It is NOT terminal.

There is no cure.

The tendency to develop the disease can be inherited.

It is an auto-Immune disorder.

The initial flare of this disease lasts anywhere from a few months to 11 months.

It can and does go into remission anywhere from weeks to years.

Symptoms include but are not limited to:

Arthritis (swelling of the joints).

Psoriatic Arthritis PA. (nail psoriasis, pitted and ridged nails).

IBD (Inflammatory Bowel Disease).

Iritis, Uveitis (inflammation of the Eyes). Vision problems with Iritis

or Conjunctivitis, blurred vision, sensitive to bright light.

Keratoderma Blennorrhagica (Skin Lesions).

This is a very simple/basic explanation. Most of the information here I've gotten from the RISG list server archives. As you'll be able to tell I'm no Medical Scientist. The reason for this FAQ is that when I know what is happening to me I can accept it much easier. I've created this to give members and visitors to the RISG web page a better idea of just what's happening to them.

Two of the most commonly used Medications.

Descriptions from RXMED

Eyes.

You didn't really catch the disease, The disease is your body's reaction to an antigen (germ). The actual disease is your body's immune system reacting to an antigen (germ) which quite probably isn't in your system anymore.

Antigen: Foreign substance introduced into the body. Toxins, bacteria, foreign blood cells.

How did I get the antigen? (trigger)

That's hard to say, most people don't ever find out how or when they received the antigen. The antigen is also referred to as the trigger for the purposes of discussing these diseases because they trigger the immune system to react albeit unnecessarily. That's also why Reiter's Syndrome is known as reactive arthritis because the inflammation you have is from your immune system REACTING to the antigen (trigger). Anyway, you could have gotten it in several ways.

The two most common ways are:

Chlamydia through sexual contact or Salmonella food poisoning.

Other Infectious agents most commonly involved in reactive arthritis:

BACTERIAL MICROORGANISMS

Enteric:

--Salmonella enteritidis, typhymurium, heidelberg, cholereses, saint paul, montevideo, agona.

--Yersinia enterocolitica

--Helicobacter jejuni (formerly Campylobacter)

--Clostridium difficile

Genitourinary:

--Chlamydia trachomatis

--Ureaplasma urealyticum

--Neisseria gonorrhea

Cutaneous:

--Propionibacterium acne

--Borrelia burgdorferi

Respiratory:

--Streptococcus pyogenes (hemolyticus), Group A

--Chlamydia pneumoniae

Other:

--Brucella sp.

--Neisseria meningitidis

--Mycobacterium tuberculosis

PARASITES

--Loa (filaria sp.)

--Giardia lamblia

--Entamoeba histolytica

--Blastocystis hominis

--Strongyloides stercolaris

--Taenia saginata

VIRUSES

--Hepatitis B, A, C

--Parvovirus B-19, RA-1

--Rubella

--Human immunodeficiency (HIV)

ARTHROVIRUSES

--Cytomegaloviruses

--Adenoviruses

--Human leukemia virus (HTLV-I)

What is this HLA-B27 I hear so much about?

Okay, going back to the basics. We all have a Mother and Father and we inherit one set of chromosomes from each. So this gives us each two copies of the HLA gene. We all have a region of genes responsible for creating proteins that recognize foreign material in our bodies. This region is called the "Major Histocompatibility Complex" (MHC). Within this region there are groups of genes whose codes for proteins are expressed on the on the surface of leukocytes (type of white blood cell). For this reason these proteins are called Human Leukocyte Antigen (HLA).

Gene: In a Chromosome are DNA, in DNA are genes. Among these genes are the HLA-B27 gene. (Human Leukocyte Antigen). A small section of the DNA strand that gets transcribed into mRNA messenger that get translated into amino acids sequence when correctly folded produces a protein.

Leukocytes. Also spelled leucocytes. Type of white blood cell.

Messenger Ribonucleic Acid abbreviation mRNA. RNA is similar to DNA as

it's also a chain and consists of nucleotides; unlike DNA the sugar is ribose and uracil as one of it's bases instead of thymine. Messenger Ribonucleic Acid copies the DNA's code for proteins and moves it to a specialized part of the cell. Here it assembles amino acids from the message brought by the mRNA.

Chromosome: made up of DNA and proteins.

Cell: The smallest structure of an organism that is capable of independent functioning.

HLA-B27 is a protein in a gene. The gene is also named HLA-B27 because scientists didn't want to have another name to remember. I guess you could say the gene inherited it. Medical science believes that it has a great deal to do with one’s ability to contract the disease or more accurately one’s body’s likelihood to react in a improper way to the trigger. If you are HLA-B27+ (you have the gene) your more likely to be acceptable to the trigger and develop the disease. There are many questions about this and it can get very complex so here we go.

Human Leukocyte Antigen (HLA) is one part off the equation of determining ones genetic vulnerability to the disease. Scientist have discovered that we have three kinds of HLA so they named the A,B, and C. HLA-B is the one we're interested in. Then they discovered (they just don't quit) there are several types. 27 is the one were interested in. This gives us HLA-B27. They now believe it may go even deeper in further subdivision of each variant. HLA-B27w01 often abbreviated B2701.

B gene HLA-B

27 type HLA-B27

01 subtype HLA-B27w01 or B2701

Each subtype has a different relative risk of developing the disease and to further complicate matters, one subtype in one racial group doesn't have the same effect as the same subtype in another racial group.

Up to 90% of the people with the disease are HLA-B27+ This doesn't mean if your HLA-B27+ you will get the disease. Not at all, in fact if your HLA-B27+ you still have a 97% chance you won’t.

This is how it breaks down.

Only 6% to 7% of the Caucasian population has the HLA-B27 gene, of those 97% never develop the disease. It's rare to find HLA-B27 in people of African descent.

So only 3% of the 7% do. It's very very rare. You can find out if your HLA-B27+ by a simple blood test but as you can see it's really not worth finding out with all the variants and even if you are HLA-B27+ you still have a 97% chance of not developing the disease.

I said it's part of the equation because HLA-B27 is only about 40% and that leaves 60% out there to yet be discovered. This 60% could be 100 genes each providing 0.6% each or it could be 1000 genes each providing 0.06%. It's just not known, but it's believed this 60% is what makes our immune systems prone to react to the triggers that make our immune systems tag itself as the antigen and in doing so create the symptoms that are the disease.

Okay, but now that I’m triggered and have the disease what's happening to me?

There are many theories as to what makes us go into and out of remission. Some say it's environmental and some say otherwise. But once we are no longer in remission this is how it works.

Our immune systems are made up of white blood cells. In these white blood cells is DNA.

DNA: Deoxyribonucleic Acid. The DNA molecule holds the genetic code or blueprints of the living thing it inhabits and passes this code onto the next generation. It resembles a twisted ladder and the side rails are made up of Phosphate and a sugar called deoxyribose. What would be the steps are made up of four bases that carry the genetic information called Thymine, Adenine. Guanine and Cytosine. The DNA is wrapped around proteins called Histones which keep them from getting tangled.

The white blood cells are of two principal types: granular, which have multilobed nuclei, and the nongranular, which have rounded nuclei. The granular leukocytes include neutrophils, which ingest and destroy bacteria, eosinophils, which secrete the anticoagulant heparin and the substance histamine, which stimulates inflammation.

Found in the blood stream. Proteins sticking out of the surface of the cell membrane bind to epitopes (3D shape of antigens). These proteins are HLA proteins and they tag the antigen for later recognition by our bodies. This recognition is made by looking for epitopes on the antigen that bind to the proteins on the surface of the leukocytes. Our immune systems make a vast array of these proteins (HLA) all recognizing different variations of antigens. Once attached to the epitope the body is able to determine whether the epitope is recognized or is a new foreign material. If not recognized our bodies produce more of that particular HLA to help with the immune response against the new threat.

Protein: is a long peptide chain folded up.