Vasculitis related to viral and other microbial agents

Teng, Gim Gee; Chatham, W. Winn

doi:10.1016/j.berh.2015.05.007

Cited by 37 publications

(28 citation statements)

References 161 publications

(149 reference statements)

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“…Deposition of these complexes in small arteries and glomeruli may be responsible for clinical presentations of vasculitis and nephritis [8]. In the literature, a causal relationship has only been firmly established in a few instances of vasculitis, such as chronic HBV infection and polyarteritis nodosa [9]. …”

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus induced cytoplasmic antineutrophil cytoplasmic antibody-mediated vasculitis causing subarachnoid hemorrhage, acute transverse myelitis, and nephropathy: a case report

2017

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BackgroundTransverse myelitis, subarachnoid hemorrhage, and nephropathy are established but rare complications of hepatitis B virus infection that can potentially be triggered by an antibody-mediated vasculitis as a result of a viral infection. The following is a case report detailing a patient presenting with all three of the above presentations who is cytoplasmic antineutrophil cytoplasmic antibody-positive and a chronic carrier of hepatitis B.Case presentationA 33-year-old Nepalese man presented to our hospital with headache, swelling of his body, paraplegia, and back pain that developed over a period of 10 days. Laboratory studies showed proteinuria and elevated levels of serum urea and creatinine. Viral serology was suggestive of chronic inactive hepatitis B carrier state. A computed tomography scan of his head revealed features suggestive of subarachnoid hemorrhage. Magnetic resonance imaging of his dorsal spine showed diffuse T2 high signal intensity within his spinal cord extending from second to 12th thoracic vertebral level which was suggestive of transverse myelitis. The origin of these symptoms was attributed to immune complex-mediated vasculitis after serum analysis for cytoplasmic antineutrophil cytoplasmic antibody came out positive. He was managed with steroids administered orally and intravenously and entecavir administered orally.ConclusionThis case highlights the possibility of a hepatitis B virus-induced vasculitis as the cause of subarachnoid hemorrhage, transverse myelitis, and nephropathy.

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Section: Discussionmentioning

confidence: 99%

Hepatitis B virus induced cytoplasmic antineutrophil cytoplasmic antibody-mediated vasculitis causing subarachnoid hemorrhage, acute transverse myelitis, and nephropathy: a case report

2017

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“…For PAN induced by hepatitis B infection, there are some data suggesting a benefit with corticosteroids and plasma exchange for 1 to 2 weeks before initiating antiviral therapy. 149,150 Neuropathy from HIV-associated vasculitis tends to be acute, and once remission is obtained, does not often recur. 56 Treatment approach should include initiating antiretroviral drugs, corticosteroids, and plasma exchange.…”

Section: Virus-associated Vasculitic Neuropathiesmentioning

confidence: 99%

Vasculitic Neuropathies

2019

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Vasculitic neuropathies are disorders that result from inflammation in the peripheral nerves' vascular supply, resulting in ischemic injury. These disorders may be a result of systemic inflammation or may be confined to the peripheral nervous system. Causative etiologies include primary systemic vasculitis, vasculitis secondary to other conditions such as primary connective tissue disorders, infectious, paraneoplastic, and drug-induced conditions, and nonsystemic vasculitic neuropathy. Early recognition and treatment of these conditions is imperative to prevent substantial morbidity and mortality. The goal of this review is to provide an organization of the vasculitic neuropathies and an overview of principles of diagnosis and treatment for the clinical neurologist.

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“…Leucocytoclastic vasculitis may be caused by a range of viral, fungal, bacterial and parasitic diseases. While M.Tb and HIV may cause vascular pathology independently by several mechanisms, the presence of vasculitis in the context of TB and HIV co-infection is poorly reported [54][55][56][57][58][59][60][61][62]. The co-occurrence of TB and vasculitis was first reported in 1967 [55].…”

Section: Glands (Eg) (A) (Hematoxylin and Eosin) Dilated Lymphatic (mentioning

confidence: 99%

“…Infections may cause vasculitis by direct invasion of the wall of vessels of any size or by immune mechanisms, including immune complex disease and cryoglobulinemia [54,55,56]. Leucocytoclastic vasculitis may be caused by a range of viral, fungal, bacterial and parasitic diseases.…”

Section: Glands (Eg) (A) (Hematoxylin and Eosin) Dilated Lymphatic (mentioning

confidence: 99%

Vulval Tuberculosis: The Histomorphological Spectrum in Patients with HIV Co-Infection and AIDS

Gb¹,

Ramdial²,

Nargan³

et al. 2017

J AIDS Clin Res

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Objective: Vulval tuberculosis (TB) is reported rarely. The histomorphological spectrum and diagnostic mimicry thereof in patients with concomitant HIV infection/ AIDS is unreported to date. This study aimed to appraise the histopathologic spectrum of vulval TB in HIV co-infected patients and to identify histopathological diagnostic challenges, mimicry and pitfalls.Methods: Ten year retrospective study that reappraised the histomorphological features of vulval TB in HIV-infected patients. Results:The clinical descriptions of the biopsied lesions from 19 patients that form the study cohort encompassed nodules (9), ulcers (5), hypertrophy/edema (3) and abscesses (2). The main microscopic features included necrotizing and non-necrotizing granulomatous inflammation, ulceration with a zoned inflammatory response and chronic suppurative inflammation. The necrotizing component had the typical morphology of caseative necrosis or of suppuration/karyorrhexis or an admixture of both necrosis types. Vasculitis, of varied histomorphology, was present in 15 biopsies. Infective special stains were pivotal diagnostic tools. The presence of mycobacteria on Ziehl Neelsen stains (ZNs) and absence of nonmycobacterial infective agents on additional infective stains, underpinned TB diagnosis, especially in biopsies that lacked prototypical granulomatous inflammation or of infective mimickers that manifest with a granulomatous phenotype. ZNs also confirmed mycobacteria in vasculitic foci. The absence of mycobacteria on ZNs facilitated the diagnosis of tuberculids. Conclusion:Lesions with a common clinical appearance had heterogeneous histomorphological features, while lesions with common histopathological features demonstrated divergent clinical morphology. Infective, especially Ziehl Neelsen, stains are pivotal in the histopathological work-up of infective/inflammatory vulval biopsies. It is possible that the rarely reported anergic mononuclear or abscessing features, pseudotumoral spindle cell reactions, ulcers with a zoned inflammatory response and the presence of vasculitis of varied type, are clues to the HIV-TB tissue partnership. Increased clinicopathological investigation of and reporting on vulval TB in the HIV/AIDS afflicted population is pivotal to ascertain this.

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Vasculitis related to viral and other microbial agents

Cited by 37 publications

References 161 publications

Hepatitis B virus induced cytoplasmic antineutrophil cytoplasmic antibody-mediated vasculitis causing subarachnoid hemorrhage, acute transverse myelitis, and nephropathy: a case report

Hepatitis B virus induced cytoplasmic antineutrophil cytoplasmic antibody-mediated vasculitis causing subarachnoid hemorrhage, acute transverse myelitis, and nephropathy: a case report

Vasculitic Neuropathies

Vulval Tuberculosis: The Histomorphological Spectrum in Patients with HIV Co-Infection and AIDS

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