Pyostomatitis vegetans

Pyostomatitis vegetans Report of a case and review o f the literature Frances Stahl Ballo, MD," Charles Camisa, MD," and Carl M. Mien, DDS, MSD b

Cleveland and Columbus, Ohio This report describes a 39-year-old woman with pyostomatitis vegetans and ulcerative colitis. Pyostomatitis vegetans is a rare eruption of the oral cavity characterized by tiny yellow pustules coating the surface of the friable eroded mucosa. It is considered a marker for inflammatory bowel disease. In a review of the literature, 19 of 26 cases (73%) reported were associated with gastrointestinal disturbances, predominantly inflammatory bowel disease. (J AM ACADDERMATOL1989;21:381-7.)

In 1898 Hallopeau ~ described for the first time an unusual pustular vegetating dermatosis, which he termed pyodermite vegetante. The skin lesions typically involved the axillary and genital regions, occasionally the face and scalp, and rarely the oral mucous membranes. Two of the original five cases described by HaUopeau had the pustular and vegetating eruption throughout the oral mucosa. Subsequently cases were reported by Wallhauser 2 and Goldsmith, 3 who described the presence of striking lesions of pyodermite vegetante in the oral mucosa that resembled the lesions found on the skin. In a 1949 report McCarthy 4 was the first to describe three patients who, on initial examination, demonstrated comparable lesions confined to the oral cavity. He described the lesions as soft hypertrophic folds studded with miliary abscesses with superficial areas of necrosis. In one of the three patients, the skin vegetations of Hallopeau developed the following year, facilitating clarification of the diagnosis of these oral lesions. McCarthy 4 coined the term pyostomatitis vegetans for this condition and believed it to be a variant of pyodermite vegetante. Pyostomatitis vegetans is a rare disorder, and to From the Department of Dermatology, The Cleveland Clinic Foundation," and the College of Dentistry, Ohio State University, Columbus.b Reprint requests: Charles Camisa, MD, The Cleveland Clinic Foundation, Department of Dermatology, A61, 9500 Euclid Ave., Cleveland, OH 44106,

our knowledge only 26 cases have been reported in the literature, Most of the patients in these reports had either colitis or a gastrointestinal disturbance in association with their oral disease. In fact, Van Hale et alJ recently proposed that pyostomatitis vegetans is actually a highly specific oral mucosal marker for inflammatory bowel disease. In this report we present a new case of pyostomatitis vegetans, followed by a review of the literature. CASE REPORT

A 39-year-old woman was admitted to Ohio State University Hospital in June 1986 with a 4-month history of oral ulcerations, decreased oral intake, and dehydration. Several oral surgeons had been consulted previously for treatment of the oral lesions. Therapy with oral antibiotics, acyclovir, and topical corticosteroids was unsuccessful, and no definitive diagnosis was made. The patient had been unable to take solid food for 1 month before referral to Ohio State University. She also had a 15-year history of intermittent upper abdominal cramping and diarrhea, occurring approximately 1 hour after meals, that was associated with nearly daily rectal bleeding. Barium enema and sigmoidoscopy were performed in 1971, when the patient was informed of the diagnosis of hemorrhoids and chronic diarrhea. Oral examination (on admission) revealed an eruption of yellow pustules coating the surface of the friable eroded mucosa. The areas most involved were the upper and lower buccal, facial, and lingual gingivae (Fig. 1); the upper and lower labial mucosa; and the bilateral buccal mucosa. Erosions also were seen on the internal aspects of the oral commissures. The palate and tongue were spared. External swelling of the cheeks was noted. 381

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Fig. 1. Multiple yellow pustules, 1 to 2 mm, scattered on erythematous friable gingival mucosa. "Snail tracks," where several of the pustules have coalesced, may be seen particularly on the fight upper gingiva.

Results of the remainder of the cutaneous examination, including genitalia, were normal. Rectal examination showed mild internal hemorrhoids. Laboratory studies revealed the following values: white blood cell count, 9700/mma; platelet count, 457,000/mm~; hematocrit, 30.8%; hemoglobin, 10.5 gm/dl; mean corpuscular volume, 77 ~m3; and mean corpuscular hemoglobin concentration, 34%. Results of additional studies revealed the following values: serum ferritin, 7 ng/ml; serum iron, 11 izg/dl; and total serum iron binding capacity, 330 ~tg/dl. Results of routine serum ebemistdes, urinalysis, and thyroid function tests were within normal limits. Examination of bacterial, fungal, and viral cultures of the purulent material showed no growth of pathogens. A biopsy specimen was obtained from the lower labial mucosa for both light microscopic and immunofluorescence studies. Exfoliative cytologic findings revealed acantholytic epithelial cells, eosinophils, and neutrophils (Fig. 2). Light microscopic study demonstrated intraepithelial clefts containing eosinophils and neutrophils, with a moderate chronic inflammatory cell infiltrate in the underlying connective tissue. Results of direct immunofluorescence study showed focal weak intercellular deposits of IgG and IgA and 2+ fibrinogen at the mucosal-submucosal junction. Findings from indirect immunofluorescence studies were negative for circulating autoantibodies. These results were believed to be consistent with a diagnosis of pyostomatitis vegetans. Therapy with intravenous fluids and oral prednisone (60 rag/day for 4 days) was begun. Twenty-four hours later the patient showed a dramatic response with nearly complete healing of the oral mucosa. Gastroenterology consultation was obtained. Results of a biliary echogram

were interpreted as normal. Findings from upper endoscopy revealed no abnormalities except for a small hiatal hernia. Results of colonoscopy revealed diffuse, patchy mucosal ulcerations. Examination of multiple biopsy specimens demonstrated edema and chronic inflammation with a mild scattering of polymorphonuclear leukocytes, compatible with ulcerative colitis. The patient was discharged 4 days after admission with the diagnoses of pyostomatitis vegetans, ulcerative colitis, and iron deficiency anemia. She was instructed to take prednisone, 60 mg/day, and ferrous sulfate, 325 mg three times daily. The patient returned for follow-up examination 11 days after discharge. All the lesions had healed, and the diarrhea was improved. Prednisone was decreased to 40 rag/day for 1 week and was to be tapered by 10 mg each week. One month after discharge, all gastrointestinal symptoms had resolved and the oral examination was again unremarkable. However, stool tested with guaiac was positive for occult blood. Sulfasalazine (Azulfidine) therapy (2 gin/day) was started for maintenance of the remission of the bowel disease. The patient was last seen for follow-up examination in the dermatology clinic in October 1986, approximately 4 months after she came to Ohio State University. She was asymptomatic, and the oral examination was clear except for some fine white papules seen on the upper anterior alveolar ridge. No ulcerations were noted. DISCUSSION The case we report meets the clinical, histopathologic, and immunofluorescence criteria for classification as pyostomatitis vegetans; namely, yellow-

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Pyostomatitis vegetans

383

g C

cg~:'

Fig. 2. Exfoliative cytologic findings show squamous epithelial cells (some of which resemble acantholytic cells), as well as eosinophils and neutrophils. (Papanicolaou's stain; x160.)

ish pustules on an erythematous base that correspond microscopically to eosinophil-laden microabscesses and exhibit intercellular antibodies on direct immunofluorescence study. 6 Review of the literature shows that most patients with pyostomatitis vegetans are between the ages of 20 and 59 years. Seventeen of the 27 reported cases have occurred in men. The clinical appearance of pyostomatitis vegetans is unique to lesions of the oral mucosa and often is described as slightly elevated, roundto-oval, well-demarcated miliary abscesses set on erythematous hyperplastic folds of tissue. The white-to-yellow surface of the abscesses is soft and friable and erodes easily, leaving a small ulceration. In some cases a purulent material can be expressed from the yellowish areas. 7 When several smaller erosions coalesce to form a larger area of ulceration, a "snail track" appearance may be seen. The maxillary and mandibular labial gingivae, mucobuccal fold, buccal mucosa, and labial mucosa are most commonly affected, although lesions may affect all regions of the oral cavity. Least commonly affected are the floor of the mouth and the tongue. 7,8 Some patients had fissuring of the oral mucosa. ~,7 Interestingly, pain and discomfort were not frequent complaints, despite occasionally extensive oral involvement. Of course, appearance and distribution of lesions varied to some degree among patients, as well as with the course of the disease in individual patients.

A peripheral eosinophilia and mild anemia have been associated with pyostomatitis vegetans. Fourteen of the 27 patients studies had up to 20% eosinophils on their differential white blood cell counts. Although a differential cell count was not performed for our patient, it was determined that she had an iron deficiency anemia, most likely a result of blood loss in the stool as a consequence of colitis. Other laboratory values have been reported to be normal. In the earlier literature, attention was directed toward consideration of an infectious cause because the vegetating lesions suggested a bacterial infection. Yet results of bacterial, viral, and fungal cultures typically demonstrate only normal oral flora. McCarthy and Shkiar 7 found Streptococcus viridans to be the most consistently identified organism from cultures; occasionally Staphylococcus aureus was isolated from cultures of the associated skin lesions (but never the oral lesions). Histopathologic examination of the oral lesions demonstrates the striking feature of miliary intraepithelial and/or subepithelial abscess formation containing numerous eosinophils. There is a question as to whether some of the intraepithelial abscesses reported are actually in the tips of tangentially cut dermal papillae. 6 The underlying connective tissue is infiltrated with a dense population of chronic inflammatory cells with older lesions showing less eosinophilia. Forman ~ points

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out that although acanthosis, hyperkeratosis, and areas of intraepithelial dissociation can be seen, results of the histologic examination are not consistent with a primary acantholytic disorder. Controversy over the classification of pyostomatiffs vegetans has existed since Hallopeau published his initial findings. He originaUy considered the disease to be a separate entity, but later called it a variant of pemphigus vegetans when one of his patients died of the latter. Critics of Hallopeau prefer to emphasize the localized and benign course of pyodermite vegetante to distinguish it from the generalized and occasionally fatal course of pemphigus vegetans. The belief that the two diseases are related is based on their similar histopathologic features, specifically, the intraepithelial eosinophilic pustule. The positive immunofluorescence microscopy findings in a few patients who had pyostomatitis vegetans only confounds further the question of classification. 6,1~ Ouimet et al. 1~ and Nelson et al. H were the first to report deposits of intercellular IgG on immunofluorescence microscopy studies of skin lesions in two patients who had "pyodermite vegetante de Hallopeau." In these patients circulating intercellular antibodies were detected by indirect immunofluorescence microscopy. It may be argued that these two patients had pemphigus vegetans rather than pyostomatitis vegetans, especially because bowel disease was either not mentioned in the report or was absent. Nelson ~2reported that immunofluorescence studies in a third patient yielded negative findings. To our knowledge, only three biopsy specimens removed from the oral mucosa of patients who had pyostomatitis vegetans have been previously studied by direct immunofluorescence microscopy. Results in the case reported by Van Hale et al. s were nonspecific, whereas Wray ~3found intercellular IgG in his patient's oral mucosal specimen. Hansen et al. 6 found finely granular IgG and IgA in the intercellular spaces of the epithelium and weak linear deposits of fibrinogen along the basement membrane zone. The immunoreactants and staining patterns found in the patient of Hansen et al? were identical to those reported in ours. These positive immunofluorescence microscopy results further the cause for consideration of pyostomatitis vegetans as a variant of oral pemphigus vulgaris. However, Hansen et al? pointed out (and we concur) that the pattern and distribution of immunoreactants, as well as the presence of IgA, in these

Journal of the American Academy of Dermatology patients are different from and not diagnostic of pemphigus vulgaris or pemphigus vegetans. They concluded that the weight of evidence, based on clinical findings, course, and histopathologic criteria, favored no relation between these diseases. Nelson et al, 11 and Nelson 12proposed that immunofluorescence studies should be the deciding factor in distinguishing pyostomatitis vegetans from pemphigus vulgaris. The association of bowel disease with pyostomatiffs vegetans is well known and dates back to the early work of McCarthy. 4 Most of the literature on this subject substantiates the contention that bowel disease generally antedates oral disease. It is not uncommon for various mucous membrane and skin lesions to develop in patients with inflammatory bowel disease, including aphthous stomatitis, candidiasis, erythema nodosum, and pyoderma gangrenosum. Occasionally, patients have such mild gastrointestinal symptoms that the colitis may remain undetected without directed questioning. In fact, Forman 9 advocated that the bowel should be inspected directly in all cases of pyodermite vegetante because of the minor nature of symptoms and lack of constitutional signs. Results of radiologic examination of the two patients who prompted Forman's proposal9 were later discovered to be suggestive of whole colon involvement. In 1981 Cataldo ct al.14 described the case of a patient with a very strong family history of bowel disease who denied having ulcerative colitis. Further questioning revealed a long history of diarrhea, and subsequent evaluation was consistent with a diagnosis of Crohn's disease. Both of the cases reported by Zegarelli and Kutscher8 had features of colitis; one actually underwent an appendectomy for complaints of epigastric pain without abatement of symptoms. A diagnosis of ulcerative colitis was made several years later. In 1970 Naish et al. 15 described a case of pyostomatitis vegetans and ulcerative colitis in a 26-year-old Nigerian man, an extraordinary event because each disease is very rare in the Nigerian population. The type of bowel disease occurring in cases of pyostomatitis vegetans varies. As shown in Table I, 20 of 27 (74%) patients, incIuding ours, had gastrointestinal disturbances: 13 had ulcerative colitis, 3 had Crohn's disease, 2 had chronic diarrhea, and 2 had "colitis." Bowel disease preceded the onset of oral disease by months or years in 14 of the 20 patients studied. Fifteen of the

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Pyostomatitis vegetans 385

Table I. Summary of 27 reported cases of pyostomatitis vegetans

c'I No.

Source

Year

i

McCarthy

1949

2

McCarthy

3 4 5 6

I

Agell (yr)

Sex

4

26

F

1949

4

47

M

McCarthy Hornstein Hays Zegarelli and Kutscher Zegarelti and Kutscher Marks

1949 1957 1961 1962

4 20 21 8

33 56 61 27

M M M F

1962

8

24

M

1962

22

20

M

1962

23

9

M

1963

7

27

M

1963

7

15

M

1963

7

25

M

i3 14

Leydecker and Lund McCarthy and Shklar McCarthyand Shklar McCarthy and Shklar Rocld Forman

1964 1965

24 9

59 45

M F

15

Forman

1965

9

44

F

16

Naish et al.

1970

15

26

M

17 18 19 20 21

Ouimet et al. Nelson et al. Nelson Cataldo et al. Hansen et al.

1973 1977 1978 1981 1983

10 11 12 14 6

70 70 NS 48 37

F M NS M M

22

Wray

1984

13

58

M

23 24 25

Wray Neville et al. Van Hale et al.

1984 1985 1985

13 18 5

52 47 23

M F F

26

Van Hale et al.

1985

5

24

F

27

Ballo et al.

1988

39

F

7 8 9 10 il 12

Reference

Present report

Bowel disease

Chronic diarrhea Chronic spastic colitis None Mild colitis NS Ulcerative colitis Ulcerative colitis Ulcerative colitis Diarrhea Ulcerative colitis Ulcerative colitis Ulcerative colitis NS Ulcerative colitis Ulcerative colitis Ulcerative colitis NS None NS Crohn's disease Crohn's disease or overlap Ulcerative colitis None Crohn's disease Ulcerative colitis Ulcerative colitis Ulcerative colitis

disease

site

Eosinophilia

No

Oral

18%

Yes

Gut

+

No No NS Yes

Oral NS Oral Gut

+ 4% NS 14%

Yes

Gut

Normal

Yes

Gut

13%

Yes

NS

6%-25%

Yes

Gut

NS

No

NS

NS

Yes

NS

NS

Yes Yes

NS Gut

Yes

Gut

NS 10%20% 12%

No

Gut

NS

Yes Yes NS NS No

NS Oral NS Oral Gut

16% 15% NS NS 4%

No

Gut

NS

Yes No Yes

Skin Gut Gut

NS 5% Normal

Yes

Gut

12%

No

Gut

ND

+, Eosinophilia present but percentage not specified in reference; ND, not done; NS, not stated in reference.

reported cases had concomitant cutaneous involvement. In the majority of reported cases of pyostomatitis vegetans, it is claimed that the underlying gastrointestinal disorder is ulcerative colitis. However, Crohn's disease has been regarded as an inflammatory bowel disease discrete from ulcerative colitis only since 1960. Hansen et al, 6 make

the observation that perhaps a number of the earlier cases reported to be ulcerative colitis might be classified today as Crohn's disease. Significant overlap of radiologic and histopathologic features occurs between the two diseases, rendering classification difficult if not impossible? 6 Regardless of the type, it is evident that patients with the characteristic clinical and microscopic findings of

386

Ballo et al.

pyostomatitis vegetans generally have concomitant bowel disease, albeit subclinical. Furthermore, several investigators have reported that improvement of the bowel disease often parallels improvement of the oral lesions, with or without specific therapy. 7.17 One patient had a remission of oral lesions after emergency colectomy for associated bowel disease.5 Treatment of pyostomatitis vegetans has included a wide variety of preparations given for local as well as systemic effect. Therapy for local effect has been largely unsuccessful in the control of oral lesions, although occasional reports claimed regression with application of topical corticosteroids s. ~3; however, it is usually sufficient to cause regression of associated skin lesions. One patient described by Van Hale e t al? had a complete remission after 5 weeks of therapy with dapsone, 150 mg/day. In general, however, moderate to high doses of corticostemids for systemic effect have proved to be most successful in the management of pyostomatitis vegetans. On occasion, dramatic improvement has been observed. ~8 Attempts to taper dosages often result in recurrence of the oral lesions. Administration of suLfasalazine for systemic effect, 2 to 3 gin/day, m a y give additional benefit.13. J8 The beneficial response to oral corticosteroids led one group of authors to speculate that pyostomatitis vegetans is a disease of the hypersensitivity type, similar to pyoderma gangrenosum, erythema nodosum, and uveitis associated with ulcerative colitis. 15 Whatever the pathogenesis, most authorities agree that the lesions of pyostomatitis vegetans are part of a syndrome that includes bowel disease and the skin lesions of pyodermite vegetante. 7,8.12.t4 McCarthy and Shklar 7 suggested that colitis associated with this syndrome might reflect lesions in the gastrointestinal tract similar to those found in the mouth and on the skin. However, it should be noted that the classic histologic findings of ulcerative colitis would not be in accord with this viewlg: the inflammatory response is nonspecific and consists of neutrophils, lymphocytes, maerophages, and plasma cells. Eosinophils are not a feature. The classic histopathologic finding of sarcoidal granulomas in Crohn's disease is not seen in pyostomatitis vegetans. In summary, we have presented another case of pyostomatitis vegetans that supports its strong association with inflammatory bowel disease and

Journal of the American Academy of Dermatology demonstrates direct immunofluorescence findings reminiscent of, but not specific for, pemphigus vulgaris or vegetans. This case is particularly interesting because of the rapid onset of remission (within 24 hours) in response to moderate doses of oral corticosteroids. REFERENCES 1. Hallopeau H. "Pyodermite vegetante," ihre Beziehungen zur Dermatitis herpetiformis und dem Pemphigus vegetans. Arch Dermatol Syph 1898;43:289-306. 2. Wallhauser HJF. Dermatitis vegetans: report of two cases of the Hallopeau type. Arch Dermatol Syph 1929;19:7788. 3. Goldsmith WN. A case of pyodermite vegetante (Hallopeau). Br J Dermatol Syph 1941;53:299-318. 4. McCarthy FP. Pyostomatitis vegetans: report of three cases. Arch Dermatol Syph 1949;60:750-64. 5. Van Hale M, Rogers RS, Zone JJ, Greipp PR. Pyostomatitis vegetans: a reactive mucosal marker for inflammatory disease of the gut. Arch Dermatol 1985;121: 94-8. 6. Hansen LS, Silverman S, Daniels TE. The differential diagnosis of pyostomatitis vegetans and its relation to bowel disease. Oral Surg 1983;55:363-73. 7. McCarthy D, Shklar G. A syndrome of pyostomatitis vegetans and ulcerative colitis. Arch Dermatol 1963; 88:913-9. 8. Zegarelli EV, Kutscher AH. Oral "pyoderma": report of two cases. Am J Dig Dis (NS) 1962;7:281-8. 9. Forman L. Two cases of pyodermite vegetante (Hallopeau): an r pustular and vegetating dermatitis with conjunctival, oral, and colonic involvement. Proc R Soc Med 1965;58:244-9. 10. Ouimet G, Menard A, Trudeau J-G. Immunofluorecence dans la pyodermite vegetante de Hallopeau. Union Meal Can 1973;103:1699-701. I 1. Nelson CG, Apisarnthanarax P, Bean SF, Mullins JF. Pemphigus vegetans of Hallopeau: immunoIluorescent studies. Arch Dermatol 1977;113:942-5. 12. Nelson CG. Pemphigus vegetans of Hallopoau [Letter]. Arch Dermatol 1978;114:628. 13. Wray D. Pyostomatitis vegetans. Br Dent J 1984; 157:316-8. 14. Cataldo E, Covino MC, Tesone PE. Pyostomatitis vegetans. Oral Surg 1981;52:172-7. 15. Naish JM, Batchvarov BD, Lawoyin VL. A case of ulcerative colitisand pyostomatitisvegetans in an African. Gut 1970;11:38-40. 16. Margulis AR, Gold HI, Lawson TL, et al. The overlapping spectrum of ulcerative and granulomatous colitis: a roentgenographic-pathologic study. Am J Roentgenol 1971;113:325-34. 17. Brunsting LA, Underwood LJ. Pyoderma vegetans in association with chronic ulcerative colitis. Arch Dermatol Syph 1949;60:161-72. 18. Neville BW, Smith SE, Maize JC, Laden SA, Denton WJ. Pyostomatitisvegetans. Am J Dermatopathol 1985; 7:69-77. 19. Robbins SL, Cotran RS, Kumar V. Pathologic basis of disease. 3rd ed. Philadelphia: WB Saunders, 1984:839. 20. Hornstein O. Zur Kentnis der Pyo-(Rhino-) Stomati-

Volume 21

Pyostomatitis vegetans

Number 2, Part 2

August 1989 tis vegetans. Arch Klin Exp Dermatol 1957;205:35772. 21. Hays MA. Pyostomatitis vegetans: report of a case. Oral Surg 1961;14:1053-6.

22. Marks JM. Ulcerative colitis with pyodermite vegetante. Proc R Sor Med 1962;55:1072-3. 23. Leydecker W, Lund O-E. Augenbeteiligung bei Pyosto-

matitis vegetans. Klin Monatsbl Augenheilkd 1962; 141:595-602. 24. Rockl H. Uber die Pyodermite vegetante Hallopeau aks benig'ne form des Pemphigus vegetans yon Neumann

nebst einigen Bemerkungen zur Pyostomatitis vegetans von McCarthy. Arch Klin Exp Derrnatol 1964;218:57482.

Interferon-3, as adjuvant therapy for resistant warts T. Shiohara, MD, J. Hayakawa, MD, and M. Nagashima, MD Tokyo, Japan A patient who for 26 years had common warts, which were resistant to various treatment modalities, was treated with a single intralesional injection of interferon-7 after dinitrochlorobenzene immunotherapy, became immunologic studies indicated she had failed to respond to prior treatment modallties as a result of a functional impairment of her cellular immune response. Within 1 to 2 days, not only the wart injected with interferon--/, but also other warts, became erythematous and swollen, giving a lichen planus-like appearance. Without additional injections of interferon-% all warts disappeared completely, leaving slight pigmentation. Interferon-3, would be most effective when used with, rather than instead of, other immunotherapy. (J AM ACAD DEa-~A'rOt. 1989;21:387-91.)

Cell-mediated immune responses play a central role in the regression of warts. Patients with a functional impairment of cell-mediated immune responses have an increased frequency of viral skin diseases, and they often develop warts that are refractory to conventional treatment. Immunotherapy thus appears to be a rational approach to the treatment of the resistant warts. Indeed, immunotherapy with dinitrochlorobenzene (DNCB) for warts resistant to traditional therapies has proved to be of benefit, ~ but its putative mutagenicity 2 limits its usefulness. Because of its antiviral and antiproliferative properties, as well as its immunomodulatory activities, interferons have recently received increased attention as a treatment for resistant warts. 35 Intralesional injections of interferon-o~ have been shown to be effective4,5; largescale clinical trials of interferon-3, have thus far not been reported. W e report a case in which the warts, resistant to various standard treatments for 26 From the Department of Dermatology, Kyorin UniversitySchool of Medicine. Reprint requests: T. Shlohara, MD, Department of Dermatology, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo lgl, Japan.

years, completely resolved after D N C B application, followed by a single intralesional injection of interferon-%

CASE REPORT A 46-year-old woman sought treatment at the dermatology clinic of Kyorin University Hospital for verrucae vulgares, which had been present since the age of 20 years. For 26 years she had been treated with cryotherapy with liquid nitrogen, electrocautery, keratotytic agents, and DNCB immunotherapy, with no effect. For the previous 5 years, the warts had neither increased in number and size nor changed in shape. She had not received any antiwart treatment for 2 months before her first visit. Her past medical history was remarkable for a 4-year history of Graves' disease, which had been well controlled for 2 years. She was otherwise healthy, and there was no family history of a similar eruption. Physical examination revealed 19 verrucae on the dorsal aspects of both hands. No inflammatory signs were noted in any verrucae. Results of routine laboratory blood tests were all within normal limits, except for an elevated thymol turbidity test level. Immunologic studies revealed a normal serum immunoglobulin level, a slightly elevated percentage of CD8 T cells (suppressor/ cytotoxic) (38.7%) with a normal CD4/CD8 ratio (1.02), a normal percentage of B cells, and a markedly 387