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The Paediatric Rheumatology Unit (PRU) at Vall d’Hebron University Hospital sits within the Rheumatology Department and is tasked with specialist care of locomotive system inflammatory disorders and other autoimmune diseases affecting paediatric patients. It consists of two rheumatology specialists with specific training in paediatric rheumatology disorders, Dr Estefanía Moreno Ruzafa and Dr Mireia López Corbeto, a specialist in Paediatrics with specific training in paediatric rheumatology, Dr Laia Martínez Mitjana, and a nurse specialising in rheumatic disorders in children, Julia Vivancos Pons.
The Paediatric Rheumatology Unit has always been a centre of reference within our Rheumatology Department. We have a close relationship with other paediatric units with the aim of setting up common strategies for diagnosing, treating and monitoring our patients.
The Bone Metabolism Unit (UMO) focuses on detecting, treating, and monitoring patients with metabolic bone disorders. Our specialized care comprises pathologies ranging from osteoporosis, which is the most common of these disorders, to Paget's disease and osteomalacia, and includes rare diseases like osteogenesis imperfecta.
We concern ourselves with detecting, treating, and monitoring patients with premenopausal, postmenopausal, and male osteoporosis, along with osteoporosis that can appear secondary to drugs and other diseases, such as transplants, blood and endocrine diseases, HIV infection, bariatric surgery, breast cancer, and chronic kidney failure. These pathologies can, through various mechanisms, cause osteoporosis.
The Rheumatology Department at Vall d'Hebron Hospital has a long and successful history of treating patients with immune-mediated inflammatory diseases (IMID). The IMIDs are a group of systemic illnesses that share common characteristics and are of unknown aetiology. Depending on which organ is most severely affected, different medical specialities are involved in caring for these patients. In addition, we have a wealth of experience in precision medical research in this area.
The Inflammation and Autoimmunity Unit is divided into three large departments:
Osteogenesis imperfecta (OI), also known as "brittle bone disease", is a genetic disorder that affects the production of collagen, a principal element in connective tissue and bone. These individuals easily sustain fractures, even without trauma. There are various types of OI, so symptoms can vary. In most cases, the disease is caused by a mutation in the gene coding for type I collagen.
OI can cause fragile bones, short stature, delays in growth, deformities of the spinal column and other bones, blue sclera, hearing loss, and problems with the formation of the teeth (dentinogenesis imperfecta). In its most severe form, babies die shortly after birth. There are mild forms that can manifest with premature osteoporosis.
It is a very infrequent disease and is considered rare. The estimated incidence of OI is
approximately 1 out of every 10,000-20,000 births, but we must keep in mind that the milder forms may not be diagnosed.
If a patient presents symptoms like those mentioned above, leading to the suspicion that they may have this disease, a genetic study must be carried out.
It requires a multidisciplinary approach. Treatment aims to improve the impact on quality of life and prevent complications. Physical therapy, occupational therapy, detecting and treating dental and respiratory problems, dealing with hearing loss, and surgery to correct deformities are very important. Pharmacological treatment is carried out using widely employed osteoporosis drugs.
Osteomalacia is a skeletal mineralisation disorder. The bones are soft and this causes deformation and fractures, even without trauma, especially affecting the pelvis, ribs, and spinal column. In addition, it can cause pain, especially in the spinal column, pelvis, legs, and ribs, as well as weakness in the legs. In childhood, this disorder is called rickets and it can also negatively affect growth.
In order to correctly mineralise, bones need calcium and phosphate. The absorption of these substances (especially calcium) depends on vitamin D, which is synthesized in the skin using UVB rays from the sun. Thus, osteomalacia is caused by a severe deficiency in vitamin D and/or phosphate.
The main causes of a severe vitamin D deficiency are varied and include:
Another, more infrequent cause is phosphate deficiency, either congenital (such as X-linked hypophosphataemic rickets or fibrous dysplasia) or acquired (Fanconi syndrome, tumours, IV iron administration, antiretroviral therapy, etc.).
The diagnosis will be performed based on the symptoms, blood analysis, urinalysis, and X-rays.
Treatment consists of correcting the vitamin D and calcium deficiencies and also treating the causes underlying these.
This is the second most frequent bone disorder, following osteoporosis. It affects 1.5-3% of the population over 65 years of age. It was described by Sir James Paget in 1876. In this disease, the natural process of the destruction of old bone and the formation of new bone (called bone remodelling) is abnormal and disordered. As a consequence, the bone is fragile, it increases in size, and it presents deformity. Thus, it also receives the name of deforming osteitis. It usually affects the cranium, spinal column, and the pelvis. The risk of having this disease increases with age, and it is very rare in young people.
The underlying cause is not known for sure, but it's known to have an important genetic and family component. Thus, the probability of suffering this disease increases if family member has it. It could also be associated with a viral infection like measles or rubella.
It usually does not produce symptoms. In fact, the diagnosis is usually made based on an unusually high alkaline phosphatase level or findings suggestive of the disease on imaging tests that were ordered for another reason. However, it can cause pain in the affected area that does not improve with rest due to the increase in bone, as well as redness and heat secondary to the increased number of blood vessels in that area. If it affects a joint, it can cause arthrosis. If it compresses nerve roots, it can cause sciatica or even deafness (if the head is affected). It can also cause fractures. A rare complication is the degeneration into bone cancer (osteosarcoma).
Bone scintigraphy is the nuclear medicine technique that reveals which bones are affected by the disease.
The medical treatment includes pharmaceuticals to improve pain (analgesics and anti-inflammatory agents) and pharmaceuticals that inhibit bone remodelling, such as biphosphonates (zoledronat, alendronat), which are widely used for osteoporosis. Measures to improve quality of life, such as using a cane if arthrosis is present or using hearing aids if the illness has caused deafness, are very important. If a bone or joint is a severely affected, surgery can be considered. In general, the illness responds well to treatment and has a good prognosis.
Immunotherapy has revolutionised the treatment of some cancers in recent years. The immune system's job is to recognise and eliminate tumour cells, which prevents the appearance of tumours. However, when the tumour cells evade the immune system or it is not able to contain the tumour, that is when the cancer becomes apparent. The principle underlying immunotherapy is over-activating the immune system so that it can act against tumour cells. Nevertheless, this over-activation of the immune system can favour the appearance of inflammatory autoimmune diseases such as arthritis or myositis.
These adverse effects of immunotherapy, called immune-related adverse events (irAE), can manifest in any organ in the body. In rheumatology, the most common effects are joint issues with pain and swelling (arthritis) and inflammation in the muscles in the form of myositis. Other presentations include dry eye syndrome (dry eyes with a feeling of having "sand" in them), inflammation of vessels (vasculitis), or even kidney problems (nephritis).
These effects can occur in any patient being treated with immunotherapy, but it is more commonly seen in relation to the medications nivolumab, pembrolizumab, and ipilimumab. Diagnosing it requires an evaluation by a rheumatologist, who will take the symptoms into account, along with the analytical and imaging results, to make a more precise diagnosis.
Treatment is complex, as the immunotherapy must be continued due to the cancer. The oncologist and rheumatologist must carry out a joint evaluation to decide on the best treatment. The most commonly used treatments are anti-inflammatory agents and glucocorticoids, although in more severe cases, treatment with biological drugs (such as TNF-alpha inhibitors) can be considered.
SLE is a systemic autoimmune disease. Under normal conditions, the immune system produces proteins (antibodies) to protect us from bacteria, viruses, and other foreign substances (what we call antigens). In autoimmune diseases like SLE, the immune system gets "confused" and cannot distinguish between foreign particles and our own cells, so it produces antibodies against our own body, which causes inflammation and damage to different organs.
It being a systemic disease means that it can affect most parts/organs of our body: skin, joints, kidney, lungs, etc. It is a chronic disease that has flares or flare-ups, meaning that it goes through periods where it is more active (flare-ups) and periods of inactivity.
Antiphospholipid syndrome is characterized by the appearance of thrombosis (blood clots) in any area of the body, complications during pregnancy (especially recurring miscarriages and premature births), and the presence of antibodies against phospholipids. Half of the cases of APS are associated with SLE.
SLE can affect almost every organ in the body. The most frequent symptoms are:
The most characteristic clinical manifestations of APS are thrombosis (blood clots) and serial miscarriages.
This thrombosis can trigger deep vein thrombosis in the legs, strokes or brain bleeding, myocardial infarctions, pulmonary thrombosis, ocular thrombosis, etc.
Among the complications that APS may cause during pregnancy, the most common are repeated miscarriages (mostly before week 10 of gestation), although it can also give rise to premature births (before week 34 of gestation).
Apart from the thrombosis and obstetric complications, patients with APS may also present with anaemia, kidney problems, convulsions, arrhythmia, and different kinds of skin lesions.
SLE is a disease that predominantly affects women; one man is diagnosed with this illness for every nine women. It can appear at any age, although most cases manifest between 17 and 35 years of age.
What exactly triggers the disease is unknown. It is believed that an infectious agent may initiate the disease, but at the same time, the individual must present genetic and hormonal factors for this to occur.
APS also affects women (60-80%) more than it affects men. It is unknown exactly why there are individuals who test positive for antiphospholipid antibodies but have never had thrombosis or a miscarriage, while others who are positive do have these issues.
The diagnosis for SLE is clinical and is based on three main aspects: the symptoms the patient reports, the alterations observed on the physical examination, and the results of the blood and urine analysis. There is no single test to diagnose SLE.
There are some abnormalities on a blood test that can make us suspect that a patient may have SLE. It is common for these patients to have a low number of leukocytes, lymphocytes, and/or platelets. We can also detect the presence of antinuclear antibodies (ANAs). Almost 100% of patients with SLE are positive for these, but this does not constitute a diagnosis of the disease, since healthy people or those with other illnesses can test positive.
Diagnosing APS is based on the combination of clinical characteristics mentioned previously (presence of thrombosis or obstetric problems like miscarriages or premature births) and the presence of one or more of the antibodies typically associated with the disease (lupus anticoagulant, cardiolipin antibodies, and anti-beta 2-glycoprotein antibodies).
There is no single cure for SLE, since treatment will vary for each patient based on the clinical manifestations they present. It is usually a long-term, chronic treatment. Generally speaking, anti-inflammatory agents and corticosteroids are prescribed to treat flares and immunosuppressants (hydroxychloroquine, methotrexate, azathioprine, mycophenolate, etc.) are used, based on the areas/organs affected, to treat and prevent new flare-ups. Currently, we only have one biological pharmaceutical approved for SLE, belimumab, although numerous studies are underway that aim to find new, effective drugs to treat this disease.
Treatment for APS mainly includes the administration of an anti-clotting treatment (aspirin) or anticoagulant, based on the clinical manifestations and antibody profile of the patient.
The most common diagnostic test used for suspected SLE and APS is the blood analysis, which includes testing for auto-antibodies.
Other studies and tests can also be used, based on the patient's symptoms: urinalysis to evaluate whether the kidney is affected, chest X-rays and echocardiogram when the heart or lungs are involved, renal biopsy if kidney problems are detected, skin biopsy, head CT or MRI if neurological symptoms appear, etc.
There is no specific measure we can take to prevent the appearance of SLE and APS.
Once manifested, an early diagnosis is essential for both illnesses in order to begin treatment quickly and thus avoid possible complications. Patients must regularly see and work in close collaboration with their specialists.
In addition, for both SLE and APS, it's very important to strictly control the classic cardiovascular risk factors (high blood pressure, diabetes, dyslipidaemia, obesity, and tobacco use), because they can very negatively affect the prognosis of both diseases.
Lupus-Eritematoso
American College of Rheumatology: Lupus
American College of Rheumatology: Síndrome Antifosfolípido
American College of Rheumatology: Tratamientos
Rheumatoid arthritis is a chronic inflammatory disease that primarily affects the joints, although it can also compromise other organs. There is definitely a genetic component, but its cause is unknown.
It principally manifests as pain and inflammation in the joints (hands, feet, shoulders, knees, etc.) and morning stiffness. It can be accompanied by fever, general malaise, and/or fatigue.
Untreated rheumatoid arthritis can end up causing a deterioration and deformity of the affected joints, which can cause serious disabilities. However, the early diagnosis we often perform and the quantity of drugs we have available today mean that most patients with rheumatoid arthritis can lead a practically normal life. For rheumatoid arthritis to have a good clinical evolution, an early diagnosis is very important, starting treatment as soon as possible. This is because the first years during which the illness presents are key for improving the prognosis and evolution of these patients.
The most frequent symptoms are pain and inflammation in the joints. The joints that are most commonly affected are the knuckles of the hands, wrists, and feet, but the illness can also affect any other joint in the body (elbows, shoulders, hips, knees, etc.) and morning stiffness is typically associated with it. The joints of the spinal column are usually not affected, and when this happens it is in the neck area (cervical involvement).
Apart from the symptoms in the joints, rheumatoid arthritis can give rise to other symptoms or affect other organs.
In addition, patients with rheumatoid arthritis can present other associated illnesses more often than people without arthritis. They have a higher risk of suffering from osteoporosis (decalcification of the bones) and having cardiovascular problems like myocardial infarction or stroke. This is why in patients with rheumatoid arthritis, it's extremely important to control other factors that may aggravate their condition, such as high cholesterol, diabetes, high blood pressure, tobacco use, and obesity.
It can affect any person, of any race, anywhere in the world, but it affects more women than men (approximately three women for every man), and it usually appears between the ages of 40 and 60.
The cause of the disease is unknown. What we do know is that there are different components involved in the appearance of the disease:
Therefore, rheumatoid arthritis appears when a combination of the circumstances described above occurs at the same time. Alterations in the immune system can occur in genetically predisposed individuals and can combine with hormonal and environmental factors. It is not known exactly how this process happens.
Diagnosing the illness is done in a comprehensive way, considering the symptoms reported by the patient, the physical examination, the results of the analyses, and the X-rays. It is important to keep in mind that there is no blood test or other kind of test that can diagnose rheumatoid arthritis independently; a medical evaluation of the entire situation by a rheumatology specialist will always be required.
The symptoms described by the patient are usually the ones we've described in the "symptoms" section. The physical examination usually reveals pain, inflammation, and a limited range of movement in one or more joints, and this tends to be symmetrical.
On a blood analysis, elevated inflammatory markers are often observed, such as a high erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level. Mild anaemia can also appear.
Rheumatoid factor (RF) can be tested for on a blood analysis, and 70-80% of patients with rheumatoid arthritis are positive for it. However, it's important to point out that up to 30% of healthy people without arthritis can also turn up positive, so being positive for this factor does not definitively tell us if someone has the disease.
Anti-cyclic citrullinated peptide (anti-CCP) antibody is a more specific biomarker for rheumatoid arthritis. This means that in a person with arthritis, if they are positive for this antibody, it practically confirms the diagnosis. However, if it turns up negative, the illness is not ruled out, since up to 40% of patients with rheumatoid arthritis are negative for this biomarker.
The fundamental basis for the treatment of this illness is using pharmaceuticals that we call disease-modifying drugs (DMDs). These drugs act on the cells and molecules that participate in the disease process and manage to change its natural course. We divide these into three groups: traditional, biological, and synthetic.
Besides the DMDs, another important part of treating arthritis is providing the patient with symptomatic relief. We round out treatment plans with pain relievers and conventional anti-inflammatory agents, to work in conjunction with DMDs during disease flare-ups or to provide relief while these agents take effect. They act quickly, but their effects are short-lived and disappear just hours after a dose is taken.
Within this group we also have corticosteroids, which are the most effective pharmaceuticals to quickly control joint inflammation. They can be administered orally or delivered directly to the inflamed joints as injections.
Unfortunately, there is no specific action to prevent the appearance of rheumatoid arthritis. Nevertheless, as we know tobacco use to be the only environmental factor that can contribute to the appearance of and a worse prognosis for arthritis, it is recommended that the entire population in general avoid this habit, but this is especially true for patients at risk for arthritis.
Sociedad Española de Reumatología: aprendiendo a convivir con la Artritis Reumatoide
American College of Rheumatology (ACR): la Artritis Reumatoide
American College of Rheumatology (ACR): web amb informació detallada dels tractaments més utilitzats en reumatologia
Spondyloarthritis is the name of a group of diseases whose common element is inflammation of the axial skeleton (especially the spine), although it can also affect the peripheral joints (hands, feet, knees, etc.). The following diseases are included in this group: axial spondyloarthritis (or ankylosing spondylitis, in its more advanced stage), psoriatic arthritis, arthritis related to inflammatory intestinal disease, reactive arthritis, and a subgroup of juvenile idiopathic arthritis.
The most common symptom is pain in the lower back or buttocks (inflammatory lumbar pain). This pain is characterised by worsening with rest and improving with exercise. It is associated with prolonged morning stiffness, can wake patients up in the night, and it improves with anti-inflammatory medications. It can also affect the peripheral joints; this is most common in psoriatic arthritis, which can manifest as pain and inflammation in the knuckles, wrists, feet, and other joints.
Spondyloarthritis also affects what we call the enthesis, where a tendon inserts into a bone. The most commonly affected entheses are the Achilles tendon and the epicondyles (elbows), although any tendon insertion can be affected.
Finally, these diseases also present with manifestations outside the joints, and these may be the only visible presentation of the illness. These include inflammation of the eye (uveitis), inflammatory intestinal disease (ulcerative colitis or Crohn's disease), or inflammation of the skin (psoriasis). In fact, 30% of patients with psoriasis have psoriatic arthritis and the skin lesions tend to predict the joint disease.
Spondyloarthritis can affect anyone, although it usually presents between adolescence and 50 years of age. Axial spondyloarthritis usually manifests before the age of 40, while psoriatic arthritis can start later (between 30 and 50 years of age). These affect women and men equally, even though axial spondyloarthritis is slightly more prevalent in men.
It is quite common for people who have one of these illnesses to have family members with the same disease or another spondyloarthritic condition. That is why it was decided these be grouped together, thinking that they share a common aetiology. Thus, genetics is the main cause of these diseases, with several genes identified; the most prominent is HLA-B27, which can be detected in the laboratory, making diagnosis easier. Other causes, like infectious aetiologies, have been investigated, since in many cases the disease is preceded by an infection that acts as a trigger.
The diagnosis of the disease is done in a comprehensive way, considering the symptoms the patient complains of, the physical examination, the analytical results, and the imaging (X-ray, ultrasound, MRI) results. It's important to consider that there is no one analysis or other test that can diagnose these diseases by itself; it will always require a specialist in rheumatology to perform a medical evaluation of the situation as a whole.
Since the symptoms they present can be confused with very common conditions (lower back pain) and there is no specific test that can diagnose them unequivocally, it's common for a diagnosis to take up to 10 years. It is routine for patients to visit multiple professionals and specialists (traumatologists, physical therapists, osteopaths, primary care physicians, etc.) before receiving a diagnosis.
One of the treatment pillars for spondyloarthritis is exercise and physical therapy that targets the joints. The main pharmacological options are anti-inflammatory agents, and in case these do not control the illness, the so-called disease modifying drugs (DMDs) will then be used. Within the DMDs, we use conventional DMDs, like methotrexate and sulfasalazine, and more recently we have begun using biological and synthetic DMDs, which represent an important advance in the treatment of these diseases.
Unfortunately, there is no particular action we know of that can prevent the appearance of spondyloarthritis.Nevertheless, tobacco use is one of the most important factors involved in these diseases and their progression, so avoiding tobacco is recommended. In the case of psoriatic arthritis, the fact that the skin disease often precedes the joint disease offers us a window of opportunity to identify it early and avoid its progression. Biomarkers to be able to identify it before it appears are being researched.
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