499Indian J Dermatol Venereol Leprol | September-October | Vol 74 | Issue 5

in practically all raw materials.[3] Patients in our study had significant occupational exposure to chromates, thereby increasing the risk of contact sensitivity to chromates, which could explain the high number of positive patch test reactions to potassium dichromate noted by us.

Chandrashekar Laxmisha, Senthil Kumar, Amiya Kumar Nath, Devinder Mohan Thappa

Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry,

India

Address for correspondence: Dr. Devinder Mohan Thappa, Department of Dermatology and STD, JIPMER, Pondicherry - 605

006, India. E-mail: dmthappa@gmail.com

REFERENCES

1. Holden CA, Berth-Jones J. Eczema, lichenification, prurigo and erythroderma. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook’s Textbook of Dermatology, 7th ed. Oxford: Blackwell Science; 2004. p. 17.1-17.55.

2. Li LF, Wang J. Contact hypersensitivity in hand dermatitis. Contact Dermatitis 2002;47:206-9.

3. Rietschel RL, Fowler JF Jr. Hand dermatitis due to contactants: Special considerations. Fisher’s Contact Dermatitis. 5th ed. Philadelphia: Lippincott Williams and Wilkins; 2001. p. 261-78.

4. Rietschel RL, Fowler JF Jr. Practical aspects of patch testing. Fisher’s Contact Dermatitis. 5th ed. Philadelphia: Lippincott Williams and Wilkins; 2001. p. 9-26.

5. Kishore NB, Belliappa AD, Shetty NJ, Sukumar D, Ravi S. Hand eczema-clinical patterns and role of patch testing. Indian J Dermatol Venereol Leprol 2005;71:207-8.

6. Bajaj AK. Contact dermatitis hands. Indian J Dermatol Venereol Leprol 1983;49:195-9.

7. Skoet R, Olsen J, Mathiesen B, Iversen L, Johansen JD, Agner T. A survey of occupational hand eczema in Denmark. Contact Dermatitis 2004;51:159-66.

8. Suman M, Reddy BS. Pattern of contact sensitivity in Indian patients with hand eczema. J Dermatol 2003;30:649-54.

9. Templet JT, Hall S, Belsito DV. Etiology of hand dermatitis among patients referred for patch testing. Dermatitis 2004;15:25-32.

A study of erythroderma: Clues from eosinophilia and elevated lactate dehydrogenase levels

Sir,Erythroderma, first described by Hebra in 1868, is an inflammatory disorder characterized by erythema and scaling

involving more than 90% of the body surface. It results from worsening of existing skin disease (psoriasis, atopic dermatitis), or may be caused by drugs or underlying neoplasm; or of unknown cause, with an acute or insidious onset. The prognosis is frequently related to the cause, time of evolution, onset, associated diseases, and laboratory findings.[1]

We studied records of 66 patients with erythroderma, admitted to the Department of Dermatology, Hospital General de Mexico, between 1996 and 2007. Data collected from the records comprised age at onset, time for evolution, symptoms, associated disorders, existing skin disease, drug intake, aggravating factors, and laboratory parameters (hemoglobin, total leukocyte count, erythrocyte sedimentation rate (ESR), serum proteins, serum creatinine, serum electrolytes, serum lactate dehydrogenase (LDH), blood glucose, liver function tests, urine examination, and chest x-ray). Skin biopsies were performed in all cases; lymph node biopsy, CT scan, and determination of β2 microglobulin levels were undertaken when indicated.

All records selected fulfilled inclusion criteria. The mean age at onset was 44 years (range, 15-84 years). The sample consisted of 18 female and 44 male patients. In our study, erythroderma commonly showed a gradual onset, frequently related to gradual worsening of a preexisting dermatosis (time of evolution, 6.47 + 3.7 months). Itching and chills were the most common symptoms in 100% and 75% of the patients respectively. The most common causes of erythroderma were a) psoriasis (46%), b) carbamazepine which accounted for 69% of drug-related erythroderma and c) cutaneous T-cell lymphoma for underlying neoplasm.

The most important laboratory results were hypo-albuminemia (75%), eosinophilia (35%), and elevated ESR (30%). High levels of LDH were often related to an underlying neoplasm. We also performed a correlation analysis to check for a possible association of eosinophilia and high levels of LDH with paraneoplastic erythroderma (PE) and found that these parameters were frequently associated with this type of erythroderma (497.75 ± 264.64 vs. 99.55 ± 31.46 IU/L, P ≤ 0.05). There were statistically differences in the number of blood eosinophils between patients with and without PE (1.55 ± 0.826 vs. 0.829 ± 0.179 K/mm3, P ≤ 0.05).

In patients with erythroderma related to malignancy, LDH and eosinophils levels were higher than those found in patients with erythroderma secondary to

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Indian J Dermatol Venereol Leprol | September-October | Vol 74 | Issue 5500

other causes. Buechner[2] recognized that a high level of tissue eosinophils is a prognostic factor for death in erythroderma, because there is a greater probability of it being associated with malignancy, mainly T-cell lymphoma. Similar findings on high serum levels of LDH were arrived at by Vonderheid.[3]

A gradual onset is the most frequent pattern of evolution, probably because of the relation with a preexisting dermatosis. Clinical features of the syndrome were almost identical, despite of etiology, with similar data found in other studies.[4]

Nail disease was recorded in all patients, onychodystrophy and Beau´s lines being the most frequent manifestations, probably due to the large number of cases associated with psoriasis. Skin biopsy is a helpful tool, but it always needs to be performed at more than one site to achieve diagnostic accuracy, especially in patients with gradual onset of erythroderma.

Psoriasis was the most common underlying cause of erythroderma, in accordance with previous studies.[1,4]

In the follow-up, 6 patients died, mainly because of a malignant neoplasm, which suggests that erythroderma does not increase the risk of death; nevertheless, it is a significant cause of distress for patients. We recommend performing a complete medical history to identify the underlying cause so that this cutaneous disease can be treated.

Finally, we conclude that LDH is a useful tool when erythroderma is associated with neoplasms and may be considered as a prognostic factor for death, although in the majority of cases, it is associated with a favorable prognosis.

Torres-Camacho Paula, Tirado-Sánchez Andrés, Ponce-Olivera Rosa María

Service of Dermatology, Hospital General de México, o.D., Mexico

Address for correspondence: Dr. Andrés Tirado Sánchez, Servicio de Dermatología, Hospital General de México, Dr. Balmis 148, Col.

Doctores, Deleg, Cuauhtemoc, C.P. 06720, México, D.F. E-mail: andrestiradosanchez@hotmail.com

REFERENCES

1. Pal S, Haroon TS. Erythroderma: A clinico-ethiologic study of 90 cases. Int J Dermatol 1998;37:104-7.

2. Buechner SA, Winkelmann RK. Sézary syndrome: A clinicopathologic study of 39 cases. Arch Dermatol 1983;119:979-86.

3. Vonderheid EC, Pena J, Nowell P. Sézary cell counts in

erythrodermic cutaneous T-cell lymphoma: Implications for prognosis and staging. Leuk Lymph 2006;47:1841-56.

4. Hasan T, Jansen CT. Erythroderma: A follow up of 50 cases. J Am Acad Dermatol 1983;8:836-40.

Cell phone dermatitis

Sir,Metal cases of mobile phone are newer sources of the growing list of conditions where nickel may cause contact dermatitis.

A 32-year-old man, software professional by occupation, presented to us with history of unilateral itchy red rash on left cheek for 6 weeks, which worsened in hot weather and with excessive sweating [Figure 1]. There was no history of similar lesions/atopy/metal allergies in the past. He gave history of using his mobile predominantly on the left side and often for long periods of time. He

Letters to Editor

Figure 1: Preauricular dermatitis corresponding to the area of mobile use

Figure 2: Mobile usage habit