Gulf war diagnostics and treatments
and comparison to Nam toxic chemicals
Did you serve in the military between 1985 and 2005?
Have you received Anthrax or other experimental vaccines?
Do you exhibit or suffer from any of the following symptoms?
There are recommended diagnostic procedures and treatments available for the syndrome of symptoms, frequently called Gulf War Syndrome, Persian Gulf Illnesses, or Gulf War Illnesses.
Recommended Diagnostic Procedures for Gulf War Syndrome (GWS)
It is recommended
that one be seen, diagnosed and treated by an immunologist or rheumatologist
with extensive immunology training. If suffering from neurological problems, it
is recommended one be seen
by a neurologist, also with extensive immunology training.
Autoimmune-Neurological Diseases with Connective Tissue Disorders. Many are suffering Lupus-like and thyroid autoimmune diseases. Not all develop the disease processes or symptoms the same way or at the same rate. GWS, being autoimmune has an ebb and flow action, with some days being really bad and other days not quite so bad, in symptom severity.
(These can have different degrees of severity within a constellation) - Joint pain, muscle pain, rashes, photosensitive rashes, mouth sores, hair loss anywhere on the body, lymphadenopathy, increased allergic reactions, gastrointestinal problems, Raynaud's phenomenon, autoimmune thyroid disease, Reiter's syndrome, uveitis, autonomic nervous system neuropathies, autoimmune hepatitis, Sjogren's syndrome, intermittent low grade fevers, headaches, cerebellar atrophy, cerebral atrophy, memory loss, seizures, mood swings, autoimmune cardiomyopathy, peripheral neuropathies, reactive asthma, pulmonary fibrosis, polymyositis, MS, ALS and Lupus-like syndromes.
GWS-DIAGNOSTIC TESTING PROCEDURES & APPROPRIATE TREATMENTS:
There are diagnostic testing procedures and appropriate treatments available.
GWS-APPROPRIATE DIAGNOSTIC PROCEDURES:
There are appropriate diagnostic procedures, for those GW Era Vets and others with GWS illnesses and recommended treatments, depending on the severity of the illnesses, for controlling and reducing the
symptoms and associated suffering.
GWS-RECOMMENDED DIAGNOSTIC TESTING:
Of importance is that the following tests need be done at the same time, not in a 2 tiered approach. Some may be missed if part of the tests are performed at different times. Also, if inconclusive at the
time of initial testing, it may be necessary to have the tests performed again.
FANA - used to actually detect the antibodies in the cells, thus ANA testing is sometimes referred to as fluorescent antinuclear antibody test (FANA). ...
ESR - ESR (erythrocyte sedimentation rate) is a nonspecific screening test for various diseases. This 1-hour test measures the distance (in millimeters) that red blood cells settle in un-clotted blood toward the bottom of a specially marked test tube.
*Note significant higher levels of ESR was found in the Ranch Hand study in 1987.
Also known as:
Formal name: High-sensitivity C-reactive protein
Related tests: Lipid profile, Cardiac Risk Assessment.
Some experts say that the best way to predict risk is to combine a good marker for inflammation.
CPK isoenzymes are performed when the total CPK level is elevated. Isoenzyme testing can help differentiate the source of the damaged tissue.
CPK is an enzyme found predominantly in the heart, brain, and skeletal muscle. CPK is composed of 3 isoenzymes that differ slightly in structure:
CPK-1 (also called CPK-BB) is concentrated in the brain and lungs
CPK-2 (also called CPK-MB) is found mostly in the heart
CPK-3 (also called CPK-MM) is found mostly in skeletal muscle
Because the CPK-1 isoenzyme is predominately found in the brain and lungs, injury to either of these organs (for example, stroke or lung injury due to a pulmonary embolism) are associated with elevated levels of this isoenzyme.
CPK-2 levels rise 3 to 6 hours after a heart attack. If there is no further damage to the heart muscle, the level peaks at 12 to 24 hours and returns to normal 12 to 48 hours after tissue death. CPK-2 levels do not usually rise with chest pain caused by angina, pulmonary embolism (blood clot in the lung), or congestive heart failure.
The CPK-3 isoenzyme is normally responsible for almost all CPK enzyme activity in healthy people. When this particular isoenzyme is elevated, it usually indicates injury or stress to skeletal muscle.
Rheumatoid factor -The test for rheumatoid factor (RF) is used to help diagnose rheumatoid arthritis (RA). The test may also be used to help diagnose an arthritis-related condition called Sjögren’s syndrome. About 80% to 90% of patients with this syndrome have high amounts of RF in their blood.
C3 - This is a blood test that measures one component of the complement cascade. Complement is a group of blood proteins that cause immune responses and inflammation. The complement cascade is a series of reactions that take place in the blood. There are 9 major complement components, labeled C1 through C9. This test measures C3.
(CH50, CH100, terminal complement component, or individual complement
proteins) is measured to determine if complement is involved in the
development of a number of diseases. Complement activity is also measured to
monitor how severe a disease is or to determine if treatment is working. For
example, patients with active lupus erythematosus may have low levels of C3
and C4, and these component levels may be watched as an indicator of disease
C4 - C4 level is a test that measures the concentration of a component of the complement system in the blood.
Complement activity (CH50, CH100, terminal complement component, or individual complement proteins) is measured to determine if complement is involved in the development of a disease. Complement activity is also measured to monitor how severe a disease is, or if treatment is working.
laboratory test performed most often is the immunofluorescence test for
antinuclear antibodies (ANA). This is often simply called the ANA test. It has
almost entirely replaced the older LE cell test which is more time consuming
to perform and is less accurate. The ANA test is a very sensitive one. Over
ninety-five percent of untreated lupus patients have high ANA levels in their
blood. A small number of individuals have an unusual lupus disorder with a
negative ANA test, a rash and a high sensitivity to sunlight. For most people,
however, an ANA test with negative results in several repeated tests performed
in a good laboratory is strong evidence against the diagnosis of systemic
The ANA test is not specific for lupus. This means that people with other diseases can also have a high ANA. Elevated blood ANA levels are found in a number of other disorders including some with symptoms similar to lupus.
Sometimes this leads to confusion and a diagnosis of lupus is made in someone with another disorder just because the ANA test is abnormal. Much research has been done to expand and refine the ANA test in order to help find a test more specific for lupus. Although the ANA levels in the blood are generally higher in untreated lupus patients than in patients with other diseases, this is not always so. A diagnosis of lupus, therefore, cannot be made only on the basis of a high ANA. It is helpful to know in diagnosing lupus that the ANA is actually a group of antibodies directed against different parts of cells within our bodies. in laboratories with special equipment, these antibodies can now be detected individually. Some of these individual antibodies are very specific for the diagnosis of lupus. Some of these are listed below:
Anti-ds (double-stranded) DNA antibodies. These are substances which react to the material which makes up the genes found in cells. Double stranded DNA also plays a key role in the growth and multiplication of these cells. increased blood levels of antidsDNA antibodies are found in about 70% of lupus patients, and found very infrequently in other disorders. However, the dsDNA used in the test must be prepared very carefully so that it does not contain single stranded DNA. Antibodies against this single stranded DNA are commonly found in disorders other than lupus, and can confuse the results of the test. Anti-dsDNA antibodies are more commonly found in lupus patients whose disease is active, particularly when the disease involves the kidneys or the central nervous system.
Anti-Sm (Smith) antibodies. These antibodies are named after the patient, a person named Smith, in whom they were first found. They react with another part of the cell nucleus, the central part of the cell, and are found in about 30% of lupus patients. Anti-Sm antibodies are found very rarely in disorders other than lupus.
Anti-Ro (or SS-A) antibodies. These are found in some lupus patients, particularly those with a certain type of sun-sensitivity rash. If a pregnant lupus patient has anti-Ro antibodies, it is more likely that her baby will have a certain type of congenital heart disorder. Anti-Ro antibodies are also found in a disorder called Sjogren's syndrome. Sometimes lupus can occur together with Sjogren's syndrome.
Antihistone antibodies. These antibodies are found in the blood of many lupus patients and are directed against a protein which is frequently attached to the DNA (the material of which genes are made) within the cell nucleus. These antibodies are of particular interest because they are also found in the blood of some people who have high ANA tests caused by taking certain medications. Recent evidence suggests that the antibodies in lupus patients react with different histones than do the antibodies in these individuals with high ANA tests related to medications.
Anti-RNP (ribonucleoprotein) antibodies. These antibodies occur commonly in lupus and some other disorders. Certain individuals (mainly women) develop a group of symptoms that do not point strongly to lupus or to one of the other connective tissue inflammatory diseases, but rather to a combination of several of these diseases. This has been called "mixed connective tissue disease" or "overlap syndrome". Anti-RNP antibody levels are often very high in this disorder.
other antibody tests are often performed when trying to make a diagnosis of
lupus because they help tell the difference between lupus and certain other
diseases. Antiscleroderma 70 (Scl70) antibody is found in one form of
scleroderma. Anticentromere antibodies are found in another form of
scleroderma. Anti-PM-1 and anti-Jo-1 antibodies are found in polymyositis.
Rheumatoid factor (RF) is often found in the blood of patients with rheumatoid
arthritis, a condition which can sometimes be confused with lupus. Rheumatoid
factor may also be found in the blood of about 20% of lupus patients, and in a
number of other disorders.
The levels of certain non-antibody proteins in the blood, called complement components, may be low in lupus patients, particularly when the disease is active. Low complement levels are not very helpful in diagnosing lupus, however, because they can be found in other diseases as well. Complement levels are more useful both in following the disease activity and the response to treatment of individual lupus patients.
There are many laboratory tests which measure and identify whether or not specific organ systems are affected by lupus. These can be very valuable in the care of the individual lupus patient.
CBC (look for anemia).
Many blood tests measure the amount of a particular chemical or protein in your blood, but a complete blood count checks the blood cells themselves. It measures the numbers of different types of blood cells, their sizes, and their appearance. It is a very common and useful blood test.
In general, the test measures 3 main components of blood:
Red blood cells (also called erythrocytes or RBCs). The test measures the number, size, shape, and appearance of the RBCs, and also the amount of hemoglobin in them. Hemoglobin carries oxygen from the lungs to the rest of the body. The part of the test called a hematocrit measures the percentage of your blood that is red blood cells.
White blood cells (also called leukocytes or WBCs). The total count of white cells is measured. White blood cells help the body's immune system fight infection. When the amounts of each of the different types of white blood cells are also measured, the test is called a differential. The most common types are neutrophils (also called polymorphonuclear cells, PMNs, polys, or granulocytes) and lymphocytes.
Platelets (also called thrombocytes). Platelets are not actually blood cells. They are fragments of large blood-forming cells. These fragments are essential for normal blood clotting.
Leukopenia is a decrease in the number of white blood cells circulating within blood. Common causes include:
chronic or fulminant infection
after measures designed to obliterate leukocyte population e.g. chemotherapy or radiotherapy
It can be subdivided according to the white cell population that is (most) affected:
Thrombocytopenia is the term for a reduced platelet (thrombocyte)
count. It occurs when platelets are lost from the circulation faster than they
can be replaced from the bone marrow where they are made. Thrombocytopenia may
either result from a failure of platelet production and/or an increased rate of
removal from blood.
SMA-20 (look for abnormal)
Chem-20 is a group of 20 chemical tests performed on serum (the portion of blood without cells). Electrolytes are ionized salts in blood or tissue fluids (ions are atoms or molecules that carry an electrical charge). Electrolytes in the body include sodium, potassium, chlorine, and many others.
The rest of the tests focus primarily on chemicals related to the body's metabolism and the breakdown of various substances. These are tests that evaluate the function of the liver and kidneys.
Antithyroid microsomal antibodies - this seems to correspond with an increase in TSH (Thyroid Stimulating Hormone). Now the Ranch Hand study found a linear dose response to dioxin and this TSH but because T3 and T4 did not seemed to be out of scale they concluded it was not an issue. Guess they never heard of chronic sub clinical hypothyroidism.
The antiphospholipid syndrome is a disorder of the immune system that is characterized by excessive clotting of blood and/or certain complications of pregnancy (premature miscarriages, unexplained fetal death, or premature birth) and antiphospholipid antibodies (cardiolipin or lupus anticoagulant antibodies). Patients with antiphospholipid syndrome have developed abnormal symptoms while having antiphospholipid antibodies detectable in the blood.
Antiphospholipid syndrome is also called the phospholipid antibody syndrome. Antiphospholipid syndrome has been referred to as Hughes syndrome in honor of the doctor who first described it.
It is important to note that antiphospholipid antibodies can also be found in the blood of individuals without any disease process. In fact, antiphospholipid antibodies have been reported in approximately 2 percent of the normal population. Harmless antiphospholipid antibodies can be detected in the blood for a brief period occasionally in association with a wide variety of conditions, including bacterial, viral (hepatitis, HIV), and parasite (malaria) infections. Certain drugs can cause antiphospholipid antibodies to be produced in the blood, including antibiotics, cocaine, hydralazine, procainamide, and quinine.
Anti-MAG antibodies are
associated with several forms of neuropathy
- Anti-MAG IgM antibodies were detected by ELISA in a
patient with slowly progressive peripheral neuropathy. Serum IgM
content was normal, and no M-protein was detected by serum protein
electrophoresis, immunoelectrophoresis, or immunostaining. By
immunoblot analysis, the anti-MAG antibodies were IgMk; they reacted
with human and bovine MAG but not with mouse MAG. The data suggest
that there was an anti-MAG IgM M-protein in concentration too low to
be detected by conventional techniques. Tests for anti-MAG antibodies
should be done in patients with slowly progressive neuropathy of
unknown etiology, even in the absence of detectable serum M-protein.
Sounds like this is an MS
Free and bound hydrosoluble protein extracts were prepared from
four anatomical areas of a multiple sclerosis (MS) cerebrum and from
corresponding anatomical areas of a normal (non-MS) control. Increased levels of
IgG and anti-myelin basic protein antibodies (anti-MBP) were detected in all MS
samples and they were undetectable in the controls. IgG and anti-MBP from free
(unbound) hydrosoluble protein extracts are defined as free IgG and free
anti-MBP while IgG and anti-MBP from tissue bound protein extracts are defined
as bound IgG and bound anti-MBP. IgG was purified from free protein extracts by
protein G Sepharose affinity chromatography and anti-MBP was further isolated
from purified IgG by antigen specific (MBP) Sepharose affinity chromatography.
Free and bound anti-MBP were reacted with 20 synthetic peptides of human MBP
prepared by the Fmoc method. Free anti-MBP, whether in the context of whole
protein extracts, or as purified IgG or as purified antibody was completely
neutralized by peptides #12, #15, #56 and #56* containing overall residues
75-106, partially neutralized by peptides #27, #16 and #21 containing overall
residues 61-83 and did not react with the remaining 13 peptides. Tissue bound
anti-MBP was completely neutralized only by peptides #12, #15, #56 and #56*
(overall residues 75-106) and showed no reactivity towards the remaining 16
peptides including peptides #27, #16 and #21. Synthetic peptide specificity of
free anti-MBP purified from MS cerebrum was identical to previously reported
specificity of free anti-MBP from MS cerebrospinal fluid (CSF), while tissue
bound anti-MBP, as well as bound anti-MBP from CSF had a more restricted
synthetic peptide specificity than free anti-MBP. This suggests that the most
likely epitope of anti-MBP is located between residues 84 and 95 of human MBP
just proximal to the tri-proline sequence (99-101).
Anti-neuronal antibodies - article = Neurologic complications of both the central and peripheral nervous systems occur frequently in patients with primary Sjogren's syndrome (primary SS), but the underlying cause of these complications is unknown. We studied the presence of antineuronal antibodies in relation to neurologic complications in a consecutive series of 45 patients with primary SS. Twenty-five patients had neurologic complications: 12 patients with polyneuropathy, three with psychiatric disorders, four with carpal tunnel syndrome, seven with migraine, seven with myalgia, and four with other complications (transverse myelitis, stroke, Bell's palsy, and pyramidal signs). Ten patients had more than one neurologic complication. Eleven patients had major and 14 had minor complications according to criteria used for rating neurologic complications in patients with systemic lupus erythematosus.
Antineuronal antibodies were present in six
of 11 (55%) patients with major neurologic complications and in four
of 34 (11%) of patients without major neurologic complications (p =
0.001). This difference could be attributed mainly to the group of
patients with polyneuropathy. Three of the 10 sera of patients with
positive antineuronal antibodies had antibodies reacting with a 38-kd
neuronal protein on immunoblotting, identical to the anti-Hu antibody
reactivity in paraneoplastic neurologic disease associated with
small-cell lung cancer.
For brain atrophy look for antiglutamate decarboxylase antibodies- It seems these antibodies are associated with neurological damages and forms of ataxia disorders, including Friedreich’s ataxia; multiple system atrophy, and various other immune system diseases, etc.
For those with seizures, need exists for EEG's, MRI's, CT's.
It is important to note that not all with GWS exhibit the same symptoms nor do all progress in their illnesses at the same rate. Since that is the case, not all treatments will be the same either.
Treatments are individualized to associated patient risks. Some do not respond to various medications as do others. Treatments will also vary depending on severity. All treatments should be decided upon by
one's health care provider.
Some of the recommended treatments are: non-steroidal anti-inflammatory meds, steroid creams for rashes, cortisone, Plaquenil, Prednisone, Sulphasalazine, I.V. Cytoxan, I.V. Gamma Globulin & Medrol. Use of the individual treatments or in combinations will be physician determined based on the results of testing and which syndromes or symptoms you may have. For example, those with connective tissue difficulties, such as inflammation of muscles, reduced muscle mass and strength, Polymyositis & ALS-type symptoms, I.V. Gamma Globulin may be needed.
For those with Lupus-like symptoms, Prednisone, Plaquenil, and/or I.V. Cytoxan may be required. If exhibiting Reiter's Syndrome, Sulphasalazine might be prescribed. For those with brain atrophy and/
or damage, steroids may be useful.
Present this information to your Medical Physician for his/her professional consideration.
If ignored or downplayed by your Physician, you may wish to consider seeing another Physician.
Richard G. Shuster
Viet Nam Era Veteran
Father of 3 Gulf War Era Veterans
Just mind boggling to me that we have let these lies go on and on. In the Vietnam Veterans case; none of the toxic chemicals we were exposed to can cause any of these neurotoxic symptoms or syndromes.
Now you know why I suggested antibody tests should be mandatory.
Best to all,