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Patients with distributive shock who are unresponsive to traditional vasopressors are commonly considered to have severe distributive shock and are at high mortality risk. Here, we assess the cost-effectiveness of adding angiotensin II to the standard of care (SOC) for severe distributive shock in the US critical care setting from a US payer perspective.
Short-term mortality outcomes were based on 28-day survival rates from the ATHOS-3 study. Long-term outcomes were extrapolated to lifetime survival using individually estimated life expectancies for survivors. Resource use and adverse event costs were drawn from the published literature. Health outcomes evaluated were lives saved, life-years gained, and quality-adjusted life-years (QALYs) gained using utility estimates for the US adult population weighted for sepsis mortality. Deterministic and probabilistic sensitivity analyses assessed uncertainty around results. We analyzed patients with severe distributive shock from the ATHOS-3 clinical trial.
The addition of angiotensin II to the SOC saved .08 lives at Day 28 compared to SOC alone. The cost per life saved was estimated to be $108,884. The addition of angiotensin II to the SOC was projected to result in a gain of .96 life-years and .66 QALYs. This resulted in an incremental cost-effectiveness ratio of $12,843 per QALY. The probability of angiotensin II being cost-effective at a threshold of $50,000 per QALY was 86 percent.
For treatment of severe distributive shock, angiotensin II is cost-effective at acceptable thresholds.
There have been recent calls to abandon the distinction between neurological
and psychiatric disorders on philosophical and moral grounds. Crossley and
colleagues, in this issue, meta-analyse published structural brain imaging
data and prove that they are different after all – or do they?
Symptoms of obsessive–compulsive disorder (OCD) have been described in
neuropsychiatric syndromes associated with streptococcal infections. It
is proposed that antibodies raised against streptococcal proteins
cross-react with neuronal proteins (antigens) in the brain, particularly
in the basal ganglia, which is a brain region implicated in OCD
To test the hypothesis that post-streptococcal autoimmunity, directed
against neuronal antigens, may contribute to the pathogenesis of OCD in
Ninety-six participants with OCD were tested for the presence of
anti-streptolysin-O titres (ASOT) and the presence of anti-basal ganglia
antibodies (ABGA) in a cross-sectional study. The ABGA were tested for
with western blots using three recombinant antigens; aldolase C, enolase
and pyruvate kinase. The findings were compared with those in a control
group of individuals with depression (n = 33) and
schizophrenia (n = 17).
Positivity for ABGA was observed in 19/96 (19.8%) participants with OCD
compared with 2/50 (4%) of controls (Fisher's exact test
P = 0.012). The majority of positive OCD sera (13/19)
had antibodies against the enolase antigen. No clinical variables were
associated with ABGA positivity. Positivity for ASOT was not associated
with ABGA positivity nor found at an increased incidence in participants
with OCD compared with controls.
These findings support the hypothesis that central nervous system
autoimmunity may have an aetiological role in some adults with OCD.
Further study is required to examine whether the antibodies concerned are
pathogenic and whether exposure to streptococcal infection in vulnerable
individuals is a risk factor for the development of OCD.
Conversion disorder presents a problem for the revisions of DSM–IV and ICD–10, for reasons that are informative about the difficulties of psychiatric classification more generally. Giving up criteria based on psychological aetiology may be a painful sacrifice but it is still the right thing to do.
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