The complex endocrinologic, immunologic, metabolic, and vascular changes associated with pregnancy may influence the skin in various ways. Pregnancy-specific dermatoses represent a heterogeneous group of pruritic skin diseases that have been reclassified recently as pemphigoid gestationis, pruritic urticarial papules and plaques of pregnancy (PUPPP), intrahepatic cholestasis of pregnancy, and atopic eruption of pregnancy 1. Mechanisms leading to pregnancy-specific dermatoses may be a reflection of the hormonal and immunological changes associated with pregnancy that may potentially pose a serious risk to the fetus 2. Diagnosis and timely treatment of these dermatoses are necessary as these can pose a risk to the fetus, such as prematurity and low birth weight.
In our study, we observed the frequency distribution and progression of specific dermatoses of pregnancy (Table 1) in 250 randomly selected pregnant women attending the antenatal clinic of our hospital over a period of 1 year. There are two units of the gynecology and obstetrics department at our hospital; we selected all new patients attending the antenatal clinic of one of the units on one particular day in a week, which was their outpatient department day and our free day. In total, 54.4% of patients in our study were primigravida, whereas 45.6% were multigravida.
Among the specific dermatoses, PUPPP has been described in the literature as the most common gestational dermatosis. In our study, the frequency was 1.2% and all the three women affected with PUPPP were multigravida, with the onset of lesions in the third trimester. Roger et al.3 reported the frequency to be one in 120–240 pregnancies. Of the pregnant women with PUPPP, 85.7% were primagravida in the study carried out by Kumari et al.4. In a study carried out by Rudolph et al.5, 70% of pregnant women were primigravida and 30% were multigravida. The average gestational age at the onset of eruption was reported to be 35 weeks by Holmes et al.6, which is comparable to our findings. The abdomen (especially the striae) was the most common site and papules were the most common type of lesions. The exact etiology is not known, but it has been proposed that stretching of the skin damages the connective tissue, causing subsequent conversion of nonantigenic molecules into antigenic molecules, leading to skin eruption. They reported that larger babies and increased maternal weight gain most likely lead to an increased abdominal girth. Maternal and fetal prognoses remain excellent 7. In our study, two patients were administered topical steroids and antihistaminics; however, in one patient systemic steroids had to be administered because of intractable itching. All the mothers delivered normal healthy babies without any skin rash and the maternal lesions resolved spontaneously within 6 days after delivery.
Intrahepatic cholestasis of pregnancy (ICP) was observed in two (0.8%) patients of our study. Roger et al.3 reported an incidence of 0.5%. Patients had moderate pruritus and secondarily developed excoriation marks mostly over the legs and the trunk. The time for the onset of lesions was 33 weeks of gestation in both the patients. Both patients showed abnormalities in bile acids levels in the blood. They were administered treatment in the form of topical antipruritics and 15 mg/kg/day ursodeoxycholic acid for 3 weeks. One patient followed the treatment as advised and her pruritus and laboratory test results improved; however, the second patient discontinued treatment after 1 week and presented to us at 35 weeks with fetal distress; thus, an emergency elective cesarean section was performed at the 35th week of her pregnancy. Pregnancy outcome was normal in the first patient and she delivered a healthy baby vaginally at full term. Ambros-Rudolph 1 also reported an increased risk of fetal distress with elevated bile acid levels, as was found in our study. Pruritus resolved spontaneously in both patients soon after delivery, with an average postpartum duration of 3 days. Genetic predisposition may induce an abnormal reaction to elevated female sex hormones, leading to altered liver functions and, hence, cholestasis 2.
In our study on specific cutaneous lesions in antenatal patients, two patients had prurigo of pregnancy, the frequency being two in 250 pregnancies (0.8%). Pruritus was severe and the lesions were discrete excoriated papules and nodules over the extensor surfaces of the limbs and abdomen. Lesions healed with a substantial degree of hyperpigmentation. Similar clinical characteristics have been reported by Roger et al.3 and Lawley and Yancey 8. The mean time for the onset in our patients was 26 and 28 weeks of gestations, respectively. Associated liver function tests yielded normal results and bile salt levels were not elevated, which helped rule out ICP. Both the patients were administered topical steroids and systemic antihistaminics. They had a normal vaginal delivery at full term and delivered healthy babies. There was spontaneous resolution of lesions within 4 weeks postpartum. The reason for prurigo of pregnancy is believed to be depressed cell-mediated immunity during pregnancy and a shift from Th1 to Th2 to prevent fetal rejection, which leads to atopy 9.
One of our patients had pemphigoid gestationis, which was confirmed on biopsy, the incidence being 0.4%. She was primigravida with intense itching that started at the 32nd week of gestation initially over the abdomen, later on the thighs and the forearms. Lesions were in the form of erythematous papules and annular plaques and vesicles in the periumbilical region. As the itching was severe, she had to be treated with 30 mg of deflazacort twice daily. The majority of the lesions subsided within 10 days and the old ones stopped appearing; thus, doses of the steroids were gradually reduced to 30 mg once daily until delivery and were further tapered off within 3 weeks of delivery. The mother delivered a low birth weight baby at 36 weeks of pregnancy with no skin lesions. A similar incidence of delivery of a low birth weight baby and the use of systemic steroids has been reported by Kroumponzos and Cohen 10. The pathogenesis of pemphigoid gestationis is believed to be a placental antigen cross reacting with a skin antigen 11.
Pruritus during pregnancy should never be neglected as it may be due to one of the specific dermatoses of pregnancies. Patients with pruritus should be examined thoroughly as most of the diagnoses can be made clinically, which later can be supported by laboratory investigations and skin biopsy wherever necessary 10. Involvement of the periumbilical region with papules and vesicles points toward pemphigoid gestationis 9, whereas sparing of this region and urticated lesions along striae during later stages of pregnancy favors a diagnosis of PUPPP 7. Pruritus without primary lesions and associated only with secondary excoriations supported by elevated bile acid levels in later stages of pregnancy favors the diagnosis of ICP 11. Pruritus in the early stages of pregnancy with or without elevated IgE levels points toward the diagnosis of atopic eruption of pregnancy 2. Treatment in the form of topical steroids, soothing lotions, and oral antihistaminics may suffice in the majority of patients. In patients with pemphigoid gestationis, oral steroids are required, whereas in patients with intrahepatic cholestasis, ursodeoxycholic acid is the treatment of choice to prevent maternal and fetal morbidity and mortality 12.
Jasleen Kaur: concept, design, definition of intellectual content, literature search, clinical studies, data acquisition, data analysis, statistical analysis, guarantor; Jyotika Kalsy: literature search, data analysis, statistical analysis, manuscript preparation, manuscript editing and review.
Conflicts of interest
There are no conflicts of interest.
1. Ambros-Rudolph CM. Dermatoses of pregnancy – clues to diagnosis, fetal risk and therapy. Ann Dermatol. 2011;23:265–275
2. Beard MP, Millington GWM. Recent developments in the specific dermatoses of pregnancy. Clin Exp Dermatol. 2012;37:1–5
3. Roger D, Vaillant L, Fignon A, Pierre F, Bacq Y, Brechot JF, et al. Specific pruritic diseases of pregnancy: a prospective study of 3192 pregnant women. Arch Dermatol. 1994;130:734–739
4. Kumari R, Jaisankar TJ, Thappa DM. A clinical study of skin changes in pregnancy. Indian J Dermat Venereol Leprol. 2007;73:141
5. Rudolph CM, Al-Fares S, Vaughan-Jones SA, Müllegger RR, Kerl H, Black MM. Polymorphic eruption of pregnancy: clinicopathology and potential trigger factors in 181 patients. Br J Dermatol. 2006;154:54–60
6. Holmes RC, Black MM, Dann J. A comparative study of toxic erythema of pregnancy and herpes gestationis. Br J Dermatol. 1982;106:499–510
7. Matz H, Orion E, Wolf R. Pruritic urticarial papules and plaques of pregnancy: polymorphic eruption of pregnancy (PUPPP). Clin Dermatol. 2006;24:105–108
8. Lawley TJ, Yancey KBFreedberg IM, Eisen AZ, Wolff K, et al. Skin changes and diseases in pregnancy. Fitzpatrick’s dermatology in general medicine. 19995th ed. New York McGraw-Hill:163–169
9. Wilder RL. Hormones, pregnancy, and autoimmune diseases. Ann N Y Acad Sci. 1998;840:45–50
10. Kroumpouzos G, Cohen LM. Dermatoses of pregnancy. J Am Acad Dermatol. 2001;45:1–19
11. Sachdeva S. The dermatoses of pregnancy. Indian J Dermatol. 2008;53:103–105
12. Palma J, Reyes H, Ribalta J, Hernández I, Sandoval L, Almuna R, et al. Ursodeoxycholic acid in the treatment of cholestasis of pregnancy: a randomized, double-blind study controlled with placebo. J Hepatol. 1997;27:1022–1028