Famotidine & Anti-histamines Protect Organs In (septic) Shock

This is a mouse study, but it seems revealing about the danger of high histamine in (overwhelming infectious) shock. There is a protective effect in blocking histamine action for lungs, liver and kidneys.

Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis
“Pharmacological interventions with H1- and H2-receptor antagonists indicated that both H1- and H2-receptors were involved in septic lung and liver injury, whereas only H2-receptors contributed to septic kidney injury.”

Both an H2 blocker (our friend famotidine) and an H1 blocker (Chlorphenamine, brand name Chlor-Trimeton) were each offered protection. Their combination offered more protection in reduction of some inflammatory substances.

This result raises questions about adding H1 & H2 blocking actions in extreme histamine states, for instance using cyproheptadine and famotidine together.

If this research branch looked at both histamine and serotonin in septic shock, it might be even more interesting. Chlorphenamine reportedly in an SNRI (serotonin–noradrenaline reuptake inhibitors) and so raises instead of lowering serotonin. That might help explain how chlorphenamine did not protect the kidneys. Cyproheptadine might be used to see if its organ-protective effect is better.

Perhaps reducing both excess histamine and serotonin in shock is even more helpful.

“…histamine is identified as a contributory mediator to promoting the development of organ injury in sepsis.”

“both d-chlorpheniramine and famotidine were effective in reducing septic lung and liver injury, whereas famotidine, but not d-chlorpheniramine, mitigated septic kidney injury. This suggests that, while both H1- and H2-receptors are involved in lung and liver injury, only H2-receptors contribute to kidney injury in sepsis.”

“Intriguingly, a significant risk for hospital-acquired pneumonia has been found for proton pump inhibitor (PPI) use but not H2-receptor antagonists in hospitalized patients…”