Dermatology in pregnancy

Meet the patient

A 34-year-old primigravida at 36 weeks is scratching herself raw. The eruption started inside her abdominal stretch marks and has spread to her thighs, but conspicuously spares the umbilicus. She is miserable but afebrile, and the baby is moving normally.[4][6]

Before you reach for a topical steroid, three questions sort the whole topic: how many weeks pregnant? Did itch precede the rash, or the rash the itch? And is there a primary rash at all? A pregnant patient with itch and no visible primary lesion is intrahepatic cholestasis of pregnancy until bile acids prove otherwise — not "just pregnancy itch."[1][4]

The safe triage — timing, morphology, fetal risk

Dermatology in pregnancy is not a single disease. It is the bedside problem of deciding whether a pregnant patient has a physiologic change, a pregnancy-specific dermatosis, a pre-existing dermatosis modified by pregnancy, an infection, a drug eruption, or a systemic obstetric disorder presenting through the skin.[4][6]

The safe answer in an exam is therefore not a memorised list but a reproducible triage: gestational age, whether there is a primary rash, morphology, umbilical involvement, systemic features, fetal risk, and whether the first investigation is bile acids or direct immunofluorescence.[4][6]

The fetal risk is not proportional to how dramatic the rash looks. PEP can be intensely itchy and widespread but is fetal-benign. ICP may have no visible rash at all but carries bile-acid-related fetal risk. PG can start as urticarial plaques before bullae appear, so the examiner expects a biopsy plan rather than blind reassurance. Pustular psoriasis of pregnancy may be rare, but fever, malaise, hypocalcaemia and fetal distress make it a dermatology emergency.[4][7][9][10]

[7]

The named group — and the misleading old name

The classic named group of pregnancy-specific dermatoses was reorganised by Ambros-Rudolph and colleagues into atopic eruption of pregnancy, polymorphic eruption of pregnancy, pemphigoid gestationis, and intrahepatic cholestasis of pregnancy.[6]

Modern teaching also treats pustular psoriasis of pregnancy, historically called impetigo herpetiformis, as a pregnancy-triggered severe pustular psoriasis syndrome that behaves like a maternal systemic illness rather than a benign itchy rash. The old name is a trap: it is not impetigo and not herpes.[10]

Classification — four boxes

A useful classification separates four boxes.[4][6]

[4]

Epidemiology & Risk Factors

Atopic eruption of pregnancy is the commonest pregnancy-specific itchy dermatosis, often in the first or second trimester in women with personal or family atopy, dry skin, allergic rhinitis or asthma. It may be a flare of pre-existing atopic dermatitis or a first episode of atopic eczema or prurigo during pregnancy. Because it is common, benign for the fetus and early, it is frequently tested as the diagnosis that is itchy but not obstetrically dangerous.[4][6]

PEP/PUPPP typically affects primigravidae late in the third trimester, especially with multiple gestation, rapid abdominal distension, prominent striae or excessive maternal weight gain. The association with stretching explains why the eruption often begins inside abdominal striae. It is uncomfortable but fetal-benign, and usually settles soon after delivery.[4][6]

Pemphigoid gestationis is rare. Risk is higher with prior PG, autoimmune predisposition and certain HLA associations; recurrence in later pregnancies is a high-yield counselling point, often earlier and more severe. Flares can occur postpartum or with menstruation or estrogen-containing contraception.[9]

ICP risk factors include previous ICP, family history, multiple pregnancy, hepatitis C, gallstones or underlying hepatobiliary disease, assisted reproductive technology, advanced maternal age, and ethnicity. It is primarily an obstetric liver disorder, but dermatology sees it because pruritus is the presenting symptom and there may be no rash.[1][2][5]

Pustular psoriasis of pregnancy is uncommon but dangerous, reported in women with and without known psoriasis, and may be associated with hypocalcaemia, infection triggers, medication withdrawal, stress and the immunologic-hormonal milieu of pregnancy.[10]

Pathophysiology — why each eruption looks the way it does

Physiologic pigment change is driven by estrogen, progesterone and melanocyte-stimulating influences that increase melanogenesis in predisposed sites. Melasma appears on sun-exposed facial areas because ultraviolet and visible light amplify melanocyte activity; linea nigra and areolar darkening reflect regional pigment sensitivity. Striae gravidarum arise when mechanical stretch acts on dermis whose collagen and elastic-fibre architecture is altered by pregnancy hormones. Hair often remains in anagen during pregnancy, then shifts into telogen postpartum, producing telogen effluvium several months after delivery.[4]

AEP sits on the atopic end of pregnancy immune adaptation. A Th2-skewed environment, impaired barrier function and pre-existing atopic tendency promote eczema, papules or prurigo-like lesions. It does not carry a specific fetal risk.[4][6]

PEP/PUPPP is best understood as a benign inflammatory reaction in overstretched abdominal skin — the association with primigravidity, multiple gestation, rapid distension and striae supports a stretch-related trigger. It does not cause complement-mediated blistering or fetal compromise.[4][6]

PG is the pregnancy counterpart of bullous pemphigoid. Maternal autoantibodies target BP180 (collagen XVII), especially the NC16A domain at the dermal-epidermal junction. Complement activation produces linear C3 along the basement membrane zone, then eosinophil-rich inflammation and subepidermal blistering. The placenta can express relevant antigens, and transplacental antibody passage explains transient neonatal blistering in a minority of infants.[9]

ICP is caused by impaired hepatobiliary bile-acid transport in a genetically and hormonally susceptible pregnancy. Maternal bile acids rise, producing pruritus and biochemical cholestasis. Fetal exposure to high bile-acid levels is associated with spontaneous and iatrogenic preterm birth, meconium-stained liquor and stillbirth risk; the clearest stillbirth signal in the individual patient data meta-analysis was at peak bile acids of 100 micromol/L or more.[2][7]

Pustular psoriasis of pregnancy is a systemic sterile neutrophilic pustular dermatosis. Keratinocyte and innate immune activation recruit neutrophils into epidermis, producing spongiform pustules; the systemic inflammatory load explains fever, malaise, raised inflammatory markers, electrolyte disturbance and fetal compromise. A culture-negative pustular eruption in a toxic pregnant patient should never be dismissed as a simple superficial infection.[10]

Clinical Presentation — read the timing and the morphology

The safest first history is gestational age; onset relative to pregnancy; whether itch preceded the rash or the rash preceded the itch; palms and soles; night-time itch; umbilical involvement; striae onset; blistering; fever; mucosal pain; jaundice; urine and stool colour; drug exposure; contacts with itch; psoriasis or atopy history; previous pregnancy rash; fetal movement; and systemic symptoms.[4]

Physiologic changes are common and usually asymptomatic or mildly symptomatic. Melasma appears as symmetric brown facial macules or patches, classically centrofacial, malar or mandibular. Linea nigra is a vertical hyperpigmented abdominal line. Striae are pink to violaceous linear atrophic bands on abdomen, breasts, hips and thighs. Spider angiomas and palmar erythema may appear without liver disease — but jaundice, severe itch, dark urine or pale stools should move the case out of the physiologic box.[4]

AEP presents with pruritic eczema or papules. The eczematous type affects face, neck, upper chest and flexures, with xerosis and excoriation; the papular type produces small erythematous papules on trunk and limbs, sometimes prurigo-like nodules on extensor surfaces. Onset is often before the third trimester. There is no primary blistering, no bile-acid syndrome, and no specific fetal risk.[4][6]

PEP/PUPPP is late, urticarial and striae-centred. It begins as intensely pruritic erythematous papules within abdominal stretch marks, coalescing into urticarial plaques and spreading to thighs, buttocks and limbs. The umbilicus is usually spared. Small vesicles may occur, but tense bullae should trigger PG workup. The face, palms and soles are usually spared. The mother is uncomfortable, but fever, jaundice, mucosal erosions and fetal-risk biochemistry are absent.[4][6]

The PEP-versus-PG discriminator: the umbilicus. PEP begins in striae and usually spares the umbilicus; PG commonly involves the periumbilical region and can blister. PEP has no fetal risk; PG has maternal recurrence and fetal associations.[4][9]

PG begins with intense itch and urticarial plaques, commonly around the umbilicus, before progressing to vesicles and tense bullae. It may involve trunk and limbs, including palms and soles, and often flares around delivery or postpartum. Mucosal involvement is uncommon. The danger is that early PG can look like PEP — the clues are umbilical involvement, blistering, recurrence, postpartum flare and failure to behave like a self-limited striae rash.[9]

ICP presents with pruritus without a primary rash, usually late second or third trimester. Palms and soles are classic, and night-time itch is common. Scratching can cause excoriations, prurigo nodules or secondary infection, but there is no primary eruption. Jaundice is uncommon but important. If a patient says the itch is unbearable but the skin shows only scratch marks, order bile acids rather than a stronger steroid.[1][2][3]

Pustular psoriasis of pregnancy presents as painful erythematous plaques with rings or lakes of sterile pustules, often beginning in flexures and spreading centrifugally. Fever, malaise, diarrhoea, delirium, dehydration, mucosal erosions, nail changes, hypocalcaemia, hypoalbuminaemia and secondary infection can occur. A sick pregnant patient with pustules is not a PEP patient; she needs admission and maternal-fetal assessment.[10]

Differential Diagnosis — organise by morphology

The differential is best organised by whether the patient has itch without a primary rash, urticarial plaques, eczema or papules, bullae, pustules, pigment change, or systemic illness.[4]

[4] [9] [10]

Scabies, urticaria, drug eruption, viral exanthem, contact dermatitis, tinea, bacterial folliculitis, dermatitis herpetiformis, erythema multiforme, varicella, disseminated herpes simplex, acute generalized exanthematous pustulosis and ordinary psoriasis can all occur in pregnancy. The label pregnancy-specific should be used only after the morphology and investigations fit.[4]

Clinical & Bedside Assessment

Examine the whole patient, not only the visible rash. Record gestational age, vital signs and maternal distress. Look for jaundice, dehydration, fever, sepsis, pain and reduced mobility. Inspect the umbilicus, striae, flexures, palms, soles, scalp, nails and mucosa.[4][9][10]

In itchy patients, decide whether visible marks are primary lesions or secondary excoriations. In pustular patients, assess oral mucosa, flexures and evidence of systemic toxicity. In blistering patients, keep an intact fresh blister and perilesional skin available for biopsy.[4][9][10]

The obstetric assessment should not be an afterthought. Ask about fetal movements, contractions, ruptured membranes, bleeding, prior stillbirth, prior ICP, prior PG, multiple pregnancy and current hypertensive symptoms. Dermatology diagnoses with fetal implications require obstetric or maternal-fetal medicine involvement even if the skin is the presenting complaint.[1][7][9]

Investigations — test only where tests change risk

No laboratory test is required for straightforward physiologic pigmentation, uncomplicated striae, typical mild AEP, or classic PEP in a well patient. The purpose of investigations is to exclude the dangerous mimics: ICP, PG, pustular psoriasis, infection, hepatitis, biliary disease, pre-eclampsia or HELLP, drug reaction and autoimmune disease.[4]

For suspected ICP, order serum bile acids and liver tests including ALT, AST, bilirubin and alkaline phosphatase, interpreted in the pregnancy context. Many pathways use non-fasting or random bile acids; local laboratory reference ranges matter. If symptoms are convincing but bile acids are initially normal, repeat bile acids and LFTs — itch can precede biochemical elevation. If jaundice, marked transaminase elevation, fever, right upper quadrant pain or atypical features are present, investigate other liver disease.[1][2][5]

For suspected PG, take two biopsies if possible: lesional skin for routine histology and perilesional normal-appearing skin for direct immunofluorescence. DIF classically shows linear C3 at the basement membrane zone, often with IgG. BP180 ELISA supports diagnosis and can help follow activity. Do not biopsy an old eroded blister for DIF — perilesional skin is the key sample.[9]

For suspected pustular psoriasis of pregnancy, order FBC with differential, CRP, urea and electrolytes, calcium, magnesium, phosphate, albumin, renal and liver tests, blood cultures if febrile, swabs or cultures from pustules to exclude infection, and biopsy if diagnosis is uncertain. Correctable hypocalcaemia is not a footnote — it may worsen pustular disease and maternal instability.[10]

Management — Resuscitation

Most pregnancy rashes are outpatient problems, but the red flags must be handled first. Admit or urgently co-manage with obstetrics for fever, hypotension, dehydration, painful widespread erythema, pustules, mucosal erosions, suspected sepsis, jaundice, dark urine with pale stools, reduced fetal movements, severe sleep-destroying itch with abnormal bile acids, extensive blistering, secondary infection or any known teratogenic drug exposure.[4][5][10]

In pustular psoriasis of pregnancy, resuscitation means hospital care — maternal observations, hydration, analgesia, temperature control, correction of calcium and electrolyte abnormalities, infection exclusion, venous thromboembolism risk assessment, nutrition, wound and skin barrier care, and fetal assessment. Antibiotics are not given merely because pustules exist; they are used when cultures, cellulitis, sepsis or another infection source supports them.[10]

Management — Definitive — the ladder

The definitive management ladder starts with diagnosis-specific reassurance and ends with obstetric timing decisions only when the diagnosis has fetal implications. Treat the mother, protect the fetus, avoid teratogens, and explain that pregnancy and lactation are separate prescribing decisions.[4][11][12]

AEP treatment

Treat AEP with liberal bland emollient several times daily and after washing to restore barrier function. For inflamed eczema, use a low- or moderate-potency topical corticosteroid such as hydrocortisone 1 percent cream or ointment thinly once or twice daily for 7 to 14 days, then step down to intermittent use.[4][11]

For thicker plaques on trunk or limbs, a moderate potency steroid may be used for short courses; avoid unnecessary very potent steroid use, occlusion and large cumulative quantities. Oral cetirizine 10 mg at night or loratadine 10 mg daily can be considered for itch where local obstetric advice permits; chlorphenamine at night is an alternative when sedation is acceptable. Narrowband UVB is a useful non-systemic option for widespread disease. The trap is undertreating eczema because the patient is pregnant — safe topical therapy is better than sleep deprivation, excoriation and secondary infection.[4][6][11]

PEP/PUPPP treatment

PEP management is reassurance plus itch control. Explain that the eruption is maternal discomfort rather than fetal danger and usually resolves within days to weeks postpartum. Use emollients and cool compresses.[4][11]

Apply a moderate-potency topical corticosteroid such as betamethasone valerate 0.1 percent cream thinly once daily for 1 to 2 weeks to active plaques, then reduce. Add cetirizine 10 mg daily, loratadine 10 mg daily, or a sedating antihistamine at night if sleep is severely affected and local obstetric prescribing allows. For rare severe, sleep-destroying disease, a short oral prednisolone course such as 20 to 40 mg daily for several days with taper can be used after obstetric review.[4][11]

Pemphigoid gestationis treatment

Mild PG can be treated with potent topical corticosteroid to active plaques, non-sedating antihistamine for daytime itch and careful surveillance for blistering. Moderate or severe PG needs systemic corticosteroid — commonly oral prednisolone around 0.5 mg/kg/day, increased toward 1 mg/kg/day for extensive blistering when clinically required, followed by gradual taper to the lowest dose that controls new blisters.[9][11]

Treat secondary infection if present, protect erosions with non-adherent dressings, and coordinate fetal growth and obstetric monitoring because PG is associated with prematurity and small-for-gestational-age infants. Postpartum flare is common, so do not stop follow-up at delivery.[9]

ICP treatment

ICP treatment has two parallel goals: relieve maternal itch and reduce fetal risk by bile-acid-guided obstetric planning. Start ursodeoxycholic acid when symptoms and biochemistry support ICP, often 10 to 15 mg/kg/day orally in two or three divided doses, with titration by symptoms, bile acids, tolerability and local protocol.[1][7][8]

The trap: do not oversell UDCA as fetal-protective. UDCA may improve pruritus for some patients, but PITCHES did not show a meaningful reduction in the composite adverse perinatal outcome, so UDCA is not a substitute for bile-acid surveillance and delivery planning. Emollients, a cool environment and night-time sedating antihistamine may help sleep but do not correct cholestasis.[8]

Repeat bile acids and liver tests according to local obstetric practice, stratify risk by the peak bile-acid concentration, and discuss timing of birth with obstetrics. The best-supported high-risk threshold for stillbirth is 100 micromol/L or more. Conventional fetal surveillance may be used, but it cannot reliably predict or prevent sudden ICP-related stillbirth — a reassuring CTG should not override a high bile-acid trajectory. Recheck bile acids and liver tests postpartum, often at 4 to 6 weeks, and investigate persistent abnormal results.[2][5][7]

Pustular psoriasis of pregnancy treatment

Pustular psoriasis of pregnancy requires admission and specialist care. Correct dehydration, electrolyte disturbance and hypocalcaemia; exclude infection; use bland emollients and wet wraps or non-adherent dressings for skin comfort; and begin systemic therapy when disease is moderate to severe.[10]

Oral prednisolone 30 to 60 mg daily is commonly used initially, adjusted to maternal severity and obstetric context, with taper after control. If disease is refractory, ciclosporin around 2 to 5 mg/kg/day orally can be considered with blood pressure, renal function and drug-level or toxicity monitoring. Pregnancy-compatible biologic options, especially agents with low placental transfer such as certolizumab in selected cases, require dermatology and obstetric input.[10]

The prescribing traps — teratogens

Drug pitfalls are heavily examined. Systemic retinoids are contraindicated in pregnancy; acitretin requires prolonged pregnancy avoidance after stopping because of persistence and conversion issues. Methotrexate is abortifacient and teratogenic. Mycophenolate is teratogenic. Finasteride is avoided because of male fetal genital risk.[11]

Tetracyclines are avoided, especially after early pregnancy and with prolonged use, because of fetal teeth and bone concerns. Potent topical corticosteroids are not absolutely forbidden, but high cumulative exposure, occlusion and large body-surface use should be avoided unless the benefit is clear. Breastfeeding decisions are separate: nipple exposure, infant age, prematurity, maternal dose and drug half-life matter.[11][12]

Complications & Pitfalls

AEP and PEP have no specific fetal risk, but maternal sleep loss, excoriations and secondary infection are real problems. PG is associated with prematurity, fetal growth restriction or small-for-gestational-age infants, and transient neonatal blistering from passively transferred antibodies. ICP is associated with preterm birth, meconium-stained liquor and stillbirth risk that rises most clearly with very high bile acids.[7][9][10]

Pustular psoriasis of pregnancy can cause maternal dehydration, sepsis mimic, electrolyte disturbance, hypocalcaemia, renal stress, fetal distress, preterm birth and fetal loss.[10]

Prognosis & Disposition

Physiologic changes generally improve postpartum, though melasma and striae may persist. AEP usually improves after delivery but can recur with future pregnancy or persist as atopic dermatitis. PEP usually resolves within days to weeks postpartum and recurrence is uncommon, though it can recur with multiple gestation.[3][4][9]

PG often flares around delivery or postpartum and commonly recurs in subsequent pregnancies, often earlier and sometimes more severely. ICP itch usually improves rapidly after delivery, but biochemical normalisation should be documented, and recurrence in later pregnancies is common. Pustular psoriasis of pregnancy may recur, especially in subsequent pregnancies, and requires preconception planning.[3][4][9][10]

Disposition is diagnosis- and severity-dependent. Mild AEP and PEP can be managed as outpatient dermatology or primary care with safety-netting. Suspected ICP needs prompt obstetric pathway involvement even if the mother is otherwise well. PG usually needs dermatology confirmation and obstetric coordination; extensive blistering, infection or high steroid need may require admission. Pustular psoriasis of pregnancy requires hospital admission. Any diagnostic uncertainty with fetal-risk implications should be managed upward, not by reassurance alone.[4][7][10]

Special Populations

The fetus and neonate are part of the dermatology assessment. In PG, maternal IgG can cross the placenta and produce transient neonatal blistering; neonatal lesions usually resolve as antibodies clear. In ICP, fetal risk is biochemical and obstetric rather than cutaneous; neonates do not get a rash from ICP. In pustular psoriasis of pregnancy, the fetal problem is maternal systemic illness, inflammation, placental stress and treatment complexity.[7][9][10]

Breastfeeding is not identical to pregnancy prescribing. A drug may be teratogenic during organogenesis yet have low milk transfer; another may be acceptable in pregnancy but cause infant sedation or require infant blood monitoring during lactation. Topical corticosteroids are generally compatible if not applied where the infant contacts or ingests them, especially the nipple. Loratadine or cetirizine are commonly preferred non-sedating antihistamines. Methotrexate, mycophenolate, cyclophosphamide and oral retinoids need specialist avoidance or very careful advice in breastfeeding.[12]

Immunocompromised pregnant patients require a broader differential: disseminated herpes simplex, varicella, drug eruption, fungal infection, crusted scabies and bacterial sepsis may mimic pregnancy dermatoses. Adolescents may conceal pregnancy or medication use. Multiple gestation increases PEP and ICP risk. A woman who conceives on isotretinoin, acitretin, methotrexate, mycophenolate or finasteride needs exact exposure dating, dose documentation and obstetric teratology counselling rather than vague reassurance.[5][11]

Evidence, Guidelines & Regional Differences

The Ambros-Rudolph reclassification is the historical anchor for modern specific dermatoses of pregnancy. It emphasised atopic eruption as the commonest entity and separated benign inflammatory eruptions from autoimmune blistering and cholestatic disease. Contemporary obstetric-dermatology reviews preserve this morphology-first approach because it maps directly to investigations: no test for classic PEP, bile acids for ICP, DIF for PG, and admission labs for pustular psoriasis.[4][6]

The key ICP evidence is risk stratification by bile acids. Ovadia and colleagues' aggregate and individual patient data meta-analysis showed that adverse outcomes correlate with bile-acid concentration and that stillbirth risk is most clearly increased at peak bile acids of 100 micromol/L or more. PITCHES then clarified that UDCA should not be oversold as fetal-protective. Together, these data support bile-acid monitoring and planned birth discussions rather than UDCA-only management.[7][8]

Drug guidance varies by country and changes over time. The exam-safe formulation is to name absolute contraindications, then say that pregnancy and lactation must be checked by exact agent, route, dose, timing and local teratology or LactMed-style source.[11][12]

Exam Pearls

[4] [6]

One-page exam summary

[4] [7] [9] [10]

Ward-round test

34 weeks, itchy plaques in striae, umbilicus spared. Diagnosis and fetal risk?

PEP/PUPPP. The fetus is not at increased disease-specific risk. Treat with reassurance, emollients, a topical corticosteroid and an antihistamine if needed. If the umbilicus is involved, bullae appear, or DIF is positive, the answer changes to pemphigoid gestationis. [4][9]

32 weeks, palms and soles itch at night, no rash. Next step?

Intrahepatic cholestasis of pregnancy until proven otherwise. Order serum bile acids and LFTs, repeat if initially normal but symptoms persist, assess for other liver disease when atypical, treat maternal itch, and involve obstetrics for bile-acid-guided delivery planning. The clearest stillbirth signal is peak bile acids of 100 micromol/L or more. [1][7][8]

Periumbilical urticarial plaques progressing to tense bullae at 28 weeks. Diagnosis and the confirmatory test?

Pemphigoid gestationis. The confirmatory test is perilesional direct immunofluorescence showing linear C3 at the basement membrane zone; BP180 ELISA supports it. Counsel on recurrence, possible postpartum flare, and fetal prematurity or small-for-gestational-age risk. Treat with potent topical steroid or oral prednisolone and coordinate obstetric monitoring. [9]

A pregnant patient with fever, painful flexural pustules, and a low calcium. What is this and where does she belong?

Pustular psoriasis of pregnancy (impetigo herpetiformis) — she belongs in hospital. It is a maternal-fetal emergency, not impetigo. Admit, correct the hypocalcaemia and electrolytes, exclude infection, and begin systemic therapy (prednisolone 30 to 60 mg, with ciclosporin or a pregnancy-compatible biologic if refractory) with dermatology and obstetric input. [10]

References

1. [1]Smith DD, Rood KM. Intrahepatic Cholestasis of Pregnancy Clin Obstet Gynecol, 2020.PMID 31764000
2. [2]Dajti E, Tripodi V, Hu Y, et al. Intrahepatic cholestasis of pregnancy Nat Rev Dis Primers, 2025.PMID 40707479
3. [3]Williamson C, Geenes V. Intrahepatic cholestasis of pregnancy Obstet Gynecol, 2014.PMID 24901263
4. [4]Himeles JR, Pomeranz MK. Recognizing, Diagnosing, and Managing Pregnancy Dermatoses Obstet Gynecol, 2022.PMID 36075066
5. [5]Terrault NA, Williamson C. Pregnancy-Associated Liver Diseases Gastroenterology, 2022.PMID 35276220
6. [6]Ambros-Rudolph CM, Müllegger RR, Vaughan-Jones SA, et al. The specific dermatoses of pregnancy revisited and reclassified: results of a retrospective two-center study on 505 pregnant patients J Am Acad Dermatol, 2006.PMID 16488288
7. [7]Ovadia C, Seed PT, Sklavounos A, et al. Association of adverse perinatal outcomes of intrahepatic cholestasis of pregnancy with biochemical markers: results of aggregate and individual patient data meta-analyses Lancet, 2019.PMID 30773280
8. [8]Chappell LC, Bell JL, Smith A, et al. Ursodeoxycholic acid versus placebo in women with intrahepatic cholestasis of pregnancy (PITCHES): a randomised controlled trial Lancet, 2019.PMID 31378395
9. [9]Huilaja L, Mäkikallio K, Tasanen K Gestational pemphigoid Orphanet J Rare Dis, 2014.PMID 25178359
10. [10]Seishima M, Fujii K, Mizutani Y Generalized Pustular Psoriasis in Pregnancy: Current and Future Treatments Am J Clin Dermatol, 2022.PMID 35704168
11. [11]Murase JE, Heller MM, Butler DC. Safety of dermatologic medications in pregnancy and lactation: Part I. Pregnancy J Am Acad Dermatol, 2014.PMID 24528911
12. [12]Butler DC, Heller MM, Murase JE. Safety of dermatologic medications in pregnancy and lactation: Part II. Lactation J Am Acad Dermatol, 2014.PMID 24528912