Some Laboratory Definitions of Tests Ordered

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Thought you all might like a small list of some tests along with definitions

ordered by Dr. Schoemaker.

Rosie

Laboratory:

LabCorp, Inc., Quest Diagnostics, and Specialty Laboratories, Inc., each

CLIA approved,high complexity, national laboratory facilities.

MSH: alpha melanocyte stimulating hormone (MSH) is a 13 amino acid compound

formed in the ventromedial nucleus (VMN) of the hypothalamus, solitary

nucleus and arcuate nucleus by cleavage of proopiomelanocortin (POMC) to

yield beta-endorphin and MSH.

MSH exerts inductive regulatory effects on production of hypothalamic

endorphins and melatonin. MSH has multiple anti-inflammatory and

neurohormonal regulatory functions,

exerting regulatory control on peripheral cytokine release as well as on

both anterior and posterior pituitary function. Deficiency of MSH, commonly

seen in biotoxin-associated

illnesses, is associated with impairment of multiple regulatory functions

and dysregulation of pituitary hormone release. Symptoms associated with MSH

deficiency include chronic fatigue and chronic, unusual pain syndromes.

Normal values of MSH in commercial labs (Esoterix and LabCorp) are 35-81

pg/ml.

Leptin: leptin is a 146 amino acid adipocytokine produced by fat cells in

response to rising levels of fatty acids. Leptin has peripheral metabolic

effects, promoting storage of fatty acids, as well as central effects in the

hypothalamus. Following binding by leptin to a long isoform of the leptin

receptor in the VMN, a primordial gp-130 cytokine receptor, a JAK signal

causes transcription of the gene for POMC, which is in turned cleaved to

make MSH. Peripheral cytokine responses can cause phosphorylation of a

serine moiety (instead of threonine) on the leptin receptor, creating leptin

resistance and relative deficiency of MSH production. Normal values in

commercial labs show differences between males (5-8 ng/ml) and females (8-18

ng/ml), with levels of leptin correlated with BMI.

ADH/osmolality: abnormalities in ADH/osmolality are recorded as absolute if

ADH is < 1.3 or > 8 pg/ml; or if osmolality is >295 or <275 mOsm/kg.

Abnormalities are recorded as relative if simultaneous osmolality is 292-295

and ADH < 2.3; or if osmo is 275-278 and ADH> 4.0. Symptoms associated with

dysregulation of ADH include dehydration, frequent urination, with urine

showing low specific gravity; excessive thirst and sensitivity to static

electrical shocks; as well as edema and rapid weight gain due to fluid

retention during initial correction of ADH deficits.

ACTH/cortisol: abnormalities in ACTH/cortisol are absolute if AM cortisol >

19 ug/ml or < 8 ug/ml; or if AMACTH is >60 pg/ml or < 10 pg/ml.

Abnormalities are recorded as

dysregulation if simultaneous cortisol is > 15 and ACTH is > 15, or if

cortisol is < 8 and ACTH <40. Early in the illness, as MSH begins to fall,

high ACTH is associated with few symptoms; amarked increase in symptoms is

associated with a fall in ACTH. Finding simultaneous high cortisol and high

ACTH may prompt consideration of ACTH secreting tumors, but the reality is

that the dysregulation usually corrects with therapy.

Androgens: total testosterone, androstenedione and DHEA-S provide

measurements regarding the effectiveness of gonadotrophin secretion as

influenced adversely by MSH

deficiency. Normal ranges of these hormones in males are 75-205 ng/ml for

androstenedione, 350-1030 ng/ml for testosterone and 70-218 ug/ml for

DHEA-S. Normal values for pre-menopausal women are 60-245, 10-55 and 48-247,

respectively. Postmenopausal normal ranges are 30-120, 7-40 and 48-247,

respectively.

HLA DR by PCR: LabCorp offers a standard HLA DR typing assay of 10 alleles

using a PCR sequence specific chain reaction technique. As opposed to

serologic assays for the

HLA DR genotypes, the PCR gives far greater specificity in distinguishing

individual allele polymorphisms. Linkage disequilibrium is strong in these

genotypes, with multiple

associations made to inflammatory and autoimmune disease. These genes are

part of the human major histocompatibility complex (MHC), also called the

HLA complex, located on the short arm of chromosome 6. Relative risk was

calculated, susceptible genotypes identified, compared within each group to

location and exposure.

MMP9: matrix metalloproteinase 9 (gelatinase is an extracellular

zinc-dependent enzyme produced by cytokine-stimulated neutrophils and

macrophages. MMP9 is involved in degradation of extracellular matrix; it has

been implicated in the pathogenesis COPD by destruction of lung elastin, in

rheumatoid arthritis, atherosclerosis, cardiomyopathy, and abdominal aortic

aneurysm. Cytokines that stimulate MMP9 production include IL-1, IL-2, TNF,

IL-1B, interferons alpha and gamma. MMP9 is felt to play a role in central

nervous system disease including demyelination, by generation of myelin

peptides, as it can break down myelin basic protein. MMP9 " delivers "

inflammatory elements out of blood into subintimal spaces, where further

delivery into solid organs (brain, lung, muscle, peripheral nerve and joint)

is initiated. Normal ranges of MMP9 have a mean of 150, with range of 85-322

ng/ml.

C3a and C4a: Split products of complement activation, often called

anaphylatoxins. Each activates inflammatory responses, with spillover of

effect from innate immune response to acquired immune responses and

hematologic parameters. These short-lived products are remanufactured

rapidly, such that an initial rise of plasma levels is seen within 12 hours

of exposure and sustained elevation is seen until definitive therapy is

initiated. The components increase vascular permeability, release

inflammatory elements from macrophages, neutrophils and monocytes, stimulate

smooth muscle spasm in small blood vessels and disrupt normal apoptosis.

Anticardiolipins IgA, IgM and IgG: autoantibodies often identified in

collagen vascular diseases such as lupus and scleroderma; often called

anti-phospholipids. These antibodies in high titers are associated with

increased intravascular coagulation requiring treatment with heparin and

coumadin. Lower levels titers are associated with hypercoagulability. An

increased risk of spontaneous fetal loss in the first trimester of

pregnancy is not uncommonly seen in women with presence of cardiolipin

antibodies. This problem does not have the same " dose-response " relationship

seen with levels of autoantibodies and illness as does the antiphospholipid

syndrome. Anticardiolipins are found in over 33% of children with biotoxins

associated illnesses.

Antigliadin IgA and IgG: Antibodies thought at one time to be specific for

celiac disease. With the advent of testing for IgA antibodies to tissue

transglutaminase (TTG-IgA), gliadin antibodies are most often seen in

patients with low levels of MSH. Ingestion of gliadin, the 22-amino acid

protein found in gluten (found in wheat, oats, barley and rye; often added

to processed foods) will initiate a release of pro-inflammatory cytokines in

the tissues lining the intestinal tract. This cytokine effect will often

cause symptoms within 30 minutes of ingestion that mimic attention deficit

disorder, often leading to an incorrect diagnosis. Antigliadin antibodies

are found in over 58% of children with biotoxin-associated illnesses.

Vasoactive intestinal polypeptide (VIP): neuroregulatory hormone with

receptors in suprachiasmatic nucleus of hypothalamus. This hormone/cytokine

regulates peripheral

cytokine responses, pulmonary artery pressures and inflammatory responses

throughout the body. Deficiency is commonly seen in mold illness patients,

particularly those with dyspnea on exertion.

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