![]() When PUPPP resolves, typically over an average of 4 weeks spontaneously or with delivery, there is no post-inflammatory pigment change or scarring of the skin. Mucosal involvement is usually not observed. ![]() After that, almost all patients develop more polymorphic features as the disease evolves, including widespread erythema, targetoid lesions, tiny vesicles, and eczematous patches. The eruption spreads over a matter of days, to the trunk and the extremities, but rarely involves the face, palms, or soles. The lesions can coalesce to form larger urticarial abdominal plaques often surrounded by blanched halos. The rash consists of itchy small erythematous and edematous papules and plaques usually first start in the stretch marks, typically with periumbilical sparing. Pruritic urticarial papules and plaques of pregnancy occur most often during the last month of pregnancy and only rarely appear in the postpartum period. But in one study the presence of circulating IgM anti-basement membrane zone, in 5 from 111 cases had been reported. Indirect immunofluorescence investigations for circulating IgG antibodies shows almost always negative results. Nevertheless, minimal nonspecific granular deposition of IgM, C3 or IgA along the dermal-epidermal junction or blood vessels had also been reported. Direct immunofluorescence of lesional skin is usually negative. reported epidermal changes commonly seen in the biopsies taken from patients who had lesions with various morphologies including papulovesicular rash, target-like lesions, and eczematous lesions. In the resolving stage of PUPPP, there is acanthosis with hyperkeratosis and parakeratosis. The lymphocytic infiltrate is often composed of T-helper lymphocytes with an admixture of a variable number of eosinophils and neutrophils. In early pruritic urticarial papules and plaques of pregnancy lesions, there is epidermal and upper dermal edema, and occasionally focal mild spongiosis, with a deeper dermal lymphohistiocytic perivascular infiltrate, which may resemble arthropod bite reactions. īiopsy specimens from lesional skin reveal nonspecific findings. Another hypothesis centers on fibroblast proliferation in the maternal skin, induced by a placental hormonal-type substance. High levels of progesterone, especially if multiple gestations and increased progesterone receptor immunoreactivity have been demonstrated in patients with PUPPP. An immune tolerance mechanism during subsequent pregnancies might prevent recurrence. An inflammatory response is thought to be promoted by cross-reactivity to collagen in otherwise normal-appearing skin. The mechanism by which lesions become generalized is also unclear. Additionally, there are suggestions that peripheral chimerism (deposition of fetal DNA), which occurs particularly during the third trimester, and favors skin with increased vascularity and damaged collagen, could be subsequently the target of immune reactivity. Therefore suggestions have been that rapid, late stretching of abdominal skin, occurring with a high frequency in multiple pregnancies, may lead to connective tissue damage and that the exposure of antigens within collagen could elicit an allergic-type reaction, resulting in the initial appearance of the eruption in striae. the eruption was thought to have developed in 90% of patients, as a consequence of damage to connective tissue within striae. ![]() The cause of pruritic urticarial papules and plaques of pregnancy is still unknown, although various etiological theories have been proposed, including abdominal distension, hormonal changes, placental factors and the role of fetal DNA in skin lesions of patients with PUPPP.
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