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Orbital Inflammatory Syndromes
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Jaspreet Sukhija, Savleen Kaur
Herpes zoster ophthalmicus can be triggered by reactivation of varicella zoster virus that is dormant in the trigeminal nerve ganglia. Reactivation of varicella zoster virus can be triggered by aging, an immunocompromised host, trauma, surgery, iatrogenic immunosuppression, tuberculosis, syphilis, and radiation therapy. Majority of patients with herpes zoster ophthalmicus have ocular complications, including blepharitis, keratoconjunctivitis, iritis, scleritis, and acute retinal necrosis. Ophthalmoplegia was found in 3.5–10.1% of two large herpes zoster ophthalmicus series. Among the cases with extraocular nerve palsies, oculomotor nerve palsy is the most frequent and abducens nerve palsy is the second most frequent.22,23
Viral Infections
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Overview: Herpes zoster and chickenpox (varicella) are caused by the varicella-zoster virus (VZV). The primary infection is chickenpox (varicella) during infancy or childhood. Once the patient is infected, this DNA virus stays latent in the sensory dorsal root ganglion cells. Herpes zoster is caused by reactivation of VZV. The incidence of herpes zoster increases with age and immunosuppression, especially hematologic malignancy, and HIV infection, is another risk factor.
Acute erythematous rash on the trunk and limbs
Published in Richard Ashton, Barbara Leppard, Differential Diagnosis in Dermatology, 2021
Richard Ashton, Barbara Leppard
Herpes zoster occurs in people who have previously had chickenpox. The virus, Herpes varicella-zoster, lies dormant in the dorsal root ganglion following chicken pox, and later travels down the cutaneous nerves to infect the epidermal cells. Destruction of these cells results in the formation of intra-epidermal vesicles. For several days before the rash appears, there is pain or an abnormal sensation in the skin.
Safety of current systemic therapies for nail psoriasis
Published in Expert Opinion on Drug Safety, 2023
Jonathan K. Hwang, Shari R. Lipner
Prior to initiation of tofacitinib, patients should be screened for tuberculosis, hepatitis, and HIV, as well as vaccination with recombination zoster vaccine considered [82]. Laboratory studies, including CBC, CMP, and lipid panels should be obtained at baseline and at 4–8 weeks after initiation of therapy, followed by monitoring every 3 months thereafter [87]. There are no controlled studies in pregnant women, but birth defects were reported in animal studies [75]. Data for pediatric patients is limited, but open-label psoriasis studies, as well as trials for alopecia areata and juvenile idiopathic arthritis, have demonstrated safety profiles similar to that of adults, but long-term data is still lacking [92]. For older patients (>65 years), clinical trials have shown increased risk of herpes zoster and serious infections compared to younger patients (<45 years) [78].
Bilateral Pupillary Involvement as a Clinical Presentation of Herpes Zoster Ophthalmicus
Published in Ocular Immunology and Inflammation, 2023
Yan Ma, Yuhe Tian, Xia Chen, Rupesh Agrawal, Yun Feng
VZV infection is associated with two distinct clinical diseases. primary infection usually results in varicella (chickenpox). Then the virus becomes latent in neurons of cranial nerve ganglia, dorsal root ganglia and other nervous system. The trigeminal ganglion is the most frequent site of latency for VZV.9 Years or decades later, the virus may be reactivated, resulting in herpes zoster (also named shingles). Epidemiological studies showed that a median zoster incidence of 4–4.5 per 1000 person-years.10 Herpes zoster classically results in a neurocutaneous reaction causing burning pain and rash, which can spread various parts of the body. HZO accounts for 10%–20% of herpes zoster infection,11,12 mainly affecting the first division of the trigeminal nerve. Clinical features of HZO are various from cutaneous infection limited to the eyelids to corneal ulceration or retinal disease.13
Treating psoriasis in the elderly: biologics and small molecules
Published in Expert Opinion on Biological Therapy, 2022
Matteo Megna, Luca Potestio, Gabriella Fabbrocini, Elisa Camela
Tofacitinib is an oral JAK-inhibitor that acts by inhibiting JAK-1 and JAK- 2 isoforms. It is approved for the treatment of rheumatoid arthritis but its efficacy on psoriasis is under investigation in phase III trials [70]. In a Phase III trial, the administration of tofacitinib 10 mg BID in patients with moderate-to-severe plaque psoriasis showed to be non-inferior to etanercept 50 mg twice weekly and was superior to placebo [71]. The efficacy of Tofacitinib has also been studied in 2 phase III clinical trials, where patients were randomized to two different dosage, 10 mg vs 5 mg BID [64,72]. Of the 1859 enrolled patients, 117 aged ≥65 years [64,72]. In the tofacitinib 10 mg BID treatment group, an average of 73% of elderly patients achieved PASI 75, compared to 52% of elderly patients on tofacitinib 5 mg BID, and 5% of patients on placebo at week 16 [64,72]. Moreover, the efficacy was higher than in younger population: in fact, among the patients of the first group reaching PASI 75, only 60% were aged 45–72 and 57% <45 years [64,72]. Concerning safety, elderly patients had an increased risk of herpes zoster and serious infections compared to younger population [73].