Invasive aspergillosis is a rare opportunistic infection mainly occurring in patients with a well-established risk such as neutropenia or conditions that lead to chronically impaired cellular immune responses. Systemic corticosteroids are a well-known risk factor for fungal infections. Recently, reports of invasive aspergillosis in patients treated with monoclonal biologic agents, such as tumor necrosis factor-alpha inhibitors, have been increasing. We present the case of a 47-year-old female patient with seronegative spondyloarthropathy treated with infliximab and corticosteroids. The patient presented classical symptoms of an acute lower respiratory infection, and she was treated with a β-lactam antibiotic. Infliximab administration was deferred until nine days after clinical recovery. Fourteen days after drug administration, she was admitted with a symptomatic subcortical hematoma in the left parietal region. There was a rapid neurological recovery, and there were no risk factors for haemorrhagic stroke detected. The chest X-ray revealed an oval mass with an air crescent sign, and the CT scan was suggestive of aspergilloma. Bronchoalveolar lavage cytology identified Aspergillus spp. Voriconazole was initiated and, after one month of treatment, the patient was readmitted with a left facial palsy associated with hemiparesis and dysarthria. Laboratory evaluation showed leukocytosis and elevated C-reactive protein. A severe right middle cerebral artery stroke was present on the brain CT scan. Transesophageal echocardiogram revealed large mitral valve vegetation, and the diagnosis of Aspergillus endocarditis with cerebral embolization was made. Fungal infections are challenging due to the diagnosis infrequency and paucisymptomatic natural history. Despite being crucial in the treatment of autoimmune diseases, immunosuppressive drugs increase the risk of fungal infection. It is extremely important to consider Aspergillus infection in immunosuppressed patients, and the need for prophylaxis in non-neutropenic patients with risk factors should be clarified.

Information about a real patient is presented in stages (boldface type) to expert clinicians (Drs Ribeiro, Fialho, and Boavida), who respond to the information and share their reasoning with the reader (regular type). A discussion by the authors follows.

INTRODUCTION: Pulmonary lymphangitic carcinomatosis (PLC) is a rare lung metastatic manifestation [1,2,3]. Its nonspecific presentation and imagiologic findings, often similar to interstitial lung disease (ILD), usually leads to a delayed diagnosis [1,3]. Half of the cases are associated with history of cancer, particularly adenocarcinoma [1]. CASE PRESENTATION:We describe 8 patients with PLC, with a median age of 56 years (table 1) and the majority (63%) having past history of cancer. Symptoms present at admission were progressive exertional dyspnea (63%), dry cough (50%), pleuritic chest pain (25%) and weight loss (25%). Median time from onset of symptoms until hospital admission was 25.5 days. At presentation, 75% had bilateral infiltrates in chest radiography and 50% had hypoxemia. Thoracic computed tomography findings (image 1) included ground-glass opacities in 100% of cases, mediastinal adenopathies in 25%, thickening of interlobular septae in 75% and bilateral effusion in 25%. The diagnosis of ILD was initially considered in all patients and in 3 cases corticosteroids were started, without improvement. The diagnosis of PLC was confirmed in 5 cases through lung biopsy. In the other 3, PLC was presumed through pulmonary imaging associated with histologic confirmation of a distant tumor simultaneously diagnosed. Diagnosis was delayed a median of 30 days after hospital admission. Half of the cases were associated with adenocarcinoma (1 of the lung and 3 of the stomach) and 2 with invasive breast cancer. Other less common causes were: 1 case of small cell lung cancer and 1 of hepatocellular carcinoma. In 63% PLC was the first manifestation of cancer recurrence, and in the other cases was the first presentation of the tumor. The median time of survival after the diagnosis was 36 days, despite starting antineoplastic therapy.DISCUSSION: In our case series, PLC presented with dyspnea and cough, which did not point to the original tumor site in the majority of cases. The non-specific radiographic abnormalities lead to the misdiagnosis of ILD, delaying the correct diagnosis often for more than 1 month. Moreover treatment was also postponed, worsening prognosis. Although some subtypes of ILD can present with mediastinal node enlargement and pleural effusion, these should raise suspicion of malignancy. Diagnosis confirmation of PLC typically requires lung biopsy, but given the usual rapid clinical deterioration, this step is sometimes purposely obviated and diagnosis is presumed.CONCLUSIONS: PLC is a challenging diagnosis and might be the first manifestation of malignancy, new or recurrent. Persistent and worsening dyspnea in patients with past history of cancer should prompt an extended differential diagnosis to include PLC, given the associated poor prognosis.

We report a case of a 40-year-old African male with a history of diabetes mellitus with multiple microvascular complications, having recently initiated insulin treatment with a rapid decline in glycosylated hemoglobin (HbA1c) concentration. The patient presented with a sudden onset of right thigh pain and swelling not associated with trauma. Blood work revealed elevated inflammatory markers. A presumptive diagnosis of pyomyositis was made and the patient was treated with intravenous antibiotics with no improvement. Diabetic muscle infarction was then considered and confirmed by magnetic resonance imaging of the affected thigh. As with retinopathy and neuropathy deterioration that have been described as secondary to an aggressive glycemic control, it is possible that muscle myonecrosis may have been consequent to the rapid HbA1c normalization.

Acute copper toxicity is uncommon in Western countries and is often the result of accidental consumption or a suicide attempt. We report the case of a 65-year-old man presenting to the accident and emergency department after a suicide attempt with ingestion of Bordeaux mixture, ibuprofen, acetaminophen and bleach. Primary evaluation showed caustic oesophagitis, toxic hepatitis and acute renal injury, which were treated with supportive care. During admission, he developed a non-immune haemolytic anaemia associated with high levels of copper in urine and blood. Chelation treatment with penicillamine was started and evolution was favourable after 1 month of treatment. Copper poisoning can be lethal. Prompt diagnosis and treatment are key for a favourable prognosis.