Cutaneous Lymphoid Hyperplasia and Related Entities



Cutaneous Lymphoid Hyperplasia and Related Entities


Alejandro A. Gru



INTRODUCTION

Cutaneous lymphoid hyperplasia (CLH) refers to a heterogeneous group of “reactive” T- and B-cell processes that simulate cutaneous lymphomas both clinically and/or histologically.1,2 Most CLHs consist of a mixture of reactive B and T cells along with macrophages and dendritic cells. B-cell-rich CLH exhibits unique clinical features; rare T-cell-rich cases have been described.3,4,5 CLH may be idiopathic, or it may arise in response to a wide variety of foreign antigens, including arthropod bites,6 stings, and infestations7,8; tattoos; vaccinations; trauma; injection of foreign substances; pierced ear jewelry; and drugs.9,10 Since CLH often shows striking morphologic overlap with low-grade B-cell lymphomas, and less frequently with T-cell lymphoproliferations, a careful phenotypic and molecular characterization is mandatory to exclude lymphoid neoplasia. In this chapter, we will review the main forms of CLH and will also expand on a few related entities with unique clinicopathologic features (Table 45-1).








TABLE 45-1 Cutaneous Lymphoid Hyperplasia and Related Entities





















•

Cutaneous lymphoid hyperplasia of B cells, T cells, and mixed T/B cells.


•

Borrelia burgdorferi-associated lymphocytoma cutis.


•

Atypical lymphoid hyperplasia.


•

Atypical marginal zone hyperplasia.


•

Lymphomatoid keratosis.


•

Syringolymphoid hyperplasia with alopecia.



CUTANEOUS MIXED T- AND B-CELL HYPERPLASIA

Cutaneous mixed T- and B-cell hyperplasia (mixed T–B CLH) presents both in women and men, with an average age of 54 years at presentation (range 16 to 93). The lesions typically present as nodules, plaques, and papules. Most of the lesions are located in the head and neck region, followed by the trunk, and extremities. Solitary lesions are much more common than multiple lesions.1 Many different etiologic agents have been linked to CLH (Table 45-2).








TABLE 45-2 Causes of CLH
























1.

Medications: oxaliplatin and 5-fluorouracil in advanced colon cancer11; simvastatin12; omeprazole; ranitidine13; aspirin; ramipril12,13,14; glyburide; alfuzosin; calcium channel blockers12,15; atenolol; metoprolol15; paroxetine; doxazosin mesylate1; fluoxetine and amytriptiline16; minoxidil17; antihistamines10; benzodiazepines12; minocycline13; lupron injections13; carbamazepine13; isoflavin13; doxepin13; erythromycin13; sertraline13; losartan18; gabapentin15; phenytoin19,19,20,21,22,23,24,25,26,27,28,29,30; cefuroxime; cefepime15; terbinafine; levofloxacin15; gemcitabine31; leuprolide; hepatobiliary iminodiacetic acid (HIDA) scintigraphy.


2.

Infections: Varicella-zoster-virus folliculitis promoted clonal cutaneous lymphoid hyperplasia32; tick bites33; zoster34; B. burgdorferi3, 35,36,37,38,39,40; scabies41; secondary syphilis42,43,44,45,46,47,48,49,50; leishmaniasis 51; HSV52,53,54; molluscum contagiosum55,56,57,58,59; H. pylori 60; HIV61,62,63,64,65; HPV-related in common warts66,67; orf 68; dermatophyte infections69 (Fig. 45-2); M. tuberculosis70; HTLV-1; hepatitis B/C; R. tsutsugamushi.


3.

Vaccinations71,72: hepatitis B vaccine72,73,74; hepatitis A vaccine74; influenza vaccine.75


4.

Toxicologic/Traumatic: venoms7; following feline scratches76; tattoos77,78,79,80,81; squaric acid82; following radiation therapy83; following a broken thermometer and presumptively secondary to mercury exposure.84


5.

Synchronous to other cutaneous disorders: granuloma annulare85; melanocytic nevi86; scars mimicking subcutaneous panniculitis-like T-cell lymphoma87,88; folliculitis89,90; lymphomatoid contact dermatitis; lichen sclerosus (Fig. 45-3).


6.

Autoimmune disorders: Sjögren syndrome91; lupus erythematosus.


7.

Neoplastic: spiradenoma with dense lymphoid infiltrates92; lymphoepithelioma-like carcinoma93,94,95,96,97,98,99,100; halo nevus101,102,103,104; angiosarcoma105,106; myxoinflammatory fibroblastic sarcoma; angiomatoid fibrous histiocytoma; pyogenic granuloma/lobular capillary hemangioma.







FIGURE 45-1. Persistent arthropod-bite reaction. A and B. Nodular and diffuse infiltrate in the dermis with sparing of the epidermis. The entire dermis is involved (20× and 100×, respectively). C. Grenz-zone and increased superficial dermal vascularity (200×). D. The infiltrate shows a diffuse pattern and extends within the collagen fibers (100×). E. Eosinophils are abundant in the infiltrate (200×). F. Germinal center formation can be identified (400×).






FIGURE 45-2. Cutaneous pseudolymphoma in association with a dermatophyte infection. A. Periodic acid-Schiff-positive hyphae and spores within the horny layer. B. Few periodic acid-Schiff-positive hyphae and spores within a hair follicle. (From Kash N, Ginter-Hanselmayer G, Cerroni L. Cutaneous mycotic infections with pseudolymphomatous infiltrates. Am J Dermatopathol. 2010;32:514-517, with permission.)






FIGURE 45-3. Cutaneous pseudolymphoma in association with lichen sclerosus. The findings were present in the excision specimen from a woman with squamous cell carcinoma of the vulva. A. Superficial band-like infiltrate with interface changes (20×). B. Prominent epidermotropism and marked interface changes (200×). C. The epidermotropic cells show no significant atypia (400×). D. CD3. E. CD8. The CD3:CD8 ratio is preserved. F. CD7 shows no significant loss among the T cells.

CLH can develop as a result of scabies or an arthropod bite (Fig. 45-1). Clinically, multiple pruritic firm erythematous to red-brown papules and nodules occur most commonly on the elbows, abdomen, genitalia, and axillae. Nodules following scabies may persist for many months after adequate antiscabetic therapy. The cause of the persistent nodules is not known but is thought to be a delayed-type hypersensitivity reaction to a component of the mite. Scabies mites are seldom identified in scabetic nodules.107,108,109,110


CUTANEOUS B-CELL HYPERPLASIA

Cutaneous B-cell hyperplasia (B-CLH), also known as lymphocytoma cutis (LC), is characterized by flesh-colored to plum-red dermal and subcutaneous nodules and plaques similar to cutaneous B-cell lymphomas (CBCLs).111 In idiopathic LC, the most typical sites of involvement include the face (cheek, nose, ear lobe; 50%), chest (36%), and upper extremities (14%).112,113,114,115 Lesions below the waist are infrequent.112 The female-to-male ratio is 3:1. The disease predominantly affects white populations (white/black = 9:1). Two-thirds of patients are under the age of 40 years at initial biopsy. Approximately 8% of patients are under the age of 18 years.

Two clinical forms have been reported: the more common localized form (72%) and the less frequent generalized form (28%).116,117 The localized form is usually seen as a single asymptomatic soft, doughy, or firm nodule or tumor measuring up to 4 cm in diameter; lesions may be aggregated in small clusters. Occasionally, miliary papules measuring only a few millimeters in diameter may be seen. The color varies from skin-colored to red to red-brown to red-purple. Scale and ulceration are generally absent.

Histologically, the dermis shows top heavy infiltrates of small mature lymphocytes without epidermal involvement (Fig. 45-4). The infiltrate can be nodular,118 nodular and diffuse, or predominantly diffuse (Figs. 45-5, 45-6 and 45-7). Germinal centers are typically seen with mantle zones forming well-defined follicles. The germinal centers contain a mixture of centrocytes (small cleaved lymphocytes) and centroblasts (large lymphocytes with prominent nucleoli). Polarization of the germinal centers can be seen in approximately 30% of cases. Most germinal centers also typically have tangible body macrophages and mitotic figures. Some cases can also show progressive transformation of germinal centers.119

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Nov 8, 2018 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Cutaneous Lymphoid Hyperplasia and Related Entities

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