Systemic Lupus Erythematosus

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GOod Morning!

 

Systemic Lupus Erythematosus

 

Systemic lupus erythematosus is a chronic, often life-long,

autoimmune disease that ranges from mild to severe and afflicts

mostly women. The primary characteristics of the disease are fatigue,

joint pain, and recurrent injuries in the vessels that course through

the body. Systemic lupus erythematosus (SLE) may affect widespread

sites, but it often manifests in the skin, joints, blood, and

kidneys. SLE was first described in 1828. Its name includes " lupus, "

from the Latin term for wolf, because the disease often produces a

rash that extends across the bridge of the nose and upper cheekbones

and was thought to resemble a wolf bite. The term erythematosus (from

the Greek word for red) refers to the color of the rash, and the term

systemic is used because the disease can affect organs and tissue

throughout the body.

 

Lupus is a chronic, often life-long, autoimmune disease that ranges

from

mild to severe and afflicts mostly women. The primary characteristics

of the disease are fatigue, joint pain, and recurrent injuries in the

vessels that course through the body. Systemic lupus erythematosus

(SLE) may affect widespread sites, but it often manifests in the

skin, joints, blood, and kidneys. SLE was first described in 1828.

Its name includes " lupus, " from the Latin term for wolf, because the

disease often produces a rash that extends across the bridge of the

nose and upper cheekbones and was thought to resemble a wolf bite.

The term erythematosus (from the Greek word for red) refers to the

color of the rash, and the term systemic is used because the disease

can affect organs and tissue throughout the body.

 

No treatment cures systemic lupus erythematosus, BUT many therapies

can suppress symptoms and relieve discomfort. Treatment of SLE varies

depending on the extent and severity of the disease. Milder

treatments are usually effective for symptoms such as fever,

arthritis, pleurisy, mild kidney involvement, inflammation of the

tissue surrounding the heart, headaches, and rash. More aggressive

treatment is needed if there is serious disease progression,

evidenced by the following: hemolytic anemia, low platelet count with

an accompanying rash (thrombocytopenic purpura), major involvement in

the lungs or heart, significant kidney damage, acute inflammation of

the small blood vessels in the extremities or gastrointestinal tract,

or severe central nervous system symptoms.

 

Consider this:

 

Patients have reported benefits from certain herbs, such as Essiac Tea

(used in tea and other preparations).

 

White Willow Bark is a good anti-inflamatory that works like aspirin

(it is an ingredient in aspirin) with out side effects to the stomach

or gastrointestinal tract.

 

Cultivating a healthy diet low in saturated fats and high in whole

grains and fresh vegetables and fruits is essential. Obtaining most

proteins from vegetables, particularly soy, and avoiding dairy and

meat products may help protect the kidneys. Patients should take

extra calcium and vitamin D, particularly if they are on

corticosteroids. Supplements of vitamins B12, B6, and folate may be

necessary, especially in people whose blood tests show high levels of

homocysteine. According to some studies, a diet rich in fruits and

vegetables can lower homocysteine levels.

 

Exercise is safe. Take it slow and at your own pace.

 

Certain Chinese herbal formulas and acupuncture have been very

effective in treating symptoms and regulating the immune system.

 

Studies on foods containing omega-3 fatty acids, including fish oil

and flax seed, have been showing benefits for SLE patients.

Researchers are also investigating compounds called indoles, also

known as mustard oil, which are found in broccoli, cabbage, Brussels

sprouts, cauliflower, kale, kohlrabi, collard and mustard greens,

rutabaga, turnips, and bok choy. Indoles stimulate enzymes that

convert estrogen to a more benign type. Eating vegetables certainly

will not cure SLE, but they offer many health benefits in general.

 

Patients should minimize their exposure to crowds or people with

contagious illnesses. Immunizations against influenza and

pneumococcal pneumonia are usually recommended, although flu shots

can cause flares. Careful dental hygiene is also important.

 

Simple preventative measures include avoiding overexposure to

ultraviolet rays and wearing protective clothing and sunblocks.

Allergy shots, which increase certain SLE antibodies, should be

avoided. In general, SLE patients should use only hypoallergenic

cosmetics or hair products.

 

Chronic stress has profound physical effects and influences the

progression of SLE. Patients should try to avoid undue emotional or

physical stress. Getting adequate rest of at least 8 hours and

possibly a nap during the day may be helpful. Maintaining social

relationships and healthy activities help prevent the depression and

anxiety associated with the disease.

 

Consider diffusing essential oils into the air such as Lavender,

Clary Sage or Chamomile when stressed. Yoga breath exercises, deep

breathing, makes a great difference in any stressful situation.

 

 

Andrew Pacholyk L.Ac, MSTOM

Peacefulmind.com

Alternative medicine and therapies

for healing mind, body & spirit!

[Guest guest]

Andrew Pacholyk L.Ac, MSTOM

Good evening to you,

 

Could you possibly give me more details on: acute inflammation ofthe small blood vessels in the extremities or gastrointestinal tract,or severe central nervous system symptoms. Also anything relating to the forehead and scull!! I am puzzled by my symptoms and have no answerer. Please help and advice.

 

Thank you sincerely

Magda

yogiguruji <yogiguruji wrote:

GOod Morning!Systemic Lupus ErythematosusSystemic lupus erythematosus is a chronic, often life-long,autoimmune disease that ranges from mild to severe and afflictsmostly women. The primary characteristics of the disease are fatigue,joint pain, and recurrent injuries in the vessels that course throughthe body. Systemic lupus erythematosus (SLE) may affect widespreadsites, but it often manifests in the skin, joints, blood, andkidneys. SLE was first described in 1828. Its name includes "lupus,"from the Latin term for wolf, because the disease often produces arash that extends across the bridge of the nose and upper cheekbonesand was thought to resemble a wolf bite. The term erythematosus (fromthe Greek word for red) refers to the color of the rash, and the termsystemic is used because the disease can affect organs and

tissuethroughout the body.Lupus is a chronic, often life-long, autoimmune disease that rangesfrommild to severe and afflicts mostly women. The primary characteristicsof the disease are fatigue, joint pain, and recurrent injuries in thevessels that course through the body. Systemic lupus erythematosus(SLE) may affect widespread sites, but it often manifests in theskin, joints, blood, and kidneys. SLE was first described in 1828.Its name includes "lupus," from the Latin term for wolf, because thedisease often produces a rash that extends across the bridge of thenose and upper cheekbones and was thought to resemble a wolf bite.The term erythematosus (from the Greek word for red) refers to thecolor of the rash, and the term systemic is used because the diseasecan affect organs and tissue throughout the body.No treatment cures systemic lupus erythematosus, BUT many therapiescan suppress symptoms and relieve

discomfort. Treatment of SLE variesdepending on the extent and severity of the disease. Mildertreatments are usually effective for symptoms such as fever,arthritis, pleurisy, mild kidney involvement, inflammation of thetissue surrounding the heart, headaches, and rash. More aggressivetreatment is needed if there is serious disease progression,evidenced by the following: hemolytic anemia, low platelet count withan accompanying rash (thrombocytopenic purpura), major involvement inthe lungs or heart, significant kidney damage, acute inflammation ofthe small blood vessels in the extremities or gastrointestinal tract,or severe central nervous system symptoms.Consider this:Patients have reported benefits from certain herbs, such as Essiac Tea(used in tea and other preparations).White Willow Bark is a good anti-inflamatory that works like aspirin(it is an ingredient in aspirin) with out side effects to the

stomachor gastrointestinal tract.Cultivating a healthy diet low in saturated fats and high in wholegrains and fresh vegetables and fruits is essential. Obtaining mostproteins from vegetables, particularly soy, and avoiding dairy andmeat products may help protect the kidneys. Patients should takeextra calcium and vitamin D, particularly if they are oncorticosteroids. Supplements of vitamins B12, B6, and folate may benecessary, especially in people whose blood tests show high levels ofhomocysteine. According to some studies, a diet rich in fruits andvegetables can lower homocysteine levels.Exercise is safe. Take it slow and at your own pace.Certain Chinese herbal formulas and acupuncture have been very effective in treating symptoms and regulating the immune system.Studies on foods containing omega-3 fatty acids, including fish oiland flax seed, have been showing benefits for SLE patients.Researchers are

also investigating compounds called indoles, alsoknown as mustard oil, which are found in broccoli, cabbage, Brusselssprouts, cauliflower, kale, kohlrabi, collard and mustard greens,rutabaga, turnips, and bok choy. Indoles stimulate enzymes thatconvert estrogen to a more benign type. Eating vegetables certainlywill not cure SLE, but they offer many health benefits in general.Patients should minimize their exposure to crowds or people withcontagious illnesses. Immunizations against influenza andpneumococcal pneumonia are usually recommended, although flu shotscan cause flares. Careful dental hygiene is also important.Simple preventative measures include avoiding overexposure toultraviolet rays and wearing protective clothing and sunblocks.Allergy shots, which increase certain SLE antibodies, should beavoided. In general, SLE patients should use only hypoallergeniccosmetics or hair products.Chronic stress has

profound physical effects and influences theprogression of SLE. Patients should try to avoid undue emotional orphysical stress. Getting adequate rest of at least 8 hours andpossibly a nap during the day may be helpful. Maintaining socialrelationships and healthy activities help prevent the depression andanxiety associated with the disease.Consider diffusing essential oils into the air such as Lavender,Clary Sage or Chamomile when stressed. Yoga breath exercises, deepbreathing, makes a great difference in any stressful situation.Andrew Pacholyk L.Ac, MSTOMPeacefulmind.comAlternative medicine and therapiesfor healing mind, body & spirit!********************************************* WWW.PEACEFULMIND.COM Sponsors Alternative Answers-HEALING NATURALLY- this is the premise of HOLISTIC HEALTH. Preventative and Curative measure to take for many ailments at:http://www.peacefulmind.com/ailments_frame.htm__________-To INVITE A FRIEND to our healing community, copy and paste this address in an email to them:http://www./members_add _________To ADD A LINK, RESOURCE, OR WEBSITE to Alternative Answers please Go to: http://www./links___________Community email addresses: Post message: Subscribe: - Un: - List

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Good Morning!

 

The Acute Inflammatory Reaction

 

In order to study the inflammatory reaction, it is customary to

divide into its various components. The sequence can be divided into

vascular and cellular events. Both of them mediated by chemical

factors (mediators). However, it must be remembered that the latter

is done for only academic purposes since these events occur together.

 

A. VASCULAR EVENTS

 

Immediately following an injury, there is frequently a transient

vasoconstriction of arterioles. This is mediated by nerves to the

smooth muscle within the arteriolar walls (i.e. it is a neurogenic

response). - This process is brief and usually lasts up to five

minutes.

The transient vasoconstriction is followed by the hemodynamically

more important vasodilatation of venules, capillaries, and

arterioles.

 

Opening of precapillary sphincters of arterioles.

Opening up of new capillary beds.

Opening of arterial venous shunts in capillary bed.

This results in increased blood flow to the injured area and thus, on

gross examination, the area appears red or hyperemic.

 

With very mild injuries, the vascular changes may not proceed any

further than this stage. With more severe injury, the vasodilation is

soon followed by slowing of the blood flow.

 

Vasodilatation is often accompanied by increased vascular

permeability. This refers to the outpouring of fluids and proteins

from the blood vessels. This affects firstly and predominantly

venules; however, capillaries and arterioles are also involved.

 

Local hemoconcentration - The viscosity of blood is increased as a

result of fluid loss from the vessel. This will lead to packing or

sludging of red blood cells, therefore slowing blood flow.

Occasionally, the blood flow is slowed to the point of stasis or

thrombosis (clotting). Thrombosis in vessels may also occur due to a

second mechanism in severe injuries in instances in which there is

direct damage to endothelial cells which, in turn, initiate the

formation of blood clots in the damaged areas.

 

The cellular elements in a blood vessel normally travel in a stream

in the centre of the vessel. As a result of loss of fluid because of

increased vascular permeability and of slowing of blood flow in the

vessel, the circulating cellular elements, including white blood

cells, become displaced to the periphery of vessels where they come

in to contact with the endothelial cells. This is referred to as

margination.

The process of the escape of plasma and plasma proteins along with

white blood cells from the vessel is known as exudation. This

inflammatory exudate accounts for an increase in the volume of

interstitial fluid (edema) and tissue swelling at the local site of

injury.

 

There are two events in the inflammatory response that are

responsible for the increased vascular permeability:

 

Rise in hydrostatic pressure within the microcirculation. Arteriolar

vasodilatation is followed by a rise in pressure within the

capillaries and venules. This results in the passive transport of a

large volume of fluid along with small molecules into the

interstitium.

Widening of the inter-endothelial cell junctions. These cells contain

myofibrils within the cytoplasm and these allow for contraction of

the cells. This is the mechanism by which large molecules may escape

resulting in a protein-rich exudate.

An inflammatory exudate is characterized by having:

A high specific gravity (greater than 1.020).

High protein levels - greater than 2-4 gms per dl.

Numerous cells and cell fragments.

In contrast, a transudate is due to rise in hydrostatic pressure,

reduced plasma proteins (oncotic pressure), lymphatic obstruction or

Na+ retention. It consists of fluid similar to water with a low

specific gravidity (<1.0120) with little to no protein nor cells (or

cell fragments). Transudates are NOT associated with inflammation but

with clinical situations such as: heart failure, venous obstruction,

malnutrition, among others (also see disturbances of blood flow and

body fluids section).

 

B. PERMEABILITY:

Starling's hypothesis: The normal fluid balance is maintained by two

opposing sets of forces:

 

Fluid moves out by:

osmotic pressure of interstitial fluid

intravascular hydrostatic pressure

Fluid moves in by:

osmotic pressure plasma proteins

tissue hydrostatic pressure

The balance of this movement is such that net movement under normal

conditions is quite small and is outward in direction. This excess

interstitial fluid drains into the lymphatics and no edema occurs.

Factors that increase intravascular hydrostatic pressure

(vasodilation) or decrease intravascular osmotic pressure (decreased

albumin) will give a net increase in interstitial fluid and edema

(transudate).

In inflammation, leaky endothelium (by permeability factors) cause

loss of high protein fluid (exudate) with reduction of intravascular

osmotic pressure and increased interstitial osmotic pressure causing

further impairment of return of fluid to blood vessels (venules)

producing marked inflammatory edema.

 

Normal fluid exchange depends on intact ENDOTHELIUM. Although

relatively simple, the endothelial cells are capable of secreting a

variety of substances such as prostaglandins (PGI2), coagulant factor

VIII, collagens and anticoagulant (plasminogen activator). PGI2 is a

potent vasodilator and anticoagulant

 

C. PATTERNS OF INCREASED VASCULAR PERMEABILITY:

We know of at least 5 mechanisms by which the endothelium becomes

leaky during inflammation:

 

 

Endothelial cell contraction leading to wide intercellular gaps. This

process is mediated by histamine and other chemical mediators. It is

reversible ,short lived (15–30') and occurs only in small venules

(20um to 60 um), not in capillaries or arterioles. It is not known

why venules are the only affected, however, they are known to have

more histamine receptors. This is called " immediate transient "

response.

 

Junctional retraction is cytokine mediated. It involves structural

reorganization of the cell's cytoskeleton and disruption of

endothelial cells junctions of venules. Occurs 4-6 hrs after injury

and lasts for 24 hrs or more. This has been demonstrated

experimentally using TNF & interleukin-1.

 

Direct endothelial injury with endothelial cell necrosis and

detachment. In more severe injuries such as burns, infections, cuts,

abrasions, etc. The endothelial detachment is secondary to platelet

adhesion and thrombosis. It begins immediately after the injury and

persists for hours or days. This reaction is known as " immediate

sustained " response.

 

Direct injury of endothelial cells may also induce a " delayed

prolonged leakage " that begins after a delay of 2-12 hours, lasts for

hours/days and involves capillaries and venules. The best examples

are sunburn and bacterial toxins.

 

" Leukocyte dependent endothelial injury " occurs during inflammation,

when activated inflammatory cells release toxic Oxygen species and

proteolytic enzymes causing endothelial cell detachment. This occurs

mostly in venules, pulmonary capillaries. It is usually late in the

inflammatory process.

 

" Increased transcytosis " occurs in the presence of vascular

endothelial growth factor and other mediators. They increase the

venular permeability via a vesiculovacuolar intracellular pathway.

 

Most clinically significant injuries are immediate-sustained.

 

D. CELLULAR EVENTS

" The most important feature of inflammation is the accumulation of

leukocytes in the affected tissue. "

 

Leukocytes will:

 

engulf, degrade bacteria, immune complexes and cell debris.

release lysosomal enzymes.

release chemical mediators.

release toxic radicals.

All these may help clear the inflammation but also may prolong the

inflammation and/or increase tissue injury.

Migration of Leukocytes = (Exudation)

Migration of leukocytes through vessel walls during inflammation into

adjacent tissues is the main cellular phase of acute inflammation.

Sequence of Events:

 

Margination:

when blood is viscous there is peripheral orientation of WBCs because

of sludging of RBCs (rouleaux). WBCs are pushed to periphery of

vessels because they are smaller particles (law of physics).

Pavementing & Rolling:

Normally up to 50% of PMNs are transiently marginating and sticking;

during inflammation, the % increases as well as the absolute numbers

of PMN.

 

Now it is recognized that rolling & adhesion in inflammation is the

result of interaction of adhesion molecules on leukocytes and

endothelial cell surfaces. These molecules (cell adhesion molecules =

CAM) are either expressed, induced or enhanced by chemical mediation.

CAMs are not only known to be important in inflammation, but also are

believed to be involved in the process of cell recognition and

adhesion that takes place during the organization of embryonic

tissues and organs in the cellular interactions of postnatal life.

CAMs can be subdivided into those that require Ca2+ for their

activity and those that are Ca2+ independent.

 

Although CAM-mediated cell-cell interactions are very important, we

must also remember the significance of cell-matrix interactions

particularly on cell migration, shape, etc. (see Repair).

 

In inflammation the rolling of inflammatory cells to the endothelium

is the initial step on their " way out " of the vessels. This occurs

due to alteration of expression and conformation of cell-surface

glycoproteins (CAM) in response to chemotactic agents. The group of

CAM involved in this process during inflammation are from

the " selectin family " .The adhesion molecules most important at this

stage (L-Selectin) are present on the phagocyte's surface

[inflammatory cell capable of phagocytosis such as PMNs, macrophages,

basophils, etc.]. When absent, (e.g. leukocyte adhesion deficiency, a

familial disease) there are serious infections with lack of

phagocytes at the infection site. In the endothelial cells, two main

subclasses of adhesion molecules have been described: P-Selectin and

endothelial cell-leukocyte adhesion molecules (ELAM-1 or E-Selectin).

Their number increases (upregulation) with cytokines. They interact

with the phagocyte adhesion molecules.

 

Adhesion & Emigration:

Adhesion and emigration of WBC's: The adhesion of inflammatory cells

is mediated by endothelial adhesion molecules of the immunoglobulin

superfamily, binding to integrins found on the leucocyte cell

surfaces. The endothelial adhesion molecules include ICAM-1

(intercellular adhesion molecule) and VCAM (Vascular cell adhesion

molecule). Both are up-regulated during inflammation by various

cytokines. Integrins are transmembrane glycoproteins that are also

receptors for extracellular matrix. The integrin receptors for ICAM-1

are LFA-1 (CD11a/CD18) and Mac1(CD11b/CD18), while VCAM-1 binds to

the integrin VLA-4. These integrins only adhere to their ligands when

the leucocytes are activated by inflammatory chemotactic factors.

After binding has occurred, the leucocyte moves between endothelial

cell gaps. This movement of leucocytes across the basement membrane

to the extravascular space is called diapedesis.

 

RBC migration is passive

PMNs are the first type of leukocyte to appear in the inflamed area.

This is partly due to the fact that they are faster and more

numerous. Thus, the cell type in the inflammatory response varies

with the age of the lesion and type of stimulus. In most acute

inflammations PMN predominate (early) to be later replaced by

monocytes or macrophages (days later). Exceptions: viral infections

(lymphocytes first).

This is also due to the fact that the PMN is short-lived, the

monocyte migration is sustained longer and chemotactic factors for

PMN and monocytes are activated at different periods.

 

Once in the tissues, these cells stimulate and control subsequent

inflammatory response, interact with the immune system.

 

Chemotaxis & Activation:

 

unidirectional migration of cells toward an attractant or locomotion

oriented along a chemical gradient.

chemokinesis: accelerated random locomotion of cells.

all WBCs respond to such stimuli, but PMN's and monocytes are most

reactive.

proven experimentally with the micropore filter technique of Boyden.

 

 

Chemotactic factors can be exogenous and endogenous.

 

Most Important:

Chemotactic Factors for PMN:

 

bacterial products (E. coli and staph. aureus best studied)

complement fractions (C5a)

arachidonic acid metabolites (leukotriene B4)

cytokines (chemokines)

 

E. PHAGOCYTOSIS

Involves three steps:

recognition and attachment.

engulfment.

killing and/or degradation.

1. Recognition and Attachment:

Most micro-organisms are not recognized until they are coated by

naturally occurring serum factors called opsonins. There are two well-

known opsonins: IgG and C3b. The opsonized particles attach to two

receptors in PMN or macrophages:

 

a receptor for Fc fragment of IgG (to react with IgG opsonin).

a receptor to C3b (to react with C3b opsonin).

2. Engulfment:

Pseudopods flow around organisms with complete enclosure followed by

fusion with lysosomal granules resulting in a phagolysosome. While

this takes place, leakage of enzymes and metabolic products (H2O2)

from the leukocyte into the medium occurs (regurgitation during

feeding); thus increasing the tissue damage.

 

This process of engulfment requires the presence of Ca2+ and Mg2+ and

is associated with Ca2+ transport across plasma membrane. The Ca2+

acts as a second messenger to initiate the cell events in the

microfilaments and microtubules, culminating with engulfment.

 

The biochemical events involved in phagocytosis are somewhat similar

to those of chemotaxis: it is associated with receptor-ligand

binding, phospholipase with activation, etc. and there is eventual

increase in Ca2+ in the cytosol.

 

 

3. Killing and/or Degradation:

Two types of bactericidal mechanisms:

 

Oxygen-dependent mechanisms:

With phagocytosis, there is a burst in oxygen use with increase of

glycogenolysis, increased glucose oxidase (hexose-monophosphate

shunt) and production of active oxygen metabolites

 

Oxygen-independent bactericidal mechanisms:

H+ ion from increased lactate and from action of carbonic anhydrase

produces marked reduction of intravacuolar pH, which is bactericidal.

Also due to action of substances from leukocyte granules.

 

Extracellular release of leukocyte products include:

 

Lysosomal enzymes.

Oxygen derived metabolites

Products of arachidonic acid metabolism (prostaglandins, leukotrienes)

This process takes place in 3 ways:

 

Regurgitation during feeding.

Reverse endocytosis (frustrated phagocytosis)

Cytotoxic release (following cell death).

 

 

Andrew Pacholyk, L.Ac. MSTOM

Peacefulmind.com

Therapies for healing

mind, body, spirit