Management of Seymour Fractures in Children and Adolescents: A Systematic Review and Meta-Analysis.

PURPOSE: Seymour fractures are injuries with a potentially high risk of infection and osteomyelitis. The optimal management of this pediatric open fracture is unknown. We performed a systematic review and meta-analysis to summarize the best evidence for these fractures and determine their optional management based on primary clinical studies. METHODS: A Preferred Reporting Items for Systematic Reviews and Meta-Analyses-compliant systematic review and meta-analysis was performed. A comprehensive search strategy was applied to the MEDLINE, EMBASE, Cumulative Index to Nursing and Allied Health Literature, Cochrane Library, and gray literature databases (from May 1966 to April 15, 2020). Studies describing patients under the age of 18 years with Seymour fractures were included. Treatment was grouped based on debridement and antibiotic status as well as the timing of these interventions. The primary outcome was infection. The secondary outcomes included malunion, physeal disturbance, and nail dystrophy. RESULTS: The searches helped identify 56 records, of which 10 nonrandomized studies met our inclusion criteria, comprising 352 patients and 355 fractures. Early (<48 hours) debridement was associated with significantly less risk of infection (risk ratio [RR] = 0.28 [95% CI, 0.12-0.64]) and malunion (RR = 0.25 [95% CI, 0.07-0.99]). Prophylactic (<24 hours) antibiotics significantly reduced the risk of infection (RR = 0.21 [95% CI, 0.10-0.43]). In addition, prophylactic antibiotics and debridement were associated with a 70% reduction in the risk of infection (RR = 0.30 [95% CI, 0.11-0.83]). Over one-third of patients with delayed presentation (median 8.5 days) were infected at presentation. CONCLUSIONS: The high-risk nature of Seymour fractures may be mitigated by prompt recognition and early, basic interventions, which can usually be performed in any setting. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic IV.

Learning from lawsuits: Ten-years of NHS litigation authority claims against 11 surgical specialities in England.

INTRODUCTION: Medico-legal claims are a drain on NHS resources and promote defencive practice. The litigious burden of surgery in England has not been previously described. This paper describes trends over ten years of claims made against the NHS across 11 surgical specialities. MATERIALS AND METHODS: Data were requested for all claims received by the NHS Litigation Authority (NHSLA) from 2004 to 2014. Surgical specialities included cardiothoracic, general, neurosurgery, obstetric, oral and maxillofacial (OMFS), orthopaedic, otorhinolaryngology, paediatric, plastic, urology and vascular surgery. A literature review of peer-reviewed publications was performed with search terms 'NHSLA' and 'Surgery'. RESULTS: The NHS paid out approximately £1.5 billion across 11 surgical specialities from 2004 to 2014. Orthopaedic, obstetric and general surgery received the largest number of claims per year, and paediatric surgery the least. The mean time from registration of claim with the NHSLA to settlement was 25.5 months (range 17.8 months-35 months). Neurosurgery was responsible for the highest average amount paid per claim, and OMFS the lowest. Failure/delay in treatment and/or diagnosis and failure to warn/adequately consent were the three leading types of claim. 806 never events were successfully claimed for during the ten-year period. DISCUSSION AND CONCLUSION: Sharing information and good practice should be a priority for surgical professionals. Lessons learnt from medico-legal claims are transferrable in strategic planning. This pan-speciality report has demonstrated considerable burden on the NHS and should promote improvement in practice on an individual level in addition to providing systems based recommendations to NHS and international organisations.

Defining Normal Parameters for the Male Nipple-Areola Complex: A Prospective Observational Study and Recommendations for Placement on the Chest Wall.

BACKGROUND: The nipple-areola complex (NAC) is important aesthetically and functionally for both sexes. Methods for positioning the NAC in males are less well established in the literature compared to females but are just as important. OBJECTIVES: This study aims to determine the normal parameters for the male NAC, to review literature, and to present a reliable method for preoperative placement. METHODS: Normal male patients, with no prior chest wall conditions, were prospectively recruited to participate. General demographics and chest wall dimensions were recorded-sternal notch to nipple (SNND), internipple (IND), anterior axillary folds distances (AFD), NAC, and chest circumference were measured. Comparisons were made using t test and ANOVA. RESULTS: One hundred and fifty-eight patients were recruited (age range, 18-90 years); mostly (86.7%) with normal or overweight BMI. The IND averaged 249.4 mm, the SNND averaged 204.2 mm, and the AFD averaged 383.8 mm. Areola diameter averaged 26.6 mm and for the nipple, 6.9 mm. The IND:AFD ratio was 0.65. There was no statistical difference in the IND:AFD ratio, SNND, or NAC parameters comparing different ethnic groups. The SNND increased with greater BMI (P ≤ 0.001). Using these data, we suggest ideal NAC dimensions and devised a simple method for positioning of the NAC on the male chest wall. CONCLUSIONS: This is the largest study, with the widest range in age and BMI, to date on this topic. Although fewer men than women undergo surgery to the breast, there is a growing awareness for enhancing the appearance of the male chest wall.

Growth in children with choledochal malformations: effect of the Roux loop.

PURPOSE: Excision and biliary reconstruction using a Roux loop is the current standard for choledochal malformation (CM). This is un-physiological, delivering bile beyond the duodenum and excluding a significant length of the jejunum from intestinal absorption. We investigated whether this had an effect on post-operative growth. METHODS: Retrospective case-note analysis of children surgically treated for CM. Growth variables were converted to standard deviation scores (SDS) and compared against population norms. P < 0.05 was significant. RESULTS: From 1994 to 2014, 135 children (<16 years) were identified. Median age at surgery was 3.3 (IQR 1.5-7) years. Morphology included: type 1 Cystic (n = 54, 40%), type 1 Fusiform (n = 58, 43%) and type 4 (intra and extra-hepatic) (n = 22, 16%). There was pre-operative growth failure [median weight SDS = -0.4 (-1.2 - 0.4), P = 0.0004] with a similar trend for height [SDS = -0.38 (-1.2 - 0.5), P = 0.08)]. This correlated with presentation bilirubin (r s = -0.24, P = 0.004), GGT (r s = -0.27, P = 0.002) and AST (r s = -0.27, P = 0.002) but not morphology (P = 0.82) or presentation (P = 0.4). Median follow-up was 1.9 (0.6-4.7) years, during which time both height (P = 0.73) and weight (P = 0.45) reverted to normal. CONCLUSION: This is the first report of growth in children with CM following a Roux-loop reconstruction and showed pre-operative growth failure probably attributed to a period of biliary obstruction but catch-up growth when corrected.

The optimal management of Seymour fractures in children and adolescents: a systematic review protocol.

BACKGROUND: Seymour fractures are open, displaced juxta-epiphyseal fractures of the distal phalanx, with an overlying nail bed laceration that occur in children and adolescents with an open physis. This fracture occurs rarely, but its potential consequences are clinically significant. Due to anatomical particulars and proximity to the growth plate, this open fracture may result in soft tissue infection and osteomyelitis, leading to growth arrest and persistent mallet deformity. At present, there is no consensus as to the optimal management of Seymour fractures. The objective of this study will be to systematically evaluate the existing evidence on the management of Seymour fractures in children and adolescents and to establish what are the most important factors pertaining to an uncomplicated recovery. METHODS: We designed and registered a study protocol for a systematic review of randomised controlled trials and observational studies. A comprehensive literature search will be conducted (from inception to present) in MEDLINE, EMBASE, CINAHL and Cochrane Library databases. Grey literature will be identified through searching Open Grey and dissertation databases using an exhaustive search strategy. All clinical studies examining the management of Seymour fractures will be included. The interventions (irrigation and debridement; prophylactic antibiotics) and their timings (early vs late) will be compared to no antibiotics and no debridement. Primary outcome measures will be the incidence of superficial and deep infection. Secondary outcomes will include other adverse events such mal-union, non-union, need for re-operation, physeal disturbance and nail dystrophy/atrophy. Two independent reviewers will screen all citations, full-text articles, and abstract data. Conflicts will be resolved through discussion. The study methodological quality (or bias) will be appraised using an appropriate tool. A narrative synthesis will be performed. If data permits, we will conduct random-effects meta-analysis where appropriate. DISCUSSION: This review will provide evidence for the management of Seymour fractures, based on a cumulation of existing smaller studies. Due to the rarity of this fracture pattern, included studies are expected to be mainly observational and prone to bias; however, there is value in summarising the evidence to guide clinicians. SYSTEMATIC REVIEW REGISTRATION: Systematic review registration: PROSPERO CRD42020153726.

Tryptophan hydroxylase polymorphism and suicidality in unipolar and bipolar affective disorders: a multicenter association study.

BACKGROUND: Being the rate-limiting enzyme in the biosynthesis of serotonin, the tryptophan hydroxylase gene (TPH) has been considered a possible candidate gene in bipolar and unipolar affective disorders (BPAD and UPAD). Several studies have investigated the possible role of TPH polymorphisms in affective disorders and suicidal behavior. METHODS: The TPH A218C polymorphism has been investigated in 927 patients (527 BPAD and 400 UPAD) and their matched healthy control subjects collected within the European Collaborative Project on Affective Disorders. RESULTS: No difference of genotype distribution or allele distribution was found in BPAD or UPAD. No statistically significant difference was observed for allele frequency and genotypes counts. In a genotype per genotype analysis in UPAD patients with a personal history of suicide attempt, the frequency of the C-C genotype (homozygosity for the short allele) was lower in UPAD patients (24%) than in control subjects (43%) (chi(2) = 4.67, p =.03). There was no difference in allele or genotype frequency between patients presenting violent suicidal behavior (n = 48) and their matched control subjects. CONCLUSIONS: We failed to detect an association between the A218C polymorphism of the TPH gene and BPAD and UPAD in a large European sample. Homozygosity for the short allele is significantly less frequent in a subgroup of UPAD patients with a history of suicide attempt than in control subjects.

Serotonin-2C and serotonin-1A receptor genes are not associated with psychotic symptomatology of mood disorders.

The serotonergic system is involved in both pathophysiology and treatment of mood disorders. In the present study we investigated the possible influence of the polymorphisms of the serotonin-1A and 2C receptor genes on the symptomatology of mood disorders. Eighty-four inpatients affected by mood disorders (72 bipolar and 12 major depressive disorder) were assessed by the Operational Criteria Checklist for Psychotic Illness to score their lifetime psychotic symptomatology. The subjects were also typed for 5HT1A and 5HT2C variants using polymerase chain reaction techniques. No association was found between 5HT2C and psychopathology as defined by the four symptomatologic factors used as phenotype definition (mania, depression, delusion, and disorganization) even when bipolar subjects were analyzed separately. Only one subject with the 5HT1A variant was observed. Genetic variation at the 5HT1A and 5HT2C receptor genes does not, therefore, play a major role in the pathogenesis of mood disorders symptomatology. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:161-166, 2000.

DRD4 exon 3 variants associated with delusional symptomatology in major psychoses: a study on 2,011 affected subjects.

We previously reported an association of DRD4 exon3 long allele variants with delusional symptomatology independently from diagnoses. The aim of this investigation was to study DRD4 in major psychoses and to test the association in a larger sample. We studied 2,011 inpatients affected by bipolar disorder (n = 811), major depressive disorder (n = 635), schizophrenia (n = 419), delusional disorder (n = 104), psychotic disorder not otherwise specified (n = 42), and 601 healthy controls. A subsample of 1,264 patients were evaluated using the OPCRIT checklist and differences of symptomatology factor scores among genetic variants were assessed using one-way analysis of variance (ANOVA). DRD4 allele and genotype frequencies in bipolars, schizophrenics, delusionals, and psychotic NOS were not significantly different from controls; major depressives showed a trend toward an excess of DRD4*Short and DRD4*Short/Short variants versus controls. The ANOVA on factor scores in the whole subsample of 1,264 subjects showed a significant difference on delusion factor in allele analysis (P = 0.007), and in genotype one (P = 0.018), with DRD4*Long containing variants associated with severe symptomatology. The analysis in the replication subjects only (n = 803) showed a trend in the same direction, though not reaching the significance level. This analysis in an enlarged sample suggests that DRD4*Long alleles exert a small but significant influence on the delusional symptomatology in subjects affected by major psychoses.

Serotonin-2A receptor gene is not associated with symptomatology of schizophrenia.

The serotonin receptor type 2A (5-HT2A) is a primary candidate for involvement in major psychoses. Polymorphisms within the 5-HT2A gene have recently been reported to be associated with a variety of psychopathological conditions. In the present study, we investigated the potential influence of the T102C polymorphism on the psychopathology of schizophrenia. One hundred eighty-eight inpatients affected by schizophrenia (DSM-III-R) were assessed by the Operational Criteria checklist for psychotic illness (OPCRIT) and were typed for their 5-HT2A variants by PCR techniques. Mania, depression, delusion and disorganization were the four symptomatologic factors previously derived from our psychotic population that were used to define phenotype in our sample. Genetic variants of the polymorphism under study were not associated with these symptomatologic factors, and consideration of possible stratification effects such as sex and age of onset did not reveal any association either. Our results do not, therefore, support the hypothesis that the serotonin receptor 2A gene is a liability factor for the symptomatology of schizophrenia as defined by the OPCRIT checklist. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:84-87, 2000.

Dopamine D3 receptor gene not associated with symptomatology of major psychoses.

Dopamine D3 receptor gene (DRD3) variants have been implicated in the pathogenesis of psychiatric disorders. Many studies, however, have failed to replicate the association of DRD3 with schizophrenia. A possible reason for this may lie in the definition of phenotype, which is traditionally based on psychiatric diagnosis. In this study we investigated the possibility that variants of the DRD3 gene might be associated with symptomatology in a sample of subjects affected by major psychoses. Two hundred and eleven inpatients affected by major psychoses were assessed by the Operational Criteria Checklist for Psychotic Illness (OPCRIT) and were also typed for the DRD3 variants using polymerase chain reaction techniques. Mania, depression, delusion, and disorganization were the four symptomatologic factors used as phenotype definitions. DRD3 variants were not associated with these symptomatologic factors, and consideration of possible stratification effects, such as sex and psychiatric diagnosis, did not reveal any association either.

No interaction between serotonin transporter gene and dopamine receptor D4 gene in symptomatology of major psychoses.

Previously, we reported an association of the dopamine receptor D4 (DRD4) gene with delusional symptomatology of major psychoses. However, DRD4 variants accounted for only 2% of the phenotypic variance, indicating that contributions from other genes were probable. The serotonin transporter gene is a primary candidate in major psychoses, and a functional polymorphism in the upstream regulatory region of the serotonin transporter gene (5-HTTLPR) has recently been reported to be associated with a number of psychopathological conditions. In the present study we investigated the original cohort of subjects to evaluate the 5-HTTLPR possible influence on the psychopathology of major psychoses in interaction with DRD4. Four hundred and sixty-one inpatients affected by major psychoses were assessed by the Operational Criteria Checklist for Psychotic Illness (OPCRIT) and were also typed for the 5-HTTLPR and DRD4 variants using polymerase chain reaction techniques. Mania, depression, delusion, and disorganization were the four symptomatologic factors used as phenotype definition. 5-HTTLPR variants did not significantly influence the previously reported association of DRD4 with delusional symptoms. No interaction was observed on the other symptom factors. The serotonin transporter gene does not, therefore, interact with DRD4 in determining the symptomatology of major psychoses.

Dopamine receptor D4 gene is not associated with major psychoses.

We previously reported an association between dopamine receptor D4 (DRD4) gene exon 1 variants and delusional disorder. The aim of this investigation was to study the DRD4 gene exon 1 and 3 variants in schizophrenia, delusional, bipolar, and unipolar disorders. We studied 651 inpatients affected by schizophrenia (n = 229), delusional (n = 86), bipolar (n = 210), and unipolar (n = 126) disorders (DSM III-R) and 471 healthy controls; these were typed for DRD4 variants at the first and third exon using polymerase chain reaction techniques. DRD4 variants were not associated with schizophrenic and delusional subjects even when possible confounders like gender and onset were considered. A marginal association between DRD4 exon 3 variants with unipolar (excess of DRD4*2/4, p = 0.004) and bipolar (excess of DRD4*2/4, p = 0.001) disorders was observed, both associations drop to insignificance when corrected for multiple testing. Our results exclude that coding variants of the DRD4 exon 1 and 3 may play a major role in conferring susceptibility to major psychoses; moreover, we could not replicate the association of DRD4 exon 1 variant with delusional disorder.

No interaction of GABA(A) alpha-1 subunit and dopamine receptor D4 exon 3 genes in symptomatology of major psychoses.

Previously, we reported on an association of the dopamine receptor D4 (DRD4) gene with delusional symptomatology of major psychoses. However, despite the strength of the association, it only accounted for 2% of the variance, indicating that contributions from other genes were probable. In the present study, we investigated the original cohort of subjects to evaluate the gene for the gamma-aminobutyric acid type A (GABA(A)) receptor alpha-1 subunit (GABRA1). The possible association of GABRA1 with the psychopathology of major psychoses was tested both alone and in interaction with DRD4. Four hundred and sixty-one inpatients affected by major psychoses were assessed by the operational criteria checklist for psychotic illness (OPCRIT) and were also typed for the DRD4 and GABRA1 variants using PCR techniques. Mania, depression, delusion, and disorganization were the four symptomatologic factors used as phenotype definitions. GABRA1 variants were not associated with these symptomatologic factors, and consideration of possible stratification effects such as sex and psychiatric diagnosis also did not reveal any association. GABRA1 variants did not significantly influence the association of DRD4 with delusional symptoms. No interaction was observed on the other symptom factors. The GABA(A) alpha-1 subunit gene does not, therefore, interact with DRD4 in the symptomatology of major psychoses.

GABAA alpha-1 subunit gene not associated with depressive symptomatology in mood disorders.

Considerable evidence implicates the neurotransmitter gamma-aminobutyric acid (GABA) in the biochemical pathophysiology of mood disorders. In this study, we investigated the possibility that the gene for the gamma-aminobutyric acid type A (GABAA) receptor alpha-1 subunit (GABRA1) might be associated with depressive symptomatology in a sample of mood disorder subjects. Sixty-seven inpatients affected by unipolar (n = 37) and bipolar (n = 30) disorder (DSMIV) were assessed at admission by the Hamilton depression rating scale (HAMD) and were typed using polymerase chain reaction (PCR) techniques. GABRA1 variants were not associated with depressive symptomatology, and consideration of possible stratification effects such as sex, psychiatric diagnosis and illness severity did not reveal any association either. GABAA alpha-1 subunit gene is not, therefore, associated with depressive symptomatology in mood disorder subjects.

Serotonin receptor 2A, 2C, 1A genes and response to lithium prophylaxis in mood disorders.

The aim of this study was to investigate the influence of serotonin receptors 2A, 2C and 1A gene variants on lithium prophylactic efficacy in mood disorders. One hundred and twenty-four subjects affected by bipolar (n=102) and major depressive (n=22) disorder were followed prospectively for an average of 52 months and were typed for 5-HT2A (T102C: n=111, HTP: n=104), 5-HT2C (n=110) and 5-HT1A (n=61) variants. Both 5-HT2A and 5-HT2C variants were not associated with lithium outcome. Consideration of possible stratification effects like gender, polarity, family history, age at onset and duration of lithium treatment did not influence results. No 5-HT1A gene variant was identified. 5-HT2A and 2C variants are not, therefore, associated with lithium prophylactic efficacy in mood disorders.

Tryptophan hydroxylase gene and response to lithium prophylaxis in mood disorders.

Lithium is an effective prophylactic agent in mood disorders but not all patients with mood disorders respond to lithium therapy; it is therefore necessary to identify responders prior to treatment. Clinical predictors account for about half of the variance and it is probable that genetic factors play a substantial role. The aim of this study was to investigate the possible association between the tryptophan hydroxylase (TPH) gene and prophylactic efficacy of lithium in mood disorders. One hundred and eight subjects affected by bipolar (n = 90) and major depressive (n = 18) disorder were followed prospectively for an average of 50.4 months and were typed for their TPH variant using polymerase chain reaction techniques. TPH variants were marginally associated with lithium outcome (F = 3.16; d.f.=2,105; P = 0.046). Subjects with the TPH*A/A variant showed a trend toward a worse response compared to both TPH*A/C and TPH*C/C variants. Consideration of possible stratification effects such as gender, polarity or age at onset did not influence the observed association. TPH variants may be a possible factor influencing the prophylactic efficacy of lithium in mood disorders.

Influence of 5-HTTLPR and TPH variants on illness time course in mood disorders.

The aim of our study was to investigate gene variants in the long-term outcome of mood disorders. We retrospectively studied a sample of inpatients affected by recurrent and rapid cycling mood disorders. The serotonin transporter gene-linked functional polymorphic region (5-HTTLPR) and the A218C tryptophan hydroxylase (TPH) gene variant were determined using a PCR-based technique. For 5-HTTLPR polymorphism we genotyped 435 inpatients affected by major depressive (n=153), bipolar (n=213) and rapid cycling (n=69) mood disorders and 456 controls; for TPH we genotyped 399 inpatients (MD, n=132; BP, n=203; rapid cycling n=64) and 259 controls. Random Regression Model analysis was used to investigate the longitudinal time course of the illness. 5-HTTLPR and TPH polymorphisms were not associated with mood disorders time course. However we observed an excess of 5-HTTLPR*long alleles among rapid cycling subjects compared to both controls (P=0.018) and remitting mood disorders (P=0.006). TPH frequencies did not differ between mood disorders subtypes. Our results suggest that 5-HTTLPR variants may confer a susceptibility toward rapid cycling mood disorders.

No association between serotonin-2A receptor gene polymorphism and psychotic symptomatology of mood disorders.

Abnormalities of the serotonergic system are involved in the pathophysiology of mood disorders. In the present study, we investigated the possible influence of the T102C polymorphism of the serotonin-2A receptor gene (5-HT2A, 13q14-21) on the symptomatology of mood disorders. Inpatients affected by mood disorders (n = 246, 149 bipolar, 97 major depressive disorder) were assessed with a checklist of operational criteria for psychotic illness (OPCRIT) to score their lifetime psychotic symptomatology. The subjects were also typed for 5-HT2A variants using polymerase chain reaction techniques. No association was found between this polymorphism and psychopathology as defined by the four symptomatologic factors used in phenotype definition (mania, depression, delusion and disorganization). Genetic variation at the 5-HT2A receptor gene does not, therefore, appear to play a major role in the pathogenesis of major mood disorders.

Dopamine receptor D2 and D4 genes, GABA(A) alpha-1 subunit genes and response to lithium prophylaxis in mood disorders.

Lithium is an effective prophylactic agent in mood disorders, and genetic factors are likely to modulate individual susceptibility to lithium treatment. The aim of this study is to investigate the influence of dopamine receptor D2 (DRD2), D4 exon 3 (DRD4), and gamma-aminobutyric acid type A (GABA(A)) receptor alpha-1 subunit (GABRA1) gene variants on the efficacy of lithium prophylaxis in mood disorders. Patients with mood disorders (N = 125: bipolar subtype, n = 100; major depressive disorder subtype, n = 25) were followed prospectively for an average of 53 months and were typed for DRD2 (Ser311/Cys311: n = 121, VNTR: n = 63), DRD4 (n = 125) and GABRA1 (n = 61) variants using polymerase chain reaction (PCR) techniques. DRD2, DRD4 and GABRA1 variants were not associated with response to lithium. A trend was observed toward a better outcome of DRD4* 2/4 subjects, but it was due to only two subjects. Consideration of possible stratification effects like gender, polarity, family history, age at onset and duration of lithium treatment did not reveal any association either. DRD2, DRD4 and GABRA1 variants therefore do not appear to be associated with the outcome of lithium prophylaxis in mood disorders.

Dopamine receptor D4 gene is associated with delusional symptomatology in mood disorders.

Disturbances of the dopaminergic neurotransmitter system have been implicated in the pathogenesis of depressive symptoms. Many studies have, however, failed to detect any association between genetic markers for the dopamine system and mood disorders. A possible reason for this may lie in the definition of phenotype, which is traditionally based on psychiatric diagnosis. In this study, we investigated the possibility that functional variants of the dopamine D4 receptor (DRD4) gene might be associated with depressive symptomatology in a sample of mood disorder subjects. Seventy-nine inpatients affected by bipolar (n=37) and major depressive (n=42) disorder (DSM-IV) were assessed at admission by the Hamilton Depression Rating Scale and were typed for DRD4 variants at the third exon using polymerase chain reaction (PCR) techniques. DRD4 was associated with delusional symptoms (F=5.56; d.f.=2,145; P=0.005), with DRD4*7 exhibiting higher scores when compared to DRD4*4 (P=0.006) variants. Polarity of mood disorder did not influence results significantly. The findings are in accordance with our previous report of an association of the DRD4 gene with delusional symptomatology of major psychoses. DRD4*7 should, therefore, be considered a liability factor for delusional symptoms in mood disorders.