Epipericardial Fat Necrosis: Who Should Be a Candidate?

OBJECTIVE: The objectives of the present study were to estimate the frequency of epipericardial fat necrosis among patients undergoing chest CT for chest pain and to compare the clinical and laboratory data between patients with epipericardial fat necrosis and control subjects. MATERIALS AND METHODS: A retrospective review of 7463 chest CT studies performed in the emergency department from July 2011 to December 2014 was conducted to collect data regarding patient demographic characteristics and CT findings. Twenty patients who had epipericardial fat necrosis diagnosed were defined as the main patient group. An age- and sex-matched control group was selected from patients with chest pain who underwent chest CT during the same period. Linear regression models were used to assess data, and statistical significance was expressed as p values and 95% CIs. RESULTS: We found that the frequency of epipericardial fat necrosis was 2.15% among patients who underwent chest CT for chest pain. Epipericardial fat necrosis was statistically significantly associated with a lack of medication use (p = 0.01; 95% CI, -3.33 to -0.40) and the absence of other symptoms (p = 0.005; 95% CI, -5.83 to -1.27). Epipericardial fat necrosis was most often observed as an ovoid lesion with mixed fat attenuation with little stranding in the left paracardiac region accompanied by pleural effusion. CONCLUSION: Epipericardial fat necrosis is a significant clinical condition. For patients seen in the emergency department with isolated acute chest pain but no additional clinical history, no medication history, and normal laboratory results, chest CT is recommended to support a diagnosis of epipericardial fat necrosis.

Pneumonia por Legionella após uso de Infliximabe em paciente com Artrite Reumatoide / Legionella pneumonia after infliximab in a patient with Rheumatoid Arthritis

Os antagonistas do fator de necrose tumoral (anti-TNF) têm sido utilizados com sucesso em várias doenças inflamatórias crônicas, como artrite reumatoide (AR), mas alguns estudos observaram a ocorrência de infecções por patógenos intracelulares em pacientes medicados com anti-TNF. Relatamos um caso de paciente mulher com diagnóstico prévio de AR durante 16 anos e que estava sendo medicada com várias drogas antirreumáticas modificadoras de doença (DARMDs), tendo como resultado o insucesso terapêutico, sendo em seguida tratada com infliximab. Depois de transcorridos 15 dias da segunda dose, a paciente foi acome- tida por dor torácica ventilatório-dependente, tosse seca e dispneia. Foi hospitalizada, e o diagnóstico de pneumonia por Legionella pneumophila foi confirmado pela presença do antí- geno de Legionella na urina. TNF é uma citocina inflamatória que também promove inibição do crescimento bacteriano de patógenos intracelulares, e sua inibição parece aumentar a sensibilidade a essas infecções em alguns pacientes.

The antagonists of tumour necrosis factor (anti-TNF) have been successfully used in several chronic inflammatory diseases such as Rheumatoid Arthritis (RA), but some studies have observed the development of infections by intracellular pathogens in patients using anti-TNF. We report a case of a female patient with previous diagnosis of RA for 16 years that used several disease-modifying anti-rheumatic drugs (DMARDs) that resulted in treatment failure, and then was treated with infliximab. After fifteen days of the second dose, the patient developed ventilatory-dependent chest pain, dry cough and dyspnea. She was hospitalized, and the diagnosis of pneumonia by Legionella pneumophila was confirmed by the presence of Legionella antigen in an urine test. TNF is an inflammatory cytokine that also acts inhibiting the bacterial growth of intracellular pathogens, and its inhibition seems to increase susceptibility to these infections in some patients.

[Legionella pneumonia after infliximab in a patient with rheumatoid arthritis]. / Pneumonia por Legionella após uso de Infliximabe em paciente com Artrite Reumatoide.

The antagonists of tumour necrosis factor (anti-TNF) have been successfully used in several chronic inflammatory diseases such as Rheumatoid Arthritis (RA), but some studies have observed the development of infections by intracellular pathogens in patients using anti-TNF. We report a case of a female patient with previous diagnosis of RA for 16 years that used several disease-modifying anti-rheumatic drugs (DMARDs) that resulted in treatment failure, and then was treated with infliximab. After fifteen days of the second dose, the patient developed ventilatory-dependent chest pain, dry cough and dyspnea. She was hospitalized, and the diagnosis of pneumonia by Legionella pneumophila was confirmed by the presence of Legionella antigen in an urine test. TNF is an inflammatory cytokine that also acts inhibiting the bacterial growth of intracellular pathogens, and its inhibition seems to increase susceptibility to these infections in some patients.

Pseudocisto pulmonar pós-traumático em jogador de futebol: relato de caso / Post-traumatic pulmonary pseudocyst in a soccer player: a case report

Pseudocistos pulmonares são lesões raras que se desenvolvem no parênquima pulmonar após traumas fechados e de grande energia, cujo diagnóstico se baseia na associação da história clínica com exames de imagem. Relata-se a seguir um pseudocisto pulmonar ocorrido no parênquima contralateral ao trauma em um homem de 31 anos que apresentou episódio de hemoptise após queda durante partida de futebol.

Pulmonary pseudocysts are uncommon cavitary lesions that develop in the lung parenchyma as a consequence of blunt thoracic trauma, whose diagnosis is based on an association of clinical history and imaging findings. The present report describes the case of a pulmonary pseudocyst observed in the parenchyma contralateral to the trauma site in a 31year-old man presenting with hemoptysis after falling during a soccer match.

Intractable acquired autoimmune angioedema in a patient with systemic lupus erythematosus.

Acquired angioedema is caused by different drugs and lymphoproliferative diseases, and rarely it has also been related to the presence of auto-immune disorders. We report the case of a 47 year old female with systemic lupus erythematosus (SLE) and severe cutaneous involvement who developed recurrent localized angioedema of the face, including lips and eye lids, upper limbs, and thorax, not associated with urticaria, and with reduced levels of C1 esterase inhibitor. Treatment with antimalarials, glucocorticoids, and pulse therapy with methylprednisolone associated with azathioprine did not improve her condition. The patient was also unsuccessfully treated with danazol, and she only showed clinical response after several sessions of plasmapheresis, including resolution of the extensive edema of the gastrointestinal tract.

Angioedema adquirido autoimune de difícil controle em paciente com lúpus eritematoso sistêmico / Intractable acquired autoimmune angioedema in a patient with systemic lupus erythematosus

O angioedema adquirido é causado por diferentes medicamentos e doenças linfoproliferativas, e tem sido raramente relacionado com a presença de doenças autoimunes. Descrevemos aqui uma paciente de 47 anos com lúpus eritematoso sistêmico (LES) com envolvimento cutâneo importante que desenvolveu angioedema recorrente localizado em face incluindo lábios e pálpebras, membros superiores e tórax, não acompanhado de urticária e com dosagem do inibidor de C1 esterase reduzida. A utilização de antimaláricos, glicocorticoides e pulsoterapia com metilprednisolona associada ao uso de azatioprina não determinou melhora. A paciente utilizou também danazol sem sucesso, e apresentou resposta clínica somente após ter sido submetida a múltiplas sessões de plasmaferese, ocorrendo inclusive resolução de extenso angioedema na mucosa do trato gastrointestinal.

Acquired angioedema is caused by different drugs and lymphoproliferative diseases, and rarely it has also been related to the presence of auto-immune disorders. We report the case of a 47 year old female with systemic lupus erythematosus (SLE) and severe cutaneous involvement who developed recurrent localized angioedema of the face, including lips and eye lids, upper limbs, and thorax, not associated with urticaria, and with reduced levels of C1 esterase inhibitor. Treatment with antimalarials, glucocorticoids, and pulse therapy with methylprednisolone associated with azathioprine did not improve her condition. The patient was also unsuccessfully treated with danazol, and she only showed clinical response after several sessions of plasmapheresis, including resolution of the extensive edema of the gastrointestinal tract.