[PDF] Antipyretics: mechanisms of action and clinical use in fever suppression. | Semantic Scholar (2025)

It has been established that the same inflammatory agent can induce either fever or hypothermia, depending on several factors, and that different mechanisms underlie different febrile phases.

This review explains how a variety of ethanomedical plants are available in India which are used as antipyretic and how these plants are effective to cure fever has been study in various labs.

The first evidence that 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), an endogenous ligand for peroxisome proliferator-activated receptor γ (PPARγ), can attenuate the febrile response to lipopolysaccharide (LPS) in rats via an action on the brain is provided.

The various modalities available for antipyresis were examined and the perceived beneficial effects of antipyretics against the harmful side effects, including the evaluation of morbidity or mortality advantage conferred by antipyretics were envisaged.

The molecular mechanisms of NSAIDs on the body systems are summarized in this review, which reveals the reduced risk of several cancer types and neurodegenerative diseases by prolonged use ofNSAIDs.

While there is no question that life-threatening elevations in temperature require antipyretic treatment, there is much less consensus on how to approach common fevers and this essay will focus on the effects of temperature on host defense.

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Supporting a role for P‐450 in endogenous antipyresis and antiinflammation includes evidence that (1) inducers of P‐ 450 reduce fever, (2) inhibitors of P-450 cause a larger fever, and (3) and P­450 arachidonic acid metabolites reduce fever.

There are rigid criteria which ought to be satisfied before a substance can be definitely classified as a mediator of inflammation; these are listed below.

To investigate the problem directly is virtually impossible, because every method available to reduce fever has secondary metabolic consequences: antipyretics affect the body in many ways, and even physical methods — such as sponging with cold water — result in a wide range of responses, including shivering and stimulation of the adrenal–cortical axis.

Although clinicians have long suspected that bacteremia and other severe infections might induce fevers that are less responsive to antipyretic therapy than are those associated with self‐limited infections, this concept has not held up under scientific scrutiny.

It is established that PGE2 mediates fever generation in response to both exogenous and endogenous pyrogens by acting at the EP3 receptor.

The cytokines interleukin, IL‐6, and tumor necrosis factor induce increases in body temperature via direct and indirect actions on the brain and are believed to act as endogenous pyrogens, which probably act locally to stimulate the release of a secondary circulating mediator(s) that can interact with the brain.

It is speculated that patients who would not have survived severe sepsis in the past are now being kept alive and that the occasionally high fevers seen in these patients may be maladaptive.

NSAIDs inhibit early steps in neutrophil activation as reflected by their capacity to inhibit movements of Ca and to enhance intracellular levels of cyclic AMP.

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