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Herpes Zoster Duplex Unilateralis as a manifestation of severe lymphopenia in COVID19
European Journal of Pain ( IF 3.5 ) Pub Date : 2020-12-07 , DOI: 10.1002/ejp.1709
Puneet Bhargava 1 , Heena Singdia 1 , Rachita Mathur 1 , Rohit Garg 1 , Neha Rani 1 , Shivi Nijhawan 1 , Deepika Kothari 1
Affiliation  

To the editor in chief,

SARS‐CoV2 (severe acute respiratory syndrome coronavirus‐2), a novel coronavirus was first reported in December of 2019 from Wuhan, China as an aetiological agent causing a new infectious respiratory disease (coronavirus disease 2019‐ COVID‐19). The main clinical manifestations of COVID‐19 are fever, cough, fatigue, dyspnoea and muscle aches.

Herpes zoster is characterized by several groups of painful vesicles on an erythematous base with a distribution in a unilateral dermatome involving the skin and/or mucosa. Herpes zoster is caused by varicella zoster virus which remains dormant in the sensory root ganglion contained by the immune system particularly CD lymphocytes (Wollina, 2017). This characteristic presentation is seen in an immunocompetent host. Severe forms of Herpes zoster not respecting the borders of a dermatome have been described. They are (a) Disseminated Herpes zoster that is, lesions extending over three contiguous dermatomes or lesions going outside the original dermatome. (b) Herpes zoster Duplex—here the lesions involve two non‐contiguous dermatomes. If the dermatome involved are unilateral then it is known as Herpes Zoster Duplex Unilateralis and if present bilaterally then—Herpes Zoster Duplex Bilateralis (Jung et al., 2000). The non‐contiguous variants are rare in both immunocompetent and immunocompromised host and represent a viraemic spread of VZV due to decrease in lymphocyte count and/or function. Classical Dermatomal Herpes Zoster has been described as a marker of subclinical COVID19 infection (Tartari et al., 2020). We are presenting a case of Herpes Zoster Duplex Unilateralis involving left ophthalmic division of trigeminal nerve (V1) and left Thoracic 10 (T10) dermatome in a patient of COVID19 with severe lymphopenia. A 62‐year‐old otherwise healthy male presented with highly painful vesicular lesions on an erythematous base involving the left ophthalmic division of trigeminal nerve (Day 6) and left thoracic 10 (T10) (Day 8) dermatome occurring 2 days apart. The vesicles ranged from 0.3 mm to 1 cm in size and had necrotic element at some places. Hutchinson sign was positive. A diagnosis of Herpes Zoster Duplex Unilateralis involving left ophthalmic division of trigeminal nerve and left Thoracic 10 (T10) dermatome was observed. The patient had fever (101–103°F) with malaise for preceding 5 days of appearance of vesicles. His COVID19 RT PCR test was positive (Day 8), however, evaluation for HIV status, diabetes, any immunosuppressive state and malignancy was negative. HRCT thorax showed multiple ground glass opacities in both the lungs with CT severity score being 18/30. His LDH levels were 229 units/L (normal range 135–225 U/L), D‐dimer 3,422.26 (0–500 ng/ml), IL‐6 levels 23 (normal range 0–7 pg/ml). Troponin‐T levels determined by Card test, serum ferritin levels and liver function tests were normal. Total leucocyte count was 7,100 cells/mm3 (4000–11000 cells/mm3 normal range). However differential eucocyte count showed neutrophilia (90%) and relative lymphopenia (2.2%), whereas the normal range is 20%–40%. The patient was treated according to institutional COVID19 protocol and was given piperacillin tazobactam 4.5 mg thrice a day injection, remdesivir 200 mg slow iv infusion and dexamethasone injection 4 mg once daily , low molecular weight heparin 6 mg twice a day subcutaneously for 5 days. For VZV lesions, oral acyclovir was given at a dose of 800mg five times a day for 10 days after which he recovered with mild post herpetic neuralgia. Herpes Zoster Duplex Unilateralis represents a viraemic spread of VZV, probably due to decreased immune protection. In our patient lymphocyte percentage was 2.2% representing a severe lymphopenia. We tried to look into the possible explanations: In COVID 19 patients, the inflammatory cytokine storm is likely a key factor behind the observed lymphopenia. The serum level of pro‐inflammatory cytokines, such as TNF‐α and IL‐6, have been closely correlated with lymphopenia, while recovered patients show close to normal levels of such cytokines (Mazzoni et al., 2020). Autopsy studies on lymphoid organs collected from several patients who succumbed to the disease revealed massive lymphocyte death, which was attributed to high levels of IL‐6 as well as Fas–FasL interactions. Our patient also had high IL 6 levels and clinical features suggestive of cytokine storm. COVID‐19 infection can result in exhaustion of T cells. A recent study has found both CD4+ and CD8+ T cells from COVID‐19 patients had increased cell surface expression of programmed cell death protein 1 (PD‐1) and T cell immunoglobulin and mucin domain 3 (Tim‐3), the two markers of T cell exhaustion (Diao et al., 2020). The SARS‐CoV‐2 can directly infect T cells. This infection can interfere with T cell expansion. A report suggests that some genes involved in T cell activation and function, such as MAP2K7 and SOS1 are downregulated in the T cells of severe COVID‐19 patients (Ouyang et al., 2020). All these mechanisms may be an explanation to the relative lymphopenia in our patient with an unusual presentation of Herpes Zoster.

更新日期:2021-01-16
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