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1.
British Journal of Dermatology ; 186(6):e256-e257, 2022.
Article in English | EMBASE | ID: covidwho-1956697

ABSTRACT

Pemphigoid gestationis is a rare autoimmune blistering disorder which typically presents in the second and third trimester of pregnancy. We present an interesting case of a localized flare of the condition following COVID-19 vaccination. A 33- year-old woman presented 2 weeks post partum with an acute onset bullous rash. This had started at week 35 of gestation, one day prior to the onset of labour. A pruritic rash developed on her right arm before becoming widespread, with urticated erythematous plaques and tense bullae. There was no mucous membrane involvement and the infant was unaffected. Skin biopsy showed a prominent perivascular infiltrate with numerous eosinophils, suggestive of pemphigoid gestationis. Uncharacteristically, direct immunofluorescence was negative. Her symptoms improved with 30 mg oral prednisolone and topical clobetasol propionate ointment. She received the first dose of the Pfizer SARS-CoV-2 vaccine 5 weeks after the onset of the rash and within days developed a flare of her rash around the inoculation site. To our knowledge, this is the first report of a flare of pemphigoid gestationis following COVID-19 vaccination. There are case reports of other autoimmune bullous disorders (bullous pemphigoid and pemphigus vulgaris) flaring and occurring de novo following mRNA COVID-19 vaccinations. COVID -19 vaccination has been rapidly rolled out and side-effects in patients with rare conditions are only becoming apparent as these patients are exposed to the vaccine. Knowledge of this side effect will enable us to anticipate it, counsel and treat our patients more effectively, and could help maintain vaccine uptake in this vulnerable patient group. (Figure Presented) .

2.
Journal of Paediatrics and Child Health ; 58(SUPPL 2):161-162, 2022.
Article in English | EMBASE | ID: covidwho-1916254

ABSTRACT

Background: COVID-19 can cause placental histopathological changes through associated inflammatory responses, maternal hypoxia and hypoperfusion, with subsequent placental microvasculopathy and fetal hypoxia. We hypothesise that these placental changes will cause placental insufficiency, as reflected by histopathological abnormalities and fetal distress on a cardiotocography (CTG), that correlates with disease severity. Methods: During the Delta wave, Monash Medical Centre was the only referral centre for pregnant women with COVID-19 in Victoria, Australia. Three groups undergoing caesarean section prior to the onset of labour were identified: 13 women with severe COVID-19 requiring hospitalisation, 53 with asymptomatic/ mild illness and 10 with placental insufficiency without COVID-19. CTGs and placental histology were analysed for evidence of maternal and fetal hypoxia. Results: Placental histology was obtained in 12/13 of severe, 40/53 asymptomatic/mild and 8/8 cases of placental insufficiency without COVID-19. Histopathological abnormalities were associated with COVID-19 disease severity;severe (8/12, 67%) and asymptomatic/mild (24/40, 60%) compared with 100% (8/8) in the placental insufficiency group. Maternal vascular malperfusion was seen in 58%, 15% and 75% and inflammatory changes in 17%, 30% and 0%, respectively (Table 1). Abnormal CTGs reflecting fetal hypoxia were seen in 77% of severe COVID-19 cases and in 49% with asymptomatic/mild illness (Table 2). Conclusions: Both mild/asymptomatic and severe COVID-19 illness are associated with high rates of CTG and placental abnormalities. These changes are similar to those seen with other causes of placental insufficiency. Therefore, increased surveillance and delivery from >37 weeks should be considered in women with COVID-19 in pregnancy, regardless of disease severity. (Table Presented).

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