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Year : 1995  |  Volume : 61  |  Issue : 3  |  Page : 163-164

Eosinophilic cellulitis - A case study and management with griseofulvin

Correspondence Address:
P K Sharma

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Source of Support: None, Conflict of Interest: None

PMID: 20952936

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A 47 year old hypertensive and diabetic male patient suffering from eosinophilic cellulitis (Wells syndrome) is being reported. The patient responded very well to oral griseofulvin at the time of first presentation and subsequent three recurrences in a period of three years.

Keywords: Eosinophilic cellulitis, Wells syndrome, Griseofulvin

How to cite this article:
Sharma P K, Gautam R K, Sharma A K. Eosinophilic cellulitis - A case study and management with griseofulvin. Indian J Dermatol Venereol Leprol 1995;61:163-4

How to cite this URL:
Sharma P K, Gautam R K, Sharma A K. Eosinophilic cellulitis - A case study and management with griseofulvin. Indian J Dermatol Venereol Leprol [serial online] 1995 [cited 2020 Feb 25];61:163-4. Available from: http://www.ijdvl.com/text.asp?1995/61/3/163/4189

  Introduction Top

Eosinophilic cellulitis,[1] previously termed as granulomatous dermatitis with eosinophilia, was first described by Wells in 1971.[2] Since then many cases has been reported.[3],[4] The skin shows features of acute cellutitis in the form of localised oedema and redness which spreads rapidly with central involution with occasional appearance of blisters. This is followed by infiltrative granulomatous dermal and subcutaneous mass which remains oedematous and slate-coloured for several weeks and eventually the skin competely recovers.[4] Histopathology of skin shows diffuse tissue eosinophilia and fibrinoid flame figures. Although the patients may get cured spontaneously, there was an apparent temporary improvement in two cases of suspected dermatophyte infection with griseofulvin therapy.[1]

  Case Report Top

A 47-year-old overweight male patient having moderate hypertension and diabetes mellitus suddenly started having itching, stiffness, redness, burning senstation and thickening of skin over left side of back, shoulder and upper arm. This was followed by blister formation at a few places over involved areas within two days. Similar types of three episodes have occurred in last two and a half years with spontaneous regression occurring in about 4 months without leaving any signs of the disease. The patients had diabetes mellitus which was under control with glibenclamide and diet restriction.

The skin give an appearnce of acute irritant dermatitis. The lesions were deeply erythematous, oedematous, raised plaques having ill-defined regular borders over left back, shoulder and upper arm. Besides, the back lesions had superimposed tense bullae of 10 mm - 15 mm size filled with clear fluid. The lesions were indurated but non-tender. The bulla-spread and Nickolsky signs were negative. The other parts of skin, hair and nail were normal. No focus of dermatophyte infection was seen over them clinically. Blood pressure was 160/100 mm Hg.

Tzanck smear showed eosinophils and polymorphonuclear leucoctyes. The former were in abundance. KOH preparations and culture for fungi from inguinal folds and toe webs were negative. Haemologin was 15 mg/dl; total leucocyte count 10,900/mm3; polymorphs 54%, lymphocytes 33%, eosinophils 12%, and platelets 4,00,00/mm3. After 15 and 30 days of griseofulvin therapy the eosinophil count fell to 10% and 4% respectively while leucocyte count came down to 9900 and 7000/mm3 respectively.

IgG was 1500 mg/dl, IgA 255 mg/dl, IgM 50 mg/dl. LE cells, rheumatoid factor and antinuclear factors were not detected. C1Q, C2, C3 and C4 were within normal range. Immunoflourescence studies could not be conducted. The middle and lower dermis revealed a granuloma consisting of a core of dense eosinophilic collagen with surrounding histiocytes, giant cells in pallisade formation and a dense infiltration by eosinophils around it.

The treatment with griseofuluin was commenced in the dosage of 500 mg per day in two equal divided doses. There was a significant immediate, symptomatic improvement in pruritus and stiffness. The erythema, oedema and infiltration started subsiding simultaneously in the lesions in 10 days. All the bullae subsided in this period. The involved skin looked clinically normal and recovered after a month of commencement of treatment. The treatment was stopped after another 15 days.

The first recurrence after treatment was noticed after one year. The patient again responded similarly to the same treatment. In the last three years, two more similar attacks have occurred, but each time he responded well to the griseofulvin. No maintenance therapy was given.

  Discussion Top

The clinical and histopathological features in this case were similar to those described by earlier workers.[1][2][3][4] IgA being the secretory antibody, its raised levels (255 mg/dl) could be due to recurrent infections. The associated dermatophyte infection had been reported.[4] In this case, we could not corroborate this finding. The low IgM levels could be an isolated deficiency of IgM.

The resolution of the disease immediately after the intitiation of the treatment with griseofulvin was noteworthy with reduced duration of disease. The drug was equally effective each time during the recurrence of the disease. Grieofulvin has a leucopenic effect[5] on the blood leucocytes and this may cause an amelioration from the disease. This is indirectly indicated by gradual fall in the total leucocyte and eosinophil counts.

  References Top

1.Wells GC, Smith NP. Eosinophilic cellulitis. Br J Dermatol 1979;100:101-9.  Back to cited text no. 1  [PUBMED]  
2.Wells GC. Recurring granulomatous dermatitis with eosinophilia. Trans St Johns Hosp Dermatol Soc. 1971;57:46. Quoted in, Dermatology (Moschella SL, Hurely HJ, eds). 2nd edn. WB Saunders, 1985;489-90.  Back to cited text no. 2    
3.Wells GC, Smith N. Eosinophilic cellutitis persistent cutaneous swelling with phagocytosis of eosinophilic debris. abstracted. Br J Dermatol 1978;99(supplement):11-4.  Back to cited text no. 3    
4.Spigel GT, Winkelmann RK. Wells syndrome. Arch Dermatol 1979;115:611-3.  Back to cited text no. 4  [PUBMED]  
5.Sande MA, Mandell GL. Antimicrobial agents. In: Goodman and Gilman's The pharmacological basis of theraputics (Gilman AG, Goodman LS, et al, eds). 7th edn. New York: Macmillan 1995;1224.  Back to cited text no. 5    

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