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Elephantiasis nostras of the lips
Elephantiasis nostras of the lips A case report Thomas E Sollecito, DMD, a Scott DeRossi, DMD, b Jeffery C. B. Stewart, DDS, MS, c Dominick Ettlin, MD, DMD, d and Christen Mowad, MD, e Philadelphia, Pennsylvania UNIVERSITYOF PENNSYLVANIASCHOOL OF DENTALMEDICINE Elephantiasis nostras (EN) is a clinical entity that usually presents as a persistent swelling of the lower extremities. [t has been related to recurrent lymphangitis of bacterial origin that causes a fibrosis and thickening of both epidermal and connective tissue. Although very rare, EN has been previously reported in the lips. This is the first case reported in the oral medicine literature that describes EN involving the lips. We describe the clinical features and a differential diagnosis of the lip lesions and a treatment protocol to which this patient has responded. A diagnosis of EN should be entertained in patients with chronically edematous, scaling lip lesions. (Oral Surg Oral Med Oral Pathol Endod 1997;84:297-300)
Elephantiasis nostras (EN) is a disorder of persistent lymphangitis caused by a bacterial infection that alters lymphatic channels and causes marked edema and fibrosis in the lower extremities. 1 Castellani 2,3 described this condition and differentiated it from elephatiaisis tropica, a clinical entity related to a filarial infection (Wuchereria bancrofti) that has a clinical appearance identical to that of EN. EN rarely affects the lips but has been associated with Streptococcus species of bacteria. 3 Only three cases have been reported in the recent literature and none in the oral medicine/oral pathology literature. 4-6 EN of the lips must be differentiated from other chronic lip lesions. Delay in diagnosis has the potential effect of allowing the lymphangitis to irreversibly alter proper lymphatic architecture and to result in permanent facial disfigurement. 5,6 The three published cases of EN of the face all had chronic lip lesions. In addition, treatment aimed solely at the inflammatory component, disregarding a presumed underlying infection, failed to resolve the patients lesions. 5 We present a case of a young woman with chronic lip lesions that were difficult to diagnose and treat. These lesions were extremely painful such that the patient reported a 15-pound weight loss within the month before her initial visit to the oral medicine service. We describe the course of treatment with resolution only after initiating antibiotic therapy.
aAssistant Professor Oral Medicine. bFellow Oral Medicine. CAssistant Professor Oral Pathology. dFellow Oral Medicine. eAssistant Professor Dermatology. Received for publication Jan. 29, 1997; revised March 23, 1997; accepted May 13, 1997. Copyright © Mosby-Year Book, Inc. 1079-2104/97/$5.00 + 0 7/13/83503
Fig. 1. Clinical photograph of patient's lips on presentation. Note severe edema and thick crusting.
CASE REPORT The patient was a 39-year-old white woman who was seen initially in the emergency department of the University of Pennsylvania Medical Center with significantly swollen crusted lips that were painfully burning. The patient reported her symptoms began as mild burning of the upper and lower lips after prolonged sun exposure 3 months previously. Her symptoms, over a 11/2-month period, progressed gradually to diffuse scaling and crusting with redness, swelling, and burning (Figs. 1 and 2). The patient also reported a cyclical nature of symptoms with periods of quiescence and exacerbation of 3- to 4-day intervals without any complete resolution of symptoms. She had been previously treated for a herpes simplex virus infection and a fungal infection by other clinicians without relief. She denied any significant past medical diseases including gastrointestinal, cardiac, liver, endocrine, or kidney disorders. In addition, she denied the use of any new cosmetic or oral hygiene products at the time her complications began. There was a vague history of a heart murmur that was ruled out with an echocardiogram. A review of her systems was significant for dryness and burning of the eyes, nose, and 297
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September 1997
Fig. 2. Clinical photograph of patient's lips at biopsy. Note crust has been removed. Severe inflammation can be seen.
Fig. 3. Photomicrograph of biopsy demonstrating hyperplasia and spongiosis of mucosal epithelium and submucosal chronic inflammation. (Hematoxylin-eosin stain; original magnification x62.)
throat. She denied gastrointestinal or pulmonary symptoms or other systemic problems. On physical examination there was striking edema, hard crusting, and scaling of the lips overlying a severely erythematous base, exquisitely tender to palpation. No conjunctival lesions or lesions on exposed skin surfaces were detected. No lymphadenopathy was found, and the oral mucosa was normal. Our differential diagnosis included chronic erythema multiforme caused by herpes reactivation, chronic trauma, vesiculobullous diseases, contact dermatitis, connective tissue diseases, and granulomatous diseases such as sarcoidosis, Crohn's disease, and cheilitis granulomatosa. Biopsy specimens were taken from the lower lip for both routine hematoxylin-eosin staining and direct immunofluorescent study. The biopsy specimen for routine microscopy showed a hyperplastic, stratified, squamous epithelium surfacing an inflamed and edematous submucosa (Fig. 3). Extracellular and intracellular edema of mucosal epithelium was associated with exocytosis of inflammatory cells, pri-
Fig. 4. Photomicrograph demonstrating spongiosis and lymphocyte exocytosis. (Hematoxylin-eosin stain; original magnification x125.)
marily lymphocytes (Fig. 4). Vacuolar degeneration of basal keratinocytes was evident with areas of early separation of epithelium from the underlying submucosal connective tissue. A prominent, superficial, submucosal, inflammatory infiltrate was composed largely of lymphocytes and plasma cells with scattered neutrophils and mast cells evident. Numerous ectatic vessels were associated with perivascular inflammation, although features of a vasculitis were not observed (Fig. 5). Special stains failed to disclose the presence of fnngal or bacterial organisms within tissue sections examined. Fresh tissue was submitted for direct immunofluorescence study. These sections were incubated with antibodies to human immunoglobulin G, immunoglobulin M, immunoglobulin A, and C3 and were interpreted as negative. In summary, the inicroscopic features were those of a nonspecific interface and perivascutar mucositis. Supplementary investigations included a diet/oral intake history over a 2-week period to evaluate the possibility of a contact allergen, an exhaustive laboratory evaluation to rule out connective tissue diseases, thyroid dysfunction, vitamin deficiencies, and contact allergy patch testing against common dental, cosmetic, and food materials. No abnormalities were detected with any of these investigations. Treatment was initiated immediately after biopsy was performed against a suspected erythema multiforme process caused by herpes simplex virus. The patient began a trial of 50 mg prednisone for 3 days that tapered to 0 over a 6-day period and 200 mg acyclovir five times daily for 2 weeks. Follow-up evaluation at that time showed only minimal reduction in edema, erythema, and crusting, but the patient did report some moderate reduction in burning. Subsequent trials of systemic prednisone, intralesional injections with 20 mg/cc triamcinolone, systemic acyclovir, topical corticoids, and topical antifungals brought about only insignificant decreases in the patient's signs and symptoms. The failure tO achieve even moderate success with the previously described protocol led to a reevaluation of the diagnosis. Subsequently, an exhaustive literature review of lip lesions disclosed descriptions of EN of the lips that were
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Volume 84, Number 3
Fig. 5. Photomicrograph demonstrating submucosal edema vascular ectasia and mixed inflammatory infiltrate. (Hematoxylin-eosin stain; original magnification x125.)
identical to the clinical findings in our patient. This provided a rationale for revising the working diagnosis. With a protocol described by Patterson (personal communication), the patient was administered a regimen of 500 mg dicloxacillin four times daily and 250 mg erythromycin four times daily for 2 weeks. Follow-up 1 week later showed significant (50%) reduction of scaling, edema, and erythema. The patient also reported a 50% reduction in burning of the lips. In addition to the existing regimen, topical use of clindamycin ointment and 10 to 20 mg systemic doxepin at bedtime to reduce the burning sensation was introciuced. Followup examination revealed significant reduction (95%) in the patient's signs and symptoms. The previously described regimen including the systemic antimicrobials was extended 4 more weeks until the patient was free of swelling and crusting, and only mild lip burning persisted. At that time all medications except systemic doxepin were stopped, and the patient again had significant scaling, edema, and erythema of the lips within 4 to 5 days. Subsequently, dicloxacillin and erythromycin were reinstituted at 250 mg twice daily until the swelling and crusting were completely eliminated (Fig. 6). The patient is now taking 250 mg dicloxacillin and 250 mg erythromycin every day, topical clindamycin ointment, and 20 mg doxepin at bedtime with persistent minimal burning sensation of the lips without crusting, swelling, or redness.
DISCUSSION Elephantiasis nostras is a rare disorder of persistent or recurring lymphangitis usually of the lower extremities caused by a bacterial infection) This form of elephantiasis is distinguishable from Elephantiasis tropica only by the inability to isolate Wuchereria bancrofti, a filarial infection that does not exist in a nontropical environment. 5 There have been three reported cases of EN occurring in the lips. 4-6 All of these cases were chronic in nature and debilitating to the patient. It is important to consider EN as a clinical entity in patients who have
Fig. 6. Clinical photograph of patient's lips after use of systemic antibiotics.
chronic edematous, erythematous, and scaling lips. EN will not resolve to singular steroid therapy in any preparation. Only after proper administration of appropriate antibiotic will resolution begin. Delay in diagnosis and treatment may result in continued ]ymphangitis, edema, and ultimately fibrosis of the lymphatic channels. Gross facial disfigurement may be a permanent sequela to this disease process. 5,6 Our case is similar to the three other reported cases of EN involving the lips. In all of those reported cases the chronicity of the lip lesions was apparent. 4-6 In addition, there seems to be a cyclical pattern with worsening signs and symptoms if left untreated. 5 Only after antibiotic administration do the pain, swelling, and scaling decrease. We tentatively diagnosed chronic erythema multiforme of the lips in our patient, because the histologic characteristics were consistent with this disorder. Treatment with an antiviral drug and a moderately high dose of systemic steroids did not resolve her problem. Elephantiasis nostras is thought to result from a localized bacterial infection, possibly Streptococcal in nature, which elicits a recurrent or chronic lymphocytic inflammatory infiltrate. 5 The inflammatory infiltrates may produce interface alterations and exhibit exocytosis. However, the principal pathogenic effects are thought to result from the perivascular and perilymphatic inflammation caused by the bacterial infection. Previous reports 5,6 have suggested that these changes produce marked edema that is caused by marked lymphedema and lymphatic obstruction of the affected tissues on clinical and microscopic evaluation. Isolation of bacteria, specifically Streptococcus, has been a variable finding. This variability may suggest a persistent bacterial toxin causing a strong inflammatory response. Another possibility is that the bacteria may be deeper in the connective tissue, eluding recognition by routine biopsy. Previous reports of patients with EN of
300 Sollecito et aL
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September 1997 the perioral tissues have described the histopathologic features. 4,5 As in our case, the findings have been relatively nonspecific. However, common features include the presence of mild to moderate inflammation composed largely of lymphocytes and dilatation of submucosal vessels, at least some of which appear to represent lymphatic vessels. One report 4 commented on the presence of submucosal edema, which was also a prominent feature in this case. Only after we initiated the antibiotic regimen did the patient respond. Although the antibiotic regimen chosen was empiric, it was based on a previously published protocol. After initial resolution the antibiotic regimen was discontinued. Within 4 weeks the patient reported recurring symptoms of pain, swelling, and scaling. At this return visit the patient was given antibiotic therapy alone (no systemic steroid therapy). Within days the patient reported significant response, and within weeks the lips were of normal size and appearance with only minor persistent burning. Thus we now treat the patient with low-dose tricyclic antidepressant therapy for a presumed neuropathic pain related to scarred terminal nerve branches resulting from fibrosis of the connective tissue. The patient has responded favorably to this regimen with only occasional minor burning. For lack of detailed literature about this condition, we plan to treat the patient with this regimen arbitrarily, similar to a patient with chronic acne. A differential diagnosis of a patient with chronically
swollen and scaling lips should include chronic erythema multiforme, cheilitis granulomatosa, cheilitis glandularis, contact allergy, chronic fungal infection, sarcoidosis, systemic lupus, and EN. In the appropriate clinical setting it is important to include EN as a diagnostic possibility, because early recognition and proper treatment will result in drastic, prompt, clinical resolution and may also prevent permanent facial disfigurement. REFERENCES 1. Sanders LJ, Slomsky JM, Burger-Caplan C. Elephantiasis nostras: an eight year observation of progressive nonfilarial elephantiasis of the lower extremity. Cutis 1988;42:406-11. 2. Castellani A. Elephantiasis nostras. J Trop Med Hyg 1934;37: 257-64. 3. Castellani A. Researches on Elephantiasis nostras and elephantiasis tropica with special regard to their initial stage of recurring lymphangitis. J Trop Med Hyg 1969;72:89-97. 4. Beninson J. Successful treatment of elephantiasis nostras of the lip. Angiology 1971;22:448-55. 5. Ditto AM, Patterson R. Elephantiasis nostras: a case report. J Allergy Clin Immunol 1996;97:129-31. 6. Hollander DI, Halwig JM, McKinney P, Patterson R. Elephantiasis nostras 1984. J Allergy Clin Immunol 1985;75: 450-1. Reprint requests: Thomas E Sollecito, DMD University of Pennsylvania School of Dental Medicine 4001 Sprace St. Philadelphia, PA 19104
AVAILABILITY OF JOURNAL BACK ISSUES
As a service to our subscribers, copies of back issues of Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics for the preceding 5 years are maintained and are available for purchase from the publisher, Mosby, at a cost of $10.00 per issue until inventor is depleted. The following quantity discounts are available: 25% off on quantities of 12 to 23, and one third off on quantities of 24 or more. Please write to Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, MO 63146-3318, or call (800)453-4351 or (314)453-4351 for information on availability of particular issues. If unavailable from the publisher, photocopies of complete issues are available from UMI, 300 N. Zeeb Rd., Ann Arbor, MI 48106 (313)761-4700.
Elephantiasis nostras (EN) is a disorder of persistent lymphangitis caused by a bacterial infection that alters lymphatic channels and causes marked edema and fibrosis in the lower extremities. 1 Castellani 2,3 described this condition and differentiated it from elephatiaisis tropica, a clinical entity related to a filarial infection (Wuchereria bancrofti) that has a clinical appearance identical to that of EN. EN rarely affects the lips but has been associated with Streptococcus species of bacteria. 3 Only three cases have been reported in the recent literature and none in the oral medicine/oral pathology literature. 4-6 EN of the lips must be differentiated from other chronic lip lesions. Delay in diagnosis has the potential effect of allowing the lymphangitis to irreversibly alter proper lymphatic architecture and to result in permanent facial disfigurement. 5,6 The three published cases of EN of the face all had chronic lip lesions. In addition, treatment aimed solely at the inflammatory component, disregarding a presumed underlying infection, failed to resolve the patients lesions. 5 We present a case of a young woman with chronic lip lesions that were difficult to diagnose and treat. These lesions were extremely painful such that the patient reported a 15-pound weight loss within the month before her initial visit to the oral medicine service. We describe the course of treatment with resolution only after initiating antibiotic therapy.
aAssistant Professor Oral Medicine. bFellow Oral Medicine. CAssistant Professor Oral Pathology. dFellow Oral Medicine. eAssistant Professor Dermatology. Received for publication Jan. 29, 1997; revised March 23, 1997; accepted May 13, 1997. Copyright © Mosby-Year Book, Inc. 1079-2104/97/$5.00 + 0 7/13/83503
Fig. 1. Clinical photograph of patient's lips on presentation. Note severe edema and thick crusting.
CASE REPORT The patient was a 39-year-old white woman who was seen initially in the emergency department of the University of Pennsylvania Medical Center with significantly swollen crusted lips that were painfully burning. The patient reported her symptoms began as mild burning of the upper and lower lips after prolonged sun exposure 3 months previously. Her symptoms, over a 11/2-month period, progressed gradually to diffuse scaling and crusting with redness, swelling, and burning (Figs. 1 and 2). The patient also reported a cyclical nature of symptoms with periods of quiescence and exacerbation of 3- to 4-day intervals without any complete resolution of symptoms. She had been previously treated for a herpes simplex virus infection and a fungal infection by other clinicians without relief. She denied any significant past medical diseases including gastrointestinal, cardiac, liver, endocrine, or kidney disorders. In addition, she denied the use of any new cosmetic or oral hygiene products at the time her complications began. There was a vague history of a heart murmur that was ruled out with an echocardiogram. A review of her systems was significant for dryness and burning of the eyes, nose, and 297
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September 1997
Fig. 2. Clinical photograph of patient's lips at biopsy. Note crust has been removed. Severe inflammation can be seen.
Fig. 3. Photomicrograph of biopsy demonstrating hyperplasia and spongiosis of mucosal epithelium and submucosal chronic inflammation. (Hematoxylin-eosin stain; original magnification x62.)
throat. She denied gastrointestinal or pulmonary symptoms or other systemic problems. On physical examination there was striking edema, hard crusting, and scaling of the lips overlying a severely erythematous base, exquisitely tender to palpation. No conjunctival lesions or lesions on exposed skin surfaces were detected. No lymphadenopathy was found, and the oral mucosa was normal. Our differential diagnosis included chronic erythema multiforme caused by herpes reactivation, chronic trauma, vesiculobullous diseases, contact dermatitis, connective tissue diseases, and granulomatous diseases such as sarcoidosis, Crohn's disease, and cheilitis granulomatosa. Biopsy specimens were taken from the lower lip for both routine hematoxylin-eosin staining and direct immunofluorescent study. The biopsy specimen for routine microscopy showed a hyperplastic, stratified, squamous epithelium surfacing an inflamed and edematous submucosa (Fig. 3). Extracellular and intracellular edema of mucosal epithelium was associated with exocytosis of inflammatory cells, pri-
Fig. 4. Photomicrograph demonstrating spongiosis and lymphocyte exocytosis. (Hematoxylin-eosin stain; original magnification x125.)
marily lymphocytes (Fig. 4). Vacuolar degeneration of basal keratinocytes was evident with areas of early separation of epithelium from the underlying submucosal connective tissue. A prominent, superficial, submucosal, inflammatory infiltrate was composed largely of lymphocytes and plasma cells with scattered neutrophils and mast cells evident. Numerous ectatic vessels were associated with perivascular inflammation, although features of a vasculitis were not observed (Fig. 5). Special stains failed to disclose the presence of fnngal or bacterial organisms within tissue sections examined. Fresh tissue was submitted for direct immunofluorescence study. These sections were incubated with antibodies to human immunoglobulin G, immunoglobulin M, immunoglobulin A, and C3 and were interpreted as negative. In summary, the inicroscopic features were those of a nonspecific interface and perivascutar mucositis. Supplementary investigations included a diet/oral intake history over a 2-week period to evaluate the possibility of a contact allergen, an exhaustive laboratory evaluation to rule out connective tissue diseases, thyroid dysfunction, vitamin deficiencies, and contact allergy patch testing against common dental, cosmetic, and food materials. No abnormalities were detected with any of these investigations. Treatment was initiated immediately after biopsy was performed against a suspected erythema multiforme process caused by herpes simplex virus. The patient began a trial of 50 mg prednisone for 3 days that tapered to 0 over a 6-day period and 200 mg acyclovir five times daily for 2 weeks. Follow-up evaluation at that time showed only minimal reduction in edema, erythema, and crusting, but the patient did report some moderate reduction in burning. Subsequent trials of systemic prednisone, intralesional injections with 20 mg/cc triamcinolone, systemic acyclovir, topical corticoids, and topical antifungals brought about only insignificant decreases in the patient's signs and symptoms. The failure tO achieve even moderate success with the previously described protocol led to a reevaluation of the diagnosis. Subsequently, an exhaustive literature review of lip lesions disclosed descriptions of EN of the lips that were
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY
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Volume 84, Number 3
Fig. 5. Photomicrograph demonstrating submucosal edema vascular ectasia and mixed inflammatory infiltrate. (Hematoxylin-eosin stain; original magnification x125.)
identical to the clinical findings in our patient. This provided a rationale for revising the working diagnosis. With a protocol described by Patterson (personal communication), the patient was administered a regimen of 500 mg dicloxacillin four times daily and 250 mg erythromycin four times daily for 2 weeks. Follow-up 1 week later showed significant (50%) reduction of scaling, edema, and erythema. The patient also reported a 50% reduction in burning of the lips. In addition to the existing regimen, topical use of clindamycin ointment and 10 to 20 mg systemic doxepin at bedtime to reduce the burning sensation was introciuced. Followup examination revealed significant reduction (95%) in the patient's signs and symptoms. The previously described regimen including the systemic antimicrobials was extended 4 more weeks until the patient was free of swelling and crusting, and only mild lip burning persisted. At that time all medications except systemic doxepin were stopped, and the patient again had significant scaling, edema, and erythema of the lips within 4 to 5 days. Subsequently, dicloxacillin and erythromycin were reinstituted at 250 mg twice daily until the swelling and crusting were completely eliminated (Fig. 6). The patient is now taking 250 mg dicloxacillin and 250 mg erythromycin every day, topical clindamycin ointment, and 20 mg doxepin at bedtime with persistent minimal burning sensation of the lips without crusting, swelling, or redness.
DISCUSSION Elephantiasis nostras is a rare disorder of persistent or recurring lymphangitis usually of the lower extremities caused by a bacterial infection) This form of elephantiasis is distinguishable from Elephantiasis tropica only by the inability to isolate Wuchereria bancrofti, a filarial infection that does not exist in a nontropical environment. 5 There have been three reported cases of EN occurring in the lips. 4-6 All of these cases were chronic in nature and debilitating to the patient. It is important to consider EN as a clinical entity in patients who have
Fig. 6. Clinical photograph of patient's lips after use of systemic antibiotics.
chronic edematous, erythematous, and scaling lips. EN will not resolve to singular steroid therapy in any preparation. Only after proper administration of appropriate antibiotic will resolution begin. Delay in diagnosis and treatment may result in continued ]ymphangitis, edema, and ultimately fibrosis of the lymphatic channels. Gross facial disfigurement may be a permanent sequela to this disease process. 5,6 Our case is similar to the three other reported cases of EN involving the lips. In all of those reported cases the chronicity of the lip lesions was apparent. 4-6 In addition, there seems to be a cyclical pattern with worsening signs and symptoms if left untreated. 5 Only after antibiotic administration do the pain, swelling, and scaling decrease. We tentatively diagnosed chronic erythema multiforme of the lips in our patient, because the histologic characteristics were consistent with this disorder. Treatment with an antiviral drug and a moderately high dose of systemic steroids did not resolve her problem. Elephantiasis nostras is thought to result from a localized bacterial infection, possibly Streptococcal in nature, which elicits a recurrent or chronic lymphocytic inflammatory infiltrate. 5 The inflammatory infiltrates may produce interface alterations and exhibit exocytosis. However, the principal pathogenic effects are thought to result from the perivascular and perilymphatic inflammation caused by the bacterial infection. Previous reports 5,6 have suggested that these changes produce marked edema that is caused by marked lymphedema and lymphatic obstruction of the affected tissues on clinical and microscopic evaluation. Isolation of bacteria, specifically Streptococcus, has been a variable finding. This variability may suggest a persistent bacterial toxin causing a strong inflammatory response. Another possibility is that the bacteria may be deeper in the connective tissue, eluding recognition by routine biopsy. Previous reports of patients with EN of
300 Sollecito et aL
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September 1997 the perioral tissues have described the histopathologic features. 4,5 As in our case, the findings have been relatively nonspecific. However, common features include the presence of mild to moderate inflammation composed largely of lymphocytes and dilatation of submucosal vessels, at least some of which appear to represent lymphatic vessels. One report 4 commented on the presence of submucosal edema, which was also a prominent feature in this case. Only after we initiated the antibiotic regimen did the patient respond. Although the antibiotic regimen chosen was empiric, it was based on a previously published protocol. After initial resolution the antibiotic regimen was discontinued. Within 4 weeks the patient reported recurring symptoms of pain, swelling, and scaling. At this return visit the patient was given antibiotic therapy alone (no systemic steroid therapy). Within days the patient reported significant response, and within weeks the lips were of normal size and appearance with only minor persistent burning. Thus we now treat the patient with low-dose tricyclic antidepressant therapy for a presumed neuropathic pain related to scarred terminal nerve branches resulting from fibrosis of the connective tissue. The patient has responded favorably to this regimen with only occasional minor burning. For lack of detailed literature about this condition, we plan to treat the patient with this regimen arbitrarily, similar to a patient with chronic acne. A differential diagnosis of a patient with chronically
swollen and scaling lips should include chronic erythema multiforme, cheilitis granulomatosa, cheilitis glandularis, contact allergy, chronic fungal infection, sarcoidosis, systemic lupus, and EN. In the appropriate clinical setting it is important to include EN as a diagnostic possibility, because early recognition and proper treatment will result in drastic, prompt, clinical resolution and may also prevent permanent facial disfigurement. REFERENCES 1. Sanders LJ, Slomsky JM, Burger-Caplan C. Elephantiasis nostras: an eight year observation of progressive nonfilarial elephantiasis of the lower extremity. Cutis 1988;42:406-11. 2. Castellani A. Elephantiasis nostras. J Trop Med Hyg 1934;37: 257-64. 3. Castellani A. Researches on Elephantiasis nostras and elephantiasis tropica with special regard to their initial stage of recurring lymphangitis. J Trop Med Hyg 1969;72:89-97. 4. Beninson J. Successful treatment of elephantiasis nostras of the lip. Angiology 1971;22:448-55. 5. Ditto AM, Patterson R. Elephantiasis nostras: a case report. J Allergy Clin Immunol 1996;97:129-31. 6. Hollander DI, Halwig JM, McKinney P, Patterson R. Elephantiasis nostras 1984. J Allergy Clin Immunol 1985;75: 450-1. Reprint requests: Thomas E Sollecito, DMD University of Pennsylvania School of Dental Medicine 4001 Sprace St. Philadelphia, PA 19104
AVAILABILITY OF JOURNAL BACK ISSUES
As a service to our subscribers, copies of back issues of Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics for the preceding 5 years are maintained and are available for purchase from the publisher, Mosby, at a cost of $10.00 per issue until inventor is depleted. The following quantity discounts are available: 25% off on quantities of 12 to 23, and one third off on quantities of 24 or more. Please write to Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, MO 63146-3318, or call (800)453-4351 or (314)453-4351 for information on availability of particular issues. If unavailable from the publisher, photocopies of complete issues are available from UMI, 300 N. Zeeb Rd., Ann Arbor, MI 48106 (313)761-4700.