Wolf Isotopic Response Manifesting as Postherpetic Granuloma Annulare: A Case Series

2013 ◽  
Vol 137 (2) ◽  
pp. 255-258 ◽  
Author(s):  
Roger Kapoor ◽  
Adriano Piris ◽  
Arturo P. Saavedra ◽  
Lyn M. Duncan ◽  
Rosalynn M. Nazarian

Context.— Wolf isotopic response has infrequently been reported in the literature, mainly as isolated case reports. Objective.— To aid in recognition of the occurrence of postherpetic granuloma annulare for accurate histologic interpretation of granulomatous dermatitides. Design.— We report 5 cases of patients with Wolf isotopic response manifesting as granuloma annulare, developing in a site of previous herpes zoster, and discuss the clinicopathologic findings. Results.— Previous infection with herpes zoster or herpes simplex virus was found in 5 of 5 cases reported. The differential diagnosis of a dermal lymphohistiocytic infiltrate with multinucleated giant cells includes postherpetic granuloma annulare. Conclusions.— All cases of postherpetic Wolf isotopic response reported in this series revealed granuloma annulare, with a perineurovascular or perifollicular pattern of lymphohistiocytic infiltration including multinucleated giant cells, and occurred following herpes zoster or herpes simplex infection, although herpes viral infection was not always associated with a subsequent isotopic eruption. Awareness of this entity can aid in the clinicopathologic diagnosis of granuloma annulare occurring at the site of prior herpes viral infection.

2017 ◽  
Vol 9 ◽  
pp. 365-378 ◽  
Author(s):  
Tejabhiram Yadavalli ◽  
Alex Agelidis ◽  
Dinesh Jaishankar ◽  
Kyle Mangano ◽  
Neel Thakkar ◽  
...  

2021 ◽  
pp. 616-620
Author(s):  
Maryam Bilal Haider ◽  
Brinda Basida ◽  
Anusha Bapatla ◽  
Rana Ismail ◽  
Wasif Hafeez

Herpes simplex (HSV) esophagitis is usually identified in patients with significant immunosuppressive conditions such as AIDS. Short course of immunosuppressive therapy is an uncommon risk factor for this condition. We present a case of acute gastrointestinal bleeding secondary to HSV type 1-induced esophageal ulcers. A 63-year-old woman developed acute hypoxic hypercapnic respiratory failure. Past medical history was significant for COPD for which the patient was taking short-acting bronchodilator inhalers. The patient was intubated and started on mechanical ventilation. Intravenous Solu-Medrol 40 mg Q6 was started. Hospital course was complicated by sepsis of unknown source. Empiric broad-spectrum antibiotic therapy was started. On the 11th hospital day, the patient experienced multiple episodes of coffee ground emesis. There was abdominal tenderness on physical examination. Significant laboratory results were lipase 1,911 U/L and lymphopenia (ALC = 300/mm<sup>3</sup>). Endoscopy revealed severe erosive esophagitis and multiple punched-out ulcerations of the esophagus. Empiric treatment with valacyclovir 500 mg OD was started. The patient required PEG tube insertion for dysphagia. Complete resolution of esophagitis was noted then. Immunohistochemical staining for HSV was strongly positive in the cells with inclusions. Short course of intravenous corticosteroids is an uncommon cause of HSV-1 esophagitis. Corticosteroid-induced lymphopenia impedes underlying cellular immunity, which might explain the reactivation of latent herpes and esophageal ulcer formation. Given the rarity of the disease, evidence of treatment is available from case reports only. We found complete resolution of esophageal ulcers after the patient received valacyclovir therapy for 10 days.


2003 ◽  
Vol 127 (2) ◽  
pp. 231-234 ◽  
Author(s):  
Masayuki Shintaku ◽  
Yasushi Umehara ◽  
Keiko Iwaisako ◽  
Masao Tahara ◽  
Yasushi Adachi

Abstract Lesions of the pancreas induced by viral infection have drawn relatively little attention because of their low incidence, and the histopathologic features of viral pancreatitis have not been fully elucidated. We report the autopsy findings of 2 patients, a 59-year-old woman with allergic granulomatous angiitis and a 73-year-old man with invasive pulmonary aspergillosis who had a disseminated visceral herpes simplex virus (HSV) infection. In both cases, the liver was the organ most severely affected by the viral infection. The pancreas showed multiple small foci of hemorrhagic necrosis, which were not accompanied by fat necrosis of the surrounding adipose tissue. Histopathologically, Cowdry type A intranuclear inclusions and a ground-glass appearance of the nuclei were found in many degenerated acinar cells around the necrotic foci. The gross appearance and histopathologic features of HSV pancreatitis were characteristic and, in particular, distinct from those of the more common acute hemorrhagic pancreatitis. Immunohistochemistry using an anti-HSV antibody revealed immunoreactivity in the intranuclear inclusions and ground-glass nuclei, and polymerase chain reaction analysis disclosed that the causative virus in these 2 cases was HSV-1. Herpes simplex virus pancreatitis constitutes a rare, but distinct pathologic entity among a group of acute pancreatitis diseases with diverse etiopathogenesis.


2018 ◽  
Vol 4 (1) ◽  
pp. 38-40
Author(s):  
Sundeep Chowdhry ◽  
Prashansa Jaiswal ◽  
Tapan Kumar Dhali ◽  
Akhilesh Shukla

A 3 year old girl presented with a two- day history of multiple fluid filled lesions on buttocks and back of left thigh. As informed by the child's mother, she had fever 4 days back and was irritable with pain and discomfort on back of the left thigh. The pain was episodic and radiated from buttocks to the leg. On examination, multiple fluid filled lesions of various sizes with surrounding erythema were present involving the S1, S2, S3 dermatomes extending from buttock to the sole sparing few areas in between the vesicles. On further examination of whole body, there were multiple discrete fluid filled lesions on erythematous base ranging from 0.1 to 0.3 mm diameter in size on chest, abdomen and back. Multinucleated giant cells with acantholytic cells were found in Tzank smears. Diagnosis of concurrent varicella with herpes zoster was made.Journal of Universal College of Medical Sciences (2016) Vol.04 No.01 Issue 13, Page: 38-40


1986 ◽  
Vol 6 (8) ◽  
pp. 2977-2983 ◽  
Author(s):  
L Pilon ◽  
Y Langelier ◽  
A Royal

In a previous report, herpes simplex virus type 2 (HSV-2) was shown to increase the frequency of mutation at the hypoxanthine phosphoribosyltransferase (hprt) locus of nonpermissive rat XC cells (L. Pilon, A. Royal, and Y. Langelier, J. Gen. Virol. 66:259-265, 1985). A series of 17 independent mutants were isolated after viral infection together with 12 spontaneous noninfected mutants to characterize the nature of the mutations induced by the virus at the molecular level. The DNA of the mutants isolated after viral infection was probed with cloned HSV-2 fragments representing the entire genome. In these mutants, no authentic HSV-2 hybridization could be detected. This was indicative of a mechanism of mutagenesis which did not require the permanent integration of viral sequences in the host genome. The structure of the hprt gene was determined by the method of Southern (J. Mol. Biol. 98:503-517, 1975), and the level of hprt mRNA was analyzed by Northern blots. Except for the identification of one deletion mutant in each of the two groups, the HPRT- clones showed no evidence of alteration in their hprt gene. A total of 7 of 12 spontaneous mutants and 11 of 15 mutants isolated from the infected population transcribed an hprt mRNA of the same size and abundance as did the wild-type cells. Thus, the majority of the mutants seemed to have a point mutation in their hprt structural gene. Interestingly, the proportion of the different types of mutations was similar in the two groups of mutants. This analysis revealed that HSV-2 infection did not increase the frequency of rearrangements but rather that it probably induced a general increase of the level of mutations in the cells. This type of response is thought to be compatible with the biology of the virus, and the possible mechanisms by which HSV-2 induces somatic mutations in mammalian cells are discussed.


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