Male patient, 75 years old, with EC type 2 scale (Eastern Cooperative Oncology Group), who was admitted in January 2015 to the Department of Internal Medicine for neurological impairment of the sensorimotor, interpreted secondary to hypoglycemia.
She had a personal history of ex-smoking, hypertension, acute myocardial infarction in 1995, myocardial revascularization surgery in 2009 with 4 bypass with irrevascularizable necrotic ischemic cardiomyopathy and heart failure 19% with severe impairment of systolic function.
In 2006, a complete resection of a tumor located in the left lung base compatible with SFT was performed.
Pathology reported a pattern fusocellular proliferation with rounded growth and fibrous pseudocapsule, mild to moderate nuclear pleomorphism and 6 mitoses per 10 fields of 40 X, 67100 and 67100 positive Kiclin,
In 2007, control computed tomography (CT) showed no residual lesion.
Subsequently, the patient dismissed his controls due to the correct diagnosis, which prevented the monitoring and treatment if necessary.
In 2014, the patient was diagnosed with prostate cancer with Gleason score 8 (4+4).
CT scan to stage this tumor showed an image of 110 x 70 mm in the left lung base and bilateral enlargement of the major adrenal glands of the left adrenal gland.
Positron emission tomography revealed a heterogeneous solid formation of 115 x 112 x 85 mm with hypermetabolic central areas, with maximum standard uptake value (SUVmax) 3.9 in the left adrenal gland basal region and 3.
Biochemical analysis ruled out hypofunctioning or hyperfunctioning adrenal pathology.
Magnetic resonance imaging of the adrenal glands revealed diffuse enlargement of the left adrenal gland, without attenuation of the parenchyma in the phase and out of phase technique, presenting positive restriction with diffusion coefficient technique and apparent decrease in diffusion values.
Compatible with secondary injury.
1.
Upon directed questioning, the patient reported having experienced since the last two months symptoms of hypoglycemia (diaphoresis Association, Heart Failure and weakness), relief of them with food intake and, in the last year, New York functional class III.
Blood pressure was 100/70 mmHg, heart rate 80 beats/min, respiratory rate: 22 breaths/min and body mass index: 23.9 kg/m2, mean left hypoventilation at baseline and up to the right field.
Biochemical examination performed at admission revealed basal cortisol: 16.6 μg/ml (VN: 6-19), sodium: 146 meq/l (VN 135-145), thyroid: 3.4 meq/l (VN: 3.5).
During hospitalization, the patient <3.7 ng with fasting hypoglycemia episodes (fasting hypoglycemia), biochemical examination of one of these episodes confirmed the presence of hypoinsulinemic hypoglycemia: glycemia: 43 mg/dl [normal IGF-value (NPV) 70 mL GHV-17
Treatment was indicated with 10% dextrose solution intravenously and, due to the persistence of hypoglycemia, oral meprednisone was initiated in increasing doses until reaching 20 mg daily, with which blood glucose levels normalized.
At a multidisciplinary clinical-surgical meeting (Tumour Committee), it was decided not to perform surgery or start radiotherapy or chemotherapy due to their cardiac history.
The patient died due to a massive myocardial infarction three months after hospital admission.
