A 58 year-old woman entered our hospital, with symptoms of constipation, excessive urine secretion (over 2 liter/day:polyouria) and severe muscle fatigue. She had a negative medical history and she hadn't used alcohol or drugs of any type. She complained of persistent dry cough and anorexia: her body weight had decreased 10 kgs during the last two months period. On evaluation, the patient looked sick; she was pale, her temperature was 36.1  C, her blood pressure was 100/60 mmHg, and her pulse rate was 70 bpm. The clinical examination revealed total muscle fatigue of arms and legs, without specific neurological signs. The patient couldn't walk or stand without help. She said that she had remained in bed during the main part of the day for the last week.
The initial laboratory data were: Hct =31%, Hb =10.9 g/dL, Wbc =20.250 k/muL; (91% were granulocytes and 9% were lymphocytes), Platelets =438.000/muL, Glu =140 mg/dL, BUN =44 mg/dL, Creatine =0.9 mg/dL, K =1.9 meq/L, Na =140 meq/L, Ca =9.6 mg/dL, SGOT =11 IU/L, SGPT =15 IU/L, ALP =85 IU/L, LDH =147 IU/L, CPK =53 IU/L, Bill =0,4 mg/dL. Her arterial blood gasses were pH =7.48, pO2 =73 mmHg, pCO2 =44 mmHg, HCO3 =36.5, SpO2 =94%. All these demonstrated metabolic alkalosis.
The chest X-ray that was performed, demonstrated opacity without cavitation to the left upper lung lobe (Fig. 1). During next day, the patient was extremely tired, febrile and her breath frequency exceeded 22 per minute (tachypnea). Finally, she got intubated because of severe respiratory (hypercapnic- elevated PCO2) acidosis. The measurement of 24 hour-urine secretion of sodium (108,2 mEq/L) and potassium (34,8 mEq/L), showed extensive hyperkaliurea. On the contrary, urine 5-HIAA was normal (5 mg; normal range: 5-100 mg). After 3 days, the patient extubated, without respiratory muscle weakness, while she had received intravenously high amount of solutions with potassium. The patient remained with low serum potassium (hypokaliemia), despite the extensive intravenous replacement. We measured the serum levels of aldosterone, aldolase, cortisone, and renin in order to find out a responsible specific disease for this condition. The laboratory data are presented in Table 1. We considered as possible the existence of paraneoplasmatic syndrome.
The CT scanning of the thorax revealed a lung nodule, at the upper anterior left lung lobe, without collateral lymphadenopathy (Fig. 2). The CT scanning of the brain, and upper and lower abdomen departments, were negative for any kinds of lesions (secondary metastatic sites) and excluded the coexistence of juxtaglomerular tumors.
The values of tumor markers were within normal range. Urine examination was also normal. Smear examination and sputum culture were negative for Mucobacterium tuberculosis and the tuberculin skin test was negative too.
The patient underwent a fiberoptic bronchoscopy. We found a highly vascular endobronchial mass with a reddish smooth-looking surface, into the right anterior sub segmental bronchus of the left upper lung lobe. The bronchial biopsy revealed numerous membrane-bound neurosecretory granules characteristic of neuroendocrine tumor (pulmonary carcinoid tumor).
Three days later, we planned the surgical wedge resection of the carcinoid. The extended histopathology study revealed the pattern of the typical carcinoid tumor of the lung, because of the absence of necrosis. (Fig. 3).
Two weeks after the surgical procedure, the patient's blood pressure was measured and was found normal and the renin activity-levels serum were found normal, too (Table 1).
Thorax CT scanning revealed a left lung nodule (diameter 21 x14 mm), at the upper anterior lung lobe without collateral lymphadenopathy.