Capillary leak syndrome: a cytokine and catecholamine storm?

Siddall, Eric

doi:10.1016/j.kint.2019.03.001

Cited by 8 publications

(4 citation statements)

References 5 publications

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“…There is an increasing evidence that certain catecholamines, such as epinephrine (adrenaline) and norepinephrine (noradrenaline), can be pro‐inflammatory, 99‐102 but dopamine much less so 103 . We have observed a high heart rate and significant hypertension for several hours after OHTx in some baboons, 32 and we suspect this is associated with endogenous catecholamine production, possibly associated with the inflammatory response, combined with epinephrine administered as an inotrope in the early post‐transplant period.…”

Section: What Steps Can Be Taken To Reduce the Inflammatory Response Or Its Effects After Pig Ohtx In Nhps?mentioning

confidence: 81%

A perspective on the potential detrimental role of inflammation in pig orthotopic heart xenotransplantation

Thompson

Jagdale

Walcott

et al. 2021

Xenotransplantation

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There is a critical shortage of deceased human donor organs for transplantation. The need is perhaps most acute in neonates and infants with life‐threatening congenital heart disease, in whom mechanical support devices are largely unsuccessful. If orthotopic (life‐supporting) heart transplantation (OHTx) were consistently successful in the genetically engineered pig‐to‐nonhuman primate (NHP) model, a clinical trial of bridging with a pig heart in such patients might be justified. However, the results of pig OHTx in NHPs have been mixed and largely poor. We hypothesise that a factor is the detrimental effects of the inflammatory response that is known to develop (a) during any surgical procedure that requires cardiopulmonary bypass, and (b) immediately after an NHP recipient is exposed to a pig xenograft. We suggest that the combination of these two inflammatory responses has a direct detrimental effect on pig heart graft function, but also, and possibly of more importance, on recipient baboon pulmonary function, which further impacts survival of the pig heart graft. In addition, the inflammatory response almost certainly adversely impacts the immune response to the graft. If our hypothesis is correct, the potential steps that could be taken to reduce the inflammatory response or its effects (with varying degrees of efficacy) include (a) white blood cell filtration, (b) complement depletion or inactivation, (c) immunosuppressive therapy, (d) high‐dose corticosteroid therapy, (e) cytokine/chemokine‐targeted therapy, (f) ultrafiltration or CytoSorb hemoperfusion, (g) reduction in the levels of endogenous catecholamines, (h) triiodothyronine therapy and (i) genetic engineering of the organ‐source pig. Prevention of the inflammatory response, or attenuation of its effects, by judicious anti‐inflammatory therapy may contribute not only to early survival of the recipient of a genetically engineered pig OHTx, but also to improved long‐term pig heart graft survival. This would open the possibility of initiating a clinical trial of genetically engineered pig OHTx as a bridge to allotransplantation.

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Section: What Steps Can Be Taken To Reduce the Inflammatory Response Or Its Effects After Pig Ohtx In Nhps?mentioning

confidence: 81%

A perspective on the potential detrimental role of inflammation in pig orthotopic heart xenotransplantation

Thompson

Jagdale

Walcott

et al. 2021

Xenotransplantation

View full text Add to dashboard Cite

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“…Monoclonal gammopathy is often but not always present in the idiopathic form of SCLS; the significance of paraproteinaemia is undetermined but unlikely to be the source of pathology. The underlying mechanism of SCLS has not yet been elucidated, but hypotheses suggest alteration of capillary permeability mediated by cytokines and soluble mediators such as interleukin-6, tumour necrosis factor-α, leucotrienes and vascular endothelial growth factor 7. Interestingly, investigations have also proposed that the pathophysiology of SCLS may potentially involve a combination of endothelial injury with subsequent cell contraction, alterations of endothelial cell junctions and endothelial apoptosis 8–10.…”

Section: Discussionmentioning

confidence: 99%

Systemic capillary leak syndrome secondary to decompression sickness

Mathavan

Jones

et al. 2023

BMJ Case Rep

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Systemic capillary leak syndrome is a rare derangement of endothelial function characterised by extravasation of plasma and proteins into the interstitial space. Primary capillary leak syndrome is a rare, episodic medical illness of unknown molecular pathology while secondary capillary leak syndrome may be precipitated by any number of inflammatory and infectious syndromes. Decompression sickness, a disorder of depressurisation, has been identified as a very rare trigger. We present a structured case report of systemic capillary leak syndrome secondary to decompression sickness following deep diving, informing physicians of this potential complication. No pharmacological therapy has substantial evidence in the treatment of acute systemic capillary leak syndrome. By review of current recommendations for acute management, we also emphasise an observed positive response to judicious fluid resuscitation and an oral cyclic AMP-elevating agent (ie, terbutaline).

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“…Rlddell speculated that catecholamine acts as a fuel for the activation and boosting of macrophages and neutrophils and the development of CS ( 86 ). Indeed, high catecholamine levels interact with pro-inflammatory cytokines in the progression of capillary leak syndrome and the development of MOF ( 87 ). These findings confirm the potential nexus between SS and CS in the development of MOF in patients with severe Covid-19 ( 88 ).…”

Section: Cross Talk Between Sympathetic and Cytokine Storms In Covid-19mentioning

confidence: 99%

Effects of β-Blockers on the Sympathetic and Cytokines Storms in Covid-19

et al. 2021

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a causative virus in the development of coronavirus disease 2019 (Covid-19) pandemic. Respiratory manifestations of SARS-CoV-2 infection such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) leads to hypoxia, oxidative stress, and sympatho-activation and in severe cases leads to sympathetic storm (SS). On the other hand, an exaggerated immune response to the SARS-CoV-2 invasion may lead to uncontrolled release of pro-inflammatory cytokine development of cytokine storm (CS). In Covid-19, there are interactive interactions between CS and SS in the development of multi-organ failure (MOF). Interestingly, cutting the bridge between CS and SS by anti-inflammatory and anti-adrenergic agents may mitigate complications that are induced by SARS-CoV-2 infection in severely affected Covid-19 patients. The potential mechanisms of SS in Covid-19 are through different pathways such as hypoxia, which activate the central sympathetic center through carotid bodies chemosensory input and induced pro-inflammatory cytokines, which cross the blood-brain barrier and activation of the sympathetic center. β2-receptors signaling pathway play a crucial role in the production of pro-inflammatory cytokines, macrophage activation, and B-cells for the production of antibodies with inflammation exacerbation. β-blockers have anti-inflammatory effects through reduction release of pro-inflammatory cytokines with inhibition of NF-κB. In conclusion, β-blockers interrupt this interaction through inhibition of several mediators of CS and SS with prevention development of neural-cytokine loop in SARS-CoV-2 infection. Evidence from this study triggers an idea for future prospective studies to confirm the potential role of β-blockers in the management of Covid-19.

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Capillary leak syndrome: a cytokine and catecholamine storm?

Cited by 8 publications

References 5 publications

A perspective on the potential detrimental role of inflammation in pig orthotopic heart xenotransplantation

A perspective on the potential detrimental role of inflammation in pig orthotopic heart xenotransplantation

Systemic capillary leak syndrome secondary to decompression sickness

Effects of β-Blockers on the Sympathetic and Cytokines Storms in Covid-19

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