Progress in Neuro-Psychopharmacology & Biological Psychiatry 35 (2011) 1087–1092

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Progress in Neuro-Psychopharmacology & Biological

Psychiatry
j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / p n p

Comorbid obsessive–compulsive personality disorder in obsessive–compulsive

disorder (OCD): A marker of severity
Christine Lochner a,⁎, Paul Serebro b, Lize van der Merwe c,d, Sian Hemmings e, Craig Kinnear f,
Soraya Seedat a, Dan J. Stein a,g
a
MRC Unit on Anxiety and Stress Disorders, Department of Psychiatry, University of Stellenbosch, South Africa
b
Obsessive–Compulsive Disorder Association of South Africa, South Africa
c
Biostatistics Unit, Medical Research Council, Tygerberg, South Africa
d
Department of Statistics, University of Western Cape, Bellville, South Africa
e
Department of Psychiatry, University of Stellenbosch, Faculty of Health Sciences, South Africa
f
Department of Biomedical Science, Division of Molecular Biology and Human Genetics, Faculty of Health Sciences, University of Stellenbosch, South Africa
g
Department of Psychiatry and Mental Health, University of Cape Town, South Africa

a r t i c l e i n f o a b s t r a c t

Article history: Introduction: Comorbid obsessive–compulsive personality disorder (OCPD) is well-described in obsessive–
Received 7 December 2010 compulsive disorder (OCD). It remains unclear, however, whether OCPD in OCD represents a distinct subtype
Received in revised form 25 February 2011 of OCD or whether it is simply a marker of severity in OCD.
Accepted 8 March 2011 Materials and methods: The aim of this study was to compare a large sample of OCD subjects (n = 403) with
Available online 14 March 2011
and without OCPD on a range of demographic, clinical and genetic characteristics to evaluate whether
comorbid OCPD in OCD represents a distinct subtype of OCD, or is a marker of severity.
Keywords:
Genetics
Results: Our findings suggest that OCD with and without OCPD are similar in terms of gender distribution and
Obsessive–compulsive disorder age at onset of OC symptoms. Compared to OCD − OCPD (n = 267, 66%), those with OCD + OCPD (n = 136,
Obsessive–compulsive personality disorder 34%) are more likely to present with the OC symptom dimensions which reflect the diagnostic criteria for
Severity OCPD (e.g. hoarding), and have significantly greater OCD severity, comorbidity, functional impairment, and
Subtype poorer insight. Furthermore there are no differences in distribution of gene variants, or response to treatment
in the two groups.
Conclusion: The majority of our findings suggest that in OCD, patients with OCPD do not have a highly
distinctive phenomenological or genetic profile, but rather that OCPD represents a marker of severity.
© 2011 Elsevier Inc. All rights reserved.

1. Introduction
Several studies have documented a high prevalence of obsessive–
compulsive personality disorder (OCPD) in obsessive–compulsive
disorder (OCD). Clinical studies using the DSM-III and DSM-III-R criteria
for OCPD have found OCPD comorbidity rates in OCD ranging between 6
and 31% (Baer et al., 1990; Diaferia et al., 1997; Mancebo et al., 2005).
More recent clinical studies using DSM-IV criteria have found OCPD
Abbreviations: OCPD, obsessive–compulsive personality disorder; OCD, obsessive–
compulsive disorder; OC, obsessive–compulsive; OCD − OCPD, OCD subjects without
OCPD; OCD + OCPD, OCD subjects with OCPD; DSM, Diagnostic and Statistical Manual
of Mental Disorders; SCID-I/P, Structured Clinical Interview for Axis I Disorders Patient
Version; SCID-OCSD, Structured Clinical Interview for Obsessive–Compulsive Spectrum
Disorders; YBOCS-SS, Yale–Brown Obsessive–Compulsive Severity Scale; YBOCS-CL,
Yale–Brown Obsessive–Compulsive Symptom Checklist; DYBOCS, Dimensional Yale
Brown Obsessive–Compulsive Scale; CGI, Clinical Global Impression scale; DP, Disability
Profile questionnaire; SNP's, single nucleotide polymorphisms.
⁎ Corresponding author at: PO Box 19063, Tygerberg, 7505, South Africa. Tel.: + 27
21 938 9229; fax: + 27 21 933 5790.
E-mail address: cl2@sun.ac.za (C. Lochner).
comorbidity rates ranging from 23% to 32% (Albert et al., 2004; Coles et al.,
2008; Pinto et al., 2006; Samuels et al., 2000). These rates are substantially
higher than prevalence rates of OCPD reported in community samples,
which range from 0.9% to 2.0% (Samuels et al., 2002; Torgersen et al.,
2001). A strong association between OCPD and OCD is supported by
findings that OCPD occurs more frequently in individuals with OCD than
in individuals with other anxiety disorders (e.g. panic disorder and social
phobia) (Crino and Andrews, 1996).
Growing interest in the clinical heterogeneity of OCD raises the
question of whether OCD with OCPD is a distinctive clinical subtype of
OCD, or whether OCPD is merely a marker of severity in OCD. Coles et al.
(2008) recently reported that, compared with OCD subjects without
OCPD (OCD −OCPD), OCD subjects with OCPD (OCD +OCPD) had a
significantly younger age of first onset of OC symptoms, and had higher
rates of symmetry and hoarding obsessions and cleaning, ordering,
repeating and hoarding compulsions. They concluded that OCD+ OCPD
represented a distinctive subtype of OCD. This conclusion was also
supported by their findings that subjects with OCD+ OCPD have higher
rates of comorbid anxiety disorders and avoidant personality disorder,
and significantly lower ratings of global functioning and more impaired

0278-5846/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.pnpbp.2011.03.006
1088 C. Lochner et al. / Progress in Neuro-Psychopharmacology & Biological Psychiatry 35 (2011) 1087–1092
social functioning. Additional support for a distinctive subtype of OCD
could derive from data showing that OCD patients with OCPD have
distinctive treatment responses (Cavedini et al., 1997) or distinctive
distribution of gene variants, as has been suggested for OCD with
comorbid tics or Tourette's disorder (e.g. do Rosario-Campos et al., 2005;
Grados et al., 2001).
However, some of the Coles et al. findings may not provide sufficient
support for an OCD/OCPD subtype but rather merely indicate that OCPD
in OCD reflects a more severe (OC) disorder. As illustrated by their study
findings and that of others (e.g. Diaferia et al., 1997), OC personality traits
may closely reflect OCD symptomatology – for example, having very high
standards about what is right or wrong, preoccupation with detail and
perfectionism, and hoarding (Eisen et al., 2006) – and may be best
understood as a relatively non-specific marker of symptom severity in
patients predominantly presenting with these types of OC symptoms
(Bejerot et al., 1998). A view of OCPD as an OC symptom severity marker
would be supported by findings that patients with and without OCPD
show similar clinical profiles (other than symptoms reflecting OC traits or
degree of OCD severity), respond to similar treatments (albeit perhaps
not as robustly), and show no difference in terms of genetic profiles; in
the same way that poor insight in OCD may represent a severity marker
(Matsunaga et al., 2002).
The aim of the current exploratory study was to build on previous
work investigating the relationship between OCD and OCPD. We
compared a large group of OCD subjects with and without OCPD on a
selected range of demographic variables (i.e. gender and age), clinical
characteristics — including age of onset of OCD, illness severity,
comorbidity, functional impairment and treatment response, and
polymorphisms in genes involved in monoamine function recently
hypothesized to be relevant to OCD, to evaluate whether OCD + OCPD
comorbidity can be considered a distinct subtype of OCD, or whether
OCPD is simply a marker of severity in OCD. A distinctive treatment
response or genotype distribution profile may provide support for
OCD + OCPD as a distinct OCD subtype. On the other hand, if it is
found that OCD + OCPD is characterized by similar but higher rates of
specific OC symptoms/traits and consequent increased distress and
disability, this would rather suggest that OCPD is a marker of severity
in OCD.
2. Materials and methods
2.1. Subjects
Patients with a primary diagnosis of OCD who were referred from a
wide range of sources (including the OCD Association of South Africa,
specialist psychiatrists, and community based primary care practi-
tioners), were included in the study. Patients with a history of
psychotic disorder were excluded. All participants were interviewed
by a clinical psychologist or other clinician with expertise in the field,
and met the Diagnostic and Statistical Manual of Mental Disorders
(DSM-IV) criteria (American Psychiatric Association, 1994) for OCD
on the Structured Clinical Interview for Axis I Disorders-Patient
Version (SCID-I/P) (First et al., 1998). Subjects were enrolled
irrespective of their current treatment status or phase of treatment.
Referring clinicians were contacted to establish, where possible, a
longitudinal expert opinion on the diagnostic status of referred
patients.
The present study formed part of a larger project focused on the
phenomenology and neurobiological underpinnings of anxiety dis-
orders that has been conducted over several years. The Institutional
Review Board of the University of Stellenbosch (South Africa)
approved the protocol, and all subjects provided written informed
consent after being presented with a complete description of the
study. The study was conducted in accordance with the guidelines of
the Declaration of Helsinki.
2.2. Interview
Specific demographic data, including current age and gender were
entered into the dataset. In addition to the SCID-I/P and the Structured
Clinical Interview for Axis II-Disorders (SCID-II) (First et al., 1998), the
interview also included the Structured Clinical Interview for Obses-
sive–Compulsive Spectrum Disorders (SCID-OCSD) to determine the
presence of comorbid putative obsessive–compulsive spectrum
disorders (du Toit et al., 2001). The assessment also addressed the
presence/absence of tics (current and/or past) and their nature (e.g.
motor and/or vocal).
In addition, the Yale–Brown Obsessive–Compulsive Severity Scale
(YBOCS-SS) and the Yale–Brown Obsessive–Compulsive Symptom
Checklist (YBOCS-CL) were used to allow for the assessment of the
severity and typology of obsessive–compulsive symptoms, respec-
tively (Goodman et al., 1989b). These two clinician-rated scales
represent the two major sections of the Yale–Brown Obsessive–
Compulsive Scale (YBOCS). The YBOCS-SS is composed of 10 items,
with each item rated on a five-point scale (0 — no symptoms to 4 —
extreme symptoms). There is a total obsession score (maximum total
for obsessions: 20), a total compulsion score (maximum total for
compulsions: 20), and a combined total score (maximum total score:
40). Each of the 74 items of the YBOCS-CL represents a single
obsessive or compulsive symptom. These items are sometimes
grouped together into 13 to 14 broad or major symptom categories
based on their core characteristics. The YBOCS was developed in 1986,
has very frequently been used in research and clinical settings since,
and is generally assumed to have good validity and reliability
(Goodman et al., 1989b; Goodman et al., 1989a). The Dimensional
Yale Brown Obsessive–Compulsive Scale (DYBOCS) (do Rosario-
Campos et al., 2006) was also administered and enabled assessment
of the time spent on, the levels of distress associated with, and the
impairment of functioning and relationships due to each identified
OCD symptom category. Severity scores range from 0 to 15, with 15
indicating the worst possible severity.
Patients' level of insight into the senselessness or excessiveness of
their symptoms was assessed using the relevant YBOCS-SS item
(Goodman et al., 1989b). Where applicable, response to previous or
current pharmacotherapy was assessed retrospectively. For patients
who have received an adequate trial of cognitive–behavioral therapy
(i.e. 8 sessions or more), treatment response was also assessed. In
both instances, the global improvement item of the Clinical Global
Impression (CGI) scale was used to assess treatment response;
subjects with CGI scores of 1 (‘very much improved’) or 2 (‘much
improved’) were defined as responders (Guy, 1976).
The Disability Profile questionnaire (DP) (Schneier et al., 1994)
was included in the interview to assess current and lifetime functional
impairment due to OCD in eight domains. The DP was initially
developed for use in patients with social anxiety disorder, and its
psychometric properties remain to be fully established. Nevertheless,
the scale has since been used to assess disability in patients with other
anxiety disorders as well (Mogotsi et al., 2000).
2.3. DNA extraction, single nucleotide polymorphisms (SNP's) selection
and genotyping
Venous blood (20–30 ml) was drawn from all participants and
genomic DNA was subsequently extracted from each sample using the
standard phenol/chloroform method. DNA from the South African
Caucasian subset (N = 302) of the total OCD sample (OCD + OCPD:
N = 106; OCD − OCPD: N = 196), including a subset of patients
(N = 159) from Afrikaner descent (OCD + OCPD: N = 46; OCD −
OCPD: N = 113), was genotyped. The Afrikaner population of South
Africa is of Dutch, German and French origin, and their history and
population dynamics over the past 350 years have led to a relatively
small gene pool making it especially suitable for genetics
 C. Lochner et al. / Progress in Neuro-Psychopharmacology & Biological Psychiatry 35 (2011) 1087–1092
investigations (de Jager et al., 1996; Moolman-Smook et al., 1999;
Starfield et al., 1997). Furthermore, investigations carried out in this
population have indicated evidence of strong background linkage
disequilibrium, extending over relatively large chromosomal regions
(Gordon et al., 2000; Hall et al., 2002).
Polymorphisms within serotonergic (5HTT) and dopaminergic
(COMT, MAO-A, and DRD3 and DRD4, respectively) systems were
genotyped according to previously described protocols 5-HTTLPR
(Kinnear et al., 2000); COMT rs4680 [Val158Met] (Karayiorgou et al.,
1997), MAO-A (C1460T/EcoRV) (Hotamisligil and Breakefield, 1991),
DRD4 exon III variable number of tandem repeat polymorphism
[VNTR] (Lichter et al., 1993) and DRD3 rs6280 [Ser9Cys] (Crocq et al.,
1992).
Assessment of genotypes was conducted blind to diagnosis, and by
two independent investigators. Genotypes were only used if the
genotyping results obtained by the two independent investigators
concurred. In order to ensure genotyping accuracy, replicate samples
were included in the PCR-amplification reactions and subsequent
genotyping procedures, and only assays that provided 100% concor-
dance between replicates were utilized in the analyses.
Not all participants were genotyped in the present investigation. A
major factor limiting the number of samples analyzed was the lack of
a renewable source of DNA for patients. As noted previously, the
present study forms part of a larger project that has been conducted
over a period of several years. A number of concurrent investigations
using the same samples have been performed resulting in the
depletion of some DNA samples. This explains the differences in the
number of subjects available for genotyping of the SNPs.
2.4. Data analysis
If 30% of the group of OCD − OCPD patients had a specific
characteristic (e.g. in terms of comorbidity or genotype), our group
sizes (of 136 with, and 267 without OCPD, respectively) provide 80%
power at a 5% significance level to detect a proportion of 42% or greater
(an absolute difference of 12%; a 40% increase) in the OCD+OCPD group.
Demographic, clinical and genetic findings were compared
between OCD + OCPD and OCD − OCPD patients. All descriptive
statistics were stratified between the OCPD groups. As the gender
differences were not significant, we do not provide gender-stratified
summary statistics. Logistic regression (generalized linear model with
binomial family and default logit link) was used to model the risk of
OCPD, providing the p-values in the tables. Logistic regression makes
it possible to adjust for known confounders such as age and gender by
including them in the models as covariates. The models for the
demographic and clinical variables were unadjusted. The tests for
symptom categories and comorbidities were adjusted for age and
gender, because age was found to differ significantly between the
groups, and given the role of gender in influencing the clinical
phenomenology of OCD (Lochner and Stein, 2001) and its impact on
genetic findings (Cavallini et al., 1999; Lochner et al., 2004; Nestadt
et al., 2000).
Table 1
OCD with OCPD vs. OCD without OCPD: Demographic and clinical data.
Variables
N 136
Gender, male (%)
Age, years (mean ± SD)
Employment, unemployed (%)
Age at onset of OC symptoms, years (mean ± SD)
Current (past 2 weeks) disability (DP) score (mean ± SD)
Lifetime disability (DP) score (mean ± SD)
OCD total severity (YBOCS-SS) score (mean ± SD)
a
P-values are from unadjusted logistic regression models.
1089
Because we did multiple tests on related variables on the same
group of individuals, and as there is not always a consensus on how to
appropriately adjust for this in analyses (Rodriguez-Murillo and
Greenberg, 2008), we used a token 1% as our critical significance level,
and not the usual 5%. We interpreted p-values above 1% but below 5%
as weakly significant or showing a trend toward significance.
3. Results
3.1. Demographic and clinical differences
Demographic and clinical data are summarized in Table 1. Four
hundred and three patients with a primary diagnosis of OCD (n = 403;
199 males and 204 females), with ages ranging between 18 and
75 years (mean age (SD): 35 (12)), took part in the study. One third
(34%; n = 136) of the total group presented with comorbid OCPD.
OCD + OCPD patients were significantly older than the OCD − OCPD
patients at the time of the interview. The differences in gender
distribution and age at onset of OC symptoms between OCD + OCPD
and OCD − OCD patients were not significant. In terms of clinical
phenomenology, compared to the OCD − OCPD group, those with
OCD + OCPD reported significantly more current and lifetime func-
tional impairment due to OCD. In addition, patients with the dual
diagnosis had significantly greater OCD severity. They also had
significantly higher compulsion scores (t = −3.399, p = 0.001).
The OCD + OCPD and OCD − OCPD patients currently presenting
with the different OC symptom categories (YBOCS-CL) were com-
pared (Table 2). Patients with the dual diagnosis were significantly
more likely to present with symmetry obsessions with checking,
repeating, counting, ordering, and arranging compulsions, and
hoarding obsessions with hoarding/collecting compulsions.
Further investigation of the severity of each OCD symptom
category as assessed with the D-YBOCS indicated that severity of
symmetry, ordering, counting and arranging symptoms were signif-
icantly higher in the OCD + OCPD group compared to the OCD − OCPD
group (t = −2.802, p = 0.006).
According to interviewer ratings, in comparison to the OCD− OCPD
group, patients with OCD+OCPD tended to have poorer insight into the
senselessness or excessiveness of their obsessions or compulsive
behaviors based on their beliefs expressed at the time of the interview
(t=−2.388, p =0.018).
Rates of mood, anxiety and OCD spectrum disorders were
generally higher in OCD + OCPD (Table 3). Using 1% as the threshold
for significance, we documented significantly higher rates of anorexia
nervosa (p = 0.008) in the OCD + OCPD group.
In terms of treatment history, a large number of patients (n = 322,
79.9% of the total sample) indicated that they had received one or
more medication trials for the treatment of OCD specifically. Of those,
136 (42.24%) had a good treatment response (i.e. CGI-I b=2). The
number of OCD + OCPD (n = 44, or 39.6%) and OCD − OCPD (n = 92,
or 43.6%) patients who responded to pharmacotherapy was similar
(t = 0.469, p = 0.493). Of the total sample, 155 patients indicated that
they have received an adequate trial of CBT previously and 68 of those
OCD + OCPD OCD − OCPD P-valuea
267
64 (47%) 72 (51%) 0.5757
38.1 ± 12.2 33.53 ± 12.2 0.0005
12 (9%) 11 (4%) 0.0896
18.6 ± 11.5 17.1 ± 9.2 0.1664
12.8 ± 5.7 10.9 ± 5.4 0.0046
8.6 ± 5.5 6.8 ± 4.6 0.0029
21.9 ± 7.3 19.4 ± 7.3 0.0016
1090 C. Lochner et al. / Progress in Neuro-Psychopharmacology & Biological Psychiatry 35 (2011) 1087–1092

Table 2 Table 4
OCD with OCPD vs. OCD without OCPD: OC Symptom categories. Details of the polymorphisms investigated in a Caucasian subset (N = 302): Genotype
counts and genotype.
OC symptom category OCD + OCPD OCD − OCPD P-valueb
(current)a Genes (polymorphisms)* OCD + OCPD n (%) OCD − OCPD n (%) P-valuea
n (%) n (%)
Male Female Male Female
Obsessions
Aggressive or harm-related 76 (55.9%) 139 (52.1%) 0.2028 MAO-A (C1460T/EcoRV) 0.9084
Contamination 77 (56.6%) 124 (46.4%) 0.0203 C/C 15 (65) 13 (62) 15 (58) 14 (61)
Sexual 21 (15.4%) 49 (18.4%) 0.8886 C/T – 6 (29) – 8 (35)
Hoarding/saving 41 (30.1%) 33 (12.4%) 0.0001 T/T 8 (35) 2 (10) 11 (42) 1 (4)
Religious 49 (36.0%) 71 (26.6%) 0.0178 5HTTLPR (SLC6A4) 0.8946
Symmetry 80 (58.8%) 86 (32.2%) b 0.0001 L/L 14 (29) 11 (24) 25 (30) 24 (30)
Somatic or body-focused 38 (27.9%) 84 (31.5%) 0.7022 L/S 25 (51) 21 (47) 41 (50) 35 (43)
S/S 10 (20) 13 (29) 16 (20) 22 (27)
Compulsions COMT rs4680 (Val158Met) 0.8214
Cleaning or washing 69 (50.7%) 109 (40.8%) 0.0351 AA(met158met) 10 (20) 14 (32) 19 (24) 20 (23)
Checking 102 (75%) 140 (52.4%) b 0.0001 AG(met158val) 27 (54) 22 (50) 46 (57) 44 (51)
Repeating rituals 73 (53.7%) 95 (35.6%) 0.0001 GG(val158val) 13 (26) 8 (18) 15 (19) 23 (26)
Counting 55 (40.4%) 62 (23.2%) 0.0008 DRD3 rs6280 (ser9cys) 0.6323
Ordering and arranging 72 (52.9%) 65 (24.3%) b 0.0001 AA(ser9ser) 21 (58) 15 (48) 22 (47) 22 (45)
Hoarding 41 (30.1%) 27 (10.1%) b 0.0001 AG(ser9cys) 11 (31) 12 (39) 17 (36) 21 (43)
Mental 85 (62.5%) 132 (49.4%) 0.012 GG(cys9cys) 4 (11) 4 (13) 8 (17) 6 (12)
a DRD4 (exon III VNTR) 0.2506
The Yale–Brown Obsessive–Compulsive Symptom Checklist (YBOCS-CL) were used
A4/A4 26 (58) 22 (54) 20 (41) 21 (46)
to assess obsessive–compulsive symptoms.
b A4/A7 7 (16) 5 (12) 13 (27) 9 (20)
P-values are from logistic regression models, adjusted for gender and age.
A4/A2 5 (11) 5 (12) 4 (8) 9 (20)
A4/A3 4 (9) 4 (10) 7 (14) 2 (4)
A4/A5 1 (2) 1 (2) 0 (0) 1 (2)
A7/A7 1 (2) 4 (10) 2 (4) 1 (2)
(44%) had a good treatment response (i.e. CGI-I b=2). Response rates A7/A2 0 (0) 0 (0) 0 (0) 1 (2)
to CBT were similar for OCD + OCPD (n = 24, or 46%) and OCD − OCPD A7/A3 0 (0) 0 (0) 1 (2) 0 (0)
(n = 44, or 43%) groups (t = 0.165, p = 0.684). A2/A2 0 (0) 0 (0) 1 (2) 2 (4)
A3/A3 1 (2) 0 (0) 0 (0) 0 (0)
A3/A6 0 (0) 0 (0) 1 (2) 0 (0)
3.2. Genetics
⁎MAO-A (C1460T/EcoRV): Monoamine oxidase inhibitor A (C1460T/EcoRV); MAO-A is X-
(gender) linked, so counts and frequencies for male alleles are placed next to
Details for the SNP's investigated and their genotype frequencies
corresponding homozygotes.
in the OCD + OCPD and OCD − OCPD groups are presented in Table 4. 5HTTLPR (SLC6A4): Serotonin transporter.
The mean heterozygosity for all polymorphisms was 0.47 (range: COMT rs4680(Val158Met): Catechol-O-methyltransferase rs4680 (Val158Met).
0.43 to 0.50). All of the polymorphisms were found to obey HWE, even DRD3 rs6280 (ser9cys): Dopamine receptor 3 (ser9cys).
though we were not genotyping healthy individuals. (Results not DRD4 (exon III VNTR): Dopamine receptor 4 exon III variable number of tandem repeat
polymorphism (VNTR).
shown.) The analyses were repeated in an Afrikaner subset (n = 159; OCD + OCPD: n = 46; OCD
− OCPD = n = 113); there were no significant differences between OCD + OCPD and
OCD − OCPD in terms of genotype distribution (results are not shown here).
Table 3 There were no significant differences between the OCD + OCPD and OCD − OCPD
OCD patients with OCPD vs. OCD patients without OCPD: Comorbidity rates of mood, groups in terms of genotype distribution; therefore further analyses (i.e. investigation
anxiety and OCD spectrum disorders. of allele distribution) were not done.
a
P-values are from single polymorphism logistic regression association analyses,
Comorbid psychiatric disorders OCD + OCPD OCD − OCPD P-valueb
adjusted for gender, age and comorbid depression.
(lifetime)a
n (%) n (%)

Major depressive disorder 94 (69.1%) 174 (65.2%) 0.3667

Dysthymic disorder 31 (22.8%) 46 (17.2%) 0.1726 No statistically significant differences in any of the genotype or
Bipolar disorder 4 (2.9%) 6 (2.2%) 0.7608 allele frequencies in both the Caucasian and Afrikaner subsets, also
Panic disorder with/out agoraphobia 27 (19.9%) 30 (11.2%) 0.0597 after adjusting for gender and comorbid depression, were observed
Social anxiety disorder 16 (11.8%) 24 (9%) 0.3578
Specific phobia 20 (14.7%) 36 (13.5%) 0.8270
between OCD + OCPD and OCD − OCPD patients.
Posttraumatic stress disorder 10 (7.4%) 6 (2.2%) 0.0119
Generalized anxiety disorder 28 (10.5%) 27 (19.9%) 0.0414
Hypochondriasis 9 (6.6%) 4 (1.5%) 0.0118 4. Discussion
Body dysmorphic disorder 12 (8.8%) 15 (5.6%) 0.2427
Anorexia nervosa 12 (8.8%) 5 (1.9%) 0.0008
Bulimia nervosa 11 (8.1%) 8 (3%) 0.0137 The aim of this study was to compare a large group of OCD subjects
Tics 21 (15.4%) 25 (9.4%) 0.0405 with and without OCPD on a range of demographic variables, clinical
Alcohol dependence 6 (4.4%) 6 (2.2%) 0.3421 measures and genetic variants to evaluate whether OCD + OCPD
Alcohol abuse 11 (8.1%) 21 (7.9%) 0.7516 comorbidity represents a distinct subtype of OCD, or whether OCPD is
Intermittent explosive disorder 27 (19.9%) 31 (11.6%) 0.0231
best understood as a marker of severity in OCD.
Kleptomania 10 (7.4%) 10 (3.7%) 0.1818
Trichotillomania 12 (8.8%) 11 (4.1%) 0.0433 One third of the total sample presented with comorbid OCPD. Our
Self-injury 26 (19.1%) 38 (14.2%) 0.0997 findings suggested that (i) OCD patients with and without OCPD had
Impulsive shopping 11 (8.1%) 16 (6%) 0.5160 similar gender distribution, age at onset of OC symptoms, distribution
Hypersexuality disorder 12 (8.8%) 13 (4.9%) 0.0676
of gene variants, and treatment response and ii) compared to patients
The table only includes those disorders that occur at a rate of 5% or more in the sample with OCD − OCPD, those with OCD + OCPD were more likely to
as a whole. present with the OC symptom categories which reflect the diagnostic
a
Diagnostic tools used were the Structured Clinical Interview for Axis I Disorders —
Patient Version (SCID-I/P) and the Structured Clinical Interview for Obsessive–
criteria for OCPD (e.g. hoarding), had significantly greater OCD
Compulsive Spectrum Disorders (SCID-OCSD). severity, had more comorbidity, had increased functional impairment,
b
P-values are from logistic regression models, adjusted for gender and age. and had worse insight.
 C. Lochner et al. / Progress in Neuro-Psychopharmacology & Biological Psychiatry 35 (2011) 1087–1092
These findings are consistent with those from a previous study
which found that individuals with OCD + OCPD had a greater severity
of compulsions, significantly higher rates of comorbid anxiety
disorders, significantly lower ratings of global functioning and
significantly more impaired social functioning compared to those
without OCPD (Coles et al., 2008). However, taken together with our
findings that there are no differences in genetic findings or treatment
response, we would interpret these findings as support for the
hypothesis that OCD + OCPD represents a marker of severity in OCD,
rather than a distinct subtype of OCD. While any comorbidity in OCD
may arguably also be associated with increased illness severity or
impairment, OCPD may be a relatively specific marker of severity
given its high prevalence in OCD, and its comparatively lower
prevalence in other mood and anxiety disorders (e.g. Diaferia et al.,
1997; Skodol et al., 1995).
We found that OCD + OCPD patients were more likely to present
with hoarding and symmetry, ordering, counting and arranging
symptoms compared to those without OCPD. This finding is
reminiscent of work showing that OCD with tics is associated with
particular symptom dimensions (e.g. Baer, 1994). Our finding may
thus be somewhat supportive of the hypothesis that OCD + OCPD
represents a distinctive clinical subtype of OCD. However, many of the
OC symptom dimensions found to be associated with comorbid OCPD
are precisely those which are mentioned in the diagnostic criteria for
this personality disorder. For example, in the Collaborative Longitu-
dinal Personality Disorders Study, Eisen et al. (2006) showed that
three of the eight DSM-IV OCPD criteria, i.e. – hoarding, perfectionism,
and preoccupation with detail – were significantly more frequent in
subjects with OCD than in subjects without OCD. Thus, meeting
diagnostic criteria for OCPD in OCD may also merely point to the
presence of more severe OCD symptomatology.
The study limitations should be noted. Given the retrospective
nature of this data collection, and the relatively small number of gene
variants examined, the possibility of false negative findings (type II
error) cannot be excluded (Arnold et al., 2004; Hall et al., 2003). For
example, it is possible that OCPD is a predictor of negative treatment
response (for a review, see Keeley et al., 2008). In addition, it may be
suggested that OCPD in relatives of individuals with OCD represents a
sub-clinical form of OCD (Samuels et al., 2000), and perhaps even an
endophenotype for OCD susceptibility; we did not however, include
data from relatives of OCD patients in the present investigation.
In conclusion, the majority of our findings suggest that comorbid
OCPD may be a marker of severity in OCD. It may be useful to assess
OCPD traits as well as a range of other personality traits and disorders
in patients presenting with OCD (e.g. Poyurovsky et al., 2008; Sobin
et al., 2000). The presence of OCPD is often accompanied by other
indicators of increased severity, and so points to a need for timely and
robust treatment intervention.
Acknowledgements
We are grateful to the Medical Research Council (MRC) of South
Africa and the Crossley Foundation for their support. The Obsessive–
Compulsive Disorder Association of South Africa played a crucial role
in undertaking this work.
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