There are five major dermatoses which occur in pregnancy, and some that can be precipitated by pregnancy.

Pruritus of pregnancy
Itching occurs in about 20 per cent of pregnancies. Sometimes this is in association with an inflammatory dermatosis. Often there are no physical signs, other than scratch marks, and iron deficiency must be excluded. In about 2 per cent of women itching is related to cholestasis of pregnancy, when it is termed pruritus gravidarum. The itching begins in the third trimester and affects the abdomen, palms, and soles. Liver function tests are abnormal and bile salts are raised. It resolves postpartum, but will recur in subsequent pregnancies.

Management consists of emollients and sometimes antihistamines. Chlorpheniramine is the one usually recommended for pregnancy. The non-sedating antihistamines are probably ineffective.

Polymorphic eruption of pregnancy (pruritic urticated papules and plaques of pregnancy)

This dermatosis affects 1 in 240 singleton pregnancies but is more common in multiple births, and is thus being seen more often in the context of in vitro fertilization. It is more common with a male foetus. The dermatosis usually begins in the third trimester and occasionally postpartum. It is most common in first pregnancies or the first multiple pregnancy.

The lesions usually begin in the striae on the abdomen and thighs, and then spread to the whole trunk and limbs, including the hands and feet. The lesions are raised red papules (

Plate 1) and plaques, occasionally polycyclic, and rarely may blister on the lower legs. The itching can be very severe, preventing sleep. The histopathology shows oedema, perivascular lymphocytes, and eosinophils. Immunofluorescence does not demonstrate any circulating or bound immunoreactants.

The aetiology is unknown, but there is an association with a low serum cortisol. The increased frequency in multiple births may relate to the mechanical effect of the abdominal stretching or to an increased immune complex load.

Treatment is with reassurance and emollients, for example aqueous cream and 1 to 2 per cent menthol, is helpful, but is not always sufficient. Antihistamines and moderate to very potent topical steroids, which will have significant absorption (

see Table 1), and occasionally systemic steroids or induction, may be required. The condition resolves over days to weeks after delivery. It does not usually recur. The outcome of the pregnancy is not adversely affected.

Prurigo of pregnancy
This is may affect 1 in 300 pregnancies. It commences at the end of the second or beginning of the third trimester. The eruption is scattered over the abdomen and limbs, and comprises excoriated papules. There is intense pruritus. It is essential to make sure that iron deficiency is not a contributing factor.

Histopathology shows a perivascular infiltrate with thickened epidermis. Direct and indirect immunofluorescence are negative. Treatment is with reassurance and emollients, and if this is not sufficient, with antihistamines and moderate to very potent topical steroids or occlusive coal tar or icthapaste bandages, which can be applied over topical steroids to the limbs. The condition resolves in days to weeks after delivery. It does not usually recur.

Pruritic folliculitis
This is rare and most commonly affects pregnancies with a male foetus. The lesions are pruritic papules and pustules that present in the third trimester, affect the trunk, and may spread to the limbs. Topical steroids may be helpful. Pruritic folliculitis is associated with a low birth weight.

Pemphigoid gestationis (herpes gestationis)
Pemphigoid gestationis is the most severe of the pregnancy dermatoses. It occurs in 1 in 50 000 pregnancies. The name herpes gestationis is best abandoned as the herpes refers to the herpetiform grouping of the blisters rather than herpes infection. Pemphigoid gestationis commences from the second trimester onwards and quite often in the first week postpartum (range 5 weeks gestation to 4 weeks postpartum). It usually occurs in the first and subsequent pregnancies, although 8 per cent of pregnancies are skipped.

The eruption begins around the umbilicus and spreads to the whole trunk, limbs, hands, and feet, including the palms and soles, and rarely the face. The mouth and vulva may be involved. The eruption usually commences as an annular red raised plaque around the umbilicus. The lesions comprise annular lesions, papules, and plaques. Vesicles and blisters are seen (

Plate 2). The mucosal lesions may be blisters or erosions. Pruritus is severe and sleep often impossible. Transplacental transmission to the fetus occurs in about 3 per cent of affected pregnancies, and the neonate develops transient self-limiting blisters (

Plate 3).

Histopathology demonstrates eosinophilia, subepidermal blisters, and tear-drop vesicles within the epidermis, continuous with the subepidermal blisters. Direct immunofluorescence demonstrates that C3 component of complement and IgG1 are bound at the basement membrane zone of the dermoepidermal junction. The patient’s serum has circulating IgG1 basement membrane zone antibodies that bind C3. These immunoreactants are also found at the basement membrane zone of the amnion (

Plate 4). The mothers have HLA DR 3, 4, and are C4 null, and there is an association with thyroid and less commonly other autoimmune disease.

The aetiology is only partially understood. The pathogenicity of the circulating basement membrane zone antibodies is demonstrated by transplacental transmission of the disease. The major target antigen is BP180/collagen XVII (chief epitope - the transmembrane NC16A domain) and BP230 is a further antigen. Both antigens are present in skin, mucosa, and amnion associated with the hemidesmosome and adhesion complex linking epithelium to dermis/mesenchyme, and are targets in other autoimmune blistering diseases. The placenta shows increased expression of antigen presenting cells, but it is unclear why breakdown of tolerance occurs, and why normal components of amnion and stratified squamous epithelium become antigenic.

Treatment with potent or very potent topical steroids and chlorpheniramine is sometimes successful, but usually systemic steroids, for example prednisolone 20 to 80 mg daily, are required, with the dose adjusted according to disease activity. There is usually a postpartum flare, necessitating increased steroids. The disease slowly resolves postpartum, but persists for several months. There is an increased incidence of premature births and small-for-dates babies. The classical teaching is that it recurs earlier and is more severe in subsequent pregnancies, but this has not always been our experience.