795 U/l (2–190). WBC: 6400/mm³, RBC: 2,72 /mm³ (4-5.5), Hgb: 8.6 g/dl, PLT: 114.000/mm³ (150–450), MCV: 94 fl, RDW: 16.4% (11.5–14), D dimer: 0.5 mg/l (0–0.55) and fibrinogen: 302 mg/dl (180–350). Erythrocyte morphology was normochromic normocytic. The plain abdominal radiograph in standing position reviewed in Emergency Clinic showed air-fluid levels. Colonic pseudo-obstruction was found in abdominal computerized tomography.

We consider hypopituitarism due to absent axillary hair, hypotension, hyperpotassemia and hyponatremia. Basal hormone results (8 a.m.) as below: Cortisol: 4.75 μg/dl, ACTH: 23.5 pg/ml (0–46), FT3: 0.28 pg/ml (2.1–5.2), FT4: 0.21 pg/ml (0.8–1.76), TSH: 4.8 mIU/l and Growth Hormone <0.05 ng/ml (0–8), FSH: 4.97 mlU/ml (9.7–111), LH: 1.26 mlU/ml, Estradiol: 29.2 pg/ml (20–30), Progesterone <0.2 ng/ml (0–1), DHEAS <15 μg/dl (35–430), IGF-1 (Insulin-like growth factor) <25 ng/dl (71–290), prolactin: 0.72 ng/ml (1.8–20.3) and Total Testosterone: 0.01 ng/dl (0–74). Synacthen stimulation test and glucagon stimulation test were performed. But, low serum cortisol levels were found in both stimulation tests. Afterwards, in pituitary magnetic resonance examination, partially empty sella was detected in the patient. She discharged with full remission after hormone replacement treatment.

In conclusion, SS is not a very rare condition in our developing country. However, SS is insidious condition. Because obscure of complaints and clinical findings are similar to that of many other diseases, the diagnosis of SS is delayed. Moreover, SS with unusual clinic presentation cannot be considered in differential diagnosis. In order to diagnose SS patients before occurrence of complications, as in our case, a proper anamnesis should be performed and clinical findings should be interpreted carefully.