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Meta-Analysis
. 2021 Sep 28;9(9):CD007662.
doi: 10.1002/14651858.CD007662.pub3.

Pharmacotherapy for trichotillomania

Affiliations
Meta-Analysis

Pharmacotherapy for trichotillomania

Jacob Hoffman et al. Cochrane Database Syst Rev. .

Abstract

Background: Trichotillomania (TTM; hair-pulling disorder) is a prevalent and disabling disorder characterised by recurrent hair-pulling. Here we update a previous Cochrane Review on the effects of medication for TTM.

Objectives: To assess the effects of medication for trichotillomania (TTM) in adults, children and adolescents compared with placebo or other medication.

Search methods: We searched CENTRAL, MEDLINE, Embase, PsycINFO, eleven other bibliographic databases, trial registries and grey literature sources (to 26 November 2020). We checked reference lists and contacted subject experts.

Selection criteria: We selected randomised controlled trials of medication versus placebo or other medication for TTM in adults, children and adolescents.

Data collection and analysis: We used standard methodological procedures expected by Cochrane.

Main results: Twelve studies were included. We identified 10 studies in adults (286 participants) with a mean sample size of 29 participants per trial; one study in children and adolescents (39 participants); and, one study in adults and adolescents (22 participants: 18 adults and 4 adolescents). All studies were single-centre, outpatient trials. Eleven studies compared medication and placebo (334 participants); one study compared two medications (13 participants). Studies were 5 to 13 weeks duration. We undertook meta-analysis only for opioid antagonists as other comparisons contained a single study, or reported insufficient data. Antioxidants versus placebo in adults There was little to no difference in treatment response between antioxidant (35.7%) and placebo groups (28.6%) after six weeks, based on a single trial of silymarin (risk ratio (RR) 2.25, 95% confidence interval (CI) 0.84 to 5.99; 36 participants; low-certainty evidence). We could not calculate differences in number of dropouts as there were no events in either group (18 participants; low-certainty evidence). Antioxidants versus placebo in adolescents There was little to no difference in treatment response between antioxidant (50%) and placebo groups (25%) after six weeks, based on a single trial of silymarin (RR 2.00, 95% CI 0.28 to 14.20; 8 participants; low-certainty evidence). We could not calculate differences in number of dropouts as there were no events in either group (8 participants; low-certainty evidence). Antipsychotics versus placebo in adults There may be greater treatment response in the antipsychotic group (85%) compared to the placebo group (17%) after 12 weeks, based on a single trial of olanzapine (RR 5.08, 95% CI 1.4 to 18.37; 25 participants; low-certainty evidence). We could not calculate differences in number of dropouts as there were no events in either group (25 participants; low-certainty evidence). Cell signal transducers versus placebo in adults There was little to no difference in treatment response between cell signal transducer (42.1%) and placebo groups (31.6%) after 10 weeks, based on a single trial of inositol (RR 1.33, 95% CI 0.57 to 3.11; 38 participants; low-certainty evidence). We could not calculate differences in number of dropouts as there were no events in either group (38 participants; low-certainty evidence). Glutamate modulators versus placebo in adults There is probably greater treatment response in the glutamate modulator group (56%) compared to the placebo group (16%) after 12 weeks, based on a single trial of N-acetylcysteine (RR 3.5, 95% CI 1.34 to 9.17; 50 participants; moderate-certainty evidence). We could not calculate differences in number of dropouts as there were no events in either group (50 participants; low-certainty evidence). Glutamate modulators versus placebo in children and adolescents There was little to no difference in treatment response between the glutamate modulator (25%) and placebo groups (21.1%) in children and adolescents, based on a single trial of N-acetylcysteine (RR 1.19, 95% CI 0.37 to 3.77; 39 participants; low-certainty evidence). There was little to no difference in dropouts due to adverse events between glutamate modulator (5%) and placebo (0%) groups, based on a single trial (RR 2.86, 95% CI 0.12 to 66.11; 39 participants; low-certainty evidence). Opioid antagonists versus placebo in adults There may be little to no difference in treatment response between opioid antagonist (37.5%) and placebo groups (25%) after six to eight weeks, based on two studies of naltrexone, but the evidence is very uncertain (RR 2.14, 95% CI 0.25 to 18.17; 2 studies, 68 participants; very low-certainty evidence). No data were available regarding dropouts due to adverse events. Selective serotonin reuptake inhibitors (SSRIs) versus placebo in adults There were no data available for treatment response to SSRIs. There was little to no difference in dropouts due to adverse events in the SSRI group (5.1%) compared to the placebo group (0%) after 6 to 12 weeks, based on two trials of fluoxetine (RR 3.00, 95% CI 0.33 to 27.62; 2 studies, 78 participants; low-certainty evidence). Tricyclic antidepressants (TCAs) with predominantly serotonin reuptake inhibitor (SRI) actions versus placebo in adults There may be greater treatment response in the TCAs with predominantly SRI actions group (40%) compared to the placebo group (0%) after nine weeks, but the evidence is very uncertain, based on a single trial of clomipramine (RR 5.73, 95% CI 0.36 to 90.83; 16 participants; very low-certainty evidence). There may be increased dropouts due to adverse events in the TCAs with predominantly SRI actions group (30%) compared to the placebo group (0%), but the evidence is very uncertain (RR 4.45, 95% CI 0.27 to 73.81; 16 participants; very low-certainty evidence). TCAs with predominantly SRI actions versus other TCAs in adults There may be greater treatment response in the TCAs with predominantly SRI actions group compared to the other TCAs group after five weeks, based on a single trial comparing clomipramine to desipramine (mean difference (MD) -4.00, 95% CI -6.13 to -1.87; 26 participants; low-certainty evidence). We could not calculate differences in number of dropouts as there were no events in either group (26 participants; low-certainty evidence).

Authors' conclusions: There was insufficient evidence from meta-analysis to confirm or refute the efficacy of any agent or class of medication for the treatment of TTM in adults, children or adolescents. Preliminary evidence suggests there may be beneficial treatment effects for N-acetylcysteine, clomipramine and olanzapine in adults based on four trials, albeit with relatively small sample sizes.

Trial registration: ClinicalTrials.gov NCT00993265 NCT00118014 NCT00354770 NCT00775229 NCT01875445 NCT00182507 NCT02794389 NCT03530800 NCT03797521.

PubMed Disclaimer

Conflict of interest statement

Jacob Hoffman: declares no conflicts of interest.

Taryn Williams: declares no conflicts of interest, outside of her employment by the Medical Research Council of South Africa.

Rachel Rothbart: declares no conflicts of interest.

Samuel Chamberlain: consults for Promentis, and Ieso Digital Health. He receives stipends from Elsevier for editorial work at Comprehensive Psychiatry; and at Neuroscience & Biobehavioral Reviews. Samuel Chamberlain’s role in this research was supported by a Wellcome Trust Clinical Fellowship (reference 110049/Z/15/Z).

Naomi Fineberg: declares that in the past three years, I have held research or networking grants from the European College of Neuropsychopharmacology (ECNP), UK National Institute for Health Research (NIHR), Horizon 2020, Medical Research Council (MRC) and the University of Hertfordshire. In the past three years, I have accepted travel or hospitality expenses, or both, from the British Association for Psychopharmacology (BAP), ECNP, Royal College of Psychiatrists (RCPsych), International College of Neuropsychopharmacology (CINP), International Forum of Mood and Anxiety Disorders, World Psychiatric Association, Indian Association for Biological Psychiatry, and Sun. In the past three years, I have received payment from Taylor and Francis and Elsevier for editorial duties. In the past three years, I have accepted paid speaking engagements sponsored by Abbott and Sun. Previously, I have accepted paid speaking engagements in various pharmaceutical industry‐supported symposia and have recruited patients for various pharmaceutical industry‐sponsored studies in the field of obsessive‐compulsive disorder (OCD) treatment. I lead an NHS treatment service for OCD. I hold Board membership for various registered charities linked to OCD. I give expert advice on psychopharmacology to the UK Medicines and Healthcare products Regulatory Agency (MHRA) and the UK National Institute for Health and Care Excellence (NICE).

Jonathan Ipser: declares no conflicts of interest.

Dan Stein: has received research grants or honoraria, or both, from Lundbeck and Sun.

The South Africa Medical Research Council (SAMRC) Anxiety and Stress Disorders Research Unit has received funding from most pharmaceutical companies involved with psychiatry in South Africa.

Figures

1
1
PRISMA flow diagram
2
2
Risk of bias graph: review authors' judgements about each risk of bias item presented as percentages across all included studies
3
3
Risk of bias summary: review authors' judgements about each risk of bias item for each included study
1.1
1.1. Analysis
Comparison 1: Antioxidants versus placebo in adults, Outcome 1: Treatment response
1.2
1.2. Analysis
Comparison 1: Antioxidants versus placebo in adults, Outcome 2: Reduction of TTM symptom severity
1.3
1.3. Analysis
Comparison 1: Antioxidants versus placebo in adults, Outcome 3: Reduction of comorbid symptoms of depression
1.4
1.4. Analysis
Comparison 1: Antioxidants versus placebo in adults, Outcome 4: Quality of Life ‐ functional disability
1.5
1.5. Analysis
Comparison 1: Antioxidants versus placebo in adults, Outcome 5: Tolerability of treatment ‐ Dropouts due to adverse events
2.1
2.1. Analysis
Comparison 2: Antioxidants versus placebo in adolescents, Outcome 1: Treatment response
2.2
2.2. Analysis
Comparison 2: Antioxidants versus placebo in adolescents, Outcome 2: Reduction of TTM symptom severity
2.3
2.3. Analysis
Comparison 2: Antioxidants versus placebo in adolescents, Outcome 3: Reduction of comorbid symptoms of depression
2.4
2.4. Analysis
Comparison 2: Antioxidants versus placebo in adolescents, Outcome 4: Quality of Life ‐ functional disability
2.5
2.5. Analysis
Comparison 2: Antioxidants versus placebo in adolescents, Outcome 5: Tolerability of treatment ‐ Dropouts due to adverse events
3.1
3.1. Analysis
Comparison 3: Antipsychotics versus placebo in adults, Outcome 1: Treatment response
3.2
3.2. Analysis
Comparison 3: Antipsychotics versus placebo in adults, Outcome 2: Reduction of TTM symptom severity
3.3
3.3. Analysis
Comparison 3: Antipsychotics versus placebo in adults, Outcome 3: Tolerability of treatment ‐ Dropouts due to adverse events
3.4
3.4. Analysis
Comparison 3: Antipsychotics versus placebo in adults, Outcome 4: Tolerability of treatment ‐ Common adverse events (> 20%)
4.1
4.1. Analysis
Comparison 4: Cell signal transducers versus placebo in adults, Outcome 1: Treatment response
4.2
4.2. Analysis
Comparison 4: Cell signal transducers versus placebo in adults, Outcome 2: Reduction of TTM symptom severity
4.3
4.3. Analysis
Comparison 4: Cell signal transducers versus placebo in adults, Outcome 3: Tolerability of treatment ‐ Dropouts due to adverse events
4.4
4.4. Analysis
Comparison 4: Cell signal transducers versus placebo in adults, Outcome 4: Tolerability of treatment ‐ Common adverse events (> 20%)
5.1
5.1. Analysis
Comparison 5: Glutamate modulators versus placebo in adults, Outcome 1: Treatment response
5.2
5.2. Analysis
Comparison 5: Glutamate modulators versus placebo in adults, Outcome 2: Reduction of TTM symptom severity
5.3
5.3. Analysis
Comparison 5: Glutamate modulators versus placebo in adults, Outcome 3: Reduction of comorbid symptoms of depression
5.4
5.4. Analysis
Comparison 5: Glutamate modulators versus placebo in adults, Outcome 4: Quality of Life ‐ functional disability
5.5
5.5. Analysis
Comparison 5: Glutamate modulators versus placebo in adults, Outcome 5: Tolerability of treatment ‐ Dropouts due to adverse events
6.1
6.1. Analysis
Comparison 6: Glutamate modulators versus placebo in children and adolescents, Outcome 1: Treatment response
6.2
6.2. Analysis
Comparison 6: Glutamate modulators versus placebo in children and adolescents, Outcome 2: Reduction of TTM symptom severity
6.3
6.3. Analysis
Comparison 6: Glutamate modulators versus placebo in children and adolescents, Outcome 3: Reduction of comorbid symptoms of depression
6.4
6.4. Analysis
Comparison 6: Glutamate modulators versus placebo in children and adolescents, Outcome 4: Tolerability of treatment ‐ Dropouts due to adverse eventsDropouts due to adverse events
6.5
6.5. Analysis
Comparison 6: Glutamate modulators versus placebo in children and adolescents, Outcome 5: Tolerability of treatment ‐ Common adverse events (> 20%)
7.1
7.1. Analysis
Comparison 7: Opioid antagonists versus placebo in adults, Outcome 1: Treatment response
7.2
7.2. Analysis
Comparison 7: Opioid antagonists versus placebo in adults, Outcome 2: Reduction of TTM symptom severity
7.3
7.3. Analysis
Comparison 7: Opioid antagonists versus placebo in adults, Outcome 3: Reduction of comorbid symptoms of depression
7.4
7.4. Analysis
Comparison 7: Opioid antagonists versus placebo in adults, Outcome 4: Quality of Life ‐ functional disability
7.5
7.5. Analysis
Comparison 7: Opioid antagonists versus placebo in adults, Outcome 5: Tolerability of treatment ‐ Common adverse events (> 20%)
8.2
8.2. Analysis
Comparison 8: SSRIs versus placebo in adults, Outcome 2: Reduction of TTM symptom severity
8.3
8.3. Analysis
Comparison 8: SSRIs versus placebo in adults, Outcome 3: Reduction of comorbid symptoms of depression
8.4
8.4. Analysis
Comparison 8: SSRIs versus placebo in adults, Outcome 4: Tolerability of treatment ‐ Dropouts due to adverse events
8.5
8.5. Analysis
Comparison 8: SSRIs versus placebo in adults, Outcome 5: Tolerability of treatment ‐ Common adverse events (> 20%)
9.1
9.1. Analysis
Comparison 9: TCAs with predominantly SRI actions versus placebo in adults, Outcome 1: Treatment response
9.2
9.2. Analysis
Comparison 9: TCAs with predominantly SRI actions versus placebo in adults, Outcome 2: Reduction of TTM symptom severity
9.3
9.3. Analysis
Comparison 9: TCAs with predominantly SRI actions versus placebo in adults, Outcome 3: Tolerability of treatment ‐ Dropouts due to adverse eventsDropouts due to adverse events
9.4
9.4. Analysis
Comparison 9: TCAs with predominantly SRI actions versus placebo in adults, Outcome 4: Tolerability of treatment ‐ Common adverse events (> 20%)
10.1
10.1. Analysis
Comparison 10: TCAs with predominantly SRI actions versus other TCAs in adults, Outcome 1: Treatment response
10.2
10.2. Analysis
Comparison 10: TCAs with predominantly SRI actions versus other TCAs in adults, Outcome 2: Reduction of TTM symptom severity
10.3
10.3. Analysis
Comparison 10: TCAs with predominantly SRI actions versus other TCAs in adults, Outcome 3: Reduction of comorbid symptoms of depression
10.4
10.4. Analysis
Comparison 10: TCAs with predominantly SRI actions versus other TCAs in adults, Outcome 4: Tolerability of treatment ‐ Dropouts due to adverse events
10.5
10.5. Analysis
Comparison 10: TCAs with predominantly SRI actions versus other TCAs in adults, Outcome 5: Tolerability of treatment ‐ Common adverse events (> 20%)

Update of

References

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References to other published versions of this review

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