Rarely, individuals present with multiple poromas either in one or widespread areas; these cases are termed poromatosis.Poromas present more commonly in: pregnancy; patients treated with electron therapy for mycosis fungoides; sites of chronic radiation dermatitis caused by long-term radiation exposure; patients who received chemotherapy with or with radiation therapy (these patients have often presented with poromatosis); individuals with underlying skin conditions such as hypohidrotic ectodermal dysplasia and Bowen’s disease (i.e. a form of squamous cell carcinoma that is localized to the outermost layer of the skin); and skin plaques of individuals with the congenital disease, nevus sebaceous.Poromas are usually slow growing and asymptomatic but some individuals report that their lesions are itchy, mildly tender, or  painful. An existing poroma that develops spontaneous bleeding, ulceration, sudden itching, pain, or rapid growth over a short period of time may indicate that it has become a cancerous porocarcinoma. These cancers may metastasize to local lymph nodes, nearby or distal skin sites, bones, bladder, breast, retroperitoneum, ovary, liver, lung, brain, or stomach. However, the progression of a poroma to a porocarcinoma is very rare, i.e. less than 1% of cases. Histopathology
Microscopic histopathological examinations of the tumor tissues of all poroma variants stained with hematoxylin and eosin dyes reveal: a) basophilic "poroid cells" (i.e. small, cuboid-shaped cells with oval nuclei which resemble cells in the peripheral layer of the distal portion of eccrine sweat gland ducts) that may form cords and broad columns extending downward from the epidermis; b) larger cuticular cells (i.e.
abnormal genes caused by a mutation which merges a part of the YAP1 gene fused to part of either the Nuclear protein in testis gene (also termed the NUTM1 gene) or the MAML2 gene to form the YAP1::NUTM1 and YAP::MAML2 fusion genes, respectively. Rarely, they may also contain a WWTR1::NUTM1 fusion gene. The YAP1::MAML2 fusion gene is detected in ~63% of poromas, the YAP1::NUTM1 fusion in 20.2% to 66% of poromas, and the WWTR1::NUTM1 fusion gene in 1% of poromas. YAP1  and WNTR1 fusion genes have been implicated in the initiation, aggressiveness, metastasis, and/or therapy resistance of various neoplasms. Studies are needed to determine if they play a role in the development and/or progression of poromas. Diagnosis
The great diversity, rarity, and complex terminology of poromas make their diagnosis challenging. They have been misdiagnosed as other types of skin tumors including porocarcinomas, basal cell carcinomas, pyogenic granulomas, skin tags, plantar warts (i.e. warts on the palms or soles), fibromas, hemangiomas, pigmented moles, seborrheic keratosis, trichilemmomas, melanomas, Kaposi sarcomas, and other adnexal tumors. Poromas are typically diagnosed based on their clinical presentation; microscopic histopathology showing tumor tissues consisting of poroid, cuticular, and/or clear cells; and, in unclear cases, the presence of tumor cells that express a YAP1::NUTM1, YAP::MAML2, and/or WWTR1::NUTM1 fusion gene. However, these fusion genes also occur in porocarcinomas and cannot be used to differentiate poromas from their malignant counterpart. Poromas and porocarcinomas are distinguished based on their clinical findings and histopathology, e.g.