Progesterone is a hormone responsible for pregnancy maintenance and the amount of progesterone increases in a woman’s body during pregnancy, as well as the level of female sex hormones, estrogens are also upregulated. Due to these changes the cutaneous sensitivity to external stimuli (meteorological factors, bacteria, etc.) increases. In general, all skin changes during pregnancy can be divided into three groups: physiological changes (hormone-associated), nonspecific or dermatoses that existed before pregnancy or were triggered by it, and specific pregnancy-related dermatoses, which appear during pregnancy and resolve in the postpartum period. In this brief  review, we describe the dermatoses commonly seen in pregnancy and present our own clinical examples. We hope the review will be of some practical help for dermatologists and obstetricians.

Rosacea (acne rosacea, telangiectasiasis faciei) is a relatively common chronic facial skin disorder characterized by the presence of erythema, telangiectasiasis, papulopustular eruptions, and lesions on the eyes and eyelids, and associated with angioneurosis in the areas innervated by the trigeminal nerve as well. Rosacea is a common skin disease, people of middle and old age suffer more often. 1 The prevalence of rosacea in the world ranges from 1% to 20%. 2,3 Rosacea is localized mainly in the facial skin and is associated with the occurrence of transient or persistent erythema, telangiectasiasis, papulopustular elements, and nodes. 4 In 2002, the members of National Rosacea Society (USA) have published a classification system which helps standardize the diagnosis of rosacea, recognizing the following four main subtypes depending on the primary and secondary characteristics: erythematotelangiectatic rosacea, papulopustular rosacea, phymatous rosacea, and ocular rosacea. 5 The etiology of rosacea is not fully known, but in the literature there are suggestions of causality of this disease. First of all, the development of diseases is associated with changes in the immune system. Due to an impaired permeability barrier in the stratum corneum, the release of various cytokines such as tumor necrosis factor a (TNF-a), IL-1, and IL-6 is triggered, leading to cutaneous inflammation, perhaps in an attempt of the epidermis to initiate self-repair. 6 Elevated epidermal serine protease activity occurs in rosacea and causes the deposition of cathelicidin-derived peptides in the skin. 7 These peptides have the ability to cause inflammation when injected in the skin. 8 Flushing and erythema are vascular components and represent increased numbers of erythrocytes in mildly inflamed vasculature. Chronic extravascular fluid accumulation in the superficial

The immunomorphological findings are indicative of the important role of the level of MMP-1 and MMP-9 expression that is associated with the degree of progression of skin photoaging processes. Minimal MMP-1 and MMP-9 expression was recorded even in grades III-IV photoaging and in the foci of actinic keratosis. Intense MMP-1 and MMP-9 expression was detected in malignant skin epithelial neoplasms as different clinicomorphological types of basal cell carcinoma.

Localized scleroderma (LS, morphea, limited scleroderma, focal scleroderma) is a chronic autoimmune disease characterized by a progressive damage to the connective tissue with a predominance of fibrosclerotic disorders in the skin and the subcutaneous tissue. In addition surrounding structures may be affected: fascia, muscle, and bone tissues. This review reflects the current understanding about limited scleroderma, its pathogenesis, diagnosis, new biomarkers, and information about the possibilities of its transition to systemic scleroderma. The following new biomarkers have been identified: galactosylated IgG (Ig-Gal), progranulin (PGRN), chemokine CCXL 18, various types of microRNA , periostin, and myelin basic protein (MBP). Knowledge about new biomarkers of LS will help us to explore the patients' predisposition to the development of systemic scleroderma. In addition, by acting on these biomarkers, it is possible to prevent the progression of LS in the early stages and its transition to systemic scleroderma. The review also presents the current understanding of autoantibodies in LS and their correlation with clinical signs of the disease.

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