We are the combination of four hospitals: the General Hospital, the Children’s Hospital, the Women’s Hospital and the Traumatology, Rehabilitation and Burns Hospital. We are part of the Vall d’Hebron Barcelona Hospital Campus: a world-leading health park where healthcare plays a crucial role.
Patients are the centre and the core of our system. We are professionals committed to quality care and our organizational structure breaks down the traditional boundaries between departments and professional groups, with an exclusive model of knowledge areas.
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The commitment of Vall d'Hebron University Hospital to innovation allows us to be at the forefront of medicine, providing first class care adapted to the changing needs of each patient.
Patients with Asperger’s syndrome need a stable and predictable environment that can be easily adapted. It is key to their well-being to establish routines according to their interests, organise their time, avoid inactivity or over intense activity as well as sudden changes. Although the syndrome has no cure, appropriate treatment and involving family members can improve the quality of life of patients.
People with Asperger’s syndrome may have different requirements depending on their age, surroundings and the awareness that they have of their difficulties. For this reason, they need a tailor-made programme that responds to their specific case.
The aim of these customised programmes is to:
It is important to manage their development through different disciplines. These may include cognitive treatments, social skills programmes and occupational therapy for the patient. You also have to consider guidelines on how to resolve conflicts and how to manage pyschoeducational groups for families or caregivers.
In infants, from an emotional and attitudinal point of view, it is important to learn to identify the warning signs in their mood. In this way, we can prevent difficulties in anger management and low tolerance to frustration, since they are patients with a high degree of sensitivity to criticism. Avoid punishment as much as possible and establish more positive reinforcement strategies.
All these guidelines must be established in a space where the differences the child or adolescent presents are valued positively, including their limitations, but also their possibilities and positive aspects.
In adults, many of these characteristics continue, as Asperger’s cannot be cured. In any case, personalised treatment, involving family members and good communication with professionals can allow a better quality of life.
Autoinflammatory syndromes are a group of conditions characterised by spontaneous, recurring or persistent episodes of multi-systemic inflammation. They are caused by changes to innate immunity that cause deregulation of the immune system. Autoinflammatory conditions, due to various genetic mutations, cause a pathological hyperactivity in this structure, which unleashes abnormal, continuous inflammatory activity. The number of conditions the group includes has increased since then, due to the advances in genetics and immunology.
The main symptom of many of the conditions included in the group is repeated episodes of fever, which spontaneously disappear after a few days, only to reappear again cyclically after a variable period of time. This fever is not caused by an infection and, therefore, does not respond to treatment with antibiotics or antiviral medication. Depending on the genetic defect, these conditions may be associated with a wide diversity of other manifestations, including skin, abdominal, joints, eyes or lungs.
All the conditions within the group are infrequent and have an incidence of less than 5 cases per 10,000 inhabitants, for which reason they are considered to be rare conditions. The majority appear in infancy or adolescence.
Recent progress with research has clearly shown that some fevers where the cause is not found are provoked by a genetic defect.
Depending on whether or not they have a genetic cause, they can be classified as follows:
The diagnosis is based on the clinical features of each patient’s clinical picture. Blood tests are important in diagnosing the various autoinflammatory conditions, as they enable detection of the existence of inflammation. These analyses are repeated when the child is asymptomatic to see if they have normalised. Molecular or genetic analysis enables detection of the presence of mutations involved in the development of autoinflammatory conditions which are studied in patients suspected of suffering from them according to the features of the clinical picture. The diagnosis is confirmed when the patient shows evidence of being a mutation carrier and it is often necessary to study family members too.
Treatment fundamentally depends on the type of condition and the response to the therapy chosen. For example, for familial Mediterranean fever, the treatment of choice is colchicine. Other treatments used on the various autoinflammatory conditions are cytokine inhibitors, such as IL-1 or the tumour necrosis factor α. Close monitoring of the patient is essential to prevent complications arising in the long term.
Informació pràctica com a CSUR de malalties autoinflamatòries
Hereditary angioedema is a rare genetic disease that affects approximately one in 50,000 people. It is usually an inherited disorder and is characterised by the accumulation of fluids outside the blood vessels, causing swelling of the face, hands, feet, extremities, genitals, gastrointestinal tract or the upper respiratory tract.
Because it is a low-prevalence disease with symptoms similar to those of other diseases and is therefore difficult to diagnose, it is important for there to be reference centres so that suspected and diagnosed cases can be centralised.
The inflammation that hereditary angioedema causes does not present associated itching and may last for 1 to 5 days. These symptoms are developed as a result of the malfunction of certain proteins that help maintain the normal flow of fluids through the blood vessels (arteries, veins and capillaries).
The seriousness of the disease shows a significant degree of variance. Angioedema episodes may be extremely incapacitating and have a serious effect on the patent’s quality of life. When it occurs in the region of the mouth or neck, the sufferer may die of asphyxia if they are not given preventive treatment.
In most cases symptoms start to manifest in childhood and/or puberty and continue throughout adult life.
There are different types of hereditary angioedema and they are classified according to whether or not they present a deficiency of the C1 component of the complement (C1-INH).
Swelling of the subcutaneous tissue in any part of the body, although it is most commonly found in:
Depending on the affected area, the symptoms may range from local discomfort to invalidity of the affected extremity, discomfort or pain when swallowing, voice changes, loss of voice, or dyspnoea (shortness of breath).
At one time of their life up to 50% of patients may present an episode that affects the throat, which if not immediately treated could lead to asphyxia.
Hereditary angioedema affects people who exhibit a mutation in certain genes, such as SERPING1, F12, PLG, KNG1 and ANGPT1. As it is a dominant autosomal disease, an affected patient has a 50% chance of passing it on to their children. Given that it is a genetic disorder, it is common to find that more than one member of the family is affected.
Depending on the type of mutation, it may affect men and women equally (types I and II) or women more frequently (HAE-nC1-INH). Cases of hereditary angioedema without C1-INH deficiency are usually associated with hyperoestrogenic states, such as pregnancy or the consumption of contraceptives that contain oestrogens.
The Allergology Clinic first assesses patients who present with recurring angioedema episodes and cases in which there are family members who also suffer them. Subsequently, a blood analysis is requested to determine the levels of the components of the complement, including the inhibitor of component C1 (C1-INH) and, finally, the diagnosis is completed with a genetic study.
Treatment depends on the number of attacks, the severity of the symptoms and the degree to which quality of life is affected. Treatment is always on a case-by-case basis and may be acute, which means the subcutaneous of intravenous administration of medication at the time of the angioedema attack, or preventive, to stop attacks occurring so frequently. The latter treatment is usually recommended for the patients who suffer the most episodes.
Angioedema treatments can be self-administered by the patients.
In the case of surgery, endoscopies, tooth extractions or certain dental procedures, treatment must be given in advance to prevent an attack.
Blood analysis normally forms part of the diagnostic procedure. Depending on the treatment, during monitoring it may be necessary to perform an abdominal ultrasound and draw blood for analysis.
Factors known to possibly trigger attacks should be avoided as far as possible:
Genetic predisposition to cancer is an increased risk of developing cancer due to alterations in specific genes. It is not inherited cancer, but a predisposition. Suspected when cancers occur in multiple generations, at young ages, or multiple tumors in one person. Genetic testing uses blood, saliva, or biopsy and guides early detection, prevention strategies, intensive monitoring, and sometimes prophylactic surgeries.
Cancer is characterised by excessive and uncontrolled cell growth that invades and damages tissues and organs. It is a multi-factor illness that is caused by a combination of genetic and environmental factors.
Most cancers are sporadic, but some 5 to 10% of cancer diagnoses involve a hereditary genetic origin. This means that specific genes, called cancer susceptibility genes, present germ cell abnormalities (found throughout the body) that increase the risk of developing cancer.
It's important to point out that cancer is NOT hereditary, but the predisposition to developing it is. Having genes that are associated with cancer susceptibility simply means you have a higher risk of having the disease, not that you will have cancer for sure. This genetic predisposition can be transmitted from parents to offspring, normally following an autosomal dominant inheritance pattern, meaning that there is a 50% chance of passing the gene to descendants.
In some cases, the genetic susceptibility is individual and caused by a combination of multiple genetic differences (a combination of low-risk polymorphisms or allele variants). Identifying a genetic abnormality known to increase the risk of developing cancer in a family allows its members to benefit from early cancer detection and prevention measures, as well as to seek specific, targeted treatments against that type of cancer.
There are different genes associated with an increased risk of falling ill with cancer. Among the most frequent and well known are the genes:
The genes APC and MUTYH, linked with familial adenomatous polyposis –the formation of a large number of adenomatous polyps (non-malignant tumours) in the colon– and colon cancer.
There are different clinical criteria that may arouse the suspicion that an individual has a hereditary genetic abnormality that predisposes them to certain kinds of cancer, such as:
When these criteria are detected, they are referred to the genetic assessment unit specialising in cancer, where the need to perform a genetic study to rule out the possibility of a hereditary predisposition to cancer will be determined. This multi-disciplinary unit is staffed by physicians who are specialists in hereditary cancer and genetic counsellors. Here, an individual risk assessment, genetic tests, and follow-up for the carriers of the gene are carried out.
There are different syndromes that involve a genetic predisposition to developing cancer. For example, there are different genes that can make someone have a genetic predisposition to breast cancer. The most common are:
The genetic predisposition to developing colon cancer can be divided into two types: polyposic and non-polyposic.
There are different types of polyposis colon cancer. Familial adenomatous polyposis (FAP) presents the highest risk for developing colon cancer. It is characterised by hundreds or thousands of polyps in the colon, and sometimes also throughout the entire digestive tract. These polyps are not malignant lesions, but they can degenerate and develop into cancer. Thus, individuals with FAP end up developing colon cancer if these polyps are not removed. Pathogenic alterations in the APC gene are responsible for this condition. In addition, carriers of APC gene mutations are also at risk for other tumours or conditions (hepatoblastoma, thyroid tumours, and desmoid tumours).
The main syndrome entailing a predisposition to non-polyposis colon cancer is Lynch syndrome. This syndrome entails a high risk of developing colon and endometrial cancer, along with a risk of developing ovarian, bile duct, urinary tract, and gastric cancer. It is caused by mutations in the genes that are in charge of DNA repair, specifically, those tasked with mismatch repair, namely MLH1, MSH2, MSH6, PMS2, and EPCAM.
We can also find a genetic predisposition to endocrine tumours. Pheochromocytomas and paragangliomas are rare tumours that are caused by a hereditary genetic abnormality in 40% of cases. These can be caused by abnormalities in the succinate-dehydrogenase-encoding genes (SDHx), RET gene (MEN2 syndrome),MEN1 gene,NF1 gene (neurofibromatosis type 1) or FH gene, among others.
A genetic diagnosis is usually done with a blood sample, but a saliva sample or skin biopsy can also be used. DNA (present in the nucleus of our cells) is extracted from this sample for analysis.
There are different techniques for carrying out genetic studies. Currently, at our centre, we perform gene panel studies. This entails analysing different genes linked with the genetic predisposition to cancer to rule out any abnormality in them; this is also called gene sequencing.
When a genetic abnormality is found in a family, a predictive study is carried out. This kind of study determines if an individual also presents the genetic abnormality detected in the family.
Depending on the genetic change found, different measures for early detection and prevention can be recommended. For example, individuals with a mutated BRCA1/2 gene should begin to undergo an annual breast check-up, with a breast MRI and a mammogram, from the time they are 25–30 years old. Individuals with Lynch syndrome should get annual colonoscopies from the age of 25 onward.
Depending on the type of genetic disorder, risk reduction surgeries can also be an option. For example, in individuals diagnosed with FAP, depending on the number of polyps they have, a prophylactic colectomy (removal of the colon) can be performed to reduce their risk of developing colon cancer.
Follow-up and prevention measures are determined on an individual basis in the corresponding specialist's medical consultation. Additionally, at the medical office in charge of hereditary cancer, a reproductive genetic assessment is offered, depending on the genetic abnormality.
A rare chronic blood disease that is slow to develop. It is characterised by increased platelet production and is associated with greater risk of thrombosis (clotting) and bleeding. Patients with essential thrombocythemia are usually asymptomatic and it is detected during routine blood tests. There is currently no cure for this condition and treatment is targeted at preventing complications.
It is included within the group of chronic myeloproliferative disorders, which are a type of blood cancer that is slow to develop. Its cause is not known, although there are mutations known to be associated with the condition in 80% of cases. It is not hereditary, but some families may have several members affected by it.
It is characterised by increased platelet production and is associated with greater risk of clotting in the arteries and veins, or in some cases with bleeding.
It is a chronic illness that cannot currently be cured, with a normally benign evolution. It can be effectively controlled over long periods and generally has little impact on daily activities and work. Patients with this condition have increased risk compared to the general population of developing other blood diseases, such as acute leukaemia or myelofibrosis.
Many patients show no symptoms, either when they are initially diagnosed or as the condition evolves. Different combinations of symptoms may appear, such as tiredness, itching, night time sweating, aching bones and headaches.
The severity of symptoms varies a lot depending on the patient.
It is considered a rare disease, with a low incidence of 1.5-3 cases per 100,000 inhabitants. It mainly affects people aged 60-70 years and to a lesser extent young people. It is more common in women
It is normally diagnosed through blood tests that show a sustained increase in platelet count.
A bone marrow biopsy can be performed for diagnosis, which, together with the analysis, will allow the determination of risk factors for the progression of the disease, which in turn guide treatment.
It is usually associated with genetic mutations that support diagnosis.
Administering antiplatelets or drugs to reduce the number of platelets is not always indicated.
The aim of treatment is to prevent complications due to clotting and bleeding, as well as controlling the symptoms related to this condition. Depending on the risks and symptoms, the haematologist will therefore determine when to start treatment.
There are special circumstances, such as pregnancy, in which a multidisciplinary approach is required.
It is usually controlled by analysis.
The most important thing is to prevent clotting complications associated with this condition by controlling cardiovascular risk factors (high blood pressure, dyslipidaemia, smoking, obesity, sedentary lifestyle) and following the treatment recommended by your haematologist.
Cystic fibrosis is a genetic disorder that affects the lungs, the digestive system and other organs in the body. Affects the cells that produce mucus, sweat and digestive enzymes. Bodily secretions that are usually fluid and not viscous become more viscous. Instead of acting as a lubricant, the viscous secretions form layers, especially in the lung and pancreas. Patients with cystic fibrosis have a much higher level of salt in their sweat than normal.
The age at which symptoms appear varies, depending on the intensity of the disease in each person. Currently screening for cystic fibrosis is conducted in the first few days of a baby’s life, allowing a diagnosis to be made within a month of birth, much earlier than symptoms are likely to develop. Normally, symptoms appear within the first few months or years of life, although in some patients they may appear during adolescence or in adulthood. There has been an improvement in the quality of life of patients with cystic fibrosis compared to previous decades. Although cystic fibrosis requires daily treatment measures to control it, patients can still go to school and work.
The most common symptoms in small children are fatty deposits, delay in gaining weight, and repeated bronchitis and respiratory infections. Older children and adults may suffer from sinusitis, diabetes, pancreatitis or fertility problems.
It affects children and adults more or less severely depending on whether the illness has a mild or severe form of manifestation.
All new-borns are screened using a blood test to detect immunoreactive trypsinogen.
The sweat test (amount of salt in the sweat) is an important diagnostic test. It is done by stimulating the skin to increase sweat and measuring the amount of chloride secreted. In cystic fibrosis there is an increased amount of chloride and sodium.
Diagnosis is confirmed using genetic testing to look for mutations of the CFTR gene (Cystic Fibrosis Transmembrane conductance Regulator). This gene is involved in the passage of salt through the membranes of the body.
It is very important that patients be attended in a specialised multidisciplinary Unit.
There is currently no definitive cure, although there is a lot of research in this field and in the future it is probable that we will be able to change the natural course of this illness with new drugs that come onto the market.
Treatment is aimed at maintaining lung function, avoiding respiratory infections and improving the absorption of foods and nutrition. Breathing exercises are essential. These breathing exercises maintain adequate ventilation of the lungs and in some cases are accompanied by inhalation of a solution of sodium chloride, other fluidifying substances or antibiotics.
The relevant preventive vaccinations should be administered (flu, pneumococcal, etc.). The Cystic Fibrosis Unit designs a treatment plan for each patient, which varies over time and according to the evolution of the condition.
From a digestive point of view, pancreatic function can be helped by taking pancreatic enzymes orally and promoting the absorption of foods.
In some cases, if the disease is very advanced, a lung transplant may be needed. Treatments are improving all the time and need to be administered less and less frequently.
Screening for immunoreactive trypsinogen in the blood, the sweat test, genetic analysis.
Complementary tests that may be useful include blood tests to look at vitamin levels, among other things, chest x-ray, chest CAT scan, functional respiratory tests (spirometry) and stool analysis.
Early detection is currently a reality and allows early treatment as symptoms develop.
Acute leukemia is a blood cancer characterized by the rapid proliferation of immature cells in the bone marrow, preventing the normal production of blood cells. It is a serious disease that requires urgent treatment with chemotherapy and often stem cell transplantation.
Acute leukaemia involves abnormal cell growth in the haematopoietic system characterised by significant proliferation and accumulation of immature cells, firstly in the bone marrow and subsequently in the blood, with a great degree of clinical and biological heterogeneity.
Acute leukaemias are clonal proliferations (tumour cells that originate from a single initial cell and accumulate various genetic mutations that result in development of the disease) of altered blood stem cells. In normal circumstances, multipotent stem cells give rise to haematopoietic cells, which give rise to blood cells via a process of cell proliferation and differentiation mediated by the cell’s own mechanisms and by the surrounding tissues. Under normal conditions, blood cells migrate to the blood and tissues and are indispensable for the body to function correctly.
In acute leukaemias, the accumulation of different genetic and molecular alterations gives rise to the progressive accumulation of these cells, which substitute normal blood cells in a process known as "hiatus leukemicus", whereby progenitor cells (blasts) do not mature and accumulate in the bone marrow and peripheral blood. The symptomatology may be very mild and non-specific initially, resulting mainly from the lack of blood cells and sometimes from tissue infiltration. These are very serious diseases that require chemotherapy treatment to control them and often a transplant of bone marrow progenitor cells.
In many cases there are at first no major symptoms. Any symptoms there are mainly derive from the lack of blood cells and include tiredness, bleeding, infections and on rare occasions lack of appetite, bone pain, breathing difficulty or neurological symptoms. A physical examination may reveal palpitations, bruises, bleeding from mucus membranes, fever, infiltration of gums or other organs (skin, spleen, liver, etc.).
The average age for acute leukaemia is generally 67 years, but it can affect people of any age. Acute leukaemia is the most common cause of abnormal cell growth in children, with lymphoid leukaemia being the most common. Myeloid leukaemia is more common in the adult population.
A suspected diagnosis is reached in a number of ways, including clinical history, physical examination and a blood test. The diagnosis is confirmed using bone marrow aspiration in which we study neoplastic cells (blasts) under a microscope, as well as conducting multiparametric flow cytometry, cytogenetic analysis and molecular biology tests.
Based on chemotherapy. New drugs are currently being developed, such as immunotherapy or treatment against specific biological alterations (personalised treatment). If not contraindicated, a transplant of haematopoietic progenitor cells may be required once the response has been reached. Therapeutic strategies are adapted on the one hand to the patient’s situation (age, concomitant diseases, etc.) and on the other hand to the biological characteristics of the disease.
Full blood test and bone marrow aspiration.
Unfortunately, there is no way of preventing acute leukaemia from developing. The mechanisms that lead to a person developing this disease are not exactly known. We do know some factors that may be related, such as chemotherapy or radiotherapy in the past or exposure to certain toxins. A predisposition in some congenital diseases has also been observed, as well as cases where there is a family history of the disease.
The most common form is chronic myeloid leukaemia and this sheet refers exclusively to this form of leukaemia. It is a form of abnormal cell growth (neoplasia) that originates in immature multipotent blood cells (stem cells) and gives rise to red blood cells, platelets and white blood cells.
It is characterised by cellular proliferation of white blood cells with cytogenetic alteration that consists of the appearance of an abnormal chromosome known as the Philadelphia chromosome. The Philadelphia chromosome is also seen in other processes, such as acute lymphoblastic leukaemia, and diagnostic differentiation is required to distinguish which process is occurring. Chronic myeloid leukaemia may also involve red blood cell and platelet disorders, and is characterised by its chronicity. This disease serves to illustrate the revolution that has taken place in the last few years with targeted therapies in abnormal blood cell growth.
These are not very specific: Usually marked by tiredness, anaemia, loss of appetite.
This disease has a low incidence (1-1.5/100,000 pop./yr) and low mortality (more than 90% survival in the last 5 years). It mostly affects middle-aged people (40-50 years), although it can occur at any age.
A physical examination often reveals spleen growth. Blood tests show a very significant increase in white blood cells and bone marrow aspiration should be conducted to confirm. Genetic and molecular biology tests are also conducted.
The treatment most used is tyrosine-kinase inhibitors. It is an oral, chronic and relatively well tolerated treatment, including Imatinib: it is the first drug that was described, and the most commonly used. Side effects include submalar skin pigmentation (aesthetic problems), nausea and vomiting, which are often mild.
As there is some resistance to this drug, new drugs need to be developed to stop the other proliferation pathways of the affected cells.
Physical examination, blood test, bone marrow aspiration.
Kidney diseases affect the ability of the kidneys to filter blood, regulate minerals and blood pressure, and produce red blood cells. Early detection, medical monitoring, and appropriate treatments can slow progression and prevent serious complications.
Kidney disease encompasses a wide range of conditions that compromise the normal functioning of the kidneys. Their main purpose is to purify the blood of different composites, regulate their composition of mineral salts and acidity and contribute to the normal formation and maintenance of bones. They also support the creation of red blood cells and regulate arterial pressure.
Is measured by the stage of renal insufficiency, which increases from 1 to 5; the most advanced stage at which the kidneys have ceased to function. During stages 1 to 4 there are different medical treatments that can slow or compensate for renal insufficiency. At stage 5, patients have to undertake extrarenal purification techniques such as haemodialysis or peritoneal dialysis. In this case, the possibility of a kidney transplant will always be considered, which would allow a normal life free from dialysis but would require taking immunosuppressant medication to prevent rejection of the transplanted organ.
The treatment of kidney failure has four fundamental pillars: controlling high blood pressure when present, managing elevated urea levels, addressing mineral salt imbalances (sodium, potassium, calcium, phosphorus, magnesium), and controlling acidosis and anemia.
Renal insufficiency is usually detected with a simple blood test. Symptoms tend to be tiredness and generally feeling unwell caused by a build-up of urea, anaemia or both factors together. The patient may also have a headache if their arterial pressure is high.
All age groups. In childhood, there is often a genetic cause. In adults, it may be due to other illness such as diabetes, immune diseases or infectious diseases. It may also manifest due to the late appearance of genetic diseases in adults.
Renal insufficiency is diagnosed with a simple blood test. Establishing the cause of the renal insufficiency is more complicated. Often, a kidney biopsy and genetic testing will be needed.
Typical tests include blood tests, ultrasound, nuclear magnetic resonance imaging, kidney biopsy and genetic testing.
Initial treatment consists of substituting or compensating for the aforementioned alterations. During later stages, haemodialysis or peritoneal dialysis may be used, and in the case of terminal renal insufficiency, a kidney transplant may be carried out; from a deceased or a living donor.
Drinking a reasonable amount of water a day contributes to good kidney function.
Minority diseases, also called rare diseases, are those that affect between 5% and 7% of the population. They are very varied, affecting different parts of the body with a wide range of symptoms that change both between diseases and within the same disease.
It is estimated that some 30 million people in the EU, 3 million in Spain, and around 350,000 in Catalonia suffer from one.
The complexity of most rare diseases requires multidisciplinary care involving expert professionals from different medical specialties, personalized nursing management, psychological support, and social work, among other services.
At Vall d’Hebron, more than 200 specialist professionals care for over 40,000 patients with rare diseases. We are one of the hospitals in Spain that treats the highest number of rare conditions and one of the leading centers in Europe in this field. As of 2025, we are part of 20 European Reference Networks for rare diseases (ERN), 43 Spanish reference centers (CSUR), and the 12 expertise networks of the Department of Health (XUEC). This makes the hospital a highly specialized center for caring for these diseases throughout the entire life journey—from birth to adulthood—through a networked system that allows sharing resources and expertise with other hospitals and centers in the region.
The professionals across the various units and centers aim to improve patient access to diagnosis, information, and personalized care, as well as support research through:
The Rare Diseases Committee aims to establish a common framework for rare disease care at the hospital, identify and align the different initiatives (clinical, training, and research), deploy prioritized action lines, and monitor and evaluate outcomes in order to propose and implement improvements.
The concentration of patients with rare diseases increases knowledge and promotes research. Our Research Institute (VHIR) is a leader in both basic and clinical research. More than 14 basic research groups focus on studying rare diseases to improve diagnosis and develop new therapeutic approaches. We are the center in Spain with the highest number of clinical trials involving orphan drugs, including gene therapies, and we have a leading unit dedicated to the development of advanced therapies.
For more information, you can contact the rare disease team at: minoritaries@vallhebron.cat
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