We reported a case of a 36-year-old woman who presented with cough, dyspnea, hypereosinophilia, multiple pulmonary nodules and mediastinal lymphadenopathy. The percentage of eosinophils in bronchoalveolar lavage fluid (BALF) was as high as 65%. Pathogenic tests and cytologic examination of BALF were negative. Transbronchial lung biopsy and endobronchial ultrasound-guided transbronchial needle aspiration revealed only eosinophil infiltration. As the patient responded poorly to high-dose corticosteroids, a surgical lung biopsy was performed. The pathological diagnosis was angioimmunoblastic T-cell lymphoma. The patient received chemotherapy and achieved a partial response. Her eosinophil count returned to the normal range, and the pulmonary nodules on chest CT partially resolved.
本文报道1例36岁女性患者，主要表现为咳嗽、气短、外周血嗜酸性粒细胞显著升高，胸部CT显示双肺多发结节、纵隔淋巴结肿大。先后两次支气管镜检查，镜下表现正常，肺泡灌洗液嗜酸性粒细胞比例升高，经支气管镜肺活检及纵隔淋巴结针吸活检提示肺组织及淋巴结内嗜酸性粒细胞浸润。因足量糖皮质激素治疗效果欠佳，行外科肺活检明确诊断为血管免疫母细胞性T细胞淋巴瘤。患者接受化疗后病情部分缓解，外周嗜酸性粒细胞降至正常，肺内结节明显减少。.

Eosinophilic gastroenteritis (EGE) is a rare disease characterized by tissue eosinophilia and can affect any part of gastrointestinal (GI) tract from the esophagus to the rectum, although stomach and small intestine are sites most frequently involved. We hereby describe an unusual case of eosinophilic gastroenteritis affecting the stomach, small intestine, colon and rectum involving the mucosa and serosa. A twenty-oneyearold student presented with fever, diarrhea, ascites and right pleural effusion. Total leucocyte count was high with marked eosinophilia. Ascitic and pleural fluid were exudates with low adenosine deaminase (ADA) level and predominant eosinophils. Biopsy specimens of the stomach, duodenum, ileum, colon and rectum showed dense eosinophilic infiltration of lamina propria. Based on the constellation of clinical features and investigations, a diagnosis of EGE was made, and therapy with prednisone was started. Symptoms and peripheral eosinophilia rapidly resolved. It is thus imperative to diagnose this disease early and institute the necessary treatment.

UNASSIGNED: Junctional epidermolysis bullosa (JEB) is a rare, incurable, devastating, and mostly fatal congenital genetic disorder characterized by painful blistering of the skin and mucous membranes in response to minor trauma or pressure. JEB is classified roughly into 2 subtypes: JEB-Herlitz is caused by mutations on genes encoding laminin-332. The authors present a patient consulted with a suspicion of primary immunodeficiency due to skin sores that started at the age of 1 month and a history of 3 siblings who died with similar sores, who was diagnosed with JEB-Herlitz after detecting a homozygous LAMC2 gene mutation in WES analysis. Microscopic evaluation of hematoxylin and eosin-stained sections showed vesicle formation with subepidermal separation, which is accompanied by striking neutrophil and eosinophil leukocyte infiltration both in the vesicle and papillary dermis (eosinophil-rich inflammatory infiltrate). Such a histopathological finding has been rarely reported in this condition.

Amikacin liposome inhalation suspension (ALIS) is known to cause drug-related pneumonitis, which has been described as \"hypersensitivity pneumonitis (HP)\". However, its clinical and pathological characteristics have never been reported. We retrospectively evaluated 18 patients treated with ALIS. Three (16.7%) patients developed HP-pattern pneumonitis on high-resolution computed tomography. Serum eosinophil counts were elevated up to above 1000/μL in these three patients, which decreased with ALIS discontinuation only. Of note, the specimen obtained by transbronchial lung cryobiopsy in one patient revealed a mild degree of lymphocyte and eosinophil infiltration. Rather, the findings of acute lung injury such as an edematous thickening of the alveolar walls, and an accumulation of foamy degenerative macrophages in the alveolar lumina was prominent. A pulmonary alveolar proteinosis reaction was also observed. HP-pattern pneumonitis due to ALIS may pathologically correspond to acute lung injury and a pulmonary alveolar proteinosis reaction despite increasing serum eosinophil counts.

NK/T-cell lymphoma (NKTCL) is a highly aggressive malignant tumour with a very poor prognosis, which often poses diagnostic difficulties due to the non-specificity of its clinical presentation. NK/T-cell lymphoma with eosinophilic hyperplasia syndrome is extremely rare. This article describes a patient with NKTCL misdiagnosed as vasculitis who presented with sinusitis, abdominal pain, anorexia, and lung shadows. Additionally, the patient exhibited extremely high eosinophilia levels, which led to a further misdiagnosis of eosinophilic granuloma. We describe the clinical features, diagnostic methods and differential diagnosis of lymphoma and highlights the importance of a multidisciplinary approach in accurate diagnosis and treatment.

Kimura disease (KD), also known as eosinophilic lymphogranuloma, is a rare chronic inflammatory or allergic disease. It can present with immune-related diseases such as nephrotic syndrome, asthma, and ankylosing spondylitis. In this study, we report a case of KD combined with immunoglobulin A nephropathy that first presented as a mass in the inguinal region, followed by recurrent renal involvement. Previous reports suggested that renal involvement caused by KD was due to direct infiltration of eosinophils; however, in this case, no eosinophil infiltration was found in the renal tissue after renal biopsy. This observation reminds us to approach the case from an immune-related molecular perspective to investigate the exact cause of renal damage due to KD.

Eosinophilic oesophagitis (EoE) is a chronic immune and antigen-mediated disease characterized by symptoms related to oesophageal dysfunction, and histologically, is marked by eosinophilic infiltrate in the oesophageal mucosa. It is prevalent in developed countries and considered rare in developing countries. There is an interplay of allergic and genetic factors in the aetiology of EoE. This is a report of EoE in a 15-year-old female adolescent in Nigeria who presented to the University of Calabar Teaching Hospital with recurrent vomiting, abdominal pain, weight loss, and dysphagia. She had received treatment for Gastro-oesophageal disease three years earlier and was lost to follow-up. Weight on admission was 39 kg and height 170 cm with a BMI below the 3rd centile. Peripheral blood showed an eosinophil count of four percent. The abdominal computed tomography (CT) scan and upper gastrointestinal (GI) series were normal. Faecal antigen for H. pylori and ova for stool parasites were negative. Histologic findings of proximal and distal oesophageal mucosal biopsies showed greater than 20 eosinophils per high power field. The histology of the stomach and duodenum were normal. She was initially treated with a protein pump inhibitor, with no improvement. Swallowed fluticasone propionate and eliminating peanuts, wheat, egg, and milk from her diet were introduced. Symptoms improved with the patient no longer vomiting and had an increase in weight gain. She was discharged to follow up. This case shows that EoE occurs in developing countries, but diagnosis may be missed. There is a need for a high index of suspicion among gastroenterologists in patients with symptoms suggestive of GERD not responding to therapy.

A woman in her early 60s was referred with dysphagia and chest pain to a tertiary referral centre specialising in oesophageal disorders. Cardiac symptom origin and sinister oesophageal pathology had been excluded at her local hospital in NHS Scotland. Under multidisciplinary team oversight, reinvestigation of mucosal pathology and oesophageal motility ultimately uncovered both Type III achalasia and eosinophilic oesophagitis. This case demonstrates the benefit of including provocative testing during high-resolution manometry to reproduce relevant dysphagia and the importance of stopping proton-pump inhibitors long enough to uncover excessive eosinophils which could otherwise be masked. Ultimately, tailored management for both conditions separately was required to achieve symptoms resolution.

Pulmonary infiltrates with eosinophilia are a heterogeneous group of disorders that are characterized by pulmonary infiltrates on chest radiograph and elevated levels of eosinophils in the peripheral blood. Among patients with these disorders, reports of either allergic bronchopulmonary aspergillosis (ABPA) or tropical pulmonary eosinophilia (TPE) are common. However, the simultaneous occurrence of ABPA and TPE is not often reported. We present the case of a young man with a history of asthma who was diagnosed with ABPA and TPE. Initially, the patient exhibited a partial response to treatment of ABPA, but persistent symptoms and eosinophilia led to suspicion and subsequent diagnosis of TPE. With implementation of antifilarials and steroids, the patient experienced satisfactory clinical and serological improvements. This case underscores the importance of considering multiple diagnoses in patients with overlapping symptoms and highlights the need for comprehensive management strategies in complex lung diseases.

BACKGROUND: The advent of biologics has resulted in major progress in the treatment of severe T2 high asthmatics. There are currently several classes of biologics approved for severe asthma including anti-immunoglobulin E, anti-interleukin-5/interleukin 5R, anti-interleukin 4/interleukin 13R, and anti-thymic stromal lymphopoietin.
METHODS: Here we report the case of a 55-year-old Caucasian man with severe eosinophilic atopic asthma, who sequentially benefited from a treatment with mepolizumab, an anti-interleukin-5 monoclonal antibody, followed by treatment with dupilumab, an anti-interleukin-4/interleukin-13R antibody, the switch being justified by a flare-up of dermatitis while on mepolizumab. Overall, the patient has been followed for 72 months, including 42 months on mepolizumab and 30 months on dupilumab. Close monitoring of exacerbations, asthma control, lung function, asthma quality of life, and biomarkers shows that both biologics reduced asthma exacerbation and provided an improvement in asthma control and quality of life, with the patient achieving remission after 30 months on dupilumab. However, the effects of the two biologics on the biomarkers were very different, with mepolizumab controlling eosinophilic inflammation and dupilumab reducing serum immunoglobulin E and fractional exhaled nitric oxide levels.
CONCLUSIONS: The originality of this case resides in the description of clinical status and biomarker evolution after a sequential use of mepolizumab and dupilumab in a severe atopic eosinophilic asthmatic. It shows that mepolizumab reduces exacerbation and improves asthma control by curbing eosinophilic inflammation whereas dupilumab provides asthma remission without controlling airway eosinophilic inflammation.