[Lung carcinoma with paraneoplastic hyponatremia and hypercalcemia]

Among the numerous paraneoplastic syndromes of the lung carcinoma, metabolic manifestations are of the particular clinical relevance. They are the consequence the prominent neurosecretory activity of certain peptides and hormones, mostly within amine precursor uptake and decarboxylation (APUD) secretion. Small cell lung carcinoma is the most common cause of paraneoplastic syndromes. Ectopically produced proteins by the tumor are structurally similar but biologically less active than the "true" hormones, which may be clinically manifested by absent, less frequent or milder symptoms of the hormonal imbalance.

Malignant hyponatremia may be caused by arginine-vasopressin imbalance within the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), or by hypersecretion of the atrial natriuretic peptide (ANP). Beside the postural hypotension, clinical picture is characterized by neurological symptoms caused by plasma hypo-osmolality, resulting in detection of the occult pulmonary neoplasm as well as post-therapeutic exacerbation of the small cell carcinoma.

Malignant hypercalcemia is the most common paraneoplastic endocrine syndrome. In about 80% of the lung carcinomas without hone metastases it is caused by an increase of the parathyroid hormone-releasing protein (PTH-rP) in interaction with certain cytokines, products of the autochthonous neuroendocrine tumor secretion, predominantly in the squamous cell carcinoma. The cells expressing PTH-rP show coexpression of some neuroendocrine products.

Different degrees of hypercalcemia cause heterogenous manifestations--from fatigue, anorexia, hone pains through polyuria, polydipsia, gastrointestinal complaints all the way to confusion, lethargy, coma and death. In addition to prevention of the intravascular volume overload, the treatment occasionally necessitates substitution of calcitonin possibly with plicamycin and gallium nitrate.