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Immunology

Immunology (9)

CELLS OF THE IMMUNE SYSTEM

Written by
Published in Immunology
Saturday, 15 July 2017 11:00
The major cells of the immune system are lymphocytes. Lymphocytes that are critical for immune reactions are of two types namely B-cells and T-cells. Both cells develop from stem cells located in the liver of the foetus and in bone marrow cells of adults.
 
The lymphocytes which are differentiated in the bone marrow are B-cells. The lymphocytes that migrate to thymus and differentiate under its influence are called T-cells. The young lymphocytes migrate to lymphoid tissues such as spleen, lymph nodes and tonsils where they undergo final maturation. Matured lymphocytes circulate in the body fluids. T-cells are responsible for cellular immunity and B-cells produce antibodies about 20 trillion per day.
 
Both components require antigens to trigger them into action but they respond differently.
 
Antigens
 
An antigen is a substance when introduce into an individual, stimulates the production of an antibody with which it reacts. Antigens are large molecules of proteins or polysaccharides. Some of the antigens are the parts of microorganisms others include pollen, egg white, certain fruits, vegetables, chicken, feathers etc.

Antibodies
 
Antibodies are protein molecules called immunoglobulin (Ig). They are produced by lymphocytes. The antibodies inactivate antigens. An antibody  consists of four amino acid chains bounded together by disulphide bonds. Of the four chains two are long, heavy chains and two are short, light chains. All of them are arranged in the shape of the letter ‘Y’. The tail portion of antibody having two heavy chains is called constant fragment (Fc). On the tip of each short arm, an antigen- binding fragment (Fab) is present which specifically hold antigen.
 
Antibody immunity10
 
Based upon the five types of heavy chains, the immunoglobulin's are classified into five major types. Light chains are similar in all types of Immunoglobulin's.
 
TYPES OF IMMUNOGLOBULIN'S
 
lgG is the most important long acting antibody representing about 80% of the antibodies. The second important antibody is IgM. IgA is called secretory antibody, found in tears, saliva and colostrum, (the first milk secreted by mother). IgD serves as a receptor site at the surface of B cells to secrete other antibodies. IgE plays an important role in allergic reactions by sensitizing cells to certain antigens.
 
iimmunoglobulin types12

Blood Eosinophil Level Predicts Severity of Asthma

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Published in Immunology
Tuesday, 18 October 2016 21:28

Asthma represents a significant clinical and economic burden to the US healthcare system. Along with other clinical manifestations of the disease, elevated sputum and blood eosinophil levels are observed in patients experiencing asthma exacerbations. The aim of this study was to evaluate the association between blood eosinophil levels and asthma severity defined using Expert Panel Report 3 guidelines.

Among 1,144 patients with an asthma diagnosis, 60 % were classified as having moderate-to-severe asthma. Twenty four percent of patients with moderate-to-severe asthma and 19 % of patients with mild asthma had an elevated peripheral eosinophil count (p = 0.053). Logistic regression showed that moderate-to-severe asthma was associated with 38 % increased odds of elevated eosinophil level (OR 1.38, 95 % CI: 1.02 to 1.86, p = 0.04).

Patients with moderate-severe asthma are significantly more likely to have an elevated peripheral eosinophil count than patients with mild asthma

Read More: Value of Peripheral Blood Eosinophil Markers to Predict Severity of Asthma

How do you die from multiple myeloma?

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Published in Immunology
Tuesday, 18 October 2016 11:17

Multiple Myeloma: Early Death Common and Preventable

Improved survival among patients with multiple myeloma is one of the most impressive cancer treatment success stories in recent years.

A decade ago, patients survived an average 3 to 4 years following a multiple myeloma (MM) diagnosis, but median survival times have doubled and continue to improve, said multiple myeloma researcher Shaji Kumar, MD, of Mayo Clinic, Rochester, Minnesota.

This is due largely to the introduction of novel biologic therapies and greater use of autologous stem cell transplant. While there is still no cure for the neoplastic plasma-cell disorder, these treatments now routinely prolong initial remission and survival.

Early death remains common

Considered a rapidly fatal disease just a decade ago, MM is now considered more of a chronic condition for many, but not all, patients, Kumar said in a telephone interview.

Early death remains a significant and under-recognized problem in multiple myeloma, especially among patients with serious comorbidities or those who are very old. These patients often do not receive today’s gold-standard treatments, and that is a problem, Kumar said.

“About a quarter of patients will die within the first 2 to 3 years of diagnosis, for a number of reasons,” Kumar said, adding that he believes early mortality among multiple myeloma patients could be reduced by a third or even half if strategies to identify and treat those most at-risk were systematically applied.”

“Do’s and Don’ts” in early treatment

These strategies were outlined by Kumar and colleagues from Mayo Clinic and the University of Alabama at Birmingham in a recent analysis, published ahead of print by the American Journal of Hematology.

“Multiple myeloma is not a rare disease, but it is not commonly seen by oncologists in general practice,” analysis co-author Luciano J. Costa, MD, of the University of Alabama at Birmingham said. “Some may see only 1 or 2 of these patients a year, so we felt it was important to highlight some key strategies for reducing early death rates in this population.”

In a separate population analysis of 30,324 multiple myeloma patients published late in 2014, Kumar, Costa and colleagues found that while early mortality–defined as death within a year of MM diagnosis–has decreased over time, it still occurred in 28.6% of patients diagnosed in the U.S. between 1993 and 2010.

The incidence of early death among patients diagnosed before the age of 65 was 17.6% and incidence among older patients was 35.3%.

Majority of MM patients are age 65+

“About two-thirds of patients are 65 or older when diagnosed, so this at-risk group represents the overwhelming majority of patients,” Costa said. “And most of these older patients are not dying from refractory disease.”

Instead, Costa said he believes many die because they are either not getting optimal therapies or because they are very ill from co-morbid diseases at the time of their diagnoses.

These very ill or elderly patients have typically been excluded from multiple myeloma clinical trials, so there is little to guide physicians treating them.

This is why careful risk stratification and identification of co-morbidities immediately following a MM diagnosis is critical, Kumar noted.

“We need to manage the myeloma in the context of the other things going on with the patient,” he said.

The strategy for managing newly diagnosed MM outlined by Costa, Kumar and colleagues included a series of “do’s” and “don’ts” derived from their experience treating patients with the bone marrow cancer. Their aim was not to present comprehensive recommendations for treatment, but, instead, to focus on strategies designed to avoid early complications and death.

Among the recommended “do’s” and “don’ts”:

Do institute prompt systemic therapy

The researchers’ 2014 analysis revealed that the risk of early death was higher when novel MM drugs were not used as part of treatment.

While physicians may be tempted to focus on supportive care for conditions that accompany MM, such as hypercalcemia, bone lesions, renal failure and anemia, the researchers wrote that these treatments should not replace systemic therapy.

“It is crucial to keep in mind that ultimate symptom control or reversal of complication can only be obtained with systemic treatment, and none of the supportive measures above precludes prompt initiation of systemic therapy,” they wrote.

Do treat hypercalcemia aggressively

Approximately 1 in 5 patients develop hypercalcemia, resulting from increased activation of osteoclasts. The researchers noted that the “prompt and effective management of hypercalcemia is imperative to prevent early mortality in newly diagnosed MM.”

They added that in cases of mild hypercalcemia, aggressive rehydration with normal saline along with corticosteroids should suffice, as long as hydration is carefully monitored to avoid congestive heart failure.

In moderate to severe cases (serum calcium >12 mg/dL), an ECG is recommended to rule out arrhythmias. In addition to hydration and corticosteroids, the researchers recommended anti-bone resorption therapies, and they noted that results from two separate trials in patients with malignancy-related hypercalcemia found zoledronic acid to be superior to pamidronate for normalizing calcium levels.

Drugs that cause hypercalcemia should also be avoided, as well as drugs that can worsen neurological status in the setting of concurrent hypercalcemia, “to allow adequate assessment of neurological status.”

Do avoid and manage infections

Infections are the most common cause of early death in MM patients. One study found that 45% of deaths within 2 months of diagnosis were associated with infections. A population-based study from Sweden showed a 7- to 10-fold increase in bacterial and viral infection risk in MM patients, compared to the general population.

The use of prophylactic antibiotics to prevent infections in MM remains controversial, and the researchers noted that routine prophylaxis is not advised. They did, however, recommend the use of TMP-SMX to prevent fungal pneumonias in patients treated with 20 mg/d or more of prednisone. They also recommended prophylactic use of acyclovir or valacyclovir for patients receiving proteasome inhibitors (PIs) that disrupt normal T-cell immunity.

“For all patients receiving bortezomib and for that matter even newer PIs such as carfilzomib, we recommend administering antiviral prophylaxis with acyclovir 400 mg twice daily or valacyclovir 500 mg once a day,” they wrote.

Do avoid thromboembolic events (VTE)

This risk increases with age, and patients with blood cancers such as MM have an especially high risk for clot-related events. The researchers recommend educating all newly diagnosed patients on the warning signs for the development of VTEs. They also recommend the use of VTE prophylaxis in all newly diagnosis MM patients receiving IMiD-immunomodulator therapies.

“In MM patients who develop a thrombosis upon initiating treatment, it is reasonable to hold their treatment and resume after they are therapeutically anticoagulated,” the researchers wrote. “This level of anticoagulation may be continued for the remainder of the duration of MM-directed therapy as long as the risk of serious bleeding complications is deemed acceptable.”

Remaining “do’s” and “don’ts” recommended in the analysis included:

  • Do address comorbidities and manage pain.
  • Don’t postpone systemic therapy to address localized lesions.
  • Don’t administer prolonged courses of high-dose corticosteroids.
  • Don’t change well-tolerated therapy due to perceived suboptimal response if clinical benefit is shown.
  • Don’t administer radiation when symptoms can be managed with systemic therapy.
  • Don’t administer inferior treatment solely based on advanced age of performance status.

“In recent years we have seen an explosion in the number of available therapies for multiple myeloma, but older, sicker patients may not be getting these treatments,” Costa said. “Since about two-thirds of newly diagnosed patients are age 65 or older, it is important to address the issue of suboptimal treatment in this population.”


By Salynn Boyles
Reviewed by Alan S. Weinstein, MD, FACP, Medical Director (retired), Virtua Fox Chase Cancer Program, Marlton, NJ


Source: MEDPAGE TODAY: Multiple Myeloma: Early Death Common and Preventable

Status of laboratory testing for HIV

Written by
Published in Immunology
Monday, 17 October 2016 10:41

Two years have passed since the CDC finally published guidelines addressing HIV laboratory testing and officially endorsed the “new” HIV laboratory testing algorithm. Although many had become aware of the algorithm in the four years prior, and had adopted it to various degrees, this was the final word on this long-awaited guidance. The algorithm gained visibility prior to the official endorsement mainly because it had been heavily referenced in CDC publications and numerous scientific articles.

Advantages of the new algorithm

Why is the new algorithm superior to the old algorithm? First, the new algorithm emphasizes the use of an antigen/antibody (Ag/Ab) combination assay to screen for HIV infection, as the first step. The use of this more advanced technology (fourth generation) provides improved detection of acute HIV-1 infection because antigen/antibody combination assays not only detect established infection in those who have seroconverted, but can also diagnose HIV infection prior to seroconversion by detecting p24 antigen. Fourth generation assays detect acute HIV infections, on average, five to seven days earlier than the third generation, antibody-only assays.

Second, substituting the HIV-1/HIV-2 differentiation assay for the Western blot in the second step allows for correct identification of HIV-2 infection and earlier detection of HIV-1 infection, compared to the Western blot.

Third, the official addition of nucleic acid testing (NAT) is used to rule out acute HIV-1 infection, which is necessary because although HIV-1/HIV-2 differentiation assays can detect HIV infection on average a few days earlier than the Western blot, none of these can detect HIV infection prior to seroconversion.

There is ample evidence that the new algorithm has increased detection of acute HIV-1 infections, due to the use of Ag/Ab combination assays. This is important both for the patient, who can receive prompt treatment that improves health outcome, and also from a public health perspective, because it reduces disease transmission. Many laboratories now have access to a fourth generation assay, since they are offered by multiple vendors on a variety of automated platforms.

The data are not yet in as to whether the new algorithm has resulted in a significant increase in yield of HIV-2 diagnoses; this would provide critical information regarding prevalence and transmission of HIV-2 infections in the United States.

Challenges of the new algorithm

The new algorithm, however, has presented some real challenges for the laboratory. The biggest adjustment to adopting the new algorithm has been replacing the Western blot with an HIV-1/HIV-2 differentiation assay. The only assay with this capability until recently was the Multispot (Bio-Rad). However, the Multispot is no longer available and will be replaced with Bio-Rad’s Geenius. Although the Geenius is also a single use test (FDA-cleared) for confirming reactive HIV screen results and differentiating between HIV-1 and HIV-2 antibodies, it differs from the Multispot in a number of important aspects. The test uses either recombinant or synthetic peptides corresponding to four HIV-1 antigens, gp160, gp41, p31 and p24, and two corresponding to HIV-2 antigens, gp140 and gp36. There are eight possible interpretations based on the pattern observed. Performance characteristics are comparable to Multispot. Sensitivity is 100 percent for both assays, and specificity values are 99.1 percent and 96.3 percent for the Multispot and Geenius, respectively. The results can be read within 30 minutes and are interpreted using an automated cassette reader, therefore eliminating inter-observer subjectivity. The cassette system also allows for placement of a bar code label on each specimen, improving sample tracking. Additionally, because software is necessary for interpretation, the results are digitally captured, automatically recorded, and stored.

However, because the new HIV-1/HIV-2 differentiation assay requires an additional investment in the reader/software component, beyond the cost of the reagents, there is some concern that some small hospital laboratories will revert to sending out supplemental HIV testing to a reference laboratory. It should also be noted that, although adoption of the new algorithm has grown significantly, there is still substantial demand for Western blot testing. Importantly, when a third or fourth generation assay was used for screening, an indeterminate or negative Western blot should also be followed up with NAAT.

There is also much confusion regarding appropriate use of the fourth generation rapid HIV test. Although at first glance it would appear that this assay can be used in lieu of the laboratory based Ag/Ab combination assay and serve as the entry point into the algorithm, that is not the current CDC recommendation. Citing insufficient evidence for such an approach, the CDC suggests that a preliminary positive result obtained with any rapid test, including an antigen/antibody combination rapid test, must be followed up with a laboratory-based antigen/antibody combination assay.

Fifth generation testing

The horizon appears even more complicated now that the “fifth generation” HIV testing is available. This technology is currently offered only by one vendor, but it has the ability to differentiate between antigen, HIV-1 and HIV-2 antibody-positive specimens. While this simplifies the answer with regard to HIV infection status for the patient, there are no guidelines as to how to proceed with follow-up testing. For example, if the sample is positive for antigen only, then the logical follow-up would be to send out for NAT testing, as there is no reason to test with the supplemental HIV-1/HIV-2 differentiation assay that only detects antibodies. If the sample is positive for HIV-2 only, is it appropriate to follow up with the HIV-1/HIV-2 differentiation assay, because the fifth generation test is FDA-approved as a screen only and a supplemental test is needed? Fifth generation technology presents further complications to the algorithm and more complexity for the laboratory in terms of appropriate follow-up and interpretation for clinicians.

Last, one unintended consequence of the new algorithm is the effect on HIV surveillance programs. Ideally for the purpose of HIV surveillance, public health departments would like to have the final answer as to whether a patient has HIV-1, HIV-2, or acute HIV-1 infection, once the HIV testing algorithm is complete. The problem is that this is almost impossible because testing is almost always fragmented and different steps of the algorithm are performed in different laboratories. Often primary institution laboratories have the ability to perform the screening, even with a fourth generation Ag/Ab combination assay, but cannot complete the remainder of the algorithm. The sample is then sent to the reference laboratory, and that laboratory has to determine how to interpret the results without having the screen results. How to report a partial result and make it clear to the clinician that additional testing is needed and also satisfy public reporting needs is much more difficult in the context of the new algorithm, for both the primary and reference laboratory.

In summary, many technological advances have been made that importantly improve detection of HIV-2 and acute HIV-1 infections. These advances are beneficial for both the patient and society. Although most clinicians and laboratories are now familiar with and support the implementation of the algorithm, laboratories are challenged more than ever to provide appropriate test result interpretation and utilization as well as adequate public health reporting for HIV.

References

  1. "Laboratory Testing for the Diagnosis of HIV Infection: Updated Recommendations". BioScience.pk Digital Library Database. Centers for Disease Control and Prevention (CDC). Published June 27, 2014.

    About the author: Patricia Slev, PhD, DABCC, is Associate Professor of Pathology (Clinical), University of Utah and Medical Director of the Serologic Hepatitis and Retrovirus Laboratory, Core Immunology Laboratory and Co-Director Microbial Immunology Laboratory,  at ARUP. Board certified by the American Board of Clinical Chemistry, Dr. Slev’s research interests are immunogenetics and pathogen interactions, particularly HIV and viral hepatitis.

Source: Medical Laboratory Observer: The status of laboratory testing for the diagnosis of HIV infection

In what could be a major step forward in our understanding of how cancer moves around the body, researchers have observed the spread of cancer cells from the initial tumour to the bloodstream.

The findings suggest that secondary growths called metastases 'punch' their way through the walls of small blood vessels by targeting a molecule known as Death Receptor 6 (no, really, that's what it's called). This then sets off a self-destruct process in the blood vessels, allowing the cancer to spread.

According to the team from Goethe University Frankfurt and the Max Planck Institute in Germany, disabling Death Receptor 6 (DR6) may effectively block the spread of cancerous cells - so long as there aren't alternative ways for the cancer to access the bloodstream.
 
"This mechanism could be a promising starting point for treatments to prevent the formation of metastases," said lead researcher Stefan Offermanns.
 
Catching these secondary growths is incredibly important, because most cancer deaths are caused not by the original tumour, but by the cancer spreading.
 
To break through the walls of blood vessels, cancer cells target the body's endothelial cells, which line the interior surface of blood and lymphatic vessels. They do this via a process known as necroptosis - or 'programmed cell death' - which is prompted by cellular damage.
 
According to the researchers, this programmed death is triggered by the DR6 receptor molecule. Once the molecule is targeted, cancer cells can either travel through the gap in the vascular wall, or take advantage of weakening cells in the surrounding area.

Neutrophil disorders and their management

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Published in Immunology
Tuesday, 27 September 2016 13:49
Neutrophil disorders are an uncommon yet important cause of morbidity and mortality in infants and children. This article is an overview of these conditions, with emphasis on clinical recognition, rational investigation, and treatment.

Neutrophil disorders
  • Disorders of neutrophil number (neutropenia)
  • Disorders of neutrophil function
Neutrophil disorders are an uncommon, yet important, cause of morbidity and mortality in infants and children and should be considered when investigating children for immunodeficiency. They are especially likely when the clinical presentation includes features such as oral ulcers and gingivitis, delayed separation of the umbilical cord, uncommon infections such as hepatic or brain abscesses, uncommon organisms such as S marcescens or Pseudomonas spp, or when the individual has features of syndromic conditions associated with neutropenia or neutrophil dysfunction. All patients with recurrent oral infections, skin abscesses, perianal and perirectal abscesses, poor wound healing, sinopulmonary infections, or deep visceral abscesses should be evaluated for defects in phagocyte function. Appropriate investigations can lead to specific diagnoses, and general and specific management measures can reduce both mortality and morbidity and permit genetic counselling and antenatal diagnosis in some cases.

Read more: Neutrophil disorders and their management

Cholinesterase Tests

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Published in Immunology
Thursday, 28 April 2016 21:55
Cholinesterase testing has two main uses:
  • It can be used to detect and diagnose organophosphate pesticide exposure and/or poisoning. It may also be used to monitor those who may be at increased risk of exposure to organophosphate compounds, such as those who work in agricultural and chemical industries, and to monitor those who are being treated for exposure. Typically, tests for red blood cell acetylcholinesterase (AChE) and serum pseudocholinesterase (PChE) are used for this purpose.
  • It can be used several days prior to a surgical procedure to determine if someone with a history of or family history of post-operative paralysis following the use of succinylcholine, a common muscle relaxant used for anesthesia, is at risk of having this reaction. In these cases, the test for pseudocholinesterase is usually used. A second test, referred to as a dibucaine inhibition test, may be done to help determine the extent to which the activity of the enzyme is decreased.
 
When is it ordered?
People who work with organophosphate compounds in the farming or chemical industries may be routinely monitored to assess any adverse exposure, once baseline levels have been established. Cholinesterase testing can also be used to assess any acute exposure to these compounds, which can cause neuromuscular damage. Toxicity can follow a rapid absorption of the compound in the lungs, skin, or gastrointestinal tract. The symptoms of toxicity are varied depending on the compound, quantity, and the site of exposure. Early symptoms may include:
  • Headache, dizziness
  • Nausea
  • Excessive tearing in the eyes, sweating and/or salivation
 
As the effects of the poisoning worsen, some additional symptoms may appear:
  • Vomiting, diarrhea
  • Dark or blurred vision due to constricted pupils
  • Muscle weakness, twitching, lack of coordination
  • Slowed breathing leading to respiratory failure, requiring lifesaving ventilation
  • In serious cases, seizures, coma, and death
 
Pre-operative screening for pseudocholinesterase activity is advised if a person or a close relative has experienced prolonged paralysis and apnea after the use of succinylcholine for anesthesia during an operation.
 
What does the test result mean?
In monitoring for occupational pesticide exposure
Following exposure to organophosphate compounds, AChE and PChE activity can fall to about 80% of normal before any symptoms occur and drop to 40% of normal before the symptoms become severe. Those who are regularly exposed to these compounds may be monitored for toxic exposure by establishing a baseline activity level and then testing on a regular basis to watch for a significant reduction on activity of acetylcholinesterase or pseudocholinesterase.
 
In testing for acute pesticide exposure/poisoning
Significantly decreased cholinesterase activity levels usually indicate excessive absorption of organophosphate compounds. Pseudocholinesterase and RBC acetylcholinesterase activity are usually decreased within a few minutes to hours after exposure. Pseudocholinesterase activity may regenerate in a few days to weeks, while acetylcholinesterase activity will remain low for as long as one to three months. Both plasma and RBC activities are immediately affected by pesticide exposure but, upon removal from exposure, AChE and PChE regenerate at different rates since AChE is produced in blood cells, which have a lifespan of 120 days, whereas PChE is produced in the liver, with a half-life of about two weeks.
 
In testing for succinylcholine sensitivity
About 3% of people have low activity levels of pseudocholinesterase due to an inherited deficiency and will have prolonged effects from the muscle relaxant succinylcholine. Total quantitative pseudocholinesterase levels will be evaluated prior to surgery for patients with a history or family history of prolonged apnea after use of this drug. Low activity levels of pseudocholinesterase levels indicate that these people may be at increased risk of experiencing prolonged effects of the muscle relaxant. A second test, the dibucaine inhibition test, may also be performed to help characterize the degree of a person's sensitivity to the drug. The lower the result from a dibucaine inhibition test, the greater the risk of drug sensitivity.
Reduced cholinesterase levels can also be caused by chronic liver disease and malnutrition. Total cholinesterase activity can be lowered in a number of other conditions, including pregnancy, renal disease, shock, and some cancers.
 
Is there anything else I should know?
If someone unexpectedly has prolonged apnea after surgery, testing for succinylcholine sensitivity may be performed; however, the sample should be obtained after 24 to 48 hours have elapsed following the surgery to avoid interference by any drugs given during the surgery that could affect the results. Drugs called cholinesterase inhibitors may have a moderate benefit in those with early diagnosed Alzheimer's disease.

Serum Angiotensin Converting Enzyme

Written by
Published in Immunology
Thursday, 28 April 2016 21:18
Angiotensin-converting enzyme (ACE) is an enzyme that helps regulate blood pressure. An increased blood level of ACE is sometimes found in sarcoidosis, a systemic disorder of unknown cause that often affects the lungs but may also affect many other body organs, including the eyes, skin, nerves, liver, and heart., This test measures the amount of ACE in the blood.
 
A classic feature of sarcoidosis is the development of granulomas, small tumor-like masses of immune and inflammatory cells and fibrous tissue that form nodules under the skin and in organs throughout the body. Granulomas change the structure of the tissues around them and, in sufficient numbers, they can cause damage and inflammation and may interfere with normal functions. The cells found at the outside borders of granulomas can produce increased amounts of ACE. The level of ACE in the blood may increase when sarcoidosis-related granulomas develop.
 
The angiotensin-converting enzyme (ACE) test is primarily ordered to help diagnose and monitor sarcoidosis. It is often ordered as part of an investigation into the cause of a group of troubling chronic symptoms that are possibly due to sarcoidosis.
 
Sarcoidosis is a disorder in which small nodules called granulomas may form under the skin and in organs throughout the body. The cells surrounding granulomas can produce increased amounts of ACE and the blood level of ACE may increase when sarcoidosis is present.
 
The blood level of ACE tends to rise and fall with disease activity. If ACE is initially elevated in someone with sarcoidosis, the ACE test can be used to monitor the course of the disease and the effectiveness of corticosteroid treatment.
 
A health practitioner may order ACE along with other tests, such as AFB tests that detect mycobacterial infections or fungal tests. This may help to differentiate between sarcoidosis and another condition causing granuloma formation.
 
When is it ordered?
An ACE test is ordered when someone has signs or symptoms that may be due to sarcoidosis, such as:
  • Granulomas
  • A chronic cough or shortness of breath
  • Red, watery eyes
  • Joint pain
 
This is especially true if the person is between 20 and 40 years of age, when sarcoidosis is most frequently seen.
 
When someone has been diagnosed with sarcoidosis and initial ACE levels were elevated, a health practitioner may order ACE testing at regular intervals to monitor the change in ACE over time as a reflection of disease activity.
 
What does the test result mean?
An increased ACE level in a person who has clinical findings consistent with sarcoidosis means that it is likely that the person has an active case of sarcoidosis, if other diseases have been ruled out. ACE will be elevated in 50% to 80% of those with active sarcoidosis. The finding of a high ACE level helps to confirm the diagnosis.
 
A normal ACE level cannot be used to rule out sarcoidosis because sarcoidosis can be present without an elevated ACE level. Findings of normal ACE levels in sarcoidosis may occur if the disease is in an inactive state, may reflect early detection of sarcoidosis, or may be a case where the cells do not produce increased amounts of ACE. ACE levels are also less likely to be elevated in cases of chronic sarcoidosis.
 
When monitoring the course of the disease, an ACE level that is initially high and then decreases over time usually indicates spontaneous or therapy-induced remission and a favorable prognosis. A rising level of ACE, on the other hand, may indicate either an early disease process that is progressing or disease activity that is not responding to therapy.

Acetylcholine Receptor (AChR) Antibody

Written by
Published in Immunology
Saturday, 23 April 2016 13:06
An acetylcholine receptor (AChR) antibody test is used to help diagnose myasthenia gravis (MG) and to distinguish it from other conditions that may cause similar symptoms, such as chronic muscle fatigue and weakness.
 
AchR antibodies hinder the action of acetylcholine, a chemical (neurotransmitter) that transmits messages between nerve cells. The antibodies do this in three major ways:
  • "Binding" antibodies attach to the acetylcholine receptors on nerve cells and may initiate an inflammatory reaction that destroys them.
  • "Blocking" antibodies may sit on the receptors, preventing acetylcholine from binding.
  • "Modulating" antibodies may cross-link the receptors, causing them to be taken up into the muscle cell and removed from the neuromuscular junction.
Three different types of tests are available to determine which of these may be the problem in a particular individual. However, the test that measures "binding" antibodies is most commonly used because it is generally rare for the other two tests to be positive without the "binding" test being positive as well. These other tests may be used when a doctor strongly suspects myasthenia gravis and the "binding" test is negative.
 
One or more of the AChR antibody tests may be ordered as part of a panel of tests that may also include a striated muscle antibody test to help establish a diagnosis. Depending upon results, an anti-MuSK (muscle-specific kinase) antibody test may also be ordered. The AChR antibody test may be ordered initially as a baseline test and then as indicated to evaluate MG disease activity and/or response to therapy.
 
People with MG often have an enlarged thymus gland and may have thymomas (typically benign tumors of the thymus). Located under the breastbone, the thymus is an active part of the immune system during childhood but normally becomes less active after puberty. If a thymoma is detected, such as during a chest computed tomography (CT) scan done for a different reason, then an AChR antibody test may sometimes be used to determine whether the person has developed these antibodies.
 
When is it ordered?
The AChR antibody test may be ordered when a person has symptoms that suggest MG, such as:
  • Drooping eyelid
  • Double vision
  • Decreased eye movement control
  • Difficulty swallowing, chewing, with choking, drooling and gagging
  • Slurred speech
  • Weak neck muscles
  • Trouble holding up head
  • Difficulty breathing
  • Difficulty walking and an altered gait
  • Specific muscle weakness but normal feelings/sensations
  • Muscle weakness that worsens with sustained effort and improves with rest
When a person has been diagnosed with MG, an AChR antibody test may be ordered occasionally to evaluate MG disease activity and/or response to therapy.
 
An AChR antibody test may sometimes be ordered when a thymoma is detected.
 
What does the test result mean?
AChR antibodies are not normally present in the blood. They are autoantibodies and their presence indicates an autoimmune response.
 
If a person has AChR antibodies and symptoms of MG, then it is likely that the person has this condition.
 
AChR antibodies may be seen with some thymomas, in people who are being treated with drugs such as penicillamine, with some small cell lung cancers, with autoimmune liver disease, and with Lambert-Eaton myasthenic syndrome (a condition associated with interference with the release of acetylcholine from the nerve ending).
 
A negative test result does not rule out MG. Up to 50% of those with ocular MG (affecting only eye-related muscles) and about 10-15% of those with generalized MG will be negative for AChR antibodies.
 
In general, the greater the quantity of AChR antibody, the more likely a person is to have significant symptoms, but the test results cannot be used to evaluate the severity of symptoms in a specific person.

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