Dermatology: Practical and Conceptual Original Article | Dermatol Pract Concept. 2025;15(4):5980 1 Ultraviolet-Induced Fluorescence and Sub-Ultraviolet Reflectance Dermatoscopy of Grover’s Disease (Transient Acantholytic Dermatosis): A Retrospective Single-Center Cohort Study Paweł Pietkiewicz1,2,3, Cristian Navarrete-Dechent4, Adarsha Adhikari5, Carmen Cantisani6, Mohamad Goldust7, Natalia Salwowska2,8, Norbert Kiss9 1 Centrum Medyczne Zwierzyniecka, Poznań, Poland 2 Polish Dermatoscopy Group, Poznań, Poland 3 Unitelematica Leonardo da Vinci, Zug, Switzerland 4 Department of Dermatology, Melanoma and Skin Cancer Unit, Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile 5 Medical Private Practice, Pokhara, Nepal 6 UOC of Dermatology, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, “Sapienza” University of Rome, Italy 7 Department of Dermatology, Yale University, School of Medicine, New Haven, Connecticut, USA 8 Department of Dermatology, School of Medicine, Medical University of Silesia, Katowice, Poland 9 Department of Dermatology, Venereology and Dermatooncology, Semmelweis University, Budapest, Hungary Key words: Dermoscopy, Skin imaging, Grover’s disease, Ultraviolet, Skin cancer Citation: Pietkiewicz P, Navarrete-Dechent C, Adhikari A, et al. Ultraviolet-Induced Fluorescence and Sub-Ultraviolet Reflectance Dermatoscopy of Grover’s Disease (Transient Acantholytic Dermatosis): a Retrospective Single-Center Cohort Study. Dermatol Pract Concept. 2025;15(4):5980. DOI: https://doi.org/10.5826/dpc.1504a5980 Accepted: July 30, 2025; Published: October 2025 Copyright: ©2025 Pietkiewicz et al. This is an open-access article distributed under the terms of the Creative Commons Attribution- NonCommercial License (BY-NC-4.0), https://creativecommons.org/licenses/by-nc/4.0/, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original authors and source are credited. Funding: None. Competing Interests: None. Authorship: All authors have contributed significantly to this publication. Corresponding Author: Paweł Pietkiewicz MD, PhD, Unitelematica Leonardo Da Vinci, 6300 Zug, Switzerland. ORCID ID: 0000-0001- 7262-2456. E-mail: pietkiewicz.pp@gmail.com Introduction: Grover’s disease (GD) is a rare acantholytic skin disorder typically characterized by pruritic vesicular or keratotic truncal papules, most commonly affecting older Caucasian males. Ultraviolet-induced fluorescence dermatoscopy (UVFD) and sub-ultraviolet reflectance dermatoscopy (sUVRD) are novel imaging techniques with potential diagnostic value in dermatology. Objectives: The objective of this study was to evaluate the dermatoscopic patterns of GD using UVFD and sUVRD techniques. ABSTRACT 2 Original Article | Dermatol Pract Concept. 2025;15(4):5980 Introduction Grover’s disease (GD), also known as transient acantholytic dermatosis, was first described by the American dermatol- ogist Ralph Weir Grover in 1970 [1]. This rare acanthol- ytic disorder manifests as moderately pruritic vesicular or keratotic papules [2]. In its classic form, the lesions are dis- tributed over the trunk, mainly the chest, whereas extensive variants affect additional skin sites [3]. Despite being termed “transient”, GD may last from weeks to years, with a ten- dency to seasonal, periodic recurrence. It is more common in males (2.4:1 M/F ratio) of Caucasian origin, and the mean age at onset of GD is 61 years [4]. It has been speculated that GD involves acrosyringia [4] and is related to an increased risk of malignancy [5]. Dermatoscopy is a noninvasive diagnostic method useful in both neoplastic and general dermatology (non-neoplastic diseases) [6], including GD. Dermatoscopy allows for the vi- sualization of structures invisible to the naked eye and im- proves diagnostic accuracy when compared to the naked eye examination. GD features quasi-specific clues (shared with Darier’s disease) seen with conventional non-contact polar- ized dermatoscopy (CD), namely central, yellow-to-brown polygonal scale (erosion), surrounded by a whitish halo, further outlined with a pinkish area [7,8] (Figure 1A-F). Ultraviolet-induced fluorescence dermatoscopy (UVFD) and sub-ultraviolet reflectance dermatoscopy (sUVRD) are two novel dermatoscopy modes that are commercially available [8]. The former utilizes ultraviolet (365nm)-excited fluores- cence of the fluorophores [9,10], whereas the latter is based on reflectance and absorption of purple light (405nm) in the skin [8]. To date, little is known about UVFD and sUVRD features of GD in the literature. In the present study, we sought to explore the demo- graphic data in GD patients, evaluate the dermatoscopic patterns of GD using UVFD and sUVRD techniques, and compare them to the polarized dermatoscopy findings (Figure 2A-D). Materials and Methods In this retrospective single-center cohort study, performed between January 2023 and December 2024 in Poznań, Po- land, we explored the patterns of UVFD/sUVRD in consec- utive cases of pathology-confirmed GD in adults. Exclusion criteria consisted of other overlapping dermatoses of similar presentation and any treatment or cosmetic application six weeks before the examination. A Dermlite DL5 dermato- scope (Dermlite, San Juan Capistrano, CA, USA) paired with a smartphone camera was used for UVFD image acquisition. A Casio DZ-D100 Dermocamera (Casio, Tokyo, Japan) was used to obtain sUVRD photographs. Both devices were used to collect clinical and CD photographs as a part of routine examinations. For UVFD we assessed the presence of polygo- nal scales (bright or dark) and greenish background, whereas in sUVRD we assessed the presence of hyporeflective polyg- onal scale, hyperreflective halo, hyperreflective eccrine mi- crocircles, and vascular pattern at the periphery (dots, lines looped distributed radially, or none). CD evaluation included the presence of central polygonal scale, white intermediate area, peripheral pink area, eccrine microcircles, and vessels (dots, lines looped distributed radially, or none). All images used for the quantitative study remained unprocessed. All evaluations were performed by two investigators; a third in- vestigator served as a referee and resolved discrepancies. Statistical Analysis Differences in the visibility of clues between CD, UVFD, and sUVRD were statistically assessed with z-test, whereas com- parisons in visibility of acrosyringial involvement between Methods: A retrospective observational single-center cohort study was conducted including consec- utive adult patients diagnosed with GD. Dermatoscopic images were obtained using a Dermlite DL5 dermatoscope paired with a smartphone for UVFD and a Casio DZ-D100 Dermocamera for sUVRD. Results: Among the 23 investigated patients (15 females, 8 males; mean age 49.13 years), UVFD images frequently showed central polygonal bright scales with a greenish background. sUVRD im- ages demonstrated hyporeflective polygonal scales, hyperreflective halos, and vascular patterns at the periphery. sUVRD was superior to UVFD and CD in the detection of semi-specific polygonal scales in GD. Eccrine duct involvement was observed in 76.31% of sUVRD images and 57.89% of match- ing conventional polarized dermatoscopy images. Contrary to the existing literature, female patients represented a higher percentage of the cohort. Twelve GD patients (52.2%) had a personal history of skin cancer. Conclusion: UVFD and sUVRD effectively characterized the unique features of GD lesions. Our findings suggest that GD may affect younger individuals and females more frequently than previously reported, potentially indicating underdiagnosis in this population. Incorporating dermatoscopy into routine examinations may improve the detection and management of GD. Original Article | Dermatol Pract Concept. 2025;15(4):5980 3 matching cases imaged with CD and sUVRD were assessed with McNemar’s test. Relations between the number of le- sions (≤3 for solitary, >3 for multiple), presence of symptoms, sex (M/F), and age (<60 years, ≥60 years) were assessed with chi-squared tests. Statistical analysis was performed using Python v3.11.4 (SciPy v1.11.4, Seaborn v0.13.2). P-values <0.05 were considered statistically significant for all tests. The study was approved by the Scientific Ethics Com- mittee for Health Sciences of Pontificia Universidad Católica de Chile (Approval #211213001). The informed consent to publication form was signed by the patients whose im- ages were included in this study. The data underlying this article are available at Harvard Dataverse at https:// doi.org/10.7910/DVN/S9KOMP. The manuscript was pre- pared in alignment with the STROBE guidelines. Results A total of 2,484 medical records from a single private derma- tology clinic were evaluated to identify unique GD patients. There were 980 first-visit patients, 1,400 returning visits, and 104 prescription visits. We included 23 unique patients with GD (fifteen females, eight males; mean age 49.13 years, min. 27, max. 81 years), corresponding to 0.11% first-time visits (Table 1). Multiple lesions (>3) were present in 62.5% of male vs. 46.47% of female patients, yet the differences between sexes were not statistically significant (chi-squared test; P=0.775). Although all patients ≥60 years and only 42.11% of patients <60 years had multiple lesions, this trend did not prove to be statistically significant (chi-squared test; P=0.12). A total of 60 lesions were photographed as part of the routine examination (mean, 2.68 images per patient; Figure 2. Dermatoscopic presentation of solitary Grover’s disease lesion in a renal transplant patient: (A) Clinical presentation of an isolated papule on a left shoulder (white arrowhead); (B) Contact polarized dermatoscopy dis- playing yellow polygonal serous crust (black arrowhead) surrounded by white outline (red arrowhead) over a pink area (red arrowhead). Note the white clods of eccrine duct ostia (yellow arrowheads) (DL5 paired with iPhone 6, original magnification 10×); (C) Ultraviolet-induced fluorescence dermatoscopy showing central polygonal bright scale (black arrowhead) over greenish background (red arrowhead) (DL5 paired with iPhone 6, original magnifi- cation 10×); (D) Sub-ultraviolet reflectance dermatoscopy showing central hyporeflective polygonal scale (black arrowhead) outlined with hyperreflective halo (white arrowhead); Background was marked with red arrowhead (Casio DZ-D100 Dermocamera, original magnification 10×). Radially arranged linear looped vessels and dotted vessels can be seen at the lesion’s periphery. Of note, hyperreflective microcircles of eccrine duct openings, both within the erosion and peripheral inflammatory area, remain intact (yellow areas). (Figure © Paweł Pietkiewicz) Figure 1. Presentation of Grover’s disease in an atypical setting: (A) Grouped papules located on a chest of a 38-year-old male (white arrowhead); (B) Contact polarized dermatoscopy displaying yellow po- lygonal serous crusts (black arrowheads) surrounded by white outlines (white arrowheads), located over a common pink area (red arrowhead) (Casio DZ-D100 Dermocamera, original magnification 20×); (C) Mul- tiple disseminated papules on a back of a 70-year old female (Casio DZ-D100 Dermocamera, original magnification 20x); (D) Polygonal brown-orange crust (black arrowhead) surrounded by white zone of acanthosis (white arrowhead), located over a pink area (red arrowhead) (Casio DZ-D100 Dermocamera, original magnification 80×); (E) Sol- itary lesion on abdomen of a 45-year-old female (white arrowhead); (F) Polygonal brownish crust (black arrowhead) surrounded by white outline of acanthosis over a pink area (red arrowhead) (DL5 paired with iPhone 6, original magnification 10×) (Figure © Paweł Pietkiewicz). 4 Original Article | Dermatol Pract Concept. 2025;15(4):5980 quality of life, a correct and prompt diagnosis is of para- mount importance. GD has been reported to predominantly affect males (M/F ratio of 2.4:1), with a peak incidence at 48 to 61 years of age [4,15]. Interestingly, even though the mean age and incidence in our study matched previous re- ports, females were more commonly affected than males (M/F ratio of 0.53). In the authors’ opinion, this discrepancy may be incidental due to a relatively small study group or may originate from the demographic differences between patients attending private and public healthcare, particularly before midday. Female predominance in this particular set- ting could be explained by the fact that working males are reluctant to seek private health screening [16]. Even though the literature data suggest that the majority of patients with typical presentation are symptomatic [3], only a minority of our patients were aware of the lesions or complained of 60 non-contact polarized images, 55 UVFD, 40 sUVRD); 21.74% of patients were symptomatic (4/15 females, 1/8 males), yet no statistically significant difference was found between the sexes (chi-squared test; P=0.43). Derma- toscopy patterns for all the different light modes are pre- sented in Table 2. sUVRD was superior to UVFD (95.00% vs 76.36%; z-test: P=0.0139) and CD (95.00% vs 78.33%; z-test: P=0.022) in detecting semi-specific central polygo- nal scales. There was no significant difference in this aspect when comparing UVFD and CD (z-test: P=0.801). Eccrine duct opening involvement within the central scale or peripheral inflammatory area was detected in 80% sUVRD and 30% of conventional CD dermatoscopy images. When considering only sUVRD images (N=40), pale micro- circles of eccrine duct openings were detected in 43.75% matching CD images, making sUVRD superior in this regard (McNemar’s test; P<0.001). A total of 12 GD patients (52.2%) had a personal his- tory of concomitant or past skin cancer: basal cell carcinoma (BCC) (30.4%), melanoma (26.1%), and squamous cell car- cinoma (SCC) (13.0%). In 13 cases (56.5%), GD was de- tected during total body dermatoscopy. Discussion GD is an epidermal acantholytic disorder resulting from the loss of cell-cell adhesion due to desmosome instability and aggravated by heat, sweating, or microbial imbalance [11]. Other contributing factors are exposure to ultraviolet radi- ation, immunosuppression, organ transplantation, HIV, me- chanical trauma, hospitalization, prolonged bedrest, renal failure, exposure to honeybee venom, and a number of medi- cations, including cancer therapeutics [3,12-14]. Considered by some to be a rare dermatosis, it typically affects 0.1% of the total population. As the disease can greatly impact the Table 2. Ultraviolet-Induced Fluorescence, Sub-Ultraviolet Reflectance, and Conventional Non-Contact Polarized Dermatoscopic Clues of Assessed Lesions of Grover’s Disease (N=60). UVFD (N=55) Feature N (%) Central polygonal bright scale 42 (76.36) Central polygonal dark scale 1 (1.82) Greenish background 47 (85.45) sUVRD (N=40) Feature N (%) Central hyporeflective polygonal scale 38 (95.00) Hyperreflective halo 33 (82.50) Hyperreflective eccrine microcircles 32 (80.00) Vascular pattern (overlap possible) Radially distributed linear looped vessels 20 (50.00) Peripheral dots 14 (35.00) None 13 (32.50) Polarized dermoscopy, non-contact (N=60) Feature N (%) Central yellow-to-brown polygonal scale 47 (78.33) White intermediate area 50 (83.33) Peripheral pink area 53 (88.33) Pale eccrine microcircles 18 (30.00) Vascular pattern (overlap possible) Radially distributed linear looped vessels 17 (28.33) Peripheral dots 22 (36.67) None 28 (46.67) Abbreviations: F: female; N: number of cases; M: male; sUVRD: sub-ultraviolet reflectance dermatoscopy; UVFD: ultraviolet- induced flu. Table 1. Demographic and Clinical Data of the Study Group. Demographics (N=23) Parameter Value Mean Age (years) 49.13 M/F Ratio 0.53 Symptomatic (%) 21.74 Lesion distribution by site (N=60) n (%) Chest 40 (66.67) Abdomen 7 (11.67) Back 5 (8.33) Flank 5 (8.33) Thigh 2 (3.33) Arm 1 (1.67) Original Article | Dermatol Pract Concept. 2025;15(4):5980 5 lentigo-like or Dowling-Degos-like basal hyperpigmenta- tion) [19-21], porokeratotic (oblique parakeratotic columns located over areas of agranulosis, occasional dyskeratotic cells in the upper epidermis, and basal vacuolar degenera- tion) [21,22], epidermolytic hyperkeratosis [21,23-25], ve- sicular (intraepidermal vesicles with minimal spongiosis or acantholysis on their sides) [23], lichenoid (vacuolar de- generation and scarce interface dermatitis, with occasional dyskeratotic keratinocytes and barely recognizable acan- tholysis) [23], and dysmaturative (dysmaturated keratino- cytes with polymorphic nuclei and slight hyperchromasia) [21,26]. Some authors have previously suggested that GD may begin at or involve acrosyringia [4,14,27–29]. Eccrine duct ostia can be visualized under dermatoscopy and play a role in several skin disorders [30–34]. In our study, pale microcircles of eccrine duct openings were detected either within the central scale or peripheral inflammatory area in the minority of CD images but in the majority of sUVRD images (Figure 1 and Table 2), which could support their role in disease etiopathogenesis. Our observations require further verification in larger studies. The relationship between GD and malignancy, includ- ing skin cancer, has recently been suggested by some au- thors [5,15]. In a study on 72 GD patients, 16.67% had a history of skin neoplasm, not otherwise specified [15]. On the other hand, GD may mimic keratinocytic cancers, par- ticularly actinic keratosis/intraepithelial SCC, with actinic keratosis-like morphology (epithelial buds with atypia), nu- clear pleomorphism, keratinocyte dysmaturation, and gran- ular layer alteration (large and prominent cells) [26,35] or BCC (trichoblastic proliferation-like areas) [26]. A number of cases and case series describing the link with skin neo- plasms have been published to date [36-38]. There are no na- tional registry-based estimations of the skin cancer incidence pruritus and burning sensation. We speculate that many pa- tients may present with few recurrent oligosymptomatic or asymptomatic lesions, including with extra-truncal involve- ment, making the disease likely underdiagnosed, neglected, or mistaken for other conditions and thus underreported when based only on naked-eye physical examination. It is also possible that the specific sampling bias–e.g., type of practice (frequent full body checks and using a dermatoscope as a part of routine examination regardless of the cause and higher vigilance)–was responsible for the increased detection of GD. Based on the reported M/F ratio, we speculate that the neglected population may include middle-aged females, and to a lesser extent, middle-aged males. This underrepre- sentation may result from a mismatch between age group and the male predominance previously reported in the lit- erature, leading clinicians to overlook the disease in these groups. Although future studies are required to investigate these hypotheses, caution concerning oligosymptomatic pa- tients, particularly outside previously reported risk groups, is advised. Inflammoscopy (dermatoscopy of non-neoplastic der- matoses) is becoming an indispensable part of medical ex- amination in the field of dermatology [17]. There is also greater interest in the description of the dermatoscopic features of non-neoplastic dermatosis. Two novel imaging techniques based on ultraviolet and close-to-ultraviolet light illumination – namely, UVFD and sUVRD – have been intro- duced over the last five years. Until now, only a single case of GD has been characterized by UVFD. In a review paper on both methods, the authors described a central polygonal bright scale imposed over a darker background seen under UVFD. This finding was confirmed in our study. These struc- tures correspond to serum-induced bluish/greenish excited fluorescence of the serous scale and inflammatory infiltrate, respectively, seen as a yellow-to-brown polygonal scale with a whitish outline and pink background visualized with CD (Figure 1) [8]. On the other hand, sUVRD in the assessed GD cases showed a hyporeflective polygonal scale (likely due to the trace of hemoglobin with a peak absorption at 405 nm) surrounded by a hyperreflective outline of acanthosis and mildly hyperreflective area of inflammation, frequently with a vascular pattern of looped and/or dotted vessels (Figure 1). There are four main histopathologic patterns of GD: Darier-like (with focal acantholytic dyskeratosis, Figure 3), pemphigus vulgaris-like, or pemphigus foliaceus-like (featur- ing few acantholytic keratinocytes over suprabasilar clefts), Hailey–Hailey-like (displaying numerous acantholytic ke- ratinocytes over suprabasilar clefts), and spongiotic pat- tern (with acantholytic keratinocytes within the spongiotic foci) [18]. Other, less common patterns include lentiginous patterns (presenting with papillomatosis with some solar Figure 3. Pathology of Darier-like Grover’s disease exhibits su- prabasal acantholysis with apoptotic (yellow arrowheads) and dyskeratotic cells (black arrowheads) (H+E routine stain, original magnification 200×). 6 Original Article | Dermatol Pract Concept. 2025;15(4):5980 the incidence, age at onset, and particularly the M/F ratio in our study group. Despite the high prevalence of skin cancer in our cohort, the study was not designed for this objective and may represent referral bias. No control group was in- cluded. Future studies should utilize central registries for the assessment of skin cancer risk in GD patients. Conclusions We present CD, UVFD, and sUVRD features in a series of consecutive GD patients. Our findings indicate that GD commonly involves acrosyringia. In some populations, the disease may affect more females and younger patients than previously reported in the literature. Along with the oligo- or asymptomatic course of the disease, these factors may contribute to a lower detection rate. We have demonstrated that sUVRD, but not UVFD, was superior to CD in detect- ing semi-specific polygonal scales in GD. Including derma- toscopy in general dermatology practice may contribute to optimizing the diagnosis and management of GD patients. References 1. Grover RW. Transient acantholytic dermatosis. Arch Dermatol. 1970;101:426–34. PMID: 5440816. 2. Sousou JM, Fritsche JM, Fernandez BR, Tummala MR, Scott R. Management and Treatment of Grover’s Disease: A Case Report and Review of Literature. Cureus. 2022;14:e24082. DOI:10.7759/cureus.24082. PMID: 35573509. 3. Gantz M, Butler D, Goldberg M, Ryu J, McCalmont T, Shinkai K. Atypical features and systemic associations in extensive cases of Grover disease: A systematic review. J Am Acad Dermatol. 2017;77:952-957.e1. DOI:10.1016/j.jaad.2017.06.041. PMID: 28918973. 4. Weaver J, Bergfeld WF. Grover disease (transient acanthol- ytic dermatosis). Arch Pathol Lab Med. 2009;133:1490–4. DOI:10.5858/133.9.1490. PMID: 19722762. 5. Nedelcu R, Dobre A, Turcu G, et al. Grover’s Disease Asso- ciation with Cutaneous Keratinocyte Cancers: More than a Coincidence? Int J Mol Sci. 2024;25:9713. DOI:10.3390 /ijms25179713. PMID: 39273660. 6. Errichetti E, Zalaudek I, Kittler H, et al. Standardization of dermoscopic terminology and basic dermoscopic parameters to evaluate in general dermatology (non-neoplastic dermatoses): an expert consensus on behalf of the International Dermos- copy Society. Br J Dermatol. 2020;182:454–67. DOI:10.1111 /bjd.18125. PMID: 31077336. 7. Errichetti E, De Francesco V, Pegolo E, Stinco G. Dermoscopy of Grover’s disease: Variability according to histological subtype. J Dermatol. 2016;43:937–9. DOI:10.1111/1346-8138.13298. PMID: 26892381. 8. Pietkiewicz P, Navarrete-Dechent C, Togawa Y, et al. Appli- cations of Ultraviolet and Sub-ultraviolet Dermatoscopy in Neoplastic and Non-neoplastic Dermatoses: A Systematic Review. Dermatol Ther. 2024;14:361–90. DOI:10.1007/s13555 -024-01104-4. PMID: 38358617. among targeted treatment-naive skin cancer GD patients. Among nine such patients reported in the literature, all nine had a history of BCC, three of SCC, and one of melanoma [5,15,37,39]. Cumulative sun damage and immunosuppres- sion may be the main contributing factors to the link be- tween GD and skin cancer. It is also important to differentiate between “primary” GD developing in skin cancer patients and GD-like reaction caused by skin cancer-targeting drugs, including recombinant human IL-4, immune checkpoint inhibitors, BRAF inhib- itors, Hedgehog inhibitors, EGFR inhibitors, or other che- motherapeutics [38,40-49]. Interestingly, a recent national registry-based study from Sweden reported an increased risk of keratinocyte carcinoma (BCCs and SCCs combined, and BCC only) in Darier’s disease, which belongs to the same spectrum of acantholytic dermatoses [50]. Although clini- cally distinct from GD, both entities may feature overlapping dermatoscopic and histopathologic features and share com- mon mechanisms of pathogenesis, including overexpression of yes-associated protein (YAP) [51], which is involved in de- velopment of keratinocytic tumors [52,53]. Moreover, gene sequencing of GD lesions identified an acquired mutation of ATP2A2 [54], a defective gene responsible for Darier’s disease [55,56]. In our dataset, 52.2% of GD patients had a history of skin cancer. On the other hand, over a half of our GD cases were detected during total body dermatoscopy, making the results hard to extrapolate to a wider popula- tion. Nonetheless, we believe that these findings necessitate further research to better understand the interplay between GD and skin cancer. The exact mechanism by which keratinocytes detach from each other in GD is probably multifactorial, involving hyperactivated ERK pathway and claudin family of proteins [5,11]. Even though GD is not considered to be an auto- immune blistering dermatosis, desmosome disruption may result in epitope spreading. This mechanism is likely respon- sible for concomitance of GD and pemphigus foliaceus [57] and of GD and bullous pemphigoid [58]. Desmosomal pro- teins are involved not only in maintaining cell-cell adhesion but also participate in signal transduction, regulation of ex- pression of proteins, and cell behavior [59-61]. Limitations Our study has some limitations. For socioeconomic reasons, the results obtained in a setting of Caucasian patients from a single private Central European dermatology practice fo- cusing mainly on skin cancer screening may not be repre- sentative of the general population. Fair skin types, higher sun damage, previous history of skin cancer, and/or history of other malignancies may be responsible for increased skin cancer risk in this group. All these factors may have biased Original Article | Dermatol Pract Concept. 2025;15(4):5980 7 24. Fernández-Figueras MT, Puig L, Ariza A. Epidermolytic Hyperkeratosis: One More Pattern of Grover Disease. Am J Dermatopathol. 2015;37(9):734-5. DOI:10.1097/DAD .0000000000000223. PMID: 25436919. 25. Bardazzi F, Pepe F, Malosso M, et al. Epidermolytic hyperker- atosis: one more pattern of Grover disease. Int J Dermatol. 2020;59(11):e422-e423. 10.1111/ijd.15055. PMID: 32686086. 26. Aljarbou OZ, Asgari M, Al-Saidi N, Silloca-Cabana EO, Alathamneh M, P Sangueza O. Grover Disease With Epider- mal Dysmaturation Pattern: A Common Histopathologic Find- ing. Am J Dermatopathol. 2018;40(9):642-646. DOI:10.1097 /DAD.0000000000001112. PMID: 29443699. 27. Hashimoto K, Moiin A, Chang MW, Tada J. Sudoriferous acrosy- ringeal acantholytic disease. A subset of Grover’s disease. J Cutan Pathol. 1996;23:151–64. DOI:10.1111/j.1600-0560.1996. tb01289.x. PMID: 8721450. 28. Antley CM, Carrington PR, Mrak RE, Smoller BR. Grover’s disease (transient acantholytic dermatosis): relationship of ac- antholysis to acrosyringia. J Cutan Pathol. 1998;25:545–9. DOI:10.1111/j.1600-0560.1998.tb01738.x. PMID: 9870673. 29. Joshi R, Taneja A. Grover’s Disease with Acrosyringeal Acan- tholysis: A Rare Histological Presentation of an Uncommon Disease. Indian J Dermatol. 2014;59:621. DOI:10.4103/0019 -5154.143548. PMID: 25484405. 30. Abraham LS, Piñeiro-Maceira J, Duque-Estrada B, Barcaui CB, Sodré CT. Pinpoint white dots in the scalp: Dermoscopic and his- topathologic correlation. J Am Acad Dermatol. 2010;63:721–2. DOI:10.1016/j.jaad.2009.12.011. PMID: 20846575. 31. Rudnicka L, Olszewska M, Rakowska A, Slowinska M. Trichoscopy update 2011. J Dermatol Case Rep. 2011;5:82. DOI:10.3315/jdcr.2011.1083. PMID: 22408709. 32. Tomich LM, Pieper JB, Stern AW. Comparing dermoscopy and histological examination of normal equine skin. Vet Dermatol. 2018;29:170-e63. DOI:10.1111/vde.12511. PMID: 29143381. 33. Pietkiewicz P, Giedziun P, Idziak J, Todorovska V, Lewandowicz M, Lallas A. Diagnostic Accuracy of Hyperpigmented Micro- circles in Dermatoscopy of Non-Facial Non-Acral Melanomas: A Pilot Retrospective Study using a Public Image Database. Dermatology (Basel) 2023;239:976–87. DOI:10.1159/000533820. PMID: 37666232. 34. Kuczara A, Waśkiel-Burnat A, Rakowska A, Olszewska M, Rud- nicka L. Trichoscopy of Androgenetic Alopecia: A Systematic Re- view. J Clin Med. 2024;13:1962. DOI: 10.3390/jcm13071962. PMID: 38610726. 35. Kotzerke M, Mitri F, Enk A, Toberer F, Haenssle H. A Case of Extensive Grover’s Disease in a Patient with a History of Multiple Non-Melanoma Skin Cancers. Case Rep Derma- tol. 2021;13(3):553-557. DOI: 10.1159/000519168. PMID: 35082618. 36. Fawcett HA, Miller JA. Persistent acantholytic dermatosis re- lated to actinic damage. Br J Dermatol. 1983;109(3):349-54. DOI:10.1111/j.1365-2133.1983.tb03552.x. PMID: 6615722. 37. Mokni M, Aractingi S, Grossman R, et al. Persistent acantho- lytic dermatosis: sex-related differences in clinical presenta- tion? Acta Derm Venereol. 1993;73(1):69-71. DOI:10.2340 /00015555736971. PMID: 8095759. 38. Horn TD, Groleau GE. Transient acantholytic dermatosis in im- munocompromised febrile patients with cancer. Arch Dermatol. 1987;123(2):238-40. PMID: 3813598. 9. Pietkiewicz P, Navarrete-Dechent C, Goldust M, Korecka K, Todorovska V, Errichetti E. Differentiating Fordyce Spots from Their Common Simulators Using Ultraviolet-Induced Fluorescence Dermatoscopy—Retrospective Study. Diagnostics. 2023;13:985. DOI:10.3390/diagnostics13050985. PMID: 36900129. 10. Errichetti E, Pietkiewicz P, Bhat YJ, Salwowska N, Szlązak P, Stinco G. Diagnostic accuracy of ultraviolet-induced fluores- cence dermoscopy in non-neoplastic dermatoses (general der- matology): A multicentric retrospective comparative study. J Eur Acad Dermatol Venereol. 2024. DOI:10.1111/jdv.19795. Online ahead of print. PMID: 38288676. 11. Simpson CL, Tiwaa A, Zaver SA, et al. ERK hyperactivation in epidermal keratinocytes impairs intercellular adhesion and drives Grover disease pathology. JCI Insight. 2024;9(21):e182983. DOI:10.1172/jci.insight.182983. PMID: 39325541. 12. Awe O, Pavlidakey P, Kole L, Kissel R. Drug-induced Grover’s disease: a case report and review of the literature. Int J Der- matol. 2022;61(5):591-594. DOI:10.1111/ijd.15803. PMID: 34302358. 13. Haniff S, Butler ME, Abou-Jaoude EA, Lenahan ML. An Unusual Trigger of Grover’s Disease (GD). Cureus. 2023;15(6):e40648. DOI:10.7759/cureus.40648. PMID: 37476136. 14. Quirk CJ, Heenan PJ. Grover’s disease: 34 years on. Australas J Dermatol. 2004;45(2):83-6; quiz 87-8. DOI:10.1111/j.1440 -0960.2004.054_1.x. PMID: 15068451. 15. Davis MD, Dinneen AM, Landa N, Gibson LE. Grover’s dis- ease: clinicopathologic review of 72 cases. Mayo Clin Proc. 1999;74:229-34. DOI:10.4065/74.3.229. PMID: 10089990. 16. Mursa R, Patterson C, Halcomb E. Men’s help-seeking and en- gagement with general practice: An integrative review. J Adv Nurs. 2022; 78(7):1938-1953. DOI:10.1111/jan.15240. PMID: 35384022. 17. Zalaudek I, Lallas A, Moscarella E, Longo C, Soyer HP, Argenziano G. The dermatologist’s stethoscope—traditional and new applications of dermoscopy. Dermatol Pract Concept. 2013;3:67. DOI:10.5826/dpc.0302a11. PMID: 23785649. 18. Chalet M, Grover R, Ackerman AB. Transient acantholytic der- matosis: a reevaluation. Arch Dermatol. 1977 Apr;113(4):431-5. PMID: 848971. 19. Cooper SM, Dhittavat J, Millard P, Burge S. Extensive Grover’s- like eruption with lentiginous ‘freckling’: report of two cases. Br J Dermatol. 2004;150(2):350-2. DOI:10.1111/j.1365-2133 .2004.05778.x. PMID: 14996109. 20. Girard C, Durand L, Guillot B, Gildhou JJ, Bessis D. Persistent ac- antholytic dermatosis and extensive lentiginous ‘freckling’: a new entity? Br J Dermatol. 2005;153(1):217-8; author reply 218. doi: 10.1111/j.1365-2133.2005.06666.x. PMID: 16029360. 21. Fernández-Figueras MT, Puig L, Cannata P, et al. Grover dis- ease: a reappraisal of histopathological diagnostic criteria in 120 cases. Am J Dermatopathol. 2010;32(6):541-9. DOI:10.1097 /DAD.0b013e3181c80cf9. PMID: 20526170. 22. Montoya C, Arias LM, Salazar M, Flórez HA. Porokeratosis-Like Grover Disease: More Than an Acantholytic Pattern. Actas Der- mosifiliogr (Engl Ed). 2019;110(4):332-334. DOI:10.1016/j .ad.2018.02.032. PMID: 30409379. 23. Bearden JN, Essary LR, Cockerell CJ. Grover disease with fea- tures of epidermolytic hyperkeratosis. Am J Dermatopathol. 2014;36(4):358-9. DOI:10.1097/DAD.0b013e318282247d. PMID: 23435360. 8 Original Article | Dermatol Pract Concept. 2025;15(4):5980 51. Roth-Carter QR, Burks HE, Ren Z, et al. Transcriptional profil- ing of rare acantholytic disorders suggests common mechanisms of pathogenesis. JCI Insight. 2023;8(16):e168955. DOI:10 .1172/jci.insight.168955. PMID: 37471166. 52. Shin E, Kim J. The potential role of YAP in head and neck squa- mous cell carcinoma. Exp Mol Med. 2020;52(8):1264-1274. DOI:10.1038/s12276-020-00492-9. PMID: 32859951. 53. Debaugnies M, Sánchez-Danés A, Rorive S, et al. YAP and TAZ are essential for basal and squamous cell carcinoma ini- tiation. EMBO Rep. 2018 Jul;19(7):e45809. DOI:10.15252 /embr.201845809. PMID: 29875149. 54. Seli D, Ellis KT, Goldust M, et al. Association of Somatic ATP2A2 Damaging Variants With Grover Disease. JAMA Dermatol. 2023;159(7):745-749. DOI:10.1001/jamadermatol.2023.1139. PMID: 37195706. 55. Sakuntabhai A, Ruiz-Perez V, Carter S, et al. Mutations in ATP2A2, encoding a Ca2+ pump, cause Darier disease. Nat Genet. 1999;21(3):271–277. DOI:10.1038/6784. PMID: 10080178. 56. Jacobsen NJ, Lyons I, Hoogendoorn B, et al. ATP2A2 mutations in Darier’s disease and their relationship to neuropsychiatric phe- notypes. Hum Mol Genet. 1999;8(9):1631–1636. DOI:10.1093 /hmg/8.9.1631. PMID: 10441325. 57. Magdaleno-Tapial J, Valenzuela-Oñate C, Martínez-Doménech Á, et al. Coexistence of Pemphigus Foliaceus and Grover Dis- ease After a Radical Surgery for Basal Cell Carcinoma. Am J Dermatopathol. 2019;41(10):744-746. DOI:10.1097 /DAD.0000000000001419. PMID: 31094720. 58. Ellenbogen E, Geller S, Azrielant S, et al. Grover disease and bul- lous pemphigoid: a clinicopathological study of six cases. Clin Exp Dermatol. 2019;44(5):524-527. DOI:10.1111/ced.13789. PMID: 30264538. 59. Rehman A, Huang Y, Wan H. Evolving Mechanisms in the Pathophysiology of Pemphigus Vulgaris: A Review Emphasiz- ing the Role of Desmoglein 3 in Regulating p53 and the Yes- Associated Protein. Life (Basel). 2021;11(7):621. DOI: 10.3390 /life11070621. PMID: 34206820. 60. Müller L, Hatzfeld M, Keil R. Desmosomes as Signaling Hubs in the Regulation of Cell Behavior. Front Cell Dev Biol. 2021;9:745670. DOI:10.3389/fcell.2021.745670. PMID: 34631720. 61. Pietkiewicz P, Gornowicz-Porowska J, Bowszyc-Dmochowska M, et al. Discordant expression of desmoglein 2 and 3 at the mRNA and protein levels in nodular and superficial basal cell carcinoma revealed by immunohistochemistry and fluorescent in situ hybridization. Clin Exp Dermatol. 2014;39(5):628-35. DOI:10.1111/ced.12355. PMID: 24934917. 39. Dobre A, Nedelcu R, Turcu G, et al. A rare case of Grover dis- ease associated with multiple BCCs Proceedings of the European Academy of Dermatology & Venereology Congress, Amsterdam, The Netherlands. 25–28 September 2024. Abstract no 1731. 40. Mahler SJ, De Villez RL, Pulitzer DR. Transient acantholytic dermatosis induced by recombinant human interleukin 4. J Am Acad Dermatol. 1993;29(2 Pt 1):206-9. DOI: 10.1016/0190 -9622(93)70169-t. PMID: 8335740. 41. Plachouri KM, Florou V, Georgiou V, Georgiou S. Cutaneous Side Effects of Modern Targeted Therapy and Immunotherapy in Patients with Dermatological Malignancies. Cancers (Basel). 2023;15(12):3126. DOI: 10.3390/cancers15123126. PMID: 37370736. 42. Caplash G, Curragh DS, Halliday L, Huilgol SC, Selva D. Re- port of cutaneous side effects of vismodegib treatment. Clin Exp Ophthalmol. 2020;48(1):123-125. DOI: 10.1111/ceo.13651. PMID: 31569297. 43. Koelzer VH, Buser T, Willi N, et al. Grover’s-like drug eruption in a patient with metastatic melanoma under ipilimumab ther- apy. J Immunother Cancer. 2016;4:47. DOI:10.1186/s40425 -016-0151-z. PMID: 27532022. 44. Munoz J, Guillot B, Girard C, Dereure O, Du-Thanh A. First re- port of ipilimumab-induced Grover disease. Br J Dermatol. 2014; 171(5):1236-7. DOI:10.1111/bjd.13058. PMID: 24749658. 45. Uemura M, Fa’ak F, Haymaker C, et al. A case report of Grover’s disease from immunotherapy-a skin toxicity induced by inhibi- tion of CTLA-4 but not PD-1. J Immunother Cancer. 2016;4:55. DOI:10.1186/s40425-016-0157-6. PMID: 27660709. 46. Chu EY, Wanat KA, Miller CJ, et al. Diverse cutaneous side effects associated with BRAF inhibitor therapy: a clinico- pathologic study. J Am Acad Dermatol. 2012;67(6):1265-72. DOI:10.1016/j.jaad.2012.04.008. PMID: 22609219. 47. Pinto-Pulido EL, Polo-Rodríguez I, González-Cañete M, Medina- Expósito I, Vélez-Velázquez MD, Medina-Montalvo S. Asso- ciation of bullous pemphigoid and Grover disease induced by immune checkpoint therapy. An Bras Dermatol. 2024;99(5): 775-777. DOI:10.1016/j.abd.2023.07.018. PMID: 38876966. 48. Tscharner GG, Bühler S, Borner M, Hunziker T. Grover’s dis- ease induced by cetuximab. Dermatology. 2006;213(1):37-9. DOI:10.1159/000092836. PMID: 16778425. 49. Afvari S, Chiu MW. Grover disease associated with docetaxel chemotherapy. JAAD Case Rep. 2022;29:86-88. DOI:10.1016/j .jdcr.2022.08.047. PMID: 36199674. 50. Peltonen S, Inci R, Gilstedt M, Polesie S, Kallionpää R. Patients with Darier disease have an increased risk of keratinocyte carci- noma. J Invest Dermatol. 2024;144:S271. DOI:10.1186/s13023 -024-03497-z. PMID: 39681873.