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2.
Artigo em Inglês | MEDLINE | ID: mdl-31325311

RESUMO

OBJECTIVES: The number of innate immune system disorders classified as systemic autoinflammatory diseases (SAID) has increased in recent years. More than 70% of patients with clinical manifestations of SAID did not receive a molecular diagnosis, thus being classed as so-called undifferentiated or undefined SAID (uSAID). The aim of the present study was to evaluate a next-generation sequencing (NGS)-based clinically oriented protocol in patients with uSAID. METHODS: We designed a NGS panel that included 41 genes clustered in seven subpanels. Patients with uSAID were classified into different groups according to their clinical features and sequenced for the coding portions of the 41 genes. RESULTS: Fifty patients were enrolled in the study. Thirty-four patients (72%) displayed recurrent fevers not consistent with a PFAPA phenotype. Sixteen patients displayed a chronic inflammatory disease course. A total of 100 gene variants were found (mean 2 per patient; range 0-6), a quarter of which affected suspected genes. Mutations with a definitive diagnostic impact were detected in two patients. Patients with genetically negative recurrent fevers displayed a prevalent gastrointestinal, skin and articular involvement. Patients responded to steroids on demands (94%) and colchicine, with a response rate of 78%. CONCLUSION: Even with a low molecular diagnostic rate, a NGS-based approach is able to provide a final diagnosis in a proportion of uSAID patients with evident cost-effectiveness. It also allows the identification of a subgroup of genetically negative patients with recurrent fever responding to steroid on demand and colchicine.

4.
J Clin Immunol ; 39(5): 476-485, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31144250

RESUMO

OBJECTIVES: Mutations affecting the TMEM173 gene cause STING-associated vasculopathy with onset in infancy (SAVI). No standard immunosuppressive treatment approach is able to control disease progression in patients with SAVI. We studied the efficacy and safety of targeting type I IFN signaling with the Janus kinase inhibitor, ruxolitinib. METHODS: We used DNA sequencing to identify mutations in TMEM173 in patients with peripheral blood type I IFN signature. The JAK1/2 inhibitor ruxolitinib was administered on an off-label basis. RESULTS: We identified three patients with SAVI presenting with skin involvement and progressive severe interstitial lung disease. Indirect echocardiographic signs of pulmonary hypertension were present in one case. Following treatment with ruxolitinib, we observed improvements of respiratory function including increased forced vital capacity in two patients, with discontinuation of oxygen therapy and resolution of echocardiographic abnormalities in one case. Efficacy was persistent in one patient and only transitory in the other two patients. Clinical control of skin complications was obtained, and one patient discontinued steroid treatment. One patient, who presented with kidney involvement, showed resolution of hematuria. One patient experienced increased recurrence of severe viral respiratory infections. Monitoring of peripheral blood type I interferon signature during ruxolitinib treatment did not show a stable decrease. CONCLUSIONS: We conclude that targeting type I IFN receptor signaling may represent a promising therapeutic option for a subset of patients with SAVI syndrome and severe lung involvement. However, the occurrence of viral respiratory infection might represent an important cautionary note for the application of such form of treatment.

6.
EMBO J ; 37(23)2018 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-30420557

RESUMO

A set of glutamylases and deglutamylases controls levels of tubulin polyglutamylation, a prominent post-translational modification of neuronal microtubules. Defective tubulin polyglutamylation was first linked to neurodegeneration in the Purkinje cell degeneration (pcd) mouse, which lacks deglutamylase CCP1, displays massive cerebellar atrophy, and accumulates abnormally glutamylated tubulin in degenerating neurons. We found biallelic rare and damaging variants in the gene encoding CCP1 in 13 individuals with infantile-onset neurodegeneration and confirmed the absence of functional CCP1 along with dysregulated tubulin polyglutamylation. The human disease mainly affected the cerebellum, spinal motor neurons, and peripheral nerves. We also demonstrate previously unrecognized peripheral nerve and spinal motor neuron degeneration in pcd mice, which thus recapitulated key features of the human disease. Our findings link human neurodegeneration to tubulin polyglutamylation, entailing this post-translational modification as a potential target for drug development for neurodegenerative disorders.

7.
Blood ; 132(22): 2362-2374, 2018 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-30254128

RESUMO

ARPC1B is a key factor for the assembly and maintenance of the ARP2/3 complex that is involved in actin branching from an existing filament. Germline biallelic mutations in ARPC1B have been recently described in 6 patients with clinical features of combined immunodeficiency (CID), whose neutrophils and platelets but not T lymphocytes were studied. We hypothesized that ARPC1B deficiency may also lead to cytoskeleton and functional defects in T cells. We have identified biallelic mutations in ARPC1B in 6 unrelated patients with early onset disease characterized by severe infections, autoimmune manifestations, and thrombocytopenia. Immunological features included T-cell lymphopenia, low numbers of naïve T cells, and hyper-immunoglobulin E. Alteration in ARPC1B protein structure led to absent/low expression by flow cytometry and confocal microscopy. This molecular defect was associated with the inability of patient-derived T cells to extend an actin-rich lamellipodia upon T-cell receptor (TCR) stimulation and to assemble an immunological synapse. ARPC1B-deficient T cells additionally displayed impaired TCR-mediated proliferation and SDF1-α-directed migration. Gene transfer of ARPC1B in patients' T cells using a lentiviral vector restored both ARPC1B expression and T-cell proliferation in vitro. In 2 of the patients, in vivo somatic reversion restored ARPC1B expression in a fraction of lymphocytes and was associated with a skewed TCR repertoire. In 1 revertant patient, memory CD8+ T cells expressing normal levels of ARPC1B displayed improved T-cell migration. Inherited ARPC1B deficiency therefore alters T-cell cytoskeletal dynamics and functions, contributing to the clinical features of CID.

8.
Eur J Paediatr Neurol ; 22(4): 725-728, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29709427

RESUMO

Pseudoxanthoma elasticum (PXE) is a rare genetic disorder characterized by fragmented and mineralized elastic fibers in the mid-dermis of the skin, eye, digestive tract and cardiovascular system. Clinical presentation includes typical skin lesions, ocular angioid streaks, and multisystem vasculopathy. The age of onset varies considerably from infancy to old age, but the diagnosis is usually made in young adults due to frequent absence of pathognomonic skin and ocular manifestations in early childhood. We report two children with PXE presenting with isolated multisystem vasculopathy and early-onset stroke. In the first patient, diagnosis was delayed until typical dermatologic alterations appeared; in the second patient, next-generation sequencing (NGS) study led to early diagnosis and specific follow-up, underlying the crucial role in idiopathic pediatric stroke of early genetic testing using NGS-based panels.


Assuntos
Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética , Pseudoxantoma Elástico/complicações , Pseudoxantoma Elástico/diagnóstico , Pseudoxantoma Elástico/genética , Acidente Vascular Cerebral/genética , Adolescente , Pré-Escolar , Feminino , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Masculino , Mutação
9.
Clin Immunol ; 187: 33-36, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-29030294

RESUMO

Mutations of the COPA gene cause an immune dysregulatory disease characterised by polyarticular arthritis and progressive interstitial lung disease with pulmonary haemorrhages. We report the case of a young girl that presented at age 3 with polyarticular arthritis, chronic cough and high titer rheumatoid factor. Radiologic imaging showed interstitial lung disease with tree-in-a-bud nodules and air-filled cysts. Targeted genetic analysis of COPA gene showed the reported c.698G>A mutation. The patient was lost to follow up for 3years during which therapy was discontinued with the development of joint damage and deformities. Analysis of peripheral blood showed activation of type 1 interferon pathway, which was also confirmed in 4 previously reported COPA patients. Our observations underline the importance of early treatment in COPA disease to avoid loss of joint function. Furthermore, our results suggest a role for type 1 interferon in disease pathogenesis opening the possibility for targeted therapeutic approaches.

11.
Nat Commun ; 8(1): 2176, 2017 12 19.
Artigo em Inglês | MEDLINE | ID: mdl-29259162

RESUMO

Microbial nucleic acid recognition serves as the major stimulus to an antiviral response, implying a requirement to limit the misrepresentation of self nucleic acids as non-self and the induction of autoinflammation. By systematic screening using a panel of interferon-stimulated genes we identify two siblings and a singleton variably demonstrating severe neonatal anemia, membranoproliferative glomerulonephritis, liver fibrosis, deforming arthropathy and increased anti-DNA antibodies. In both families we identify biallelic mutations in DNASE2, associated with a loss of DNase II endonuclease activity. We record increased interferon alpha protein levels using digital ELISA, enhanced interferon signaling by RNA-Seq analysis and constitutive upregulation of phosphorylated STAT1 and STAT3 in patient lymphocytes and monocytes. A hematological disease transcriptomic signature and increased numbers of erythroblasts are recorded in patient peripheral blood, suggesting that interferon might have a particular effect on hematopoiesis. These data define a type I interferonopathy due to DNase II deficiency in humans.


Assuntos
Desoxirribonucleases/deficiência , Endodesoxirribonucleases/deficiência , Doenças Hereditárias Autoinflamatórias/enzimologia , Interferon-alfa/imunologia , Transdução de Sinais/imunologia , Adolescente , Antivirais/farmacologia , Criança , Desoxirribonucleases/genética , Desoxirribonucleases/imunologia , Endodesoxirribonucleases/genética , Endodesoxirribonucleases/imunologia , Eritroblastos/imunologia , Feminino , Perfilação da Expressão Gênica , Hematopoese/imunologia , Doenças Hereditárias Autoinflamatórias/sangue , Doenças Hereditárias Autoinflamatórias/genética , Doenças Hereditárias Autoinflamatórias/imunologia , Humanos , Interferon-alfa/sangue , Interferon-alfa/metabolismo , Masculino , Mutação , Fosforilação , RNA Mensageiro/análise , Fator de Transcrição STAT1/metabolismo , Fator de Transcrição STAT3/metabolismo , Análise de Sequência de RNA , Regulação para Cima/efeitos dos fármacos
12.
Ann Rheum Dis ; 76(10): 1648-1656, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28522451

RESUMO

OBJECTIVES: To analyse the prevalence of CECR1 mutations in patients diagnosed with early onset livedo reticularis and/or haemorrhagic/ischaemic strokes in the context of inflammation or polyarteritis nodosa (PAN). Forty-eight patients from 43 families were included in the study. METHODS: Direct sequencing of CECR1 was performed by Sanger analysis. Adenosine deaminase 2 (ADA2) enzymatic activity was analysed in monocyte isolated from patients and healthy controls incubated with adenosine and with or without an ADA1 inhibitor. RESULTS: Biallelic homozygous or compound heterozygous CECR1 mutations were detected in 15/48 patients. A heterozygous disease-associated mutation (p.G47V) was observed in two affected brothers. The mean age of onset of the genetically positive patients was 24 months (6 months to 7 years). Ten patients displayed one or more cerebral strokes during their disease course. Low immunoglobulin levels were detected in six patients. Thalidomide and anti-TNF (tumour necrosis factor) blockers were the most effective drugs. Patients without CECR1 mutations had a later age at disease onset, a lower prevalence of neurological and skin manifestations; one of these patients displayed all the clinical features of adenosine deaminase 2deficiency (DADA2) and a defective enzymatic activity suggesting the presence of a missed mutation or a synthesis defect. CONCLUSIONS: DADA2 accounts for paediatric patients diagnosed with PAN-like disease and strokes and might explain an unrecognised condition in patients followed by adult rheumatologist. Timely diagnosis and treatment with anti-TNF agents are crucial for the prevention of severe complications of the disease. Functional assay to measure ADA2 activity should complement genetic testing in patients with non-confirming genotypes.


Assuntos
Adenosina Desaminase/deficiência , Adenosina Desaminase/genética , Peptídeos e Proteínas de Sinalização Intercelular/deficiência , Peptídeos e Proteínas de Sinalização Intercelular/genética , Livedo Reticular/genética , Poliarterite Nodosa/genética , Acidente Vascular Cerebral/genética , Adolescente , Idade de Início , Estudos de Casos e Controles , Criança , Pré-Escolar , Análise Mutacional de DNA , Feminino , Heterozigoto , Homozigoto , Humanos , Imunoglobulinas/sangue , Imunossupressores/uso terapêutico , Lactente , Itália , Livedo Reticular/tratamento farmacológico , Livedo Reticular/enzimologia , Masculino , Linhagem , Poliarterite Nodosa/tratamento farmacológico , Poliarterite Nodosa/enzimologia , Acidente Vascular Cerebral/enzimologia , Talidomida/uso terapêutico , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Adulto Jovem
13.
Clin Exp Rheumatol ; 35(3): 516-517, 2017 May-Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28339360

RESUMO

OBJECTIVES: In 1966, Goldbloom et al. described two children who developed a peculiar clinical picture characterized by intermittent daily bone pain in the lower limbs, fever spikes, increased acute phase reactants and dysproteinaemia. The syndrome occurred two weeks after a group A ß-haemolytic streptococcus infection. So far, only a few cases have been reported in the medical literature in English. METHODS: We report two further cases of Goldbloom's syndrome with a review of the literature in English. RESULTS: Our two patients lived in the same Italian region and presented their syndrome onset a week apart. Early use of STIR MRI revealed an atypical metaphyseal hyperintensity in the femurs and tibias. X-ray showed periosteal hyperostosis. A short cycle of corticosteroids led to rapid recovery of symptoms and disappearance of bone changes. CONCLUSIONS: The reported cases highlight a likely under-recognised post-streptococcal inflammatory periosteal reaction and emphasise the diagnostic utility of the newer imaging modalities.


Assuntos
Fêmur/diagnóstico por imagem , Hipergamaglobulinemia/sangue , Hipoalbuminemia/sangue , Imagem por Ressonância Magnética , Periostite/diagnóstico por imagem , Infecções Estreptocócicas/complicações , Tíbia/diagnóstico por imagem , Corticosteroides/uso terapêutico , Biomarcadores/sangue , Criança , Diagnóstico Precoce , Feminino , Fêmur/microbiologia , Humanos , Hipergamaglobulinemia/diagnóstico , Hipergamaglobulinemia/tratamento farmacológico , Hipergamaglobulinemia/microbiologia , Hipoalbuminemia/diagnóstico , Hipoalbuminemia/tratamento farmacológico , Hipoalbuminemia/microbiologia , Periostite/tratamento farmacológico , Periostite/microbiologia , Valor Preditivo dos Testes , Prednisona/uso terapêutico , Infecções Estreptocócicas/diagnóstico , Infecções Estreptocócicas/microbiologia , Síndrome , Tíbia/microbiologia , Resultado do Tratamento
14.
JIMD Rep ; 37: 37-43, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28247337

RESUMO

Leigh syndrome (LS) is an early-onset progressive neurodegenerative disorder, characterized by a wide clinical and genetic heterogeneity, and is the most frequent disorder of mitochondrial energy production in children. Beside its great variability in clinical, biochemical, and genetic features, LS is pathologically uniformly characterized by multifocal bilateral and symmetric spongiform degeneration of the basal ganglia, brainstem, thalamus, cerebellum, spinal cord, and optic nerves. Isolated complex I deficiency is the most common defect identified in Leigh syndrome. In 2011, the first child with a mutation of NDUFA10 gene, coding for an accessory subunits of complex I, was described. Here, we present an additional description of a child with Leigh syndrome harboring a homozygous mutation in NDUFA10, providing insights in clinical, biochemical, and neuroradiologic features for future earlier recognition.

15.
Lancet ; 389(10072): 909-916, 2017 03 04.
Artigo em Inglês | MEDLINE | ID: mdl-28162781

RESUMO

BACKGROUND: Little evidence-based information is available to guide the treatment of oligoarticular juvenile idiopathic arthritis. We aimed to investigate whether oral methotrexate increases the efficacy of intra-articular corticosteroid therapy. METHODS: We did this prospective, open-label, randomised trial at ten hospitals in Italy. Using a concealed computer-generated list, children younger than 18 years with oligoarticular-onset disease were randomly assigned (1:1) to intra-articular corticosteroids alone or in combination with oral methotrexate (15 mg/m2; maximum 20 mg). Corticosteroids used were triamcinolone hexacetonide (shoulder, elbow, wrist, knee, and tibiotalar joints) or methylprednisolone acetate (ie, subtalar and tarsal joints). We did not mask patients or investigators to treatment assignments. Our primary outcome was the proportion of patients in the intention-to-treat population who had remission of arthritis in all injected joints at 12 months. This trial is registered with European Union Clinical Trials Register, EudraCT number 2008-006741-70. FINDINGS: Between July 7, 2009, and March 31, 2013, we screened 226 participants and randomly assigned 102 to intra-articular corticosteroids alone and 105 to intra-articular corticosteroids plus methotrexate. 33 (32%) patients assigned to intra-articular corticosteroids alone and 39 (37%) assigned to intra-articular corticosteroids and methotrexate therapy had remission of arthritis in all injected joints (p=0·48). Adverse events were recorded for 20 (17%) patients who received methotrexate, which led to permanent treatment discontinuation in two patients (one due to increased liver transaminases and one due to gastrointestinal discomfort). No patient had a serious adverse event. INTERPRETATION: Concomitant administration of methotrexate did not augment the effectiveness of intra-articular corticosteroid therapy. Future studies are needed to define the optimal therapeutic strategies for oligoarticular juvenile idiopathic arthritis. FUNDING: Italian Agency of Drug Evaluation.


Assuntos
Artrite Juvenil , Metotrexato , Corticosteroides , Humanos , Injeções Intra-Articulares , Itália , Estudos Prospectivos , Resultado do Tratamento
16.
Front Immunol ; 8: 2015, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29434583

RESUMO

Primary immunodeficiencies with selective susceptibility to EBV infection are rare conditions associated with severe lymphoproliferation. We followed a patient, son of consanguineous parents, referred to our center for recurrent periodic episodes of fever associated with tonsillitis and adenitis started after an infectious mononucleosis and responsive to oral steroid. An initial diagnosis of periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis syndrome was done. In the following months, recurrent respiratory infections and episodes of keratitis were also observed, together with a progressive reduction of immunoglobulin levels and an increase of CD20+ cells. Cell sorting and EBV PCR showed 25,000 copies for 100,000 leukocytes with predominant infection of B lymphocytes. Lymph node's biopsy revealed reactive lymphadenopathy with paracortical involvement consistent with a chronic EBV infection. Molecular analysis of XIAP, SHA2D1A, ITK, and CD27 genes did not detect any pathogenic mutation. The patients underwent repeated courses of anti-CD20 therapy with only a partial control of the disease, followed by stem cell transplantation with a complete normalization of clinical and immunological features. Whole exome sequencing of the trio was performed. Among the variants identified, a novel loss of function homozygous c.163-2A>G mutation of the CD70 gene, affecting the exon 2 AG-acceptor splice site, fit the expected recessive model of inheritance. Indeed, deficiency of both CD27, and, more recently, of its ligand CD70, has been reported as a cause of EBV-driven lymphoproliferation and hypogammaglobulinemia. Cell surface analysis of patient-derived PHA-T cell blasts and EBV-transformed lymphoblastoid cell lines confirmed absence of CD70 expression. In conclusion, we describe a case of severe chronic EBV infection caused by a novel mutation of CD70 presenting with recurrent periodic fever.

17.
Mol Cytogenet ; 9: 78, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27766118

RESUMO

BACKGROUND: Deletions of the long arm of chromosome 18 cause a common autosomal syndrome clinically characterized by a protean clinical phenotype. CASE PRESENTATION: We report on a 16-month-old male infant affected by fever attacks apparently unrelated with any infectious or inflammatory symptoms, growth retardation, bilateral vertical talus, congenital aural atresia, dysmorphisms, mild psychomotor delay, and peculiar neuroradiological features. Array-CGH analysis revealed one of the smallest 18q22.3q23 interstitial deletions involving five genes: TSHZ1, ZNF516, ZNF236, MBP, and GALR1. CONCLUSIONS: Herein we focus on previously unreported heralding symptoms and neuroradiological abnormalities which enlarge the spectrum of 18q deletion syndrome demonstrating that a small deletion can determine a complex phenotype.

18.
Pediatr Rheumatol Online J ; 14(1): 35, 2016 Jun 04.
Artigo em Inglês | MEDLINE | ID: mdl-27260006

RESUMO

Defective regulation of type I interferon response is associated with severe inflammatory phenotypes and autoimmunity. Type I interferonopathies are a clinically heterogenic group of Mendelian diseases with a constitutive activation of this pathway that might present as atypical, severe, early onset rheumatic diseases. Skin vasculopathy with chilblains and livedo reticularis, interstitial lung disease, and panniculitis are common. Recent studies have implicated abnormal responses to nucleic acid stimuli or defective regulation of downstream effector molecules in disease pathogenesis. As observed for IL1-ß and autoinflammatory diseases, knowledge of the defects responsible for type I interferonopathies will likely promote the development of targeted therapy.


Assuntos
Artrite Juvenil/imunologia , Doenças Autoimunes/imunologia , Interferon Tipo I/imunologia , Doenças da Aorta/genética , Doenças da Aorta/imunologia , Artrite Juvenil/diagnóstico , Doenças Autoimunes/diagnóstico , Doenças Autoimunes/genética , Doenças Autoimunes/terapia , Doenças Autoimunes do Sistema Nervoso/diagnóstico , Doenças Autoimunes do Sistema Nervoso/imunologia , Hipoplasia do Esmalte Dentário/genética , Hipoplasia do Esmalte Dentário/imunologia , Homozigoto , Humanos , Interferon Tipo I/genética , Lúpus Eritematoso Sistêmico/diagnóstico , Lúpus Eritematoso Sistêmico/genética , Lúpus Eritematoso Sistêmico/imunologia , Metacarpo/anormalidades , Metacarpo/imunologia , Doenças Musculares/genética , Doenças Musculares/imunologia , Mutação/genética , Mutação/imunologia , Malformações do Sistema Nervoso/diagnóstico , Malformações do Sistema Nervoso/imunologia , Odontodisplasia/genética , Odontodisplasia/imunologia , Osteocondrodisplasias/genética , Osteocondrodisplasias/imunologia , Osteoporose/genética , Osteoporose/imunologia , Proteoma/genética , Proteoma/imunologia , Doenças Raras/diagnóstico , Doenças Raras/imunologia , Doenças Raras/terapia , Transdução de Sinais , Calcificação Vascular/genética , Calcificação Vascular/imunologia
19.
Clin Exp Rheumatol ; 34(3): 527-30, 2016 May-Jun.
Artigo em Inglês | MEDLINE | ID: mdl-27268780

RESUMO

OBJECTIVES: Eosinophilic fasciitis is an uncommon scleroderma-like disorder characterised by induration and thickening of skin and soft tissue, usually associated with peripheral eosinophilia, poorly characterised in childhood. METHODS: We report 3 paediatric cases of eosinophilic fasciitis showing unusual clinical and histopathological features with a review of the literature. RESULTS: All cases presented progressive motility impairment started from upper limbs with no skin abnormalities. All cases showed systemic inflammatory involvement and 2 patients had acute complications. Two patients developed disabling outcomes despite appropriate treatments. CONCLUSIONS: Eosinophilic fasciitis may present unusual clinical and histopathological features during childhood and requires early recognition in order to prevent acute complications and disabling outcomes.


Assuntos
Contratura , Eosinofilia , Fáscia/patologia , Fasciite , Glucocorticoides/administração & dosagem , Metotrexato/administração & dosagem , Modalidades de Fisioterapia , Antirreumáticos/administração & dosagem , Pré-Escolar , Contratura/diagnóstico , Contratura/etiologia , Contratura/prevenção & controle , Diagnóstico Diferencial , Diagnóstico Precoce , Eosinofilia/sangue , Eosinofilia/complicações , Eosinofilia/diagnóstico , Eosinofilia/fisiopatologia , Eosinofilia/terapia , Fasciite/sangue , Fasciite/complicações , Fasciite/diagnóstico , Fasciite/fisiopatologia , Fasciite/terapia , Feminino , Humanos , Imagem por Ressonância Magnética/métodos , Resultado do Tratamento
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