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Clinical Updates

Skin Modifications During Pregnancy

Selim Aractingi, Sau Nguyen

Tuesday, March 07, 2006

Pregnancy-related skin modifications are diverse. They include physiological consequences that are linked to the hormonal, immunological, and vascular modifications induced by pregnancy, as well as several others signs that may signify the presence of a disease that requires diagnosis and treatment. Therefore, when facing a pregnant woman asking for advice about skin signs or symptoms, the successive questions you should ask are:

  1. Do these signs or symptoms correspond to physiological modifications linked to pregnancy?
  2. If not, do they correspond to cutaneous disorders specifically related to the pregnancy or are they related to a condition that is independent from the pregnancy?
  3. Is treatment available or needed?

If treatment is needed, consideration of the fetus is warranted, even for topical treatment.

Signs and Symptoms Corresponding to Physiological Dermatoses

Pigmentary Changes
Pigmentary disorders, affecting 85-95% of pregnant women, are the most frequently encountered modifications linked to pregnancy.1 As expected for other abnormalities of pigmentation, these are more obvious in genetically pigmented individuals. These changes are usually local and may begin early in pregnancy. They are linked to several biological phenomena, including the increased production of α-melanocyte-stimulating hormone (α-MSH), estrogens and progesterone, and sun exposure.

Hyperpigmentation of the linea alba is the most commonly observed pigmentation change (75% of cases), and it is called linea nigra. It usually extends from the pubis to the umbilicus but sometimes may reach the xyphoid appendix.2 This pigmentation almost always clears after delivery, although some minor changes may remain.

Chloasma is a symmetrical, non-homogeneous hyperpigmentation involving the front and/or the malar and/or the mandibular areas of the face. It usually begins after the first trimester and is worsened by sun exposure. Its occurrence ranges from 5-75% of pregnant women.3 The major problem is that it regresses slowly and inconstantly. It may last up to 6-18 months after delivery, and flares may still occur with sun exposure even long after the pregnancy ends. There are three types of chloasma according to the depth of the pigment deposition, the prognosis being poorer when melanin deposition occurs in the dermis. Treatment should be given only after delivery, and it should rely on the combination of photoprotection and topical depigmenting agents, primarily hydroquinone 2-5%. Oral contraception should be handled with caution as it may trigger new flares.

Nipple pigmentation affects 40% of pregnant women, and it may involve the areola alone or it may include the surrounding skin. Axillary and/or inguinal pigmentation are rare. Finally, the vulva may also become pigmented.

The pathogenesis of striae is not certain. It could result from hormonal changes - including steroids - on extracellular matrix production by dermal fibroblasts.4 Striae are easily recognized by the patient. They may be narrow or wide, their width sometimes reaching up to 2 cm. Initially inflammatory, the striae ultimately become white and atrophic and develop in 60-90% of pregnant women.1-3 The main sites are the abdomen and thighs, followed by breasts and then the buttocks. Striae involve preferentially young primagravada and begin during the third trimester. No preventive technique has been validated up until now. Restorative measures may be considered only after delivery; they may rely on topical retinoids and/or the pulse dye laser.

Vascular Disorders
Most of the following vascular abnormalities reflect the biological activity of high levels of estrogens on endothelial cells, leading to their proliferation.

The spider nevus is easy to recognize, having a central erythematous "arteriole" and radiating thin-walled vessels. Compression of the central vessel temporarily obliterates the lesion with blanching of the spider "legs". When released, the threadlike vessels quickly refill with blood from the central arteriole. These lesions predominate on the upper half of the body (eyebrows, face), but some may also occur on the hands. Most of these (75%) regress after delivery.1,2

Unilateral nevoid telangiectasia consists of acquired patches of superficial telangiectases in a unilateral linear distribution. These are plain, sometimes with a blanching halo surrounding each lesion, occurring primarily on the thorax and face. The diagnosis is based on clinical findings and their evolution is toward spontaneous regression after delivery.

Palmar erythema is another consequence of the vascular proliferation that occurs with pregnancy, described in 30-60% of pregnant women.1 Some authors have discriminated between a diffuse form and a more restricted erythema involving only finger pulps, thenar, and hypothenar protuberances.

Venous circulation is altered during pregnancy, frequently leading to the development of multiple signs and symptoms. The pathogenesis of venous insufficiency is multifactorial and relies on hypervolemia that alters valvular continence. There is decreased velocity of venous flow, resulting in increased venous pressure and compression of iliac veins by a dilated uterus. Venous insufficiency induces lower limb edema with pain, varicose veins, rarely thrombophlebitis, and purpura. Pregnant women should be informed of this risk.

This is a peculiar skin modification in this context: Indeed, it is still "physiological" as it is the consequence of hormonal estroprogestative changes in pregnancy, but it may be visible enough to require a treatment. Acne is found in 23% of pregnancies with a variable severity.2 The main issue for pregnancy-associated acne is the choice of therapeutic options. In summary, retinoids - including topical ones - and the cyclines are contraindicated throughout pregnancy. In contrast, benzoyl peroxide and oral and topical erythromycin or zinc are allowed.

Other Signs and Symptoms
Many other modifications may occur during pregnancy:

  • Gingivae hyperplasia and occasional bleeding may occur.
  • Nail growth may be accelerated, leading to shiny, delicate nails. Distal onycholysis is possible.
  • Modifications of the hair follicle cycle may occur, with a slower shift from anagen to telogen hair, allowing the impression of more hair. In the same way, hypertrichosis alone - without hirsutism - is possible. Following pregnancy, rapid hair loss, termed telogen effluvium, may occur.
  • An increase in acrochordons - skin tags - during pregnancy is classically reported in textbooks. However, original series have not reported this hallmark.

Signs and Symptoms Related to Specific Dermatoses of Pregnancy

A peculiar characteristic of pregnancy is the fact that there are skin conditions that are chronologically linked to this period. This means that these diseases appear only during pregnancy and that they resolve after delivery.

The frequency of intra-hepatic cholestasis of pregnancy (IHCP) varies, ranging from 0.02% of pregnancies series up to 2.4% of pregnancies in specific countries, such as Chile or China. Its pathogenesis is unknown, but most authors speculate that it could result from abnormalities in bile secretion, related to estrogens. This condition is usually limited to isolated pruritus without skin lesions. However, itching may lead to excoriations or linear crusts, and those are present in up to one-third of patients with IHCP.5,6 Many patients have elevated levels of serum biliary acids, with subsequent increases in transaminases. Obtaining an early diagnosis is mandatory as prolonged cholestasis may induce fetal consequences that are linked to the accumulation of biliary salts in the child's brain. Pregnant women with IHCP are therefore followed closely to prevent fetal distress. In addition, treatments such as cholestyramine or ursodesoxycholic acid may be given.

Pemphigoid gestationis (PG), formerly herpes gestationis, is a fascinating model of autoimmunity restricted to pregnancy. Previously, PG was considered to be very rare, occurring in only 1 out of 50,000 pregnancies. This figure results from series published when PG was considered only if a blistering eruption was present. However, this appears to be wrong. Indeed, more recent studies - in which direct immunofluorescence was done on skin blisters, as well as papular eruptions - finally revealed that PG affected 1 in 1,600 pregnancies.6,7

This discrepancy demonstrates that PG was commonly non-blistering. The disease begins in the third trimester, usually on the abdomen, in the periumbilical area, then disseminates. Itching is intense and lesions may indeed be blisters, but, as stated above, may also include arciform plaques and papules. Diagnosis requires a skin biopsy. Histology is not specific, showing dermal edema, mononuclear infiltrate together with eosinophils and usually dermo-epidermal detachment. However, direct immunofluorescence discloses the linear deposits of immunoreactants, C3 more frequently than Ig, at the dermal-epidermal junction. Serum analysis shows the presence of antibodies that react against the 180kd BPAG 2 antigen. In the future, the routine use of the BP180 Elisa may allow sparing of skin biopsy. Classical analyses of the anti-epidermal complement binding antibody has been abandoned.

PG may flare after delivery or may occur for the first time after delivery. An important point is that PG displays usual recurrences during subsequent pregnancies (50-70%).2 Such recurrences may also occur in patients with a history of PG after treatment with oral contraceptives in 20-50% of cases.8 Pathogenesis is linked to the development of autoantibodies targeting the 180kd antigen of the dermal epidermal junction. Affected women have susceptibility genes for autoimmune diseases: 43-45% of PG females are HLA DR3/DR4 versus 3% in control population, and 90% of PG females have a C4 null allele.9 Another point is that placentas of women with PG disclose the abnormal expression of classical HLA class I antigens, these antigens being usually absent at this site.10 There is reactivity of the woman's sera with the placental villosities.11

Therefore, the speculative statement of pathogenesis is as follows: HLA class I paternal antigens are aberrantly expressed on the placenta; women prone to autoimmunity mount an immune humoral reaction against some of these; some these anti-paternal HLA I antibodies cross-react with the cutaneous 180 kd antigen; and pemphigoid develops. The fact that the disease does not usually relapse when the father differs for subsequent pregnancies supports this hypothesis. PG is associated with some risks in pregnancy: there are higher rates of prematurity and of caesarean section. The reasons for these remain unknown, although transient blisters may be found in babies. Treatment relies usually on oral steroids (0.5 mg/kg), although limited forms - close to bullous pemphigoid - could be treated with topical steroids.

Polymorphic eruptions of pregnancy (PEP) have been individualized in the 1980s to include many entities that did not deserve to be separated.12 Therefore, PEP appeared as a disease beginning in the third trimester of pregnancy that can affect primigravida. The lesions begin as in PG on the abdomen, then usually disseminate. The immediate periumbilical skin is usually spared, and the eruption predominates in the striae. This pruritic eruption consists of papules, urticarial plaques, and more rarely vesicles.13

In the absence of treatment, spontaneous healing occurs weeks after delivery and flares are rarely noted in subsequent pregnancies (5%).6 Contraception given after delivery does not induce relapses. Biopsies have non-specific features, with a mononuclear infiltrate, sometimes eosinophils, and epidermal spongiosis. Direct immunofluorescence is mandatory: indeed, PG may present as a third trimester eruption of plaques without blisters. Therefore, determining that a cutaneous eruption developing during pregnancy is a PEP requires the absence of an immunoreactant deposition to be checked by immunofluorescence.

The pathogenesis of PEP remains unknown. Authors have proposed a role for skin distension, suggesting that cutaneous tissue would be inflamed because of mechanical distension. This hypothesis has not been confirmed.14 There is no autoimmunity in PEP. Vaughan Jones et al. have recently found a higher level of cortisol level in women with PEP.15

Our group has found abnormal trafficking of fetal cells in this disease, but these fetal cells could either trigger the disease (as in a fetal anti-maternal reaction) or, in contrast, migrate into the skin to repair established damage.16 This last hypothesis is in line with other findings in which fetal cells appear to differentiate into various phenotypes in peripheral tissues in order to participate in lesion repair. Whatever the cause, PEP has no deleterious consequences for the mother or the baby and treatment relies on topical steroids and antihistamines.


Many other items could be added to this relatively short list. Some are pre-existing skin conditions that may worsen during pregnancy, such as lupus erythematosus or dermatomyositis. In contrast, others (such as psoriasis) may improve during pregnancy. Skin infections such as syphilis, rubella, parvovirus B19, toxoplasmosis, varicella, and others could induce embryonic and/or fetal diseases and should be recognized early. This highlights the essential role of dermatologists in this context: to allow an early diagnosis.

The prognosis of melanoma is similar to that of non-pregnant women, but a delay in diagnosis seems to happen, possibly due to co-founding factors. Of note, there are no mole modifications during pregnancy and quantitative measurements of nevi have not shown any "physiological" growth of nevi.17 Therefore, every modification of melanocytic lesions during pregnancy should be interpreted with caution and not considered to be a physiological growth of moles.

Finally, prescribing treatments, including topical ones, is always delicate and it is important to always check recent information of drug agencies before administration as recommendations change frequently, even for some old molecules.


  1. Winton GB, Lewis CW. Dermatoses of pregnancy. J Am Acad Dermatol. 1982;6(6):977-98.
  2. Estève E, Saudeau l, Pierre F, et al. Signes cutanés physiologiques au cours de la grossesse normale: étude de 60 femmes enceintes. Ann Dermatol Venereol. 1994;121:227-31.
  3. Wade T, Wade SL, Jones HE. Skin changes and diseases associated with pregnancy. Obstet Gynecol. 1978;52(2):233-42.
  4. Henry F, Pierard Franchimont C, Pans A, et al. Striae distensae of pregnancy. An in vivo biomechanical evaluation. Int J Dermatol. 1997;36(7):506-8.
  5. McDonald JA. Cholestasis of pregnancy. J Gastrol Enterol. 1999;14(6):515-8.
  6. Roger D, Vaillant L, Fignon A, et al. Specific pruritic diseases of pregnancy. A prospective study of 3192 pregnant women. Arch Dermatol. 1994;130(6):734-9.
  7. Zurn A, Celebi CR, Bernard P, et al. A prospective immunofluorescence study of 111 cases of pruritic dermatoses of pregnancy: IgM anti-basement membrane zone antibodies as a novel finding. Br J Dermatol. 1992;126(5):474-8.
  8. Schornick JK, Black MM. Secondary autoimmune diseases in herpes gestationis (pemphigoid gestationis). J Am Acad Dermatol. 1992;26(4): 563-6.
  9. Schornick JK, Artlett CM, Jenkins RE, et al. Complement polymorphism in herpes gestationis: association with C4 null allele. J Am Acad Dermatol. 1993;29(4):545-9.
  10. Bortwhick GM, Holmes RC, Stirrat GM. Placenta abnormal expression of class II MHC antigens in placentae from patients with pemphigoid gestationis: analysis of class II MHC subregion product expression. Placenta. 1988;9(1):81-94.
  11. Ortonne JP, Hsi BL, Verrando P, et al. Herpes gestationis factor reacts with the amniotic epithelial basement membrane. Br J Dermatol. 1987;117(2):147-54.
  12. Holmes RC, Black MM. The specific dermatoses of pregnancy. J Am Acad Dermatol. 1983;8(3):405-12.
  13. Aronson IK, Bond S, Fielder VC, et al. Pruritic urticarial papules and plaques of pregnancy: clinical and immunopathologic observations in 57 patients. J Am Acad Dermatol. 1998;39(6):933-9.
  14. Roger D, Vaillant L, Lorette G. Pruritic papules and plaques of pregnancy are not related to maternal or fetal weight gain. Arch Dermatol. 1990;126(11):1517.
  15. Vaughan Jones SA, Hern S, Nelson-Piercy C, et al. A prospective study of 200 women with dermatoses of pregnancy correlating clinical findings with hormonal and immunopathological profiles. Br J Dermatol. 1999;141(1):71-81.
  16. Aractingi S, Berkane N, Bertheau P, et al. Fetal DNA in skin of polymorphic eruption of pregnancy. Lancet. 1998;352(9144):1898-901.
  17. Pennoyer JW, Grin CM, Driscoll MS, et al. Changes in size of melanocytic nevi during pregnancy. J Am Acad Dermatol. 1997;36(3 Pt 1):378-82.