Rarely, constriction of an appendage by hair results in ischemia and necrosis, a phenomenon termed Hair-Thread Tourniquet Syndrome (HTTS) 1. The most commonly reported scenario is that of an infant presenting with hair wrapped tightly around a finger, toe, or genitalia. However, there are isolated reports of HTTS in adolescent and adult patients involving genitalia 2 or polypoid skin lesions, albeit without detailed histopathology 3, 4. Herein, we report clinical and histopathologic details of HTTS involving a melanocytic nevus. A 50-year-old woman presented with a lesion on her upper back that had been painful for 2 weeks. She reported a long-standing, previously asymptomatic lesion at the site. Physical examination revealed an 8 mm black papule with hair strands tightly wrapped around the base (Figure 1). The lesion was removed and submitted for pathologic evaluation. Histopathology revealed a necrotic polypoid lesion with hemorrhage and hair shafts near the base (Figure 2). In the necrotic and hemorrhagic zone of the lesion, there were dermal aggregates of cells with focal pigmentation superficially, most consistent with necrotic nevic melanocytes. In a viable area at the base of the shave biopsy, there was focal scar and a rare focus of intact dermal melanocytes with nevic cytology. While the degree of tissue effacement affecting the necrotic portion of the lesion precluded definitive characterization, the foci of intact nevus cells and the overall architecture of the lesion were most consistent with a polypoid melanocytic nevus with extensive necrosis and embedded hair shafts at the base. The limitations of analyzing necrotic cells were discussed with the clinician, and clinical follow-up was pursued for management. At 5 years of follow-up, there has been no recurrence at the biopsy site. Hair tourniquets predominantly affect digits and genitalia of infants 1. This phenomenon is extremely rare in adults and limited to case reports without substantial dermatologic or pathologic detail. In one case, hair-thread tourniquet syndrome (HTTS) involved a polypoid lesion, stated to be a hemangioma, on the upper back of an adult female 3. A Spanish-language report documented a 35-year-old woman with a melanocytic nevus affected by a hair tourniquet 4; while no histopathology photos were presented for this case, the clinically photographed nevus does not appear dusky or necrotic. The hair tourniquet was removed, and 1 month later the lesion was excised and examined histopathologically to reveal, reportedly, a melanocytic nevus. Like our case, both of these reported patients presented with symptomatic protuberant lesions with hair wrapped around the base. In the absence of deliberate ligation, the pathogenesis for hair tourniquets of cutaneous tumors is presumed to be the spontaneous coiling and cinching of long hair shafts around the base of a polypoid lesion. One proposed factor is the dynamics of hair with wetting and drying: a wet hair entraps the base of a lesion and then, upon drying, it contracts, thereby ligating the lesion 2. While not represented in literature, other pedunculated skin growths such as acrochordons and polypoid melanomas conceivably could be strangulated through torsion of the peduncle. Histopathologic examination of skin affected by ischemia shows a spectrum of changes dependent on duration of ischemia and the interval between ischemia and biopsy 5. Classic histopathologic changes of “coma blister,” secondary to vascular obstruction from external pressure, include subepidermal blistering with epidermal necrosis and necrosis of adnexal structures, especially sweat glands, with a variable, often scant, degree of associated inflammation 6. A large review of various clinical and experimental models of ischemic skin injury noted a wide variety of histopathologic changes in ischemic skin, ranging from early changes of dermal inflammatory (often neutrophilic) infiltrates, edema, and basal epidermal vacuolization to epidermal separation to eventual necrosis of epidermis and cutaneous adnexal structures 5. Late changes include fibrosis and atrophy of hair follicles and sebaceous glands 5. To the authors' knowledge, the histologic effects of ischemia on melanocytic proliferations have not been reported beyond references to coagulative necrosis within tumorigenic melanomas. Given the obvious source of injury in our case, we were able to observe necrotic cells with shrunken eosinophilic cytoplasm, focally pigmented in the superficial aspect, and pyknotic nuclei (Figure 2C). We interpreted the histologic changes as most compatible with a diagnosis of necrotic polypoid melanocytic nevus based on the architecture, the presence of intact nests of banal nevic cells at the base (Figure 2D), and the limitation of lesional pigmentation to the superficial aspect of the necrotic component (Figure 2C), a feature suggestive of melanocytic maturation. Importantly, the presence of a zone of ischemic necrosis within a melanocytic lesion may preclude definitive exclusion of the diagnosis of nevoid melanoma. The histopathologic recognition of this morphologic variant of melanoma, largely defined by its architectural mimicry of a melanocytic nevus, relies on careful assessment for cellular density, cytologic atypia, mitotic activity, and other subtle features which would be lost in necrotic foci. As such, a descriptive diagnosis followed by a careful discussion of diagnostic limitations may be warranted for cases with ischemic effacement. In the case reported here, the pathology report noted the limitations of analyzing necrotic cells, prompting further discussion with the dermatologist who performed the biopsy. In addition to ischemia, melanocytic nevi may also undergo a variety of forms of external injury leading to a spectrum of secondary histopathologic changes. The most well-studied phenomenon is that of recurrent nevus after biopsy. Within the affected area marked by scar, melanocytes, often with epithelioid pigmented cytology, may show crowded growth along the base of a flattened epidermis, as well as scattered arrangement within the upper epidermal layers (pagetoid scatter) 7. Important features distinguishing recurrent nevus from melanoma are the confinement of the crowded and pagetoid growth to the zone of scar, the lack of marked nuclear pleomorphism, and, in some cases, the presence of a banal nevus adjacent or deep to the scar. Review of histologic slides from the previously sampled nevus is a worthwhile exercise to support benignity. Nonetheless, recurrent nevus and melanoma, especially with regressive fibrosis, may show considerable histopathologic overlap 7. Nonsurgical injury may also correlate with various histopathologic alterations in nevi. In a study of 92 nevi with a history of “trauma,” pagetoid scatter, analogous to that seen in recurrent nevi, was noted in a minority of cases, while most reported changes affected non-melanocytic surrounding structures and included parakeratosis, acanthosis, ulceration, granulation tissue, and telangiectasia 8. Ultraviolet radiation promotes pagetoid scatter 9. Laser therapy for hair removal may incidentally injure melanocytic lesions, affecting the histopathologic appearance; a few reports document acute changes reminiscent of those seen after electrocautery, with epidermal detachment and extensive cytologic distortion, rendering superficial lesions uninterpretable 10. The melanocytic lesion reported here highlights a unique mechanism of ischemic injury and the associated histopathologic changes. Accurate diagnosis relies on prudent clinicopathologic correlation and careful histopathologic evaluation of areas unaffected by injury. The authors have nothing to report. The authors have nothing to report. The authors declare no conflicts of interest. Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.
Batheja et al. (2026) studied this question.