Urticaria, an inflammatory skin disorder affecting up to 20% of the global population, manifests as the development of pruritic wheals (commonly known as hives), angioedema, or a combination of both; these symptoms are triggered by the release of histamine and other mediators from mast cells in the skin.¹ Among the range of urticarial presentations, chronic spontaneous urticaria (CSU) is a particularly distressing skin condition characterized by recurrent, intensely itchy wheals; angioedema; or the coexistence of both symptoms.² CSU can be challenging because of its spontaneous nature and lack of an identifiable cause; it may persist for more than 6 weeks and profoundly reduce quality of life (QOL) among affected patients.³ Whereas many individuals endure daily or near-daily symptoms for years, other individuals experience multiple episodes interspersed with brief symptom-free intervals.^2,4

A prominent feature of CSU is its association with angioedema, observed in approximately 40% to 50% of patients with CSU; around 10% of patients primarily experience angioedema as the main symptom. However, the diagnosis of CSU is complex because it commonly involves both wheals and angioedema.⁴ Furthermore, discrepancies often arise between physician and patient reports of angioedema: approximately 40% of patients with inadequately controlled CSU report angioedema, even when their physician does not concur with this assessment.⁵

These diagnostic challenges underscore the need for a comprehensive and nuanced approach to the identification and management of this prevalent and vexing skin condition. This article unravels the complex diagnostic aspects of CSU by providing insights into its clinical manifestations, testing modalities, differential diagnoses, and the underlying mechanisms that involve mast cells and immunoglobulin E (IgE).

Epidemiology

CSU occurs in approximately 1% of the global population; its prevalence is increasing.² Global estimates for urticaria in 2017 indicated that there were approximately 86 million existing cases, with an annual occurrence of about 160 million new cases.¹ In the United States, around half a million individuals are affected by chronic urticaria, constituting a prevalence of 0.23%.⁶

In children, the estimated prevalence of CSU is 1.4%, whereas it is 0.9% in adults. This prevalence exhibits geographical disparities, such that rates are higher in Latin America and Asia than in Europe and North America.³ The epidemiology of CSU displays a degree of diversity similar to the affected populations. CSU tends to occur in women aged 30 years and older; it is most prevalent in this population. Furthermore, disparate prevalences have been noted among various ethnicities, emphasizing the importance of a nuanced diagnostic approach that considers demographic differences.¹ Figure 1 illustrates the prevalence and impact of CSU.^1-5

QOL Implications

In addition to the statistical considerations, it is important to recognize the profound impact of CSU on QOL among adult and pediatric patients, as well as their families. The relentless cycle of daily or near-daily episodes of hives and angioedema, accompanied by intense itching, results in decreased productivity and an increased burden of psychological comorbidities. More than 20% of patients with CSU miss at least 1 hour of work per week, leading to a 27% loss of overall productivity. The economic and humanistic burdens of CSU reverberate throughout healthcare systems, affecting patients, their families, and their partners. Consequently, there is an increasingly urgent need to enhance diagnostic precision and develop improved treatment options for individuals affected by the complexities of CSU.²

Mast Cells and IgE in CSU

These seemingly innocuous symptoms of CSU belie its complex underlying pathogenesis. The onset of wheals and angioedema results from a cascade of events triggered by mast cell degranulation,¹ leading to sensory nerve activation, vasodilation, and increased vascular permeability.⁴ This process culminates in the pruritic, raised, and erythematous skin lesions that characterize CSU.^1,4

Mast cells and IgE antibodies play pivotal roles in CSU development. Mast cells (ie, immune cells) in the skin initiate inflammation when activated through various receptors, including high-affinity IgE receptor (FcεRI), mas-related G protein-coupled receptor-X2 (MRGPRX2), complement 5a receptor (C5aR), protease-activated receptor 1 (PAR1), protease-activated receptor 2 (PAR2), chemoattractant receptor-homologous molecule expressed on T helper 2 cells (CRTh2), and cytokine receptors. The interaction between stem cell factor (SCF) and its receptor KIT (CD117) drives mast cell differentiation and proliferation. The activation of FcεRI involves multiple cytoplasmic signaling proteins, leading to mast cell activation and the release of histamine and other mediators, which ultimately cause CSU symptoms.¹

Further complicating the clinical picture, CSU is associated with the infiltration of various immune cells at wheal sites. These cellular infiltrates include basophils, eosinophils, neutrophils, monocytes, and T lymphocytes, similar to a late-phase cutaneous reaction. The cytokine profile within these infiltrates is biased toward a T helper 2 (Th2) immune response, but it also involves Th1 and Th17 cells and their associated cytokines. Eosinophils interact with mast cells by secreting SCF in response to mast cell activation, thereby promoting mast cell proliferation and differentiation. Eosinophil movement from the blood to the skin involves chemokines, which are potential therapeutic targets. The intricate crosstalk between eosinophils and mast cells, combined with the involvement of the coagulation cascade, adds complexity to CSU pathogenesis.⁴

CSU involves dermal mast cell activation and the release of inflammatory mediators; IgE contributes to these processes in direct and indirect ways. The direct effect is attributed to the presence of autoantigen-specific IgE, which is known as type I autoimmunity. The indirect effect is associated with low levels of IgE due to IgE-specific IgG, which is known as type IIb autoimmunity.⁷ The identification of these antibodies helps to diagnose autoimmune CSU, a process that can be complicated by the existence of overlapping endotypes.¹

In addition to IgE-dependent pathways, IgE-independent mast cell activation has a crucial role in CSU.¹ Mast cells can be activated by various ligands including C5a, neuropeptides, and cytokines, providing multiple pathways for eventual mast cell degranulation.⁴ These intricate interactions highlight the complexity of CSU pathogenesis.

Diagnosis and Clinical Presentation

The diagnosis of CSU is a complex process, primarily based on the exclusion of other potential causes. It begins with a comprehensive patient history and physical examination, focusing on details such as symptom patterns, triggers, medication use, allergies, family history, and associations with angioedema. The subsequent diagnostic journey may involve various tests, including a complete blood count (CBC), erythrocyte sedimentation rate (ESR) assessment, and measurements of the levels of C-reactive protein (CRP), liver enzymes, and thyroid-stimulating hormone (TSH). The scope of testing may vary depending on a particular patient’s clinical indications.³

Additional evaluations may include skin biopsies, physical challenge tests, complement component (C3 and C4) measurements, stool analyses, urinalysis, chest radiography, autoantibody assays, and serum protein electrophoresis. Infection-related investigations may be considered if clinically warranted, such as tests for Helicobacter pylori (H pylori), hepatitis B, hepatitis C, or malignancy. In some cases, investigational assays (eg, autologous serum skin tests and the detection of antibodies to the IgE receptor or Fc region of IgE) may offer insights into the mechanisms underlying CSU pathogenesis. Notably, there is no correlation between the number of tests performed and the likelihood of determining the underlying pathogenesis.³

CSU requires the exclusion of other conditions with similar presentations. Key differential diagnoses include physical urticarias, such as symptomatic dermographism, cholinergic urticaria, and cold urticaria, which often exhibit distinct clinical features and triggers.¹ Careful analysis, symptom evaluation, and diagnostic testing are essential to distinguish these conditions from CSU. Table 1 details various characteristics of CSU.¹

Conclusion

CSU is a multifaceted condition with clinical manifestations that extend far beyond the skin surface. The central role of mast cells and the intricate interactions with IgE add layers of complexity to the understanding of CSU pathogenesis. Mast cells can be activated through IgE-dependent or independent mechanisms, leading to the release of histamine, cytokines, and other mediators responsible for the characteristic symptoms of CSU.

As the understanding of CSU improves, researchers seek to refine diagnosis and treatment strategies, which will ultimately alleviate the burden of this particularly distressing skin condition. These collective efforts hold the promise of personalized care and improved QOL for patients with CSU, offering hope for a symptom-free future.

References

1. Kolkhir P, Giménez-Arnau AM, Kulthanan K, Peter J, Metz M, Maurer M. Urticaria. Nat Rev Dis Primers. 2022;8(1):61. doi:10.1038/s41572-022-00389-z

2. Kolkhir P, Muñoz M, Asero R, et al. Autoimmune chronic spontaneous urticaria. J Allergy Clin Immunol. 2022;149(6):1819-1831. doi:10.1016/j.jaci.2022.04.010

3. Greiner B, Nicks S, Adame M, McCracken J. Pathophysiology, diagnosis, and management of chronic spontaneous urticaria: a literature review. Clin Rev Allergy Immunol. 2022;63(3):381-389. doi:10.1007/s12016-022-08952-y

4. Kaplan A, Lebwohl M, Giménez-Arnau AM, Hide M, Armstrong AW, Maurer M. Chronic spontaneous urticaria: focus on pathophysiology to unlock treatment advances. Allergy. 2023;78(2):389-401. doi:10.1111/all.15603

5. Metz M, Vadasz Z, Kocatürk E, Giménez-Arnau AM. Omalizumab updosing in chronic spontaneous urticaria: an overview of real-world evidence. Clin Rev Allergy Immunol. 2020;59(1):38-45. doi:10.1007/s12016-020-08794-6

6. Lang DM. Chronic urticaria. N Engl J Med. 2022;387(9):824-831. doi:10.1056/NEJMra2120166

7. Maurer M, Kolkhir P, Moñino-Romero S, Metz M. The crucial role of IgE as a predictor of treatment response to omalizumab in chronic spontaneous urticaria. J Allergy Clin Immunol Pract. 2023;11(8):2390-2391. doi:10.1016/j.jaip.2023.06.026

Posted by Haymarket’s Clinical Content Hub. The editorial staff of MPR played no role in this content’s preparation. 

Reviewed November 2023

Postpartum depression (PPD) is among the most common and most under-recognized peripartum morbidities. In 2018, at least 1 in every 7 live births was associated with PPD.¹ Incidence of PPD may have increased during the COVID-19 pandemic; this may reflect COVID-19-related gaps in health care resources, underfunding of research on peripartum conditions, decreased social support for breastfeeding, and maternal fears of infection.^2,3 Incidence of PPD in the United States (US) is shown in Figure 1.^4,5

Peripartum mental health conditions were the most common cause of preventable pregnancy-related deaths among 14 states reporting data from 2008 to 2017; patients representing 15% of those deaths had PPD, either exclusively or comorbid with other mental health conditions.⁶ Untreated PPD can disrupt the mutual regulatory interchange between mothers and infants, which can impair infants’ social-relational development and interfere with their ability to regulate their physiological, affective, and interactional states.⁷ Screening for depression during pregnancy and the postpartum period may help alleviate depressive symptoms in women with PPD and reduce the prevalence of PPD at the population level.⁸

Diagnostic Criteria

The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) specifies 9 symptoms in its criteria for major depressive disorder; diagnosis requires the presence of 5 of these symptoms⁹:

• Depressed mood;
• Anhedonia;
• Thoughts of worthlessness or guilt;
• Sleep disturbance;
• Change in appetite or weight;
• Impaired concentration or memory;
• Fatigue or low energy;
• Psychomotor agitation or depression; or
• Recurring thoughts of suicide or death.

Additional relevant symptoms may be useful as indicators for PPD screening. These include¹⁰:

• Frequent tearfulness;
• Low interest in or sense of bonding with the baby, or feeling anxious about the baby;
• Feeling oneself to be a bad parent; and
• Fear of self-harm or harming the baby.

Such symptoms must be present on most days for a postpartum period of at least 2 weeks, cause clinical impairment, and are not due to other causes.¹¹ However, the onset of PPD symptoms during the postpartum period is variably defined. The International Classification of Diseases 10th revision (ICD-10) specifies symptom onset within 6 weeks postpartum, the DSM-5 specifies onset during pregnancy or within 4 weeks postpartum, and the World Health Organization (WHO) stipulates onset during pregnancy through 12 months postpartum.^11,12

Predisposing and Protective Factors

Risk factors for PPD may include^1,3,10:

• Prenatal and antenatal depression and anxiety;
• Prior history of depression;
• Low self-esteem;
• Child care stress;
• Obstetric complications;
• Maternal pain during pregnancy;
• Pre-existing postpartum blues;
• Maternal disability;
• Unintended pregnancy; and
• Lower family income.

Protective factors, meanwhile, include positive parenting-related attitudes, better pre-pregnancy self-reported health, informal social supports, a sense of community belonging, exclusive breastfeeding, and having a partner who does not have depression.^3,10

Differential Diagnosis

Diagnosticians must distinguish PPD from postpartum blues, or “baby blues,” which are very common in postpartum but are of shorter duration than PPD; this state tends to occur during the first 2 weeks postpartum and presents more mildly than PPD, as it does not seriously impair functioning.¹⁰

Conversely, clinicians also must be watchful for more severe or dangerous psychiatric postpartum conditions such as postpartum psychosis. This is considered a variant of bipolar disorder that coincides with the tremendous hormonal shifts that occur after delivery, and symptoms tend to present within 4 weeks from delivery. Patients with postpartum psychosis are at higher risk for suicide and infanticide than are those with depressive disorders without psychosis.^9,13

Postpartum anxiety is associated with PPD. In 1 moderately large cohort, anxiety was present in approximately 20% of mothers with PPD at 2 months postpartum, compared with 1.3% of recent mothers without PPD. Similarly, postpartum obsessive-compulsive symptoms are also associated with PPD and in that cohort were estimated to co-occur in almost 26% of recent mothers with PPD, compared with 8.4% of recent mothers without PPD.¹⁴ Other associated conditions include panic attacks and post-traumatic stress disorder, the latter particularly in mothers who experienced complications in pregnancy or delivery.¹⁰ Clinicians should obtain thyroid function panels to rule out thyroid disease, which may cause depression and anxiety symptoms.^11,15 They also should review any medications or other substances that can produce depressive symptoms and ask about any history of discontinuation of antidepressant medication.^9,10

Barriers to Identification

In 2015, the American College of Obstetricians and Gynecologists (ACOG) recommended at least 1 perinatal screening for depression.¹⁶ The US Preventive Services Task Force and the Council on Patient Safety in Women’s Health Care recommend at least 1 prepartum and 1 postpartum screening.¹⁷ Furthermore, in 2019, the American Academy of Pediatrics affirmed its own recommendation of screenings at 1-, 2-, 4-, and 6-months postpartum to coincide with typical timing of peak risk of PPD.¹⁸ As no-show rates for postpartum visits are high in many communities, screening for PPD may be integrated into non-obstetrical settings, such as visits to the emergency department for well-baby care or evaluation.⁹

However, in the US, it remains highly variable at the state and territory level whether providers ask about depression in the postpartum period. Among 31 US sites reporting such data, the percentage of women who reported that a health care provider had asked about postpartum depressive symptoms ranged from 51.3% in Puerto Rico to 90.7% in Alaska.¹⁹ Racial disparities in postnatal screening for depression have persisted as well; Black, Asian, and other non-White patients were less likely to be screened at 1 studied multicenter health care system, even though these patients are more likely to be affected by PPD.^17,19

It is currently unclear whether communications such as ACOG’s 2015 recommendation have increased implementation of postpartum mental health screening. The publication of the ACOG recommendation alone was not associated with a significant increase in the diagnosis of PPD in the following year, although the prevalence of provider inquiry about depressive symptoms during a postpartum visit increased from 84% to 88% among 22 reporting US sites between 2016 and 2018.^16,19 This may be partially due to the fact that many health care providers who may follow the mother through the peripartum period, such as internists, pediatricians, and psychiatrists, are less likely to be directly influenced by the ACOG screening guidelines despite being well-situated to provide maternal mental health screenings.¹⁶

Another potential barrier to the uptake of screening recommendations may be uncertainty regarding diagnostic criteria, as PPD is not represented by a distinct diagnostic code in the DSM-5, but rather is composed of a code for major depressive disorder and a specifier for “with peripartum onset.”¹¹ The diagnostic criteria regarding onset timing also may exclude affected mothers, as some individuals may continue to present with symptoms through 2 years postpartum.²⁰ Clinicians may face additional barriers, such as lack of clarity on how to refer patients with diagnoses, time limitations, trouble identifying and using accurate assessment tools, and lack of access to appropriate community mental health services. The barriers patients face in obtaining screening for PPD may include time constraints and stigma associated with mental health conditions.⁹

The gold standard for diagnosis of PPD requires a structured interview that would evaluate all components of PPD, as defined by the DSM-5.⁹ However, this may not be viable for busy OB/GYN clinicians during a clinical encounter, as time constraints may require them to triage such patients for referral to mental health specialists. This requires a screening tool that can be administered briefly and inexpensively. A variety of validated screening questionnaires, as described below, are available for this purpose.

Screening Tools

When considering a PPD screening tool, important factors such as ease of administration and availability in a patient’s primary language should be considered. A questionnaire that is self-administered, as opposed to administered by a clinician as an interview, may provide patients with a greater sense of privacy.⁹

The Edinburgh Postnatal Depression Scale (EPDS) is the most commonly used questionnaire to screen for PPD.²¹ Unlike most validated depression-related questionnaires, it was developed specifically to detect PPD. With 10 items, it typically takes about 5 minutes to complete and is simple to score.²² The cutoff score to identify possible PPD varies in published literature; a meta-analysis of 121 articles indicated that a cutoff score of 11 or higher maximized combined sensitivity and specificity.²³

A 3-question subscale of the EPDS aimed at evaluating anxiety has been investigated with respect to the established validity of the full 10-question scale; a single, short-term study indicated that the sensitivity and reliability of this subscale was highly comparable to that of the 10-question scale.²⁴

The Patient Health Questionnaire-9 (PHQ-9) was adapted to be a simplified, self-administered version of the Primary Care Evaluation of Mental Disorders (PRIME-MD) that can both diagnose depression and provide an estimate of depression severity.²⁵ The PHQ-9 is a screening tool for peripartum psychiatric conditions that consists of 9 items, and it has been validated in large samples of women.⁹

A subscale of the PHQ-9, the Patient Health Questionnaire-2 (PHQ-2), has been recommended as an optional prescreening prior to administering the PHQ-9. The PHQ-2 consists of the first 2 questions of the PHQ-9, which address depressed mood and anhedonia. A meta-analysis of 44 primary studies indicated that combined use of the PHQ-2 (with a cutoff score of 2 or higher out of a maximum 6) plus the PHQ-9 (with a cutoff score of 10 or higher) resulted in sensitivity similar to that obtained with the PHQ-9 alone but with slightly higher specificity.²⁶

The Postpartum Depression Screening Scale (PDSS), a 35-item scale, was developed specifically for PPD and evaluates patients across the following 7 domains: (1) sleeping and eating disturbances, (2) anxiety and insecurity, (3) emotional lability, (4) mental confusion, (5) loss of self, (6) guilt and shame, and (7) suicidal thoughts.⁹

Several other tools previously used to screen for depression are now used to screen for peripartum mental health, including the Beck Depression Inventory II (BDI-II), the Center for Epidemiologic Studies Depression Scale (CES-D), and the Zung Self-Rating Depression Scale.⁹

It is not currently possible to identify a single “best” screening tool because accuracy, including sensitivity and specificity, vary in parallel with differing methodologies across validation studies. In particular, timing of screening administration, recruited participants, scoring methodologies, and cutoff scores tend to be heterogenous across studies²⁷; all of these influence accuracy measures within screening tools. A brief description of screening questionnaires commonly used for PPD can be found in Table 1.^9,26

References

1. Alhusen JL, Hughes RB, Lyons G, Laughon K. Depressive symptoms during the perinatal period by disability status: findings from the United States Pregnancy Risk Assessment Monitoring System. J Adv Nurs. 2023;79(1):223-233. doi:10.1111/jan.15482

2. Shuman CJ, Peahl AF, Pareddy N, et al. Postpartum depression and associated risk factors during the COVID-19 pandemic. BMC Res Notes. 2022;15(1):102. doi:10.1186/s13104-022-05991-8

3. Gopalan P, Spada ML, Shenai N, et al. Postpartum depression—identifying risk and access to intervention. Curr Psychiatry Rep. 2022;24(12):889-896. doi:10.1007/s11920-022-01392-7

4. Centers for Disease Control and Prevention. Prevalence of selected maternal and child health indicators for all PRAMS sites, Pregnancy Risk Assessment Monitoring System (PRAMS), 2012-2015. Reviewed April 22, 2022. Accessed April 26, 2023. https://www.cdc.gov/prams/prams-data/mch-indicators/states/pdf/2015/PRAMS-All-Sites-2012-2015-508.pdf

5. Centers for Disease Control and Prevention. Prevalence of selected maternal and child health indicators for all Pregnancy Risk Assessment Monitoring System (PRAMS) sites, 2016–2020. Reviewed March 28, 2023. Accessed April 12, 2023. https://www.cdc.gov/prams/prams-data/mch-indicators/states/pdf/2020/All-Sites-PRAMS-MCH-Indicators-508.pdf

6. Trost SL, Beauregard JL, Smoots AN, et al. Preventing pregnancy-related mental health deaths: insights from 14 US maternal mortality review committees, 2008–17. Health Aff (Millwood). 2021;40(10):1551-1559. doi:10.1377/hlthaff.2021.00615

7. Paris R, Bolton R, Weinberg M. Postpartum depression, suicidality, and mother-infant interactions. Arch Womens Ment Health. 2009;12(5):309-321. doi:10.1007/s00737-009-0105-2

8. O’Connor E, Rossom RC, Henninger M, Groom HC, Burda BU. Primary care screening for and treatment of depression in pregnant and postpartum women: evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2016;315(4):388-406. doi:10.1001/jama.2015.18948

9. Learman LA. Screening for depression in pregnancy and the postpartum period. Clin Obstet Gynecol. 2018;61(3):525-532. doi:10.1097/GRF.0000000000000359

10. Wells T. Postpartum depression: screening and collaborative management. Prim Care. 2023;50(1):127-142. doi:10.1016/j.pop.2022.10.011

11. Kroska EB, Stowe ZN. Postpartum depression: identification and treatment in the clinic setting. Obstet Gynecol Clin North Am. 2020;47(3):409-419. doi:10.1016/j.ogc.2020.05.001

12. Holm DML, Wohlfahrt J, Rasmussen MLH, Corn G, Melbye M. A quantitative comparison of two measures of postpartum depression. BMC Psychiatry. 2022;22(1):202. doi:10.1186/s12888-022-03836-z

13. Sit D, Rothschild AJ, Wisner KL. A review of postpartum psychosis. J Womens Health (Larchmt). 2006;15(4):352-368. doi:10.1089/jwh.2006.15.352

14. Miller ES, Hoxha D, Wisner KL, Gossett DR. The impact of perinatal depression on the evolution of anxiety and obsessive-compulsive symptoms. Arch Womens Ment Health. 2015;18(3):457-461. doi:10.1007/s00737-014-0476-x

15. Stewart DE, Vigod SN. Postpartum depression: pathophysiology, treatment, and emerging therapeutics. Annu Rev Med. 2019;70:183-196. doi:10.1146/annurev-med-041217-011106

16. Leboffe EN, Pietragallo HC, Liu G, Ba D, Leslie D, Chuang CH. The impact of the 2015 ACOG screening guidelines on the diagnosis of postpartum depression among privately insured women. J Affect Disord. 2023;328:103-107. doi:10.1016/j.jad.2023.02.020

17. Sidebottom A, Vacquier M, LaRusso E, Erickson D, Hardeman R. Perinatal depression screening practices in a large health system: identifying current state and assessing opportunities to provide more equitable care. Arch Womens Ment Health. 2021;24(1):133-144. doi:10.1007/s00737-020-01035-x

18. Earls MF, Yogman MW, Mattson G, Rafferty J; Committee on Psychosocial Aspects of Child and Family Health. Incorporating recognition and management of perinatal depression into pediatric practice. Pediatrics. 2019;143(1):e20183259. doi:10.1542/peds.2018-3259

19. Bauman BL, Ko JY, Cox S, et al. Vital signs: postpartum depressive symptoms and provider discussions about perinatal depression — United States, 2018. MMWR Morb Mortal Wkly Rep. 2020;69(19):575-581. doi:10.15585/mmwr.mm6919a2

20. Vogeli JM, Hooker SA, Everhart KD, Kaplan PS. Psychometric properties of the postpartum depression screening scale beyond the postpartum period. Res Nurs Health. 2018;41(2):185-194. doi:10.1002/nur.21861

21. Moraes GP, Lorenzo L, Pontes GAR, Montenegro MC, Cantilino A. Screening and diagnosing postpartum depression: when and how? Trends Psychiatry Psychother. 2017;39(1):54-61. doi:10.1590/2237-6089-2016-0034

22. Cox JL, Holden JM, Sagovsky R. Detection of postnatal depression. Development of the 10-item Edinburgh Postnatal Depression Scale. Br J Psychiatry. 1987;150:782-786. doi:10.1192/bjp.150.6.782

23. Levis B, Negeri Z, Sun Y, Benedetti A, Thombs BD; DEPRESsion Screening Data (DEPRESSD) EPDS Group. Accuracy of the Edinburgh Postnatal Depression Scale (EPDS) for screening to detect major depression among pregnant and postpartum women: systematic review and meta-analysis of individual participant data. BMJ. 2020;371:m4022. doi:10.1136/bmj.m4022

24. Kabir K, Sheeder J, Kelly LS. Identifying postpartum depression: are 3 questions as good as 10? Pediatrics. 2008;122(3):e696-e702. doi:10.1542/peds.2007-1759

25. Spitzer RL, Kroenke K, Williams JB. Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. JAMA. 1999;282(18):1737-1744. doi:10.1001/jama.282.18.1737

26. Levis B, Sun Y, He C, et al. Accuracy of the PHQ-2 alone and in combination with the PHQ-9 for screening to detect major depression: systematic review and meta-analysis. JAMA. 2020;323(22):2290-2300. doi:10.1001/jama.2020.6504

27. Ukatu N, Clare CA, Brulja M. Postpartum depression screening tools: a review. Psychosomatics. 2018;59(3):211-219. doi:10.1016/j.psym.2017.11.005

Posted by Haymarket’s Clinical Content Hub. The editorial staff of MPR had no role in this content’s preparation.

Reviewed May 2023