Adult onset immunoglobulin A vasculitis (Henoch-Schonlein purpura) with alveolar hemorrhage

Niknam, Negin; Ha, Lawrence; Gautam-Goyal, Pranisha

doi:10.1016/j.idcr.2018.03.006

Cited by 4 publications

(4 citation statements)

References 6 publications

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“…(8) Streptococcal-associated leukocytoclastic vasculitis is usually tied to group A streptococcus. (9,10) Lastly, the case highlights the importance of infectious etiologies in the differential diagnosis of vasculitis -especially in the setting of infectious risk factors. In our case, there was preceding immunosuppression and hypogammaglobulinemia stemming from the renal disease which predisposed to the disseminated infection.…”

Section: Discussionmentioning

confidence: 97%

Disseminated Group G Streptococcus mimicking systemic vasculitis with skin, lung, and eye manifestations: A Case Report.

Bartels

Pham

2022

Preprint

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Background: Group G streptococcal species can represent normal human flora as asymptomatic colonization. In the setting of infection, group G streptococcus can invade multiple structures and present broadly including bacteremia, toxic shock syndrome, endocarditis, septic arthritis, osteomyelitis, necrotizing skin infections, pharyngitis, and others. Severe cases tend to be more common in patients of increasing age or with chronic illnesses. Here we report a case of disseminated group G streptococcus mimicking systemic vasculitis. Case Presentation: A 41-year-old white male was hospitalized with a five-day history of fevers, chills, painful bilateral leg rash, generalized arthralgias, and right eye redness, pain and severe vision loss. Medical history was significant for minimal change disease treated with prednisone and cyclosporine. On admission, he was noted to be cushingoid with edematous erythema at the left hand, and bilateral lower limb rash. The right eye was inflamed with hypopyon. Laboratory studies demonstrated mild leukocytosis, modest thrombocytopenia, hyponatremia, hyperglycemia, with elevated CRP and creatinine. Urinalysis was positive for proteinuria, microscopic hematuria, and pyuria. CT chest demonstrated right upper lobe consolidation. There was concern for systemic vasculitis and cellulitis of the left hand. Intravenous methylprednisolone and empiric antibiotics were initiated. Ophthalmology was consulted for right uveitis and aspirated fluid from the anterior chamber. Dermatology biopsied the lower limb rash and identified leukocytoclastic vasculitis. Pulmonology performed bronchoscopy and bronchoalveolar lavage of the right upper lobe. Prior renal pathology was re-reviewed. Rheumatology was consulted due to suspicions for systemic vasculitis. Lancefield group G streptococcus was ultimately cultured from multiple blood samples, bronchoalveolar lavage fluid and right eye aspirate. There was no evidence of endocarditis on imaging. It was concluded that the source of the bacteremia and disseminated infection was most likely the left-hand cellulitis. Conclusions: To our knowledge, we present the first case of disseminated Group G streptococcal infection presenting with the constellation of bacteremia, endophthalmitis, focal mass-like lung consolidation, and leukocytoclastic vasculitis of lower extremities. The multi-organ distribution mimicked a systemic small vessel vasculitis. This case highlights the importance of infectious etiologies in the differential diagnosis of vasculitis – especially in the setting of infectious risk factors.

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Section: Discussionmentioning

confidence: 97%

Disseminated Group G Streptococcus mimicking systemic vasculitis with skin, lung, and eye manifestations: A Case Report.

Bartels

Pham

2022

Preprint

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“…Several documents have reported that the inflammatory response and OS are crucial contributors to HSP pathogenesis, 9,[54][55][56] in which the abnormal activation of TLR4 signal get closely involved. 8,19,57 When microorganisms (bacteria, viruses, etc.)…”

Section: Discussionmentioning

confidence: 99%

Protection of Proanthocyanidins Against HSP Serum-Induced Inflammation and Oxidative Stress on Human Umbilical Vein Endothelial Cells

Liu,

Wang,

Guo

et al. 2024

CCID

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Background Immune-mediated inflammation and oxidative stress play pivotal roles in Henoch-Schonlein purpura (HSP), primarily through the TLR4/MyD88/NF-κB pathway. Proanthocyanidins (PCs) exert anti-inflammatory and antioxidant effects by regulating some signals like TLR4/MyD88/NF-κB. Previous research uncovered that PCs could alleviate purpura-like lesions and pathological changes on rats likely through attenuating inflammation and OS damage. The mechanism of PCs on HSP deserves further investigation. Objective To clarify the potential mechanism of PCs to HUVECs induced by the serum of HSP patients. Methods HUVECs were randomly divided into blank, control, model, and low-, medium-, and high-concentration PCs group. Then, 25% HSP serum was assigned to the latter four groups, while 25% serum from healthy subjects to control group and serum-free culture medium to blank one. The last three groups separately received different concentrations of PCs. In addition, TAK-242, a TLR4 inhibitor, was applied to investigate the effect of TLR4-related signals in PCs against HSP serum-induced damage. Finally, inflammatory and OS-related parameters were detected by using cytological/molecular-biological techniques. Results Treated with HSP serum later, the levels of immuno-inflammatory and oxidative indicators obviously went up (P < 0.05), and those of antioxidants remarkably went down (P < 0.05). PCs, however, reversed above phenomena (P < 0.05). Moreover, TLR4, MyD88 and NF-κB proteins/genes highly expressed in the model group; but significantly fell off in the presence of PCs (P < 0.05). Amazingly, all of above indicators showed no significant difference among the groups of different PCs concentrations (P > 0.05). These alterations likewise occurred after TAK-242 pretreatment with or without PCs, ie a notable drop of TLR4, MyD88 and NF-κB appeared in TAK-242 presence, few differences existing when compared to the PCs groups. Conclusion PCs effectively protect HUVECs from inflammatory and OS damage provoked by HSP serum via blocking TLR4/MyD88/NF-κB signals.

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“…To the best of our knowledge, the pathogenesis of HSP has not been completely elucidated; however, immune imbalance and oxidative stress (OS) that induce IgA-mediated vascular damage may be involved ( 5 , 6 ). It is also hypothesized that toll-like receptor (TLR)4/myeloid differentiation primary response gene 88 (MyD88)/nuclear factor-κB (NF-κB) signaling is involved ( 7 ). Various treatments have been applied to HSP, including anti-inflammatory drugs, anti-histamine, vitamin C, calcium, corticosteroids, cytotoxic drugs and immunosuppressants, as well as blood-activating and stasis-resolving medicines ( 8-10 ).…”

Section: Introductionmentioning

confidence: 99%

Proanthocyanidins: A novel approach to Henoch‑Schonlein purpura through balancing immunity and arresting oxidative stress via TLR4/MyD88/NF‑κB signaling pathway (Review)

et al. 2023

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Henoch-Schonlein purpura (HSP), a recurrent and immunoglobulin (Ig)A-mediated vasculitis, presents not only as skin lesions but also as systemic involvement that can be life-threatening. Although the etiology of HSP remains unknown, immune imbalance and oxidative stress (OS) are primary contributors to its pathogenesis, alongside the abnormal activation of Toll-like receptor (TLR)/myeloid differentiation primary response gene 88 (MyD88)/nuclear factor-κB (NF-κB) pathway. TLRs, especially TLR4, stimulate downstream signaling molecules such as NF-κB and proinflammatory cytokines, which are released when TLRs combine with the key adapter molecule MyD88. This leads to the activation of T helper (Th) cell 2/Th17 and overproduction of reactive oxygen species (ROS). The function of regulatory T (Treg) cells is suppressed in the process. Th17/Treg imbalance then produces various inflammatory cytokines to promote proliferation and differentiation of B cells and the secretion of antibodies. IgA is secreted, and it binds to vascular endothelial surface receptors where the complex induces injury of the vascular endothelial cells. Additionally, excessive ROS creates OS that leads to an inflammatory response and vascular cell apoptosis or necrosis, thereby contributing to vascular endothelial damage and HSP occurrence. Proanthocyanidins are active compounds naturally enriched in fruits, vegetables and plants. Proanthocyanidins have diverse properties, including anti-inflammatory, antioxidant, antibacterial, immunoregulatory, anticarcinogenic and vascular protective effects. Proanthocyanidins are used in the management of various diseases. Proanthocyanidins regulate T cells, equilibrate immunity and arrest OS by inhibiting the TLR4/MyD88/NF-κB signaling pathway. Considering the pathogenesis of HSP and the properties of proanthocyanidins, the present study hypothesized that these compounds may potentially lead to HSP recovery through modulating the immune equilibrium and preventing OS by inhibiting the TLR4/MyD88/NF-κB pathway. To the best of our knowledge, however, little is known about the positive effects of proanthocyanidins against HSP. The present review summarizes the potential of proanthocyanidins to treat HSP.

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Adult onset immunoglobulin A vasculitis (Henoch-Schonlein purpura) with alveolar hemorrhage

Cited by 4 publications

References 6 publications

Disseminated Group G Streptococcus mimicking systemic vasculitis with skin, lung, and eye manifestations: A Case Report.

Disseminated Group G Streptococcus mimicking systemic vasculitis with skin, lung, and eye manifestations: A Case Report.

Protection of Proanthocyanidins Against HSP Serum-Induced Inflammation and Oxidative Stress on Human Umbilical Vein Endothelial Cells

Proanthocyanidins: A novel approach to Henoch‑Schonlein purpura through balancing immunity and arresting oxidative stress via TLR4/MyD88/NF‑κB signaling pathway (Review)

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