Pruritus in Pregnancy

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Pruritus is a commonly described symptom during pregnancy. Despite its high prevalence, it is often considered trivial but causes significant patient discomfort. It is important to assess and investigate the patient thoroughly as some conditions have a detrimental outcome for both mother and fetus. There is extensive literature on pruritus due to pregnancy-specific dermatoses, however, the evaluation of pruritus merits a broader approach. Various other conditions such as certain infections, systemic diseases, and pre-existing dermatological conditions should also be considered. Awareness of these conditions in obstetricians will also ensure adequate treatment and timely referral, if necessary. The purpose of this article is to describe the etiology, clinical features, diagnostic approach, and management of pruritus in pregnancy.

Keywords : Pruritus · Pregnancy · Pregnancy-specific dermatoses · Antihistamines · Atopy

Pruritus is an unpleasant sensation causing a desire to scratch [1]. The prevalence of pruritus in pregnancy ranges between 18 and 40% [1]. Pruritus is chronic if symptoms last longer than 6 weeks. Chronic pruritus is an overlooked symptom but is responsible for impairment in quality of life. Conventionally, the discussion of pruritus in pregnancy has been focused on pregnancy-specific dermatosis. However, coexistent dermatological disorders and underlying neurologic, psychological, and systemic conditions are also responsible for pruritus in sizeable expectant populations. Table 1 illustrates the various etiological factors responsible for pruritus in pregnancy. This article aims to provide a comprehensive review of the etiology, pathophysiology, clinical features, investigations, and management of pruritus in pregnancy.

Physiological Causes of Pruritus

Pregnancy is a complex physiological state resulting in several dermatological changes. Striae gravidarum (stretch marks) are seen in the second and third trimesters in > 90% of patients in pregnancy. They are linear pink-purple atrophic bands that develop perpendicular to skin tension lines over the abdomen, breasts, thigh, and buttocks and cause pruritus occasionally. The proposed pathophysiology appears to be related to stretching of the abdominal skin that causes activation of dermal nerve endings [2]. Xerosis (dry skin), hyperactivity of eccrine sweat and sebaceous glands, and hypoactivity of apocrine glands are other physiological causes of pruritus [1]. Awareness of the physiological causes helps avoid unnecessary diagnostic evaluation, dermatological referral, or over-treatment.

Pathological Causes of Pruritus

While there are many pathological causes of pruritus during pregnancy, dermatoses that are unique to pregnancy are most familiar to obstetricians. Table 1 provides the most up-to-date classification of pregnancy-specific dermatosis.

Pregnancy‑Specific Dermatosis

Polymorphic Eruption of Pregnancy
Polymorphic eruption of pregnancy or ‘Pruritic urticarial papules and plaques of pregnancy’ (PUPPP), is a benign, self-resolving, inflammatory disorder of pregnancy with onset in the third trimester or post-partum. An association has been reported with multiple gestations and excessive maternal weight gain [3]. Etiology Hormonal, immunological, and abdominal distension are presumed etiological factors; however, damage to the connective tissue occurring during stretching is the most likely cause [3]. Clinical features Pruritic papules appear over the abdomen, initially within the striae. Lesions progressively spread to involve the buttocks and proximal thighs and coalesce to form plaques. Occasionally, a generalized involvement is apparent. Umbilical sparing is the hallmark feature. In the later course, the rash may become vesicular, targetoid, eczematous, or simply present as widespread erythema. The condition resolves within 4–6 weeks irrespective of obstetric management or delivery. Diagnostic evaluation Differential diagnoses include pemphigoid gestationis, contact dermatitis, and atopic dermatitis. A careful history and physical examination are the key to diagnosis as investigations, including histology and immunofluorescence, are unlikely to be helpful. Umbilical sparing is an important clinical clue as it is not seen with other conditions.

Treatment Management is mainly with topical corticosteroids and antihistamines (Table 2). Emollients may provide significant alleviation of symptoms. Maternal and fetal prognosis The prognosis remains unaffected by this condition with no recurrence in subsequent pregnancies.

Pemphigoid Gestationis

Pemphigoid gestationis (PG), also known as ‘herpes gestationis’ is a rare pregnancy-specific autoimmune blistering disease with an incidence of 1:2000–1:60,000 pregnancies [1]. Its incidence is dependent on the prevalence of human leukocyte antigen (HLA) haplotypes DR3 and HLA DR4. It commonly presents during the third trimester and postpartum. Associations have been reported with trophoblastic tumors, particularly choriocarcinoma and hydatidiform mole [1]. It predisposes affected individuals to the development of other autoimmune conditions such as Graves’ disease. Etiology Autoantibodies target bullous pemphigoid antigen 180 (BP180) which is found in the basement membrane of the skin, placental tissue, and fetal membranes. It is interesting to note that the placenta is the primary site of autoimmunity and not the skin. The mechanism of blister formation involves anti-placental IgG antibodies cross-reacting with BP180-2 proteins in the skin leading to complement activation with subsequent deposition of immune complexes, chemotaxis of eosinophils to the site, and degranulation. This process destroys the basement membrane and causes bulla formation.

Declarations
Conflict of interest Nil.

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