RESUMO
The rapid emergence of the novel coronavirus [SARS-CoV2] and the coronavirus disease 2019 [COVID-19] has caused significant global morbidity and mortality. This is particularly concerning for vulnerable groups such as pregnant women with inflammatory bowel disease [IBD]. Care for pregnant IBD patients in itself is a complex issue because of the delicate balance between controlling maternal IBD as well as promoting the health of the unborn child. This often requires continued immunosuppressive maintenance medication or the introduction of new IBD medication during pregnancy. The current global COVID-19 pandemic creates an additional challenge in the management of pregnant IBD patients. In this paper we aimed to answer relevant questions that can be encountered in daily clinical practice when caring for pregnant women with IBD during the current COVID-19 pandemic. PODCAST: This article has an associated podcast which can be accessed at https://academic.oup.com/ecco-jcc/pages/podcast.
Assuntos
Betacoronavirus , Infecções por Coronavirus/prevenção & controle , Doenças Inflamatórias Intestinais/terapia , Pandemias/prevenção & controle , Pneumonia Viral/prevenção & controle , Complicações na Gravidez/terapia , Betacoronavirus/isolamento & purificação , COVID-19 , Teste para COVID-19 , Técnicas de Laboratório Clínico , Infecções por Coronavirus/complicações , Infecções por Coronavirus/diagnóstico , Progressão da Doença , Feminino , Humanos , Imunossupressores/uso terapêutico , Doenças Inflamatórias Intestinais/complicações , Pneumonia Viral/complicações , Pneumonia Viral/diagnóstico , Gravidez , Medição de Risco , SARS-CoV-2 , Índice de Gravidade de DoençaRESUMO
BACKGROUND: Anti-adalimumab antibodies (AAA) are associated with loss of clinical response (LOR). Addition of an immunomodulator has been shown to reverse immunogenicity and regain response with infliximab monotherapy. Similar data on adalimumab are lacking. AIM: To study the impact of immunomodulator addition on the emergence of AAA and LOR among adalimumab therapy patients. METHODS: The databases of three tertiary medical centres were reviewed to identify patients who developed AAA during adalimumab monotherapy with resultant LOR, and received an immunomodulator as a salvage combination therapy. All sera were prospectively analysed using previously described ELISA assays. Clinical response was determined using appropriate clinical scores. Elimination of AAA, designated as 'sero-reversal', elevation of drug levels and regained clinical response were the sought outcomes. RESULTS: Twenty-three patients (21 Crohn's disease, and 2 ulcerative colitis) developed AAA with subsequent LOR and were thereafter prescribed an immunomodulator as salvage therapy (thiopurine n = 14, methotrexate n = 9). Eleven patients (48%) underwent sero-reversal with gradual elimination of AAA, increase in drug trough levels and restoration of clinical response (median time to sero-reversal 5 months). In 12 patients (52%), immunogenicity and loss of response could not be reversed. There was no difference between responders and nonresponders in the type of immunomodulators used or baseline clinical characteristics. CONCLUSIONS: In almost half of inflammatory bowel disease patients developing anti-adalimumab antibodies and loss of response, established immunogenicity of adalimumab can be gradually reversed by the addition of immunomodulator therapy with restoration of a clinico-biological response. However, these observations need to be confirmed with larger studies.
Assuntos
Adalimumab/uso terapêutico , Anti-Inflamatórios/uso terapêutico , Formação de Anticorpos/efeitos dos fármacos , Colite Ulcerativa/tratamento farmacológico , Doença de Crohn/tratamento farmacológico , Fatores Imunológicos/uso terapêutico , Adalimumab/efeitos adversos , Adulto , Anti-Inflamatórios/efeitos adversos , Anticorpos/sangue , Azatioprina/uso terapêutico , Colite Ulcerativa/sangue , Doença de Crohn/sangue , Feminino , Humanos , Masculino , Mercaptopurina/uso terapêutico , Metotrexato/uso terapêutico , Resultado do Tratamento , Adulto JovemRESUMO
AIM: Tenesmus in rectal prolapse leads to a vicious circle of straining with deterioration of prolapse. The primary phenomenon triggering this may be rectal hypersensitivity. We aimed to assess whether treatment with tricyclic antidepressants (TCAs) may break the vicious circle and improve tenesmus. METHOD: A retrospective review was carried out of patients with rectal prolapse and severe tenesmus who were poor surgical candidates or had refused surgery. They were treated at our tertiary centre with low dose tricyclic antidepressants. RESULTS: Twenty-three (18 female) patients were included, with mean age 75.3 (±SD 14.6) years. The mean duration of symptoms was 10.8 (± 8.6) months. Full-thickness rectal prolapse was diagnosed in 16 (70%) patients while seven (30%) had mucosal or incomplete prolapse. Ten (43%), eight (35%) and five (22%) patients were treated with nortriptyline (25 mg daily), amitriptyline (10 mg daily) and desipramine (25 mg daily). After a mean follow-up of 9.05 (± 8.2) months, 14 (61%) patients reported significant improvement in symptoms, five (22%) had a partial response, three (13%) were lost to follow-up and one (4%) failed to respond. The response rates for nortriptyline, desipramine and amitriptyline were 90%, 100% and 62.5%. CONCLUSION: To the best of our knowledge this is the first report to address the symptomatic, conservative treatment of tenesmus in patients with rectal prolapse. TCAs may be an acceptable option for poor surgical candidates or patients refusing surgery.
Assuntos
Antidepressivos Tricíclicos/administração & dosagem , Doenças Retais/tratamento farmacológico , Prolapso Retal/complicações , Idoso , Idoso de 80 Anos ou mais , Amitriptilina/administração & dosagem , Defecação/efeitos dos fármacos , Desipramina/administração & dosagem , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Nortriptilina/administração & dosagem , Doenças Retais/etiologia , Doenças Retais/psicologia , Prolapso Retal/patologia , Prolapso Retal/psicologia , Estudos Retrospectivos , Resultado do TratamentoAssuntos
Hematemese/terapia , Melena/terapia , Ácidos Oleicos/efeitos adversos , Soluções Esclerosantes/efeitos adversos , Escleroterapia/efeitos adversos , Infarto do Baço/induzido quimicamente , Seguimentos , Hematemese/complicações , Hérnia Hiatal/complicações , Humanos , Injeções Intralesionais , Masculino , Melena/complicações , Pessoa de Meia-Idade , Ácidos Oleicos/administração & dosagem , Soluções Esclerosantes/administração & dosagem , Infarto do Baço/diagnóstico por imagem , Tomografia Computadorizada por Raios XRESUMO
Familial Mediterranean fever (FMF) is an inherited disease whose manifestations are acute but reversible attacks of sterile inflammation affecting synovial and serosal spaces. The FMF gene (MEFV) was recently cloned, and it codes for a protein (pyrin/marenostrin) homologous to known nuclear factors. We previously reported the deficient activity of a C5a/interleukin (IL)-8 inhibitor, a physiologic regulator of inflammatory processes, in FMF serosal and synovial fluids. We now describe the concomitant expression of MEFV and C5a/IL-8-inhibitor activity in primary cultures of human fibroblasts. Fibroblasts grown from synovial and peritoneal tissues displayed C5a/IL-8-inhibitor activity that could be further induced with phorbol myristate acetate (PMA) and IL-1 beta. Very low levels of chemotactic inhibitor were evident in skin fibroblast cultures or in peritoneal and skin fibroblasts obtained from FMF patients. MEFV was expressed in peritoneal and skin fibroblasts at a lower level than in neutrophils and could be further induced by PMA and IL-1 beta. In the FMF cultures, the MEFV transcript carried the M694V mutation, consistent with the genetic defect found in patients with this disease. MEFV was also expressed in other cell lines that do not produce C5a/IL-8 inhibitor. These findings suggest that human primary fibroblast cultures express MEFV and produce C5a/IL-8-inhibitor activity. The interrelationship between pyrin, the MEFV product, and the C5a/IL-8 inhibitor requires further investigation. (Blood. 2000;96:727-731)