Immunoglobulin and complement‐mediated glomerular diseases with an MPGN pattern of injury: Unmasking the diagnosis of lupus in a patient with hepatitis A infection

Abstract

In cases with a broad differential or atypical features, it is important to continually review the original diagnosis. Diagnosing SLE can be challenging due to its multisystem presentations; a multidisciplinary approach is beneficial.

Local and systemic autoimmune manifestations linked to hepatitis A infection

“…The development of AIH may occur in genetically susceptible people exposed to a number of environmental triggering factors such as viruses, including the HAV, xenobiotics, and drugs (16). Interestingly the presence of the HLA DRB1*1301 allele has been associated with slow HAV clearance and autoantibodies expression among Brazilian and Argentinian children with hepatitis A; HLA DRB*1301 allele, an indicator for AIH, is related with persistent liver damage after HAV infection in both pediatric and arthritis, glomerulonephritis, neurological pathologies (mononeuritis multiplex, transverse myelitis, Guillain-Barré syndrome) as well as cryoglobulinemia and vasculitis (5)(6)(7)(8)(9)(10)(11)(12)(13).…”

“…Some data suggest that HAV infection could trigger antiphospholipid syndrome development and precipitation (10) and this syndrome, beyond AIH (38), is also linked with HCC manifestations (39,40). In addition, SLE, potentially triggering by HAV (11,41), apart from AIH (42), is also associated with an increased risk of tumors including HCC (43). However, the pathophysiological background of HAV-mediated tissue damage cannot be a direct and absolute risk factor for HCC, although it could play a theoretical role at least in some subpopulations possibly implying a potential contribution to HCC (44).…”

“…HAV-related cryoglobulinemia might also trigger the development of SLE (11,41) an autoimmune connective tissue disease, connected with AIH (42). Hepatitis A-related lupus-like syndrome development is characterized by symmetrical arthralgia in the wrists, metacarpophalangeal and proximal interphalangeal joints, left-sided pleurisy, Lupus cells, and antinuclear antibodies, antibodies against double-stranded deoxyribonucleic acid, and cardiolipin (41).…”