Protein C-reactif

Protein C-reactif (C-reactive protein, CRP) are made by the liver and secreted into the bloodstream. CRP circulates in the blood for 6-10 hours after the acute inflammatory process and tissue destruction. Levels peaked within 48-72 hours. As with any test erythrocyte sedimentation rate (erithrocyte sedimentation rate, ESR), CRP is a non-specific test but the existence precedes the CRP increase during inflammation and necrosis of the LED and then immediately return to normal levels.

CRP is one of several proteins that are often referred to as acute phase proteins and used to monitor changes in the acute inflammatory phase is associated with many infectious diseases and autoimmune diseases. Some circumstances in which CRP may increase was found arthritis (rheumatoid arthritis), rheumatic fever, breast cancer, colitis, inflammatory disease stage (pelvic inflammatory disease, PID), Hodgkin's disease, SLE, bacterial infections.

CRP is also elevated in the final trimester of pregnancy, the use of intrauterine contraceptive devices and oral contraceptive drug effect.

CRP test is often performed repeatedly to evaluate and determine whether the treatment is effective. CRP is also used to monitor wound healing and to monitor post-surgical patients, organ transplant, or burns as an early detection system for possible infections.

High-sensitive CRP (hs-CRP)
This test can detect the inflammation that occurs due to the formation of atherosclerotic plaque in coronary arteries. hsCRP is a highly sensitive laboratory test for the risk of cardiovascular disease. This test is often done in conjunction with the test lipid profile (cholesterol, triglycerides, HDL, LDL). Positive hsCRP value is much lower than the standard value of serum CRP so that it becomes more useful test in detecting the risk of coronary heart disease (coronary heart disease, CHD), stroke, and peripheral arterial disease.

American Heart Association and the U.S. Centers for Disease Control and Prevention have defined risk groups as follows :

• Low risk: less than 1.0 mg / L
• Average Risk: 1.0 to 3.0 mg / L
• High risk: above 3.0 mg / L

Those values ​​are only a part of the evaluation process for kardiovaskuler.Tambahan disease risk factors to consider are the elevated levels of cholesterol, LDL, triglycerides, and glucose. In addition, smoking, high blood pressure (hypertension), and diabetes also raise the level of risk.

Procedure
CRP test can be performed manually using agglutination methods or other more advanced methods, such as sandwiches imunometri. Agglutination tests carried out by adding the latex particles coated with anti-CRP antibodies in the serum or plasma agglutination patient so that it will happen. To determine the titer of CRP, serum or plasma diluted with buffer glycine patients with multilevel dilution (1 / 2, 1 / 4, 1 / 8, 1 / 16 and so on) and then reacted with latex. CRP titer is the highest dilution that still occur agglutination.

Imunometri sandwich tests performed by measuring the intensity of colors using Nycocard Reader. Consecutive samples (serum, plasma, whole blood) and conjugate dropped on the coated membrane antibody testsspecific mononklonal CRP. CRP in the sample captured by antibodies bound to colloidal gold particle conjugates. Free conjugate was washed with wash solution (washing solution). If there is at the level of CRP in pathological samples, it will form a red-brown color in the test area with color intensity proportional to the content. Color intensity was measured quantitatively using a reader NycoCard II.

Normal reference value of CRP with imunometri sandwich method is <5 mg / L. This reference value would be different depending on each laboratory reagents and methods used.

hepatitis A (HAV)

What is hepatitis A and how is it transmitted ?

Hepatitis A is caused by the hepatitis A virus (HAV). HAV is spread through food / drink contaminated with fecal matter (stool) of an infected person enter another person's mouth. HAV is mainly transmitted through raw or inadequately cooked, handled or prepared by someone withhepatitis A (although maybe he did not know he was infected).

Drinking water or ice that is contaminated with feces is another source of infection, as well as shellfish that are not cooked enough. HAV can be transmitted through "rimming" (oral-anal sex, or between the mouth and anus). HAV is rarely transmitted through blood-to-blood.

Hepatitis A is an acute form of hepatitis, meaning do not cause chronic infection. Once we've had hepatitis A, we can not be infected again. However, we can still be infected with other hepatitis viruses.

What are the symptoms of hepatitis A?

Not all people infected with HAV will have symptoms. For example, many infants and young children infected with HAV do not experience any symptoms. Symptoms are more likely to occur in older children, adolescents and adults.

Symptoms of hepatitis A (acute hepatitis and in general) can including :

• skin and whites of the eyes become yellow (jaundice)
• Fatigue
• right-upper abdominal pain
• Loss of appetite
• Weight loss
• Fever
• Nausea
• Diarrhoea or diarrhe
• Vomiting
• Water arts such as tea and / or dirt-colored putty
• joint pain

HAV infection can also increase the levels of enzymes made by the liver to be above normal in the blood. The immune system require up to eight weeks to remove the HAV from the body. If symptoms develop, generally within two to four weeks after infection. Symptoms ofhepatitis A is generally only one week, but can be more than a month. Approximately 15 percent of people with hepatitis A have symptoms from six to nine months. Approximately one in 100 people infected with HAV may experience rapid and severe infections (so-called 'fulminant'), which - very rarely - can lead to liver failure and death.

How is hepatitis A diagnosed ?

Diagnosis of hepatitis A is confirmed by blood tests. The doctor will order these tests if we are experiencing symptoms of hepatitis A or if we want to know whether you were infected with HAV in the past. The blood test looks for two types of antibodies to the virus, which referred to as IgM and IgG (Ig stands for immunoglobulin). First, look for IgM antibodies, produced by the immune system of five to ten days before symptoms appear and usually disappear within six months. Tests also search for IgG antibodies, IgM antibodies are replaced and protect against HAV infection.

• When blood tests show negative for IgM antibodies and IgG, we probably have never been infected with HAV, and should consider getting vaccinated against HAV.
• If you are positive for IgM antibodies and negative to IgG, our chances of contracting HAV in six past month, and the immune system is being removing a virus or infection is becoming increasingly severe.
• When the tests showed negative for IgM antibodies and positive for IgG antibodies, we may be infected with HAV in an earlier time, or we already vaccinated against HAV. We are now immune to HAV.

Note : Hepatitis A is endemic in Indonesia. This means that the majority of Indonesian people ever exposed to HAV during childhood, and most likely will be immune to infection again. Because of this, most doctors HAV test is not considered beneficial for people with HIV in

Indonesia.

How to people with HIV ?

People with HIV do not have the risk of becoming infected with HAV higher

than others. However, several studies indicate that people with HIV is more likely to experience symptoms of hepatitis A for Longer term, the meaning may take longer to recover fully from hepatitis A. One other important issue to consider is that many HIV-positive people taking antiretroviral drugs can be bad for the liver. Some of these drugs can worsen the symptoms ofhepatitis A. Because of this, maybe we should stop using all drugs so that the hepatitis A began to recover or liver enzyme levels returned to normal. Talk with your doctor before any medication dismiss.

How is hepatitis A treated ?

The usual treatment for hepatitis A is a break at sleep. There are also important to drink plenty of fluids, especially when we experiencing diarrhea or vomiting. Painkillers which counter, such as ibuprofen can reduce the symptoms hepatitis A, but we should talk more check with your doctor.

When we feel we may have been exposed to HAV - for example when someone in our household recently been diagnosed with hepatitis A - we should see a doctor to discuss the benefits of immune globulin injection (also called as gamma globulin). Immune globulin contains lots of antibodies against HAV, which can help prevent the onset of disease when we are exposed to the virus. Immune globulin must be given within two to six weeks after we might have been exposed to HAV. When we receive immune globulin to preventhepatitis A, we should also receive hepatitis A vaccine (discussed below).

How can hepatitis A be prevented ?

The best way to prevent hepatitis A is vaccination. Vaccination requires two injections, usually given with a time gap of six months. Side effects of hepatitis A vaccination, if it occurs, is usually mild and may include soreness at the injection site and mild flu-like symptoms. Also available is a combination vaccine for viralhepatitis A and B. HAV vaccine is very effective - more than 99 percent of people who receive a vaccination immune to viruses and not be exposed tohepatitis A if exposed. There is little doubt that HAV vaccination in people with very low CD4 counts may not provide immunity (due to very weak immune systems), so it should be vaccinated at a CD4 count is still quite high.

When we feel we have not been infected with hepatitis A, we should discuss with your doctor. Because people with HIV often experience more severe symptoms when infected with HAV, and our heart is essential to remove the remaining end of ARV drugs, HAV vaccination is recommended for people with HIV. Vaccination is especially important for people with HIV and hepatitis B or C.

Although we have not received vaccination against hepatitis A, there are some things we can do to prevent

HAV infection:

• Avoid water, including ice, which could be contaminated with feces
• Avoid raw shellfish or undercooked
• Always wash hands with soap and water after using the room
• bathing, changing diapers and before preparing
• or eating food
• Wearing a latex barrier ('dental dam') to sex oralanal

Anti-cardiolipin Antibodies (ACA) Test

Anticardiolipin Antibodies are proteins found in the body that works against kardiolipin. Kardiolipin and other related phospholipids are lipid molecules that are usually found in cell membranes and platelets as well as having an important role in regulating blood clotting. Whenantibodies produced against kardiolipin, they will increase the risk of blood clots forming an undue (thrombosis) in the arteries and veins.

Anticardiolipin Antibodies belong to a group of antiphospholipid antibodies (APA) in conjunction with lupus anticoagulan (LA). LA causes the elongation of activated partial thromboplastin time (APTT). Clinical manifestations associated with the respective antibody appeared similar, namely thrombosis. Clinical experience suggests that venous thrombosis may be associated with LA, and arterial thrombosis is more likely associated with a high titer of ACAantibodies. Antiphospholipid antibodies are acquired abnormalities; may occur in association with systemic autoimmune disorders or by itself. Patients remain at risk for thrombosis as long as there are autoantibodies.

Clinical Problems

Elevated levels of anticardiolipin antibodies found in antiphospholipid syndrome (thrombosis of arteries and veins are recurrent, recurrent miscarriage), autoimmune diseases (SLE, HIV / AIDS), preterm labor, pre-eclampsia, intrauterine growth retardation, thrombocytopenia, malignancy (leukemia, lymphoproliferative disorders and plasmasitik, solid tumors), infections (bacteria, viruses, protozoa), neurologic events including transient ischemic attack and stroke, liver disease, and disease dermatologik (livedo reticularis, acrocyanosis, pyoderma, extensive skin necrosis). The influence of drugs: chlorpromazine, procainamide, kuinidin, penicillin, many antibiotics, phenytoin.

Procedure

Anticardiolipin antibodies consists of three kinds, namely IgM, IgG, and IgA. Tests for anticardiolipin IgM and IgG antibodies are often asked to help determine the cause of thrombosis, recurrent pregnancy loss, or thrombocytopenia. It may also be requested along with the testing of lupus anticoagulant (LA) to help investigate the cause of APTT prolonged, especially if clinical findings indicate that the patient has SLE or another autoimmune disorder. If the primary test results are normal but clinical suspicion is still there, then testing can be performed IgA anticardiolipinantibodies.

If one or more types Anticardiolipin antibodies are detected, then the same test is usually repeated at least After 6 weeks to help determine whether their presence is persistent or temporary. If the test is negative, may be retested at a later date because theseantibodies can develop at any time.

Anticardiolipin antibody testing was conducted by ELISA (Enzyme linked immunosorbent assay). Testing using an automatic analyzer has an accuracy better.

Serum specimens used were obtained by collecting venous blood in a tube and a red lid with a dizzying centrifuger to separate serum from blood cells. Avoid actions that cause hemolysis in the sample. No special preparations or restrictions on food-beverage intake in patients before sampling.

Venous Blood Sampling in Patients Posted Intravenous (IV) Lines

In order to obtain blood specimens qualified laboratory tests, the blood sampling procedure must be done correctly, from preparation equipment, the choice of anticoagulant, the selection of the location of the vein, taking up with a labeling technique (click here to see the blood sampling procedure) .

Selection of the location of the vein becomes an important concern when the patient is inserted intravenous (IV) line, for example infusion. In principle, bloodsampling should not be undertaken on an arm attached to an IV. If one arm is attached infusion, blood sampling is performed pasa infusion arm that is not installed. If the two arms attached to an IV, did capture the leg vein. So what if the entire venous access is not possible to do blood sampling? Here is a sampling of blood in patients who mounted an IV or IV-lines (examples of cases in patients with burns over 70%).

Alternative 1

If possible, do blood sampling in the arm that is attached to an IV.

Alternative 2

If it is not possible, do blood sampling in the area of ​​the foot.

Alternative 3

If there is no venous access at another location, perform blood sampling in the arm that is attached infusion by way of :

1. Ask the nurse to stop the flow of infusion for at least 2 minutes before the shooting.
2. Attach a tourniquet on the lower portion of the IV needle.
3. Perform blood sampling at a different vein from the attached infusion or at the bottom of the veins attached to the infusion.
4. Ask the nurse to restart the infusion after the specimens were collected.
5. Make a note that the specimens were collected from the terpasangi infusion arm and the type of fluid given intravenously. Write this information on lab request sheet.

Alternative 4

If there is only one venous access alone in a place that is attached infusion, then :

1. Stop the flow of infusion as the above
2. Remove the blood from the veins, discard the first 2-5 ml, and flow capacity in the next blood sample tubes.
3. Ask the nurse to restart the infusion after the specimens were collected.
4. Make a note that the specimens were collected from the terpasangi infusion arm and the type of fluid given intravenously. Write this information on lab request sheet.

Attention : Selection of alternatives 3 and 4 must be with the permission and supervision of a doctor. Phlebotomis can cooperate with the nurses for this decision procedure.

Laboratory examination of health, Rheumatoid Factor

Rheumatoid factor (rheumatoid factor, RF) are immunoglobulins that react with IgG molecules. Because the patient also contain IgG in serum, then the RF including autoantibodies. RF causative factor is not known for sure, although complement activation due to the interaction of RF with IgG play an important role in rheumatoid arthritis (rheumatoid arthritis, RA) and other diseases with positive RF. Most of the RF is IgM, but can also be IgG or IgA.

Positive RF was found in 80% of patients with rheumatoid arthritis. Very high RF levels indicate a poor prognosis with severe joint disorders and possible systemic complications.

RF often found in other autoimmune diseases, such as LE, scleroderma, dermatomyositis, but levels are usually lower than the levels of RF in rheumatoidarthritis. Low levels of RF are also found in non-immunological diseases and the elderly (above 65 years).

RF test is not used for monitoring treatment because the results of common tests remain positive, although there has been a clinical recovery. In addition, it takes about 6 months for a significant increase in titer. For the diagnosis and evaluation of RA is often used CRP test and ANA.

RF test for serum patients examined using the method of latex agglutination or nephelometry.

Reference Values

ADULT : a chronic inflammatory disease; 1/20-1/80 positive for the state of rheumatoid arthritis and other diseases;> 1 / 80 positive for rheumatoid arthritis.

CHILDREN : usually not done

Elderly : slightly increased

* Reference value may be different for each laboratory, depending on the method used.

Clinical Problems

INCREASED CONTENT : rheumatoid arthritis, LE, dermatomyositis, scleroderma, infectious mononucleosis, leukemia, tuberculosis, sarcoidosis, cirrhosis, hepatitis, syphilis, chronic infections, the elderly.

Factors that may affect the laboratory's findings :

• RF test results are often still found to be positive, regardless of whether there has been a clinical recovery.
• RF can be positive test results on a variety of clinical problems, such as collagen disease, cancer, cirrhosis of the liver.
• Elderly may have increased titers of RF, without suffering any illness.
• Due to diversity in the sensitivity and specificity of this screening test, positive findings should be interpreted based on the evidence contained in the clinical status of patients.