From the Journals

Fluoxetine tied to lower obsessive-compulsive scores among children with ASDs

Impact of the SSRI on those behaviors falls short in multiple secondary analyses

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Reconciling the limited performance

One could certainly take issue with the suggestion that this was presented as a positive trial on two levels: One, the prespecified primary outcome was not met, and two, the clinical significance (as distinct from statistical significance) of a 2-point change on that scale is problematic given the wide range of baseline scores allowed into the study.

The other thing that gets mixed up in this study is: Exactly what are obsessive-compulsive symptoms as distinct from repetitive behaviors? That question is a real challenge in this field when it comes to clinical trials for this target in autism, which tend to lump together heterogeneous repetitive behaviors.

The fact that there was absolutely no signal, or at least not a very strong one, is very challenging, considering how frequently this class of drugs is prescribed in autism.

This is not the first SSRI study for autism that’s come up empty. In this case, though, a negative study is still important because it confirms other negative studies. Another recently published study – the SOFIA fluoxetine study (J Autism Dev Disord. 2019 Jul 2. doi: 10:1007/s10803-019-04120-y) – also came up negative. SOFIA randomized 158 children to 14 weeks of fluoxetine or placebo. There were no significant differences on the primary endpoint, the Children’s Yale-Brown Obsessive-Compulsive Scale, and the placebo response rate was 41%.

However, it was clearly a heroic effort by Dr. Reddihough et al. to get this current study done: It took 7 years to get it over the finish line. This is probably because fluoxetine is so easily available. Why would a parent take a 50% chance of their child not getting a drug that might have some benefit – and that they could get without much trouble? And if it takes 7 years to complete a clinical trial, and we’re sitting around waiting for a definitive one, we are literally looking at potentially decades before we have some real answers that would inform your clinical practice in terms of this commonly prescribed drug.

As far as nailing the coffin shut on fluoxetine, I don’t think that will ever happen because some kids clearly improve. The placebo response in this population is very high. In our citalopram study (JAMA Pediatr. 2013 Nov;167[11]:1045-52), it was close to 33%. The improvement is dramatic and real, no less than any other response. If you see that response as a clinician and parent, it is very difficult to walk away from. Moreover, the population in clinical practice may be different from the population that shows up in a clinical trial specifically focused on restricted, repetitive behaviors.

One reason we may see a response in some is because SSRIs can help with anxiety, which is a common, arguably core symptom of autism. It appears to be part of the reason kids have catastrophic meltdowns when there are any changes in things they have come to expect, like a different route to school or a delay in their favorite TV show coming on. And if anxiety drives that, and an SSRI helps with anxiety, the child might be able to cope with something that would otherwise feel like the end of the world. Maybe that starts a positive feedback loop instead of a negative one, and maybe it propels more changes as the child and family experience success.

So, what are clinicians to do? The answer is still the same – they should use their best judgment about each child’s symptoms and about the risks and benefits that might occur with that individual. The fact that these trials are coming up negative for this indication in autism doesn’t mean that SSRIs might not be helpful for anxiety or depression, just as they are in the general population. I think we are back to basics. Clinicians need to use their best medical judgment according to each child’s unique needs.

These comments were adapted from an interview with Bryan H. King, MD, MBA. Dr. King is a professor of psychiatry at the University of California, San Francisco. He reported receiving personal fees from Genentech. Dr. King also commented on the study in an accompanying editorial (JAMA. 2019;322[16]:1557-8).


 

FROM JAMA

Fluoxetine appeared to lower scores for obsessive-compulsive behaviors among a group of children with autism spectrum disorders (ASDs), but the positive finding fell apart during multiple secondary analyses, Dinah S. Reddihough, MD, and colleagues have reported.

At 16 weeks, children and adolescents randomized to receive the SSRI had about a 2-point improvement on the Children’s Yale-Brown Obsessive Compulsive Scale, modified for pervasive developmental disorder (CYBOCS-PDD), compared with those taking placebo. But the finding lost significance in a multivariate analysis that accounted for a between-group difference in baseline scores – an uncontrollable variable that occurred during randomization, wrote Dr. Reddihough, of the Royal Children’s Hospital in Victoria, Australia, and coauthors.

“Moreover, repeating the analyses with multiple imputation to handle the missing data, arguably a preferable analysis, also failed to show evidence of benefit of fluoxetine compared with placebo irrespective of adjustment for the baseline imbalance,” the team noted. The study was published in JAMA.

Despite the null findings of the additional adjusted analyses, the authors held out hope for fluoxetine.

“Although cautious interpretation of the results from the primary analysis is warranted, all analyses of the primary outcome yielded 95% confidence intervals that extended well above the minimum clinically important difference of 2 points, indicating that fluoxetine may reduce the frequency and severity of obsessive-compulsive behaviors in children and adolescents with ASDs. Given the large amount of missing data, the study may have been underpowered to detect the minimum clinically important difference of 2 points.”

The study comprised 146 children (mean age, 11 years) recruited through three large practices in Australia. Children were randomized to fluoxetine or placebo for 16 weeks. Fluoxetine was weight-dosed and then titrated every week for the first month to a maximum of 20 mg/day.

The primary outcome was the difference between groups in the total score on the CYBOCS-PDD at 16 weeks. Secondary endpoints included changes on the Repetitive Behavior Scale–Revised, the Spence Children’s Anxiety Scale Aberrant Behavior Checklist–Community Version, the Clinical Global Impression Scale–Global Improvement and Efficacy Index, and a Disruptiveness Assessment.

Of the cohort, 85% were male, and 30% had an intellectual disability. The placebo group had higher scores on the Repetitive Behavior Scale–Revised and the Aberrant Behavior Checklist lethargy scale than did the fluoxetine groups.

There was a very high rate of nonadherence to study protocol, with 41% of those in the active group and 30% in the placebo group not completing the treatment regimen. The most often cited reasons for treatment discontinuation included parent decision to drop out (20 fluoxetine, 12 placebo), adverse events (5 fluoxetine, 4 placebo), and clinician decision (2 fluoxetine, 2 placebo).

The primary analysis found that scores on the CYBOCS-PDD were significantly lower in the fluoxetine group at 16 weeks; the fluoxetine group had decreased its score from 12.80 to 9.02, while the placebo group went from 13.13 to 10.89. This mean 2-point difference was statistically significant and, the authors wrote, met the minimum threshold for a clinically significant difference.

But the mean between-group difference decreased to a nonsignificant 1.17 points in the sensitivity analysis that controlled for sex, verbal ability, baseline CYBOCS-PDD, and imbalances found at baseline in some of the measures.

“Moreover, repeating the analyses with multiple imputation to handle the missing data, arguably a preferable analysis, also failed to show evidence of benefit of fluoxetine compared with placebo irrespective of adjustment for the baseline imbalance,” the team said.

There were no significant differences on any of the secondary measures.

Adverse events were similar in the active and placebo groups (45% and 42%, respectively). These included mood disturbances particularly irritability (9 fluoxetine, 12 placebo), gastrointestinal problems such as nausea and diarrhea (10 fluoxetine, 7 placebo), and sleep disorders (13 fluoxetine, 16 placebo). Two patients in the placebo group and none in the active group experienced suicidality.

Dr. Reddihough and coauthors cited the study’s high dropout rate as one of its limitations.

The study was supported by a federal grant from the Australian government. Dr. Reddihough had no financial disclosures.

SOURCE: Reddihough DS et al. JAMA. 2019;322(16):1561-9.

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