1. a tyrosine kinase inhibitor (TKI) that selectively inhibits the epidermal growth element receptor (EGFR). It functions by inhibiting intracellular phosphorylation of the tyrosine kinase associated with the EGFR1. EGFR-TKIs are currently used in the treatment of a number of solid tumors. Various cutaneous side effects of EGFR-TKIs have been reported, including acneiform eruptions, chronic paronychia, xerosis, a seborrheic dermatitis-like eruption, changes in hair consistency, and nonscarring alopecia1. The most common pores and skin manifestation is definitely a rash that has been described as a follicular or papulopustular eruption. However, significant or severe alopecia offers hardly ever been reported in individuals that receive EGFR-TKI monotherapy1,2. == CASE Statement == A 61-year-old female with metastatic non-small cell lung malignancy (NSCLC) presented with erythematous erosive patches containing pustules on her scalp. She had been using 150 mg/day time erlotinib (Tarceva) for Grosvenorine 11 weeks. Two months after starting drug administration, she experienced a slight acneiform facial eruption. By applying a topical macrolide, it improved after several days. However, about 9 weeks after taking the medicine, painful, erosive patches appeared on her scalp, which was accompanied by hair loss. Physical examination showed erythematous erosive patches with follicular pustules within the scalp (Fig. 1). No additional adverse events were observed, including xeroderma or swelling of the nails. A biopsy specimen taken from the scalp showed ruptured hair follicles and abundant perifollicular infiltrate with lymphocytes and neutrophils (Fig. 2). Bacterial and fungal staining were bad, butStaphylococcus aureuswas cultured from your pustules. Routine laboratory investigation found no significant abnormalities. == Fig. 1. == Erythematous erosive patches comprising follicular pustules within the scalp. == Fig. 2. == (A) Pores and skin biopsy from your scalp showing ruptured hair follicles (H&E, 40). (B) Abundant perifollicular infiltrate with lymphocytes and neutrophils (H&E, 200). Treatment with topical and oral steroids plus antibiotics was started and continued for Grosvenorine 5 weeks. The dose of erlotinib was decreased from 150 mg/day time to 100 mg/day time, and then the erythematous, pustular pores and skin lesion gradually improved. However, an atrophic alopecic patch developed on her scalp (Fig. 3). The final analysis was cicatricial alopecia, and the alopecic lesion remained unchanged during a 9-weeks follow-up. == Fig. 3. == Erythematous scarring, alopecic patches within the scalp. == Conversation == EGFR inhibitors have been approved for the treatment of NSCLC, pancreatic malignancy, colorectal malignancy and head and neck malignancy3. Focusing on the EGFR pathway having a small-molecule EGFR-TKI (erlotinib) or a monoclonal antibody (cetuximab) long term survival in individuals with advanced disease in both the first- and second-line settings4. EGFR inhibitors can cause a range of adverse cutaneous reactions of variable severity. The most common skin toxicity is an acneiform or papulopustular rash that primarily affects the sebaceous areas of the scalp, face, and top trunk. The rash can be itchy and, as a result, complicated by a secondary bacterial infection. The second most common pores and skin Grosvenorine toxicity affects the nails and includes symptoms such as discoloration, pitting, and paronychia3. Individuals treated with EGFR inhibitors also sometimes show hair abnormalities, like excessive eyelash dJ223E5.2 and eyebrow growth or curly/wavy hair on the face or scalp that is both good and brittle2,3. Considerable alopecia is uncommon. A literature search recognized five other instances of alopecia associated with EGFR inhibitors; but, only one case of cicatricial alopecia was reported (Table 1)1,2,5-7. == Table 1. == Published English-language reports of alopecia associated with the use of EGFR inhibitors EGFR: epidermal growth element receptor, NSCLC: non-small cell lung malignancy. The mechanism underlying the folliculocentric rash remains unclear, although it is known that EGFR inhibitors can have several adverse effects on epithelial homeostasis. EGFR is definitely strongly indicated in the basal coating of the epidermis, with lower manifestation in the lower dermal papilla, outer root sheath of the hair follicle, outer sheath of the top hair shaft, sebaceous glands, and eccrine sweat glands. Inhibiton of these EGFRs prospects to growth and migratory abnormalities that result in a papulopustular rash and impaired differentiation3,8. Several studies have shown that EGFRs perform an essential.