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Unfortunately, as expected, disease progression occurred after 8 months of clinical remission and the patient passed away ?1 year after the initial diagnosis. Discussion Hyponatremia is a common feature in oncology practice [37], occurring most frequently in patients with SCLC [38]. A quarter of all patients with SCLC were identified as having sodium [Na+] of [http://www.selleckchem.com/products/Imatinib-Mesylate.html find more] SCLC than with other malignancies [43, 44]. Four different patterns of vasopressin secretion have been identified in patients with SIADH (Figure?9): Type A is characterized by an unregulated, erratic, secretion independent of the prevailing plasma osmolality. Type B is characterized by an elevated basal secretion of vasopressin, despite normal regulation by osmolality. Type C is characterized by a ��reset osmostat�� system, whereby vasopressin is secreted at an [http://en.wikipedia.org/wiki/MERTK UNC2881] abnormally low threshold of plasma osmolality but otherwise displays a normal response to relative changes in osmolality. Type D is characterized by undetectable vasopressin levels (some of these patients may have gain-of-function mutations in the vasopressin V2 receptor) [15, 45, 46]. Figure?9: Patterns of plasma vasopressin levels where compared with plasma sodium levels in patients with SIADH [15]. Type A is characterized by unregulated secretion of vasopressin, type B by elevated basal secretion of vasopressin despite normal regulation by ... Type A vasopressin secretion tends to be usually found in [http://www.selleckchem.com/products/AP24534.html selleck compound] paraneoplastic SIADH [47]. It has been proposed that the term ��syndrome of inappropriate antidiuresis�� (SIAD) may be more suitable for this condition as not all patients with SIADH have elevated levels of vasopressin [15]. Many of these patients respond to the administration of vasopressin receptor antagonists with an aquaresis, suggesting that they have low levels of inappropriate vasopressin secretion despite the difficulty measuring such low levels. An exception is a patient group with gain-of-function mutations in the vasopressin V2 receptor��identified in infants with clinical and laboratory features consistent with the presence of SIADH but with undetectable vasopressin levels��who do not appear to respond to the administration of vasopressin receptor antagonists [45, 48]. Although this mutation appears to be a rare cause of hyponatremia at this time, the term SIAD would comprise these patients. Although SCLC is a known cause of SIADH, it must also be borne in mind that the patient in this case would have had carcinoma at the time of admission, yet his serum [Na+] had been normal.