urticarial vasculitis possibly induced by herbs

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Correspondence Maurico Goihman-Yahr, M.D., Editor Jet International M-154 PO Box 020010 Miami, FL 33102 Eruptive Melanocytic Nevi in Human Immunodeficiency Virus Infection To the Editor: Case Report A 31-year-old man was admitted to the hospital because he sutiered from chronic diarrhea. He was using intravenous drugs until 5 years before admission, and he had been well until 4 months before ad- mission when he developed weakness, weight loss, diarrhea, night sweats, and low grade fever. He had also realized the sudden appear- ance of multiple pigmented skin lesions during the last month. There was neither family nor personal history of dysplastic nevi. On physical examination he was found to have enlarged lymph nodes on laterocervical and axillary regions and multiple pigmented macular and papular lesions ranging from 2 to 10 mm over the trunk and extremities (Fig. 1). There were no other findings. Results of laboratory studies were remarkable for pancytopenia, and an enzyme-linked immunosorbent assay positive for HIV anti- bodies was subsequently confirmed by Western Blot method. The CD4 count was 400 and the CD4:CD8 ratio was 0.45. Stool examination disclosed cryptosporidium. A skin biopsy showed a compound nevus without melanocytic atypia. Therapy with Zidovudine and Spiramycin was started. The pa- tient became asymptomatic and his cutaneous lesions remained un- changed. After 9 months of follow-up he has not developed any other opportunistic infection and so far, no new nevi have appeared. Comment An important number of proliferative cutaneous disorders either neoplastic (seborrheic dermatitis, psoriasis) or neoplastic (Kaposi sarcoma, lymphoma, angiomatosis epitelioide, oral and rectal squa- mous cell carcinoma, basal carcinoma and malignant melanoma) have been associated with the human immunodeficiency virus in- fection.' Recently, the sudden appearance of multiple nevi with dys- plastic appearance has been reported.^'' Figure 1. Multiple melanocytic nevi over the back of an H1 V-infected patient. •, ,-,_.,, ... _•_•.• :.:-.-•.. We describe an HlV-seropositive patient who presented with eruptive nevi at the same time that an AIDS diagnosis was made. The occurrence of nevi either in healthy or in HIV-infected individuals is not uncommon; however, the sudden development of new nevi in a patient without personal or family history of pigmented lesions, as in this case, is unusual. Before Duvic et al.^ reported the appearance of eruptive dys- plastic nevi, there were no references about outbreaks of nevi related to HIV infection, just in a review of cutaneous lesions in the setting of AIDS where there is a case of dysplastic nevus syndrome.' The ap- pearance of dysplastic nevi in renal transplant recipients developing melanoma'' and the development of benign melanocytic nevi in children after radiotherapy or chemotherapy for malignancies' has been reported. Immunodeficiency inducing neoplasia is related to the T cell impaired function responsible for immunosurveillance. Regarding HJV-associated neoplasia it has been hypothesized that direct or indirect stimuli in growth factors result from viral replication. The melanocytic nevi proliferation has been related to the production of a growth factor by keratinocytes.' The sudden eruption of melanocytic nevi may be considered a new cutaneous picture associated with HIV infection. Isabel Betlloch, M.D. Concepcion Amador, M.D. Eusebi Chiner, M.D. Francisco Pasquau, M.D. Jose-Luis Calpe, M.D. >..; Antonio Vilar, M.D. Hospital La Vila Joiosa-Benidorm, Spain ' . - :; J References 1. Goodman DS, Teplitz ED, Wishner A, et al. Prevalence of cuta- neous diseases in patients with acquired immunodeficiency syn- drome (AIDS), or AlDS-related-complex. J Am Acad Dermatol. 1987; 17:210-220. 2. Duvic M, Lowe L, Rapini R, et al. Eruptive dysplastic nevi associated with human immunodeficiency virus infection. Arch Dermatol. 1989;!25:397-40). 3. Azon A, Vicente MA, Puig S, et al. Nevus eruptivos e infeccion por HIV. XIX Congreso Nacional de Dermatoiogia y Venereo- logia, Alicante 1990. 4. Greene MH, Young TI, Clark H. Malignant melanoma in renal transplant recipients. Lancet. 1981;1:1196-1199. 5. Hughes BR, Cunliffe WJ, Bailey CC. Excess benign melanocytic nevi after chemotherapy for malignancy in childhood. Br Med J, 1989;298:88-91. Urticarial Vasculitis Possibly Induced by Herbs To the Editor: There is a spectrum of clinical presentation of urticarial vasculitis (UV), which has been regarded as an immune complex disease,' April 1991, Vol. 30, No. 4 303

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Page 1: Urticarial Vasculitis Possibly Induced by Herbs

Correspondence

Maurico Goihman-Yahr, M.D., EditorJet International M-154PO Box 020010Miami, FL 33102

Eruptive Melanocytic Nevi in HumanImmunodeficiency Virus Infection

To the Editor:

Case Report

A 31-year-old man was admitted to the hospital because he sutieredfrom chronic diarrhea. He was using intravenous drugs until 5 yearsbefore admission, and he had been well until 4 months before ad-mission when he developed weakness, weight loss, diarrhea, nightsweats, and low grade fever. He had also realized the sudden appear-ance of multiple pigmented skin lesions during the last month. Therewas neither family nor personal history of dysplastic nevi.

On physical examination he was found to have enlarged lymphnodes on laterocervical and axillary regions and multiple pigmentedmacular and papular lesions ranging from 2 to 10 mm over the trunkand extremities (Fig. 1). There were no other findings.

Results of laboratory studies were remarkable for pancytopenia,and an enzyme-linked immunosorbent assay positive for HIV anti-bodies was subsequently confirmed by Western Blot method. TheCD4 count was 400 and the CD4:CD8 ratio was 0.45.

Stool examination disclosed cryptosporidium. A skin biopsyshowed a compound nevus without melanocytic atypia.

Therapy with Zidovudine and Spiramycin was started. The pa-tient became asymptomatic and his cutaneous lesions remained un-changed. After 9 months of follow-up he has not developed any otheropportunistic infection and so far, no new nevi have appeared.

CommentAn important number of proliferative cutaneous disorders eitherneoplastic (seborrheic dermatitis, psoriasis) or neoplastic (Kaposisarcoma, lymphoma, angiomatosis epitelioide, oral and rectal squa-mous cell carcinoma, basal carcinoma and malignant melanoma)have been associated with the human immunodeficiency virus in-fection.' Recently, the sudden appearance of multiple nevi with dys-plastic appearance has been reported.^''

Figure 1. Multiple melanocytic nevi over the back of an H1 V-infectedpatient. •, , - , _ . , , . . . _•_•.• :.:-.-•..

We describe an HlV-seropositive patient who presented witheruptive nevi at the same time that an AIDS diagnosis was made. Theoccurrence of nevi either in healthy or in HIV-infected individuals isnot uncommon; however, the sudden development of new nevi in apatient without personal or family history of pigmented lesions, as inthis case, is unusual.

Before Duvic et al.̂ reported the appearance of eruptive dys-plastic nevi, there were no references about outbreaks of nevi relatedto HIV infection, just in a review of cutaneous lesions in the setting ofAIDS where there is a case of dysplastic nevus syndrome.' The ap-pearance of dysplastic nevi in renal transplant recipients developingmelanoma'' and the development of benign melanocytic nevi inchildren after radiotherapy or chemotherapy for malignancies' hasbeen reported.

Immunodeficiency inducing neoplasia is related to the T cellimpaired function responsible for immunosurveillance. RegardingHJV-associated neoplasia it has been hypothesized that direct orindirect stimuli in growth factors result from viral replication. Themelanocytic nevi proliferation has been related to the production of agrowth factor by keratinocytes.'

The sudden eruption of melanocytic nevi may be considered anew cutaneous picture associated with HIV infection.

Isabel Betlloch, M.D.Concepcion Amador, M.D.Eusebi Chiner, M.D.Francisco Pasquau, M.D.Jose-Luis Calpe, M.D. >..;Antonio Vilar, M.D.Hospital La Vila Joiosa-Benidorm,Spain ' . - :; J

References

1. Goodman DS, Teplitz ED, Wishner A, et al. Prevalence of cuta-neous diseases in patients with acquired immunodeficiency syn-drome (AIDS), or AlDS-related-complex. J Am Acad Dermatol.1987; 17:210-220.

2. Duvic M, Lowe L, Rapini R, et al. Eruptive dysplastic neviassociated with human immunodeficiency virus infection. ArchDermatol. 1989;!25:397-40).

3. Azon A, Vicente MA, Puig S, et al. Nevus eruptivos e infeccionpor HIV. XIX Congreso Nacional de Dermatoiogia y Venereo-logia, Alicante 1990.

4. Greene MH, Young TI, Clark H. Malignant melanoma in renaltransplant recipients. Lancet. 1981;1:1196-1199.

5. Hughes BR, Cunliffe WJ, Bailey CC. Excess benign melanocyticnevi after chemotherapy for malignancy in childhood. Br Med J,1989;298:88-91.

Urticarial Vasculitis Possibly Induced by Herbs

To the Editor:

There is a spectrum of clinical presentation of urticarial vasculitis(UV), which has been regarded as an immune complex disease,'

April 1991, Vol. 30, No. 4 303

Page 2: Urticarial Vasculitis Possibly Induced by Herbs

304 International Journal of Dermatology • April 1991 Vol. 30

ranging from a benign cutaneous form to full-blown systemic dis-ease.̂ '̂ There are numerous potential antigens in the immune com-plex, such as those components from infectious agents, drugs, orother chemicals.'' Further, the antigen may be part of another sys-temic disease. The cause is not apparent in many cases. We hereindescribe a patient with localized recurrent UV that appeared to beinduced by the ingestion of herbs.

C a s e R e p o r t ':_'•• .: • - i : .: i;_

A 19-year-old woman was evaluated for recurrent episodes of urti-carial lesions on her calves persisting for longer than 24 hours. Theinitial eruption occurred 2 years before this evaluation, the seconderuption developed 1 year later in May 1989, and the third eruptionoccurred in May 1990. Each time there was some burning prurituson the affected areas with a mild arthralgia. The lesions subsidedwithin 2 weeks on the first two occasions with moderate doses ofcorticosteroids. The eruptions of urticarial lesions developed at thesame anatomic sites on each ofthe three episodes, and the symptomswere perceived to be of about the same degree. The patient deniedany previous trauma or minor injuries to the calf areas. The patienthad been in good health and had no history of allergic eruptions toany drugs. When asked about some possible causative factors forthese eruptions, the patient could only recall that she had taken herbs(the same kind of unknown ingredients), from a Chinese medicinedispensary as prescribed by a local herb doctor, for 5 days in May forthe past 3 years. She used this remedy, which acts as an energizer, tomaintain her good health. To the best of her memory, the first erup-tion had appeared 10 days after completion ofthe ingestions. Thesecond eruption had occurred on the fifth day of the ingestions. InMay 1990, she experienced the third eruption while taking the herbsfor only a few days. This remedy became the prime suspected caus-ative factor.

During the physical examination, the only pertinent findings wereconfined to the skin. Almost symmetrical lesions of annular or con-fluent urticarial eruptions were seen on the upper calves (Fig. 1).

An histologic examination ofthe urticarial erythema showed leu-kocytoclastic vasculitis (LCCV) (Fig. 2). The direct immunofluores-cent study ofthe same tissue showed a deposition of immunoglobu-lins G and M and C3 in the blood vessels ofthe upper dermis.

The erythrocyte sedimentation rate was elevated to 40 mm/h. Theresults ofthe complete blood cell count, urinalysis, and stool exami-nation were within normal limits. The pattern of serum proteinelectrophoresis, values representing liver, thyroid, and kidney func-tion, serum concentrations of immunoglobulins, and C3 and C4were all normal. The results ofthe tests for antinuclear antibodies.

r

Figure I. Annular, papular, or confluent urticarial eruptions on theupper calves.

Figure 2. The histologic picture consistent with leukocytoclastic va-sculitis (H&E, XlOO).

rheumatoid factor. Venereal Disease Research Laboratory (VDRL),and hepatitis B surface (HBs) antigen were negative. A test for serumcryoglobulin was weakly positive.

The above skin lesions of UV cleared in 1 week with dapsone (100mg/d). The patient was advised to avoid taking the herbs

DiscussionIn consideration of the clinical, laboratory, and biopsy findings,

this patient was recognized to have had episodes of a localized cuta-neous form of UV each time. With respect to the time course ofevents, the patient seemed to have had LCCV in the fashion of serumsickness,' which supposedly was precipitated by the intake of herbalantigens.

Chang Woo Lee, M.D. ;- ' '-•,'•'-•: Seon J o n g K i m , M . D . ,,!,;,,

Seoul, South Korea

References1. Mackel SE, Jordon RE. Leukocytoclastic vasculitis: A cutaneous

expression of immune complex disease. Arch Dermatol.1982; 118:296-301.

2. Gammon WR, Wheeler CE Jr. Urticarial vasculitis. Report of acase and review ofthe literature. Arch Dermatol. 1979;1 15:76-80.

3. Sanchez NP, Van Hale HM, Su WPD. Clinical and histopatho-logic spectrum of necrotizing vasculitis: Report of findings in101 cases. Arch Dermatol. I985;12I: 220-224.

4. Sam WM Jr. Hypersensitivity angiitis. J Invest Dermatol.1989;(Suppl)93:78-81.

5. Fauci AS, Haynes BF, Katz P. The spectrum of vasculitis: Clini-cal, pathologic, immunologic, and therapeutic considerations.Ann Intern Med. 1978;89:660-676.

Reichenstein Disease

To the Editor:

The review article, "A Dermatologic Gazetteer," by Drs. Andrew N.Lin and Suguru Imaeda' is an excellent and refreshing eiforl, as is thecommentary on it by Professor William D. Stewart ofthe Universityof British Columbia.^ To their list, I would like to add Reichensteindisease.

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