2025 Case Studies – Derm In-Review
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2025 Case Studies

Apr 24
Love17

April 2025 Case Study

By 2025 Case Studies

April 2025 Case Study

Author: Nikita Menta, BA1, Nidhi Shah, MD1, Karl Saardi, MD1

  1. Department of Dermatology, The George Washington University School of Medicine and Health Sciences

Patient History
A 43-year-old female presented to the clinic with several painful, erythematous, edematous plaques in addition to hyperpigmented plaques on the arms and legs, which had been present for more than 24 hours. The rash initially started about four years prior to presentation and was unresponsive to a variety of oral antihistamines and a four-month trial of omalizumab. The patient also endorsed intermittent episodes of angioedema as well as occasional low back and knee pain. She previously underwent a punch biopsy on the lower left back; hematoxylin and eosin staining demonstrated marked dermal edema, margination of neutrophils with perivascular and interstitial infiltrate including eosinophils, perivascular nuclear debris with neutrophils, and significant extravasation of erythrocytes. Exam findings are shown in Figure 1.

Based on the clinical presentation and biopsy findings, which of the following laboratory tests would be most useful in determining the prognosis of this condition?

A) Antinuclear antibodies
B) Erythrocyte sedimentation rate
C) Complement Levels
D) C-reactive protein
E) Liver function tests
F) Rheumatoid factor
G) Antithyroid antibodies

Correct Answer: C

Explanation/Literature Review:
This patient’s treatment-resistant urticarial plaques combined with histopathologic findings demonstrating perivascular nuclear debris with neutrophils and extravasation of erythrocytes are consistent with a diagnosis of urticarial vasculitis (UV). UV classically presents as recurrent, long-lasting wheal-like lesions with a predilection for the trunk and proximal extremities, accompanied by histopathologic findings of leukocytoclastic vasculitis.1 UV can present with or without angioedema. Additionally, features that help distinguish UV from chronic spontaneous urticaria (CSU) include the persistence of lesions beyond 24 hours, predominant symptoms of burning and pain compared to pruritus, and residual post-inflammatory purpura or hyperpigmentation upon healing.2,3 UV is a rare condition with an estimated incidence of 0.5 per 100,000 in the United States.4 It most commonly occurs in individuals in their 5th to 7th decades of life and demonstrates a female gender predominance.5 Regarding pathophysiology, UV is a type III hypersensitivity reaction; however, in most cases, the triggering antigen is often unidentified.6 While the majority of UV cases are idiopathic, a small percentage of cases have been associated with medications, infectious diseases, malignancies, and autoimmune diseases, commonly systemic lupus erythematosus.2

There are two main subtypes of UV, which are classified based on complement levels, the most important indicator of UV prognosis (answer choice C). Patients with normal complement levels, or normocomplementemic UV (NUV), tend to have skin-limited vasculitis. Conversely, patients with low complement levels, or hypocomplementemic UV (HUV), are much more likely to experience systemic disease.1,2 The most common systemic manifestations of HUV include arthralgia, arthritis, inflammatory eye diseases, pulmonary symptoms (mimicking asthma or COPD), gastrointestinal symptoms, and renal pathologies (proteinuria/hematuria).1 Finally, there is also a more severe subtype of HUV, called HUV syndrome (HUVS), which is defined by multiorgan involvement.1

UV is a notoriously challenging condition to treat, further complicated by the lack of standardized guidelines and randomized controlled trials. In a recent review article, H1-antihistamines, omalizumab, and immunomodulators were among the treatments with the most robust evidence in UV management.4,7 However, while H1-antihistamines were widely employed, they were only effective in improving skin lesions in 9.9% of 141 patients.7 Omalizumab demonstrated much greater efficacy, with 76% of 108 patients experiencing improvement in cutaneous symptoms and many also experiencing improvement in systemic symptoms such as arthralgia and abdominal pain.7 Among immunomodulators, systemic corticosteroids, dapsone, and hydroxychloroquine had the most substantial and strongest evidence supporting their use in addressing cutaneous and systemic symptoms of UV; however, the potential adverse effects of these drugs must be carefully considered.4,7 The aforementioned review article proposed a treatment algorithm recommending that mild UV should be approached like CSU, starting with H1-antihistamines and escalating to omalizumab, whereas moderate-to-severe UV should be managed with corticosteroids and/or other immunomodulatory agents depending on the patient profile.7 While this algorithm offers some direction, there is a critical need for high-quality, head-to-head trials to determine the optimal approach to UV management.

Incorrect answer choices:
The other laboratory tests are not indicative of prognosis but are warranted in the workup of patients with UV, particularly HUV. Inflammatory markers, specifically erythrocyte sedimentation rate (B) and C-reactive protein (D), are typically elevated in UV.1,5 Additionally, since UV can be associated with autoimmune diseases, autoimmune laboratory tests, including but not limited to antinuclear antibodies (A), rheumatoid factor (F), and anti-thyroid antibodies (G) are often included in the workup to detect or rule out underlying autoimmune diseases.5 Finally, while liver dysfunction is not a common systemic manifestation of UV, liver function tests (E) may be included alongside standard laboratory tests, such as complete blood count and basic metabolic panel, in the workup of UV.5 

References

  1. Marzano AV, Maronese CA, Genovese G, et al. Urticarial vasculitis: Clinical and laboratory findings with a particular emphasis on differential diagnosis. J Allergy Clin Immunol. 2022;149(4):1137-1149. doi:10.1016/j.jaci.2022.02.007
  2. Bolognia J, Schaffer JV, Cerroni L, Callen JP. Dermatology. Elsevier; 2025.
  3. James W. Andrews’ Diseases of the Skin. Elsevier; 2026.
  4. Kolkhir P, Grakhova M, Bonnekoh H, Krause K, Maurer M. Treatment of urticarial vasculitis: A systematic review. J Allergy Clin Immunol. 2019;143(2):458-466. doi:10.1016/j.jaci.2018.09.007
  5. Wang RX, Newman SA. Urticarial Vasculitis. Immunol Allergy Clin North Am. 2024;44(3):483-502. doi:10.1016/j.iac.2024.03.006
  6. Black AK. Urticarial vasculitis. Clin Dermatol. 1999;17(5):565-569. doi:10.1016/s0738-081x(99)00062-0
  7. Rothermel ND, Vera Ayala C, Gonçalo M, et al. Managing Urticarial Vasculitis: A Clinical Decision-Making Algorithm Based on Expert Consensus. Am J Clin Dermatol. 2025;26(1):61-75. doi:10.1007/s40257-024-00902-y
Mar 27
Love16

February 2025 Case Study

By 2025 Case Studies

February 2025 Case Study

Author: Olive Osuoji MD1
1Department of Dermatology, The George Washington University School of Medicine and Health Sciences

Patient History
A 72-year-old male female with a past medical history of hypertension, end stage renal disease s/p renal transplant, type II diabetes mellitus, peripheral arterial disease, and atrial fibrillation was admitted to the hospital with right lower extremity (RLE) pain at rest and non-healing wounds. The patient had been admitted to the hospital 2 weeks prior for RLE angiogram with angioplasty. On examination, the patient had large well-defined necrotic ulcers with surrounding erythema on the right medial leg, right heel, and dorsal foot (Figure 1) and circumferential necrosis of the second through fifth right digits (Figure 2). Bilateral lower extremity dopplers showed triphasic signals. A punch biopsy was obtained from the periphery of the ulcer and H&E staining was performed (Figure 3). Laboratory findings were noncontributory.

Based on the clinical presentation and biopsy findings, which additional stain would be most useful to confirm the etiology of the underlying disease process?

A. Periodic acid-Schiff with diastase (PAS-D)
B. Colloidal iron
C. Von Kossa
D. Trichrome
E. Methenamine Silver

        

Correct Answer: B

Explanation/Literature Review
The patient presented clinically with retiform purpura and necrotic right lower extremity ulcerations two weeks following an angiogram with angioplasty. H&E stain of the punch biopsy specimen revealed amphophilic bilaminar material resembling hydrophilic polymer gel material within a dermal vessel, consistent with hydrophilic gel embolus. DIF revealed a non-diagnostic vascular fluorescence pattern, suggesting vascular damage without an immune complex-mediated vasculitis. These combined clinical and histopathological findings led to the diagnosis of cutaneous hydrophilic polymer emboli (HPE).

Cutaneous HPE is a rare iatrogenic occlusive vasculopathy that occurs after the use of polymer-coated intravascular devices. These devices – vascular catheters, delivery sheaths, coils, guidewires, grafts, and implants – are often coated with hydrophilic polymers to reduce friction between devices and vessel walls during endovascular procedures.1-4 Despite its utility, the polymer gel coating can separate from the metallic surface of the device and embolize, causing vascular occlusion and ischemic damage. Fewer than 25 cases of HPE have been documented in the literature, but with the growing use of percutaneous endovascular procedures, recognition of HPE has increased.5

HPE can lodge in small dermal vessels, appearing clinically as erythema with pruritus, nonpalpable petechiae and purpura, livedo reticularis/racemosa, retiform purpura, acute and chronic ulcerations, hyperkeratotic and lichenified nodules, and hemorrhagic panniculitis. These lesions usually appear within 24 hours to 2 weeks of the procedure, though some cases may manifest months or even years later. Systemic complications of HPE can be severe and include pulmonary infarction, myocardial infarction, stroke, gangrene, and potentially death.1, 6

When evaluating retiform purpura and necrotic ulcers on the lower extremities, etiologies of vascular compromise should be considered. The differential diagnosis includes calciphylaxis, vasculitides (small/medium vessel, ANCA-associated, drug-induced), cryoglobulinemia, and thrombotic/thromboembolic diseases such as cholesterol emboli, antiphospholipid syndrome, DIC, TTP, septic emboli, and medication-induced thrombosis (e.g., heparin-induced thrombocytopenia).7-8

The gold standard diagnosis of HPE requires a combination of clinical findings and histopathological evidence of non-refractile, non-polarizable basophilic, amorphous material occluding mid-dermal vessels. Colloidal iron staining for acid mucopolysaccharides can be used to identify the polymer gel in HPE, but is not necessary. Colloidal iron staining can be combined with hyaluronidase digestion to differentiate between hyaluronic acid and other mucosubstances. An absence of tissue neutrophilia helps differentiate HPE from cholesterol emboli.1, 2, 6, 9

Management of cutaneous HPE prioritizes early detection to avoid unnecessary amputation. Most cutaneous lesions of HPE spontaneously resolve without treatment as the polymer material biodegrades in vivo over weeks to months, however, supportive treatment for symptoms and secondary infections may be warranted. Evidence for the role of wound care, trials of topical or oral corticosteroids, surgical resection, and antiplatelet agents is only supported by case reports.1, 6, 8

Incorrect Options 10-12

  • Periodic acid-Schiff (PAS) staining with diastase – glycogen, neutral mucopolysaccharide, and fungal stain; can be used to assist in identifying fungal organisms and inflammatory dermatoses
  • Von Kossa – calcium stain; can be used to identify calciphylaxis
  • Masson Trichrome – collagen stain; can be used to identify connective tissue abnormalities, perforating disorders, fibrosis, ischemic damage
  • Methenamine Silver – fungal stain; can be used to identify angioinvasive fungal organisms

 

References

  1. Chan KPR, Lee JSS, Lim JHL. Cutaneous Hydrophilic Polymer Embolism: An Important and Overlooked Clinical Entity. Am J Dermatopathol. 2024;46(7):452-454.
  2. Miyaoka M, Hatanaka K, Uekusa T, Nakamura N. Clinicopathological features of hydrophilic polymer emboli in Japanese autopsy cases. APMIS. 2018;126(11):838-841.
  3. Mehta RI, Mehta RI, Choi JM, Mukherjee A, Castellani RJ. Hydrophilic polymer embolism and associated vasculopathy of the lung: prevalence in a retrospective autopsy study. Hum Pathol. 2015;46(2):191-201.
  4. Barnwell SL, D’Agostino AN, Shapiro SL, Nesbit GM, Kellogg JX. Foreign bodies in small arteries after use of an infusion microcatheter. AJNR Am J Neuroradiol. 1997;18(10):1886-1889.
  5. Baudo M, Magrini E, Pernot M, et al. Hydrophilic polymer embolization after TAVI. J Cardiol. 2024;84(2):141-142.
  6. Sabzevari N, Schapiro BL, Stewart B. Necrotic leg ulcers secondary to hydrophilic polymer gel emboli. J Vasc Surg Cases Innov Tech. 2019;5(3):310-313. Published 2019 Jun 29.
  7. Georgesen C, Fox LP, Harp J. Retiform purpura: A diagnostic approach. J Am Acad Dermatol. 2020;82(4):783-796.
  8. Shefler A, Blaszak SC, Shea CR, Chadha AA. A Rare Case of Hydrophilic Polymer Embolization After Transcatheter Aortic Valve Replacement. Am J Dermatopathol. 2023;45(6):411-413.
  9. Thompson AK, Peters MS, El-Azhary RA, et al. Cutaneous microemboli from hydrophilic polymer after endovascular procedures. J Am Acad Dermatol. 2015;73(4):666-671.
  10. Elston DM, Ferringer T, Ko C, Peckham S, High WA, DiCaudo DJ. Dermatopathology. Third edition. Elsevier; 2018.
  11. Van De Vlekkert D, Machado E, d’Azzo A. Analysis of Generalized Fibrosis in Mouse Tissue Sections with Masson’s Trichrome Staining. Bio Protoc. 2020;10(10):e3629. Published 2020 May 20.
  12. Shalin SC, Ferringer T, Cassarino DS. PAS and GMS utility in dermatopathology: Review of the current medical literature. J Cutan Pathol. 2020;47(11):1096-1102.
Feb 28
Love18

January 2025 Case Study

By 2025 Case Studies

January 2025 Case Study

Author: Nathaniel Lampley, MD

Patient History
A 61-year-old male presents to your clinic with a rash on his right shin. His past medical history is significant for poorly controlled HIV. His most recent CD4+ T-cell count, and viral load were 18 and 3.3 million, respectively. The patient tells you that the rash started a few months ago as small spots that seemed to get larger and spread across his shin. He has never seen a physician for the rash and has tried no previous treatments. Examination of the right lower extremity is shown in Figure 1. A punch biopsy is performed, and histopathology is shown in Figure 2.

Which of the following immunohistochemical stains would assist in achieving a definitive diagnosis?

A) CD31
B) HHV-8
C) CK20
D) Factor XIIIa
E) GLUT1

   

 

Correct Answer: B

B) The Human herpesvirus (HHV)-8 viral stain is used to confirm the diagnosis of Kaposi’s sarcoma (KS) which is the etiology of this patient’s rash. There are 4 main types of KS: Classic, African endemic, Iatrogenic and AIDS-related.3 The patient’s history of uncontrolled HIV combined with the clinical and histopathological features presented in the question vignette should yield suspicion for KS. Histopathology of KS demonstrates an interstitial spindle cell proliferation, vascular wrapping, thin vascular spaces, extravasated RBCs, hemosiderin, and increased plasma cells.1 Application of the HHV-8 stain is especially important in the diagnosis of KS as angiosarcoma and dermatofibroma can mimic KS on histopathology.

Explanation of Incorrect Answers:

A) The CD31 stain is a marker of vascular endothelial cells and is helpful in confirming the vascular origin of tumors.2 CD31 is positive in angiosarcoma. Histopathology of angiosarcoma demonstrates poorly formed vessels filled lined by large, atypical, hyperchromatic endothelial cells that protruded into the lumen. The vascular spaces are poorly formed and leaky yielding the bruise-like clinical appearance.1

C) The CK20 stain marks Merkel cell carcinoma in the perinuclear dot pattern. It is also helpful in determining the origin of metastatic carcinomas of unknown origin as it generally correlates with adenocarcinomas that develop in organs below the diaphragm.2 Histopathology of Merkel cell carcinoma demonstrates small blue cells with scant cytoplasm and tightly packed nuclei. Nuclear molding, apoptotic cells and mitoses can also be visualized.2

D) The Factor XIIIa stain highlights dermal dendritic cells and is positive in dermatofibromas and negative in dermatofibrosarcoma protuberans (DFSP).2 Histopathology of dermatofibromas demonstrate a proliferation of fibrohistiocytic cells, ringed lipidized siderophages, peripheral collagen trapping, and overlying platelike acanthosis. Another hallmark feature of dermatofibromas is their alternating areas of hypercellularity and hypocellularity.2

E) Glucose transporter 1 (GLUT1) is a protein that is expressed in endothelial cells that have a blood-tissue barrier function. The GLUT1 stain is positive in infantile hemangiomas, but negative in both rapidly-involuting congenital hemangiomas (RICH) and non-involuting congenital hemangiomas (NICH).2 Histopathology of infantile hemangiomas demonstrates nonencapsulated masses of dense cords of mitotically active endothelial cells and pericytes with prominent basement membranes.4

References

  1. Alikhan, Ali, and Thomas L. H Hocker. Review of Dermatology (p. 435). Elsevier, 2024.
  2. Elston, Dirk M., et al. Dermatopathology (p. 133, 145, 147, 1249, 1424). Elsevier, 2019.
  3. Friedman, Adam, editor, et al. Derm In-Review 2024 Study Guide (p. 310,385). SanovaWorks, 2023.
  4. Nakayama, Hiroko. “Clinical and Histological Studies of the Classification and the Natural Course of the Strawberry Mark.” The Journal of Dermatology, vol. 8, no. 4, Aug. 1981, pp. 277–291, doi:10.1111/j.1346-8138.1981.tb02546.x.