TOPIC DISCUSSION: SIADH diagnosis

We always struggle to diagnosis this entity in few cases of hyponatremia. Measurement of AVP can prove challenging due to problems of ordering and time it takes to come back. Measurement of copeptin( a 39 amino acid glycopeptide) which is derived from the same precursor peptide as AVP and released in equimolor amounts as AVP might be measurable.  Is that been studied? You bet!

In this one prospective observational study, 106 consecutive hyponatremic patients were classified based on their history, clinical evaluation, and laboratory tests. In patients and 32 healthy control subjects, plasma copeptin concentration and standard biochemical parameters were tested for their utility of diagnosing SIADH.

Plasma copeptin levels were significantly higher in patients with hypo- and hypervolemic hyponatremia compared with SIAD (P < 0.005, respectively) and primary polydipsia (P < 0.001). The copeptin to U-Na ratio differentiated accurately between volume-depleted and normovolemic disorders (area under the receiver-operating characteristic curve 0.88, 95% confidence interval 0.81-0.95; P < 0.001), resulting in a sensitivity and specificity of 85 and 87% if a cutoff value of 30 pmol/mmol was used.  This ratio differentiated between volume-depleted and normovolemic disorders resulting in good specificity and sensitivity in this one study. It did better than copeptin alone as well. Another small swiss study felt that it added very little to the sodium balance information. I guess not much out in the literature. Lets see where this story unfolds and how this becomes real in clinical use.

Ref

http://www.ncbi.nlm.nih.gov/pubmed/18984663

http://www.ncbi.nlm.nih.gov/pubmed/21990032

TOPIC DISCUSSION: ADH and Pain?

The relationship of pain and SIADH is well documented. Severe pain can lead to inappropriate ADH production.  Why is that? Why does pain cause ADH release? Looking into the literature, not much has been studied regarding this specific question.
A single paper in 1977 from UCLA describes the effect of pain on plasma ADH concentrations. They studied patients with pain after surgery and compared to controls. Age, smoking and pain came out factors associated with increase in ADH levels. It was a nice and small study but showed that pain led to ADH increase.
Stress might not be the case, might be pain directly. Some studies have shown that stress itself without pain did not led to increase ADH.  Pain has two components:- readily localizable specific sensation that is mediated by the spinothalamic tracts and the second is the arousal of the Reticular formation , ventral thalamus and hypothalamus and perhaps ADH connection might be in this latter portion. Stimulation of the brain stem reticular formation has shown to increase ADH in animals.
When asking few academicians: some responses I got was : Flight and Fight state from an evolutionary standpoint perhaps that wants ADH to be elevated in that state and allow for the beneficial effects.
Also, ADH is produced naturally perhaps in wound healing and in these pain flight and fight situations, leads to such a response.
Interesting , not well defined and studied

Ref:
http://www.ncbi.nlm.nih.gov/pubmed/630725
http://www.ncbi.nlm.nih.gov/pubmed/6399311