The first and most common pattern (type I), accounting for approximately forty per cent of patients with SIAD, is characterised by excessive and erratic vasopressin secretion that is totally unaffected by changes in plasma osmolality. Although neoplastic conditions often demonstrate this pattern, many other causes of SIAD show the same abnormality. The pathogenesis of this type of defect is unknown, but several different mechanisms are possible. Ectopic production of vasopressin by neoplasms might be expected to cause random release. Rapidly fluctuating nonosmotic stimuli (e.g. hypotension) might also be responsible. Electrical instability of the neurogenic pathways that control vasopressin, or the neurohypophysis itself, is a further possible mechanism.
