LETTER TO THE EDITOR
Year : 2010 | Volume
: 21 | Issue : 6 | Page : 1155--1156
Disseminated "Shingles" in the nephrotic syndrome
Sunil Kumar, AP Jain
Dialysis Unit, Department of Medicine, MGIMS, Sewagram, India
Dialysis Unit, Department of Medicine, MGIMS, Sewagram
|How to cite this article:|
Kumar S, Jain A P. Disseminated "Shingles" in the nephrotic syndrome.Saudi J Kidney Dis Transpl 2010;21:1155-1156
|How to cite this URL:|
Kumar S, Jain A P. Disseminated "Shingles" in the nephrotic syndrome. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2021 Oct 18 ];21:1155-1156
Available from: https://www.sjkdt.org/text.asp?2010/21/6/1155/72316
To the editor,
Disseminated shingles is a rare entity which has been defined as more than 20 vesicles outside the area of the primary and adjacent dermatomes , and is seen especially in the immunosuppressed patient. It is caused by the varicella zoster virus (VZV) due to reactivation of the virus from dorsal root or cranial nerve ganglia. Human immunodeficiency virus infection, chronic infections, and treatment with corticosteroids are important causes of disseminated herpes zoster. We report one case of adult nephrotic syndrome on corticosteroids that developed shingles at multiple dermatomes.
A previously asymptomatic 39-year-old man presented with a 3-day history of severe pain and burning sensation over both thighs and buttocks followed a day later with development of vesicular eruptions. It was followed by the spread of vesicular eruption to involve the chest, back and abdominal wall over the next two days. The patient was a known case of the nephrotic syndrome and was on corticosteroids in a dose of 60 mg per day. The patient did not have a history of chickenpox during childhood or any recent exposure to it. There was no past history of diabetes, cardiac or pulmonary disease, or lymphoma. On examination, the patient was afebrile (37.4ºC). He had vesicles and pustules, with crusting and swelling, in the distribution of the bilateral L-1, 2, 3 dermatomes. Vesicles, pustules and scabs in various stages were also present over the trunk and extremities. The palms and soles were spared and there was no lymphadenopathy. Pulmonary, cardiovascular and abdominal examinations were normal. Complete blood count, peripheral smear, routine biochemistry, renal profile, and chest x-ray were normal. Liver function tests revealed hypoalbuminemia with serum protein of 2.5 mg/dL. Urine albumin was negative. Serology for Human Immunodeficiency Virus (HIV), Hepatitis B, and Hepatitis C were negative. The blood and vesicle cultures for VZV were negative. The patient was started on oral acyclovir, 800 mg every 8 hours. In the next 24 hours, the eruption of new vesicles ceased, the rash started to resolve and his clinical status improved. The patient was discharged on oral acyclovir 800 mg, five times daily for 14 days and is doing well on follow-up.
Shingles, also called Herpes Zoster, is due to reactivation of latent VZV from the dorsal root ganglia. It is characterized by unilateral vesicular eruptions within a dermatome. This complication of zoster has been described in immunocompromised persons (HIV, cancer, patients on corticosteroid treatment) and reported to be as common as 10 to 40%.  Our patient presented with characteristic skin findings of disseminated cutaneous herpes zoster. Dissemination occurred by second day of the eruption. In our patient, significant decrease in cellular immunity caused by treatment with steroids could have contributed to dissemination of herpes zoster. Patients with cutaneous dissemination of VZV are at risk of infection of visceral organs, particularly lungs, liver and brain. Other complications include corneal ulceration and post herpetic neuralgia. Therefore, early clinical diagnosis and aggressive treatment of disseminated herpes zoster infection in patients on steroids is important. The treatment of choice for disseminated zoster is intravenous acyclovir 10 mg/kg every 8 hours for 5-7 days, though our patient responded well to oral acyclovir.
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