Mixed Connective Tissue Disease

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Mixed connective tissue disease

Mixed connective tissue disease (MCTD) is a rare autoimmune disorder that causes signs and symptoms of other connective tissue diseases. People with mixed connective tissue disease experience features of three other diseases — lupus, scleroderma and polymyositis. For this reason, mixed connective tissue disease is sometimes referred to as an overlap disease.

Signs and symptoms of these three other diseases usually don't appear all at once. This makes diagnosing mixed connective tissue disease somewhat complicated. Often people with mixed connective tissue disease are first diagnosed with lupus. As the disease progresses and other signs and symptoms become apparent, the diagnosis is corrected.

Mixed connective tissue disease occurs most often in women and is usually diagnosed in young adults in their 20s and 30s. Children have also been diagnosed with mixed connective tissue disease.

Mixed connective tissue disease is somewhat of a controversial term among arthritis specialists (rheumatologists). Some question whether mixed connective tissue disease is its own specific disease or whether it's a precursor to another connective tissue disease.

Signs and symptoms

Mixed connective tissue disease doesn't have a unique set of signs and symptoms. Instead, people with mixed connective tissue disease usually have signs and symptoms of lupus, scleroderma and polymyositis, including:

Muscle weakness
Joint pain
Joint swelling
Swollen fingers
Mild fever
Raynaud's phenomenon — blood vessel spasms that interrupt blood flow to the fingers, toes, ears and nose
Raynaud's disease


Doctors don't know what causes mixed connective tissue disease. The disease is part of a larger group of diseases known as autoimmune disorders. When you have an autoimmune disorder, your immune system — the part of your body responsible for fighting off disease — mistakes normal, healthy cells for intruders. As a result, healthy tissue in your body is damaged, causing signs and symptoms of disease.

It isn't clear what causes your immune system to attack your body. Doctors believe a complex mix of viruses, chemicals and genetic factors may be at play.

Risk factors

Doctors don't know what puts you at risk of mixed connective tissue disease. Some research shows the disease may occur more frequently in people with a family history of connective tissue diseases. Other findings show an increased risk in people exposed to certain chemicals, including vinyl chloride and silica. More research is needed to confirm these findings.

When to seek medical advice

Signs and symptoms of mixed connective tissue disease usually begin mildly and may not prompt you to seek medical attention. But if signs and symptoms become bothersome or interfere with your daily routine, make an appointment with your doctor.

Also see your doctor if you've been diagnosed with lupus or another connective tissue disease and you begin developing new signs and symptoms.

Screening and diagnosis

Your doctor may suspect mixed connective tissue disease based on your signs and symptoms. He or she will conduct a physical exam to look for signs such as swollen hands and painful, swollen joints.

A blood test determines whether you have a certain antibody in your blood that indicates mixed connective tissue disease. The presence of this specific antibody — called U1-RNP — can confirm your doctor's suspicions.

Mixed connective tissue disease usually develops slowly, making it difficult to diagnose. As your signs and symptoms evolve over time — sometimes many years — your diagnosis may change. Many people are first diagnosed with lupus and later re-diagnosed with mixed connective tissue disease. Others begin with a diagnosis of mixed connective tissue disease only to later find they have lupus or another connective tissue disorder.


Mixed connective tissue disease and its treatment can lead to serious complications, including:

Pulmonary hypertension. High blood pressure affecting the arteries in your lungs (pulmonary hypertension) is the most common cause of death in people with mixed connective tissue disease. You might experience difficulty breathing or chest pain if you have pulmonary hypertension. People with mixed connective tissue disease usually need to take medications to control pulmonary hypertension.
Heart disease. People with mixed connective tissue disease are at risk of developing heart conditions, including enlargement of parts of the heart and inflammation around the heart (pericarditis). Your doctor may routinely monitor your heart with an electrocardiogram.

Side effects of long-term steroid use. Steroids are commonly used to manage the signs and symptoms of mixed connective tissue disease. While these medications are effective, they don't come without risks. If you take steroids, your doctor will likely monitor you for adverse effects, such as bone loss due to osteoporosis or avascular necrosis, muscle weakness and infection.
Pregnancy complications. Women with mixed connective tissue disease may experience flares during pregnancy. Babies born to women with mixed connective tissue disease are at risk of being born with a low birth weight. If you're planning to become pregnant, talk with your doctor about this risk.


No cure exists for mixed connective tissue disease, although treatments can help manage the signs and symptoms of the disease. Your treatment may vary from another person's because your signs and symptoms may be different.

While no standard treatment exists, the most common treatment for mixed connective tissue disease is corticosteroids, such as prednisone.

People with mild forms of mixed connective tissue disease may not need any treatment. You may require treatment only during flares or you may require constant medication. Work with your doctor to ensure that your signs and symptoms are adequately controlled.

Coping skills

Living with a chronic disease that has no cure requires effective coping skills. Consider trying to:

Find out as much as you can about mixed connective tissue disease. Learn as much as you can about the disease. Ask your doctor and other health care team members for assistance in locating reliable resources. The more you know about the disease, the easier it is to understand what's happening to your body.

Take care of yourself. Control your health as best you can. Eat a balanced diet with plenty of fruits and vegetables. Get exercise on days you feel up to it. Keeping your body healthy makes you better able to deal with the daily stress of living with a chronic illness. And it better prepares you to cope with your next flare.

Seek support from others. Social support helps you cope with the stress of mixed connective tissue disease. Ask your doctor about support groups in your area for people with chronic illnesses. Go online to http://www.LupusMCTD.com to connect with other people living with mixed connective tissue disease.

What is Mixed Connective Tissue Disease (MCTD)?

A few decades ago, scientists discovered that patients with a connective tissue disease had symptoms of both lupus, scleroderma, myositis, etc. These diseases are called ‘overlap-syndromes’.

 In 1969 Sharp and his co-workers found out that there is one specific type of overlap-syndrome with symptoms of lupus, scleroderma, myositis and rheumatoid arthritis, together with a large quantity of antibodies against one specific antigen, namely U1RNP. They believed it to be a distinct disease entity and called it MCTD. Meanwhile, it is known that Sjogren’s Syndrome is very common in MCTD.

It is still a matter of debate whether or not this disorder is diverse from the other overlap-syndromes. In general, however, this disorder is considered a distinct clinical entity.
Most important symptoms

*Raynaud’s phenomenon
Is basically always present in the early phase of the disease, mostly without other symptoms at the level of the fingers, unless scleroderma is also present at the onset of the disease. 

*Swollen fingers
Mostly all the fingers are swollen in the overall length and become ‘sausage-like’. Sometimes this is only temporary, but occasionally it evolves into sclerodactyly (thin fingers with hard skin and limited mobility). 

In the early phase there is painful swelling of the joints of the hands and feet like in rheumatoid arthritis. Damage to the cartilage or bone, however, is rare. As such, malformations do not occur or only seldom and the function of the joints remains intact. This kind of arthritis is comparable to the arthritis seen in lupus. 

*Muscle inflammation
In 10 to 20% of the cases, patients develop a real form of myositis, muscle inflammation (see polymyositis). Two out of three patients suffer from significant muscle pain (no weakening or paralysis), without demonstrable abnormalities in the laboratory test, electromyography or biopsy. Patients complain mostly of pain at the level of the large muscle groups of the shoulder girdle and the upper arms.

The lungs may show the same abnormalities and problems as in scleroderma. Reduced lung volume is common, sometimes reduced absorption of oxygen and rarely overpressure in the lung vessels with fatal outcome occurs.

The same complaints as in scleroderma may occur. 

Inflammation of the heart sac or pericardium (pericarditis) may be acute. Unlike in polymyositis, inflammation of the heart muscle (myocarditis), which may cause heart failure or arrhythmia, occurs rarely. These complications are very serious and may be life threatening. 

*Neurological damage
Meningitis, psychological abnormalities due to brain damage, damage to the spinal marrow or facial nerves have been described. These symptoms occur often in Sjogren’s Syndrome, which often occurs in MCTD.

*Renal involvement
Renal involvement is very rare and can be similar to the damage caused in scleroderma (especially damage to the renal blood vessels) as well as to the damage caused in lupus lupus (damage to the renal filtering units).

*Skin and mucous membranes
The skin may show symptoms of scleroderma as well as of lupus. The mucous membranes (mouth, vagina) and the eyes may be dry due to the Sjogren’s Syndrome .
Who can get MCTD and is it hereditary?
MCTD is a rare disease. In most cases the age of onset lies between 20 and 50 and 8 to 9 out of 10 patients are female. MCTD is not hereditary. There can be a difference in the disease’s genetic susceptibility: the same susceptibility often seen in lupus, rheumatoid arthritis or Sjogren’s Syndrome, can occur in combination.

External factors may also play a role. Some cases of MCTD have been described after the patients had worked professionally with PVC (polyvinylchloride).
Since MCTD overlaps (‘mixes’) different connective tissue disorders, there are many different types, and consequently, many prognoses. Complaints and symptoms depend on the organs involved, the degree of inflammation and the general degree of disease activity. In general the prognosis is favourable if the disease is adequately treated. Life expectancy is comparable to the life expectancy in lupus, i.e. favourable with a few exceptions.
The diagnosis is based on complaints, symptoms and organ involvement and on the presence of anti-U1RNP antibodies in high titre (concentration). It is the only connective tissue disease for which one specific type of antibody is necessary to make a diagnosis (at least in most centres). If the doctor suspects the diagnosis of MCTD, some additional tests like lung function tests, heart check-up, examination of the kidneys and blood pressure need to be carried out. In case of muscle complaints or nerve pains an electromyography is necessary. The results of these examinations may also contribute to a diagnosis.
Although treatments with a low dose of corticosteroids have been successful, there is no standard procedure for MCTD. The treatment is based on the type and degree of organ involvement, and can be a treatment for lupus or for scleroderma. The treatment has to be individualised for each patient.
MCTD and pregnancy
Surveys on the subject are quite different. The influence of pregnancy on MCTD or vice versa can be compared to pregnancy in lupus.
Overlapping syndromes
Besides MCTD there exist also other overlap syndromes which are less clearly definable or which do not have anti-U1RNP antibodies. As in MCTD, treatment is based on the type and degree of organ involvement and it is individualised for each patient. The evolution and prognosis are also comparable to MCTD, except that there may be more individual dissimilarities among patients.
Undefined Connective Tissue Disease (UCTD)
In the early phase of a connective tissue disease and especially at the onset of an overlap syndrome or MCTD, the symptoms can be very limited and unusual. Although the onset of a connective tissue disease can be certain in such cases, it is impossible to define the type of disease with certainty. That is why the term UCTD (= undefined connective tissue disease) is used.

Mostly Raynaud’s phenomenon, joint pains, sometimes arthritis and muscle pains are present. The evolution is very diverse: some patients remain in this phase while others evolve quickly into a real form of lupus or another type of connective tissue disease. Again, treatment has to be individualised according to each patient.


What is Systemic lupus ?

Also called: "lupus erythematosus desseminatus" (LED) or "systemic lupus erythematosus".
Systemic lupus is different from discoid lupus. Discoid lupus is mostly limited to the skin. It can occur by itself or in combination with systemic lupus.
What is systemic lupus?
Systemic lupus is a generalised autoimmune disease.
In an autoimmune disease, the immune system (=defence) partly targets itself, by producing autoantibodies that cause inflammatory diseases.
Generalised means that the autoimmunity can attack different organ systems and can cause generalised disease manifestations
Who is affected by lupus?
Basically anyone at any age, but mostly lupus strikes women of childbearing age (80 to 90%). The number of lupus patients affected by lupus also differs according to race. In the USA lupus is more common in Blacks than in Caucasians. Genetic (hereditary) factors are sure enough believed to play a role in the development of the disease.
Prevalence of lupus
Studies are scarce and results vary widely, but it cannot be denied that the number of lupus patients is increasing. Improved diagnostic measures and a better understanding of the disease are two important factors in the increase of lupus patients, but there is also an absolute rise in the incidence (= number of new patients per year of a specific disease)
Cause and heredity 
The cause remains unknown. Experts are getting convinced of the fact that inflammations and damage are caused by a reaction of autoantibodies with normal cellular components and other elements. In this process both genetic as environmental factors can play a role.

Several genetic factors are of importance, but they are unlikely to be entirely passed on. This is the reason why lupus is not a hereditary disease, although risks of developing lupus are bigger if a relative in the first degree has been diagnosed with the disease.

Ultraviolet rays are an example of an environmental factor known to trigger lupus. Although it has not been proved, viruses may also play a role in the onset of lupus. Lupus, however, is not contagious at all.
Hormones are involved as well: female hormones stimulate lupus, while male hormones protect against it. This is one of the reasons to avoid the use of the contraceptive pill.
Onset and symptoms
Possible symptoms and manifestations of lupus are very diverse. The onset of the disease is never the same: it may start off with any of the symptoms mentioned below, in a mild or severe form. Because there are so many symptoms, we have to stick to the following summary:

90 %
fatigue, arthritis and joint pain

80 %

70 %
hair loss, anaemia, swollen glands

60 %
weight loss, poor appetite, butterfly-shaped rash

50 %
inflammation of the pleura (pleuritis), inflammation of the heart sac (pericarditis), inflammation of the membrane lining the abdominal cavity (peritonitis), renal involvement, personality changes, purpura

40 %
photosensitivity, bacterial infections

30 %
ulceration of the mucous membranes e.g. aphthous ulcers, pain in the muscles or myositis (inflammation of the muscles), gastrointestinal complaints, enlargement of the liver, high blood pressure, pneumonia, myocarditis (inflammation of the heart muscle) and endocarditis (involvement of the heart valves).

20 %
Raynaud's phenomenon (turning white of the fingers), discoid lupus (skin involvement in lupus with round disc-shaped scars), inflammation of the eyes, Sjogren's Syndrome, severe renal involvement, attacks of epilepsy, psychoses, inflammation of the coronary arteries (supply of blood to the heart muscle)

10 %
hives, oedema or formation of blisters on the skin, lupus pneumonia, brain damage or damage to the spinal cord, migraine, autoimmune destruction of red blood cells, low platelet count, neuritis (inflammation of the nerves)

The diagnosis is based on complaints and/or symptoms and/or involvement of internal organs and/or abnormalities in laboratory test results. There is no single lupus test that can confirm the disease. Beginning mild forms of lupus are hard to diagnose, and sometimes diagnosis is only possible after following the evolution of the symptoms. In case of a possible onset of lupus, following up the early symptoms as well as informing the patient are very important.

Because there is no decisive test for lupus and due to the changing character of the disease, criteria have been defined to classify lupus. Their main purpose, however, is scientific research as they can only be used as a guideline to diagnose lupus. In some cases lupus can be diagnosed before the patient meets these criteria.
Must be focused on the following:

general degree of illness and complaints
internal organs involved
degree of involvement of these organs
Medications range from absolutely nothing to high doses of corticosteroids or immunosuppressive drugs.
Antimalarials and nonsteroidal anti-inflammatory drugs are frequently used.

 The basic principle to treat lupus is to react quickly with high doses of corticosteroids and/or immunosuppressive drugs if necessary and maintain the lowest dose possible during periods of low disease activity.
~Drug-induced lupus
Some 50 prescription drugs can produce symptoms of lupus, which normally disappear after the patient stops taking the medication. This does not imply, however, that these drugs are forbidden for lupus patients.

The most important ones are: Hydralasine (Neprosol), Procaïnamide (Pronestyl), Isoniazide (Rimifon), Propylthiouracil (Strumazol), d-Penicillamine (Kelatin)
The prescription drugs mentioned may have other brand names
Lupus en zwangerschap
A lupus patient is allowed to become pregnant if the disease is under control, with a low dose of medication if necessary. The safest drug during pregnancy is a low dose of corticosteroids. A lupus patient should not become pregnant without a complete check-up, given the risk for mother and child. The child may have neonatal lupus due to the presence of anti-Ro antibodies and for the mother there is the risk of a severe flare.

During pregnancy a flare may occur. In this case, it needs to be treated appropriately and the best way to do that is with corticosteroids. If you have lupus, there is a greater risk of miscarriage, often due to anti-cardiolipin antibodies (read further).

These antibodies cause the blood to clot more easily, so that small blood vessels in the placenta can get clogged up. Low weight at birth occurs more often in newborn babies of lupus patients.
~Neonatal lupus 
This is a kind of skin lupus that breaks out a few weeks after birth and disappears at the age of 6 months. It is caused by the transfer of anti-Ro antibodies through the placenta to the foetus.
In more severe cases, the heart of the foetus may be affected at about 18 weeks and the foetus may die, or the baby may be born with a congenital heart block (delayed contraction of the ventricle due to a conduction disorder, resulting in a very slow heart rate).
The survival rate of these babies varies. The children themselves do not have lupus.
Most important antibodies in lupus
Anti-Sm antibodies
About 15 % of lupus patients in Europe have anti-Sm, compared to 30 % in the USA.
It is a disease marker: this means it is only found in patients with lupus, and mostly in relatively serious cases. 
Anti-dsDNA antibodies 
Seen in about 40 % of all lupus patients. In more severe cases of lupus the percentage amounts to 80 % during a flare. These antibodies are tightly linked with lupus and lupus nephritis, though this is not 100 % the case. They occur especially in lupus nephritis, in which they are also believed to play an important role.

About 40 % of people with lupus have anti-Ro. These antibodies are linked with congenital heart block and neonatal lupus and are probably the cause of it. (read pregnancy)
Anticardiolipin antibodies
Often facilitate blood clotting, which may lead to a propensity for miscarriage and thromboses in young patients.
Antibodies against red blood cells (positive Coombtest)
kMay cause haemolysis, or the destruction of red blood cells on an autoimmune basis. Severe autoimmune haemolysis is very rare.
A whole range of other antibodies 
... of which the importance is not yet clear.
~Signs and symptoms that need immediate medical examination:
fever attacks
sudden onset of extreme fatigue
general malaise
neurological complaints
extreme headache or unexplainable mood swings
acute or subacute skin rashes
unexplainable chest pains
unexplainable abdominal pains
new complaints due to arthritis
increasing shortness of breath
presence of protein in the urine
any form of infection

~Evolution and prognosis
Systemic lupus progresses with ups and downs. Periods of serious exacerbations may alternate with periods of low disease activity, in which one may even discontinue taking medication. The patient is then said to be in remission. After menopause, lupus is likely to disappear spontaneously.
Life expectancy has increased greatly over the last 40 years and statistically almost equals a normal life span with 93 % of all patients surviving ten years after diagnosis. This improvement is due to early diagnosis and better use of medication. Even lupus nephritis can be reversed if treatment follows immediately and intensively.

The more severe forms of lupus that lead to death by affecting the brain or kidneys have become rare. Exceptionally, however, complications (mostly infections) or a neglected flare may be fatal.
Once "systemic lupus" is diagnosed, adapted drug treatment should be able to stabilise the disease. Still, lupus is to be considered a serious disorder.
Accurate compliance of medical advice together with regular medical check ups are absolutely necessary to control the disease. Clear information is in this case essential. Also contact with people from our support group, www.LupusMCTD.com can be a step forward in the process of learning how to cope with lupus.


Mixed Connective Tissue Disease (MCTD)
 Mixed connective tissue disease is an uncommon syndrome characterized by clinical features of SLE, systemic sclerosis, polymyositis or dermatomyositis, and RA and by very high titers of circulating antinuclear antibody to a ribonucleoprotein (RNP) antigen.

 Hand swelling, Raynaud's phenomenon, polyarthralgia, inflammatory myopathy, esophageal hypomotility, and pulmonary dysfunction are common. Diagnosis is by the combination of clinical features, antibodies to RNP, and absence of antibodies specific for other autoimmune diseases. Treatment is similar to that for SLE, with corticosteroids if disease is moderate or severe.

Mixed connective tissue disease (MCTD) occurs worldwide and in all races, with a peak incidence in the teens and 20s. The cause is unknown. In some patients, the disorder evolves into classic systemic sclerosis or SLE.

~Symptoms and Signs

Raynaud's phenomenon may precede other manifestations by years. Frequently, the first manifestations resemble early SLE, scleroderma, polymyositis or dermatomyositis, or RA. Whatever the initial presentation, limited disease tends to progress and become widespread, and the clinical pattern changes over time.

The most frequent finding is swelling of the hands that eventually produces a sausagelike appearance of the fingers. Skin findings include lupus or dermatomyositis-like rashes. Diffuse scleroderma-like skin changes and ischemic necrosis or ulceration of the fingertips are much less frequent in MCTD.

Almost all patients have polyarthralgias, and 75% have frank arthritis. Often the arthritis is nondeforming, but erosive changes and deformities similar to those in RA may be present. Proximal muscle weakness with or without tenderness is common.

Renal disease occurs in about 10% and is often mild but occasionally causes morbidity or mortality. A trigeminal sensory neuropathy develops more frequently in MCTD than in other connective tissue diseases.


MCTD should be suspected when additional overlapping features are present in patients appearing to have SLE, scleroderma, polymyositis, or RA. Patients should first be tested for antinuclear antibodies (ANA) and antibody to extractable nuclear antigen (ENA) and RNP antigen. If results of these tests are compatible with MCTD (eg, RNP antibodies very high), γ-globulin level, serum complement levels, rheumatoid factors, anti Jo-1 (anti histidyl t-RNA synthetase), and antibodies to the ribonuclease-resistant Smith (Sm) component of ENA, and double-stranded DNA should be tested to exclude other possible diagnoses.
Further workup depends on symptoms and signs; manifestations of myositis, renal involvement, or pulmonary involvement prompt tests of those organs (eg, CPK, MRI, electromyogram, or muscle biopsy for diagnosis of myositis).

Almost all patients have high titers (often > 1:1000) of fluorescent ANA that produce a speckled pattern. Antibodies to ENA are usually present at very high titers (> 1:100,000). Antibody to RNP is present, whereas antibody to the ribonuclease-resistant Sm component of ENA is absent.

Rheumatoid factors are frequently positive, and titers are often high. The ESR is frequently elevated.

~Prognosis and Treatment

The overall 10-yr survival rate is 80%, but prognosis depends largely on which manifestations predominate. Causes of death include pulmonary hypertension, renal failure, MI, colonic perforation, disseminated infection, and cerebral hemorrhage. Some patients have sustained remissions for many years without treatment.

General management and initial drug therapy are similar to those of SLE. Most patients with moderate or severe disease respond to corticosteroids, particularly if treated early. Mild disease is often controlled by salicylates, other NSAIDs, antimalarials, or sometimes low-dose corticosteroids. Severe major organ involvement usually requires higher doses of corticosteroids (eg, prednisone 1 mg/kg po once/day) or immunosuppressants. If patients develop features of myositis or systemic sclerosis, treatment is as for those diseases.


(Mixed Connective Tissue Disease vs. Undifferentiated Connective Tissue Disease)
Some guests & members have been requesting some clarification of the meaning of the terms "mixed connective tissue disease" (MCTD) and "undifferentiated connective tissue disease" (UCTD).

Connective tissue diseases are a special group of rheumatic diseases (diseases that feature abnormalities of the muscles and/or joints) that can be associated with arthritis. The cause(s) for the connective tissue diseases is (are) unknown. They are characterized as a group by the presence of spontaneous over-activity of the body's immune (defense) system. This over-activity results in the production of unusual antibodies that are found in the blood. The antibodies themselves may or may not cause any problems in patients with connective tissues diseases, but they are commonly found in the blood as an characteristic feature.

The connective tissues are the structural portions of our body that essentially hold the cells of the body together. These tissues form a framework, or matrix, for the body. The connective tissues are composed of two major structural protein molecules, collagen and elastin. There are many different types of collagen protein that vary in amount in each of the body's tissues. Elastin has the capability of stretching and returning to its original length - like a spring or rubber band. Elastin is the major component of ligaments (tissues that attach bone to bone) and skin. In patients with connective tissue diseases, it is common for collagen and elastin to become injured by inflammation. Diseases in which inflammation of collagen tends to occur are also referred to as collagen diseases.

The classic connective tissue diseases include systemic lupus erythematosus, rheumatoid arthritis, scleroderma, polymyositis, and dermatomyositis. Each of these diseases affects people in a characteristic way and causes typical findings that doctors can recognize during an examination. Each also has characteristic blood test abnormalities and abnormal antibody patterns. For example, systemic lupus erythematosus has dsDNA antibodies, while scleroderma has Sc170 antibodies. Additionally, each of these diseases can evolve either slowly or rapidly from very subtle abnormalities before demonstrating the classic features that help in the diagnosis.

When these conditions have not developed the classic features of a particular disease, doctors will often refer to the condition as "undifferentiated connective tissue disease," or UCTD. This designation implies that the characteristic features that are used to define the classic connective tissue diseases are not present, but that some symptoms or signs of a connective tissue disease exist. For example, a person may have a special antibody in the blood, such as antinuclear antibody and muscle pains, but no other definable features of a classic connective tissue disease. Individuals with undifferentiated connective tissue disease may never develop a fully definable condition or they may eventually develop a classic connective tissue disease.

Mixed connective tissue disease, which was first described in 1972, is "classically" considered as an "overlap," or mix, of three specific connective tissue diseases; systemic lupus erythematosus, scleroderma, and polymyositis. Patients with this pattern of illness (that is, with MCTD) have features of each of these three diseases. They also typically have very high quantities of antinuclear antibodies (ANAs) and antibodies to ribonucleoprotein (anti-RNP) detectable in their blood. The symptoms of many of these patients eventually evolve to become dominated by features of one of the three component illnesses, most commonly the scleroderma features.

It is now known, however, that overlap syndromes can involve any combination of the connective tissue diseases. Therefore, for example, patients can have a combination of rheumatoid arthritis and systemic lupus erythematosus (hence, the coined name "rhupus"). Accordingly, today, true mixed connective tissue disease is diagnosed when patients demonstrate the clinical features (exam findings) of overlap illnesses. These patients also have high amounts of ANA and anti-RNP without having such other antibodies as the dsDNA antibodies of systemic lupus erythematosus and the Scl70 antibodies of scleroderma.



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