Overview of Fever

Fever is the temporary increase in the bodys

temperature in response to some disease or illness.

A child is said to have fever when the temperature is at
or above of these levels:
- 38oC rectal temperature
- 37,5oC oral temperature
- 37,2oC axillary temperature

An adult probably has a fever when the temperature is
above 37,2 37,5 oC, depending on the time of the day

Fever is an important part of the bodys defense
against infection. Most bacteria and viruses in people
thrive best at 98,6 oF. Many infants and children
develop high fevers with minor viral illnesses.

Fever is a signal that a battle is going on in the body,
but it is a fighting for the person, not against.
Demam
Fenomena fisiologis normal yang diatur oleh sistem
saraf pusat (SSP)
Disebabkan karena pelepasan mediator inflamasi
(pirogen), stimulan seringkali berupa bakteri, virus,
jamur ataupun parasit
Demam timbul sebagai respons terhadap
pembentukan sitokin tertentu yang disebut pirogen
endogen (penghasil panas)
Aktivitas pirogen endogen berhubungan dengan
beberapa sitokin pirogenik antara lain IL-1, tumor
necrosis factor (TNF), dan IL-6

Sitogen pirogenik dilepaskan oleh beberapa sel berbeda
termasuk monosit, makrofag, sel T helper dan fibroblas
dalam berespon terhadap infeksi atau cedera jaringan.
Faktor-faktor seperti granulocyte-macrophage colony-
stimulating factor, IL-2, dan lainnya dapat menyebabkan
demam secara tidak langsung dengan cara menstimulasi
produksi sitokin-sitokin tersebut.
Pirogen endogen menyebabkan demam dengan
menghasilkan prostaglandin (PGE) yang meningkatkan set
point termoregulasi hipotalamus
Apabila sumber pirogen dihilangkan maka kadar PGE akan
turun dan akan mengembalikan set point suhu ke normal.
Aspirin dan obat anti inflamasi nonsteroid lainya
menghambat demam dengan menghambat pembentukan
prostaglandin.



How circulating endogenous pyrogens produced in the peripheral
blood interact with thermoregulatory centers in the brain such as
the preoptic area?

Main Hypotheses
IL-1 that produced locally stimulated the activation of vagus
nerve in which the information transmitted to the CNS then
as the signal arrived, the prostaglandin formed and increase
the set point of hypothalamus thermoregulator

Humoral hypotheses of fever induction
Endogenous pyrogens may: 1) interact directly with parts of the brain where
the blood-brain barrier is incomplete, 2) bind directly to cytokine-specific
receptors on brain endothelial cells, 3)be actively transported across the
blood-brain barrier

There are structures in the CNS, termed
circumventricular organs, that are highly vascular
but lack a blood-brain barrier and whose cells are in
contact with the cerebroventricular system.

One circumventricular organ, the organum
vasculosum of the lamina basalis (OVLT), is
located close to preoptiv area and appears to play a
major role in fever development.

Studies performed suggest that the OVLT functions as
a sensor for endogenous pyrogens.

The result of interactions of endogenous pyrogens
with OVLT is an increase in local levels of
prostaglandin E2 (PGE2)

Local PGE2 production activates prostaglandin
receptors in the hypothalamus

Pyrogens may work by inhibiting warm-sensitive
neurons in the POA, thus limiting heat loss and
leading to an increase in the normal
thermoregulatory set point
Sitokin Pirogenik
Infeksi/Cedera
Jaringan
Pirogen Endogen
OVLT
Increase local
level of PGE2
Aktivasi Reseptor
Prostaglandin
Increase set point
of Hypothalamus
Demam