Programmed cell death-1 (PD-1) inhibitors stimulate immune recognition of tumour cells in cancer patients, but have significant autoimmune side effects including pneumonitis. We report the case of a patient with asthma and mild eosinophilia who developed unusual pulmonary side effect of bronchiectasis, severe eosinophilia (absolute eosinophil count: 3200 c/mm3) and elevated IgE levels (7050 IU/mL; normal: <164 IU/mL) 4 months into therapy with the PD-1 inhibitor pembrolizumab. Aspergillus fumigatus IgG was elevated at 15.60 U/mL (normal: <12.01 U/mL). He responded to therapy with corticosteroids and voriconazole and was able to resume pembrolizumab thereafter with good clinical response.

in a dose of 0-02 ,ug/kg per min resulted in a significant fall in the pulmonary arterial pressure (P < 0.001), total pulmonary resistance (P < 0 001), left ventricular end-diastolic pressure (P < 0.001), and aortic pressure (P < 0.01), and an increase in the pulmonary blood volume (P < 0.01), cardiac index (P < 0.01), and heart rate (P < 0'05). No significant differences were noted in stroke volume index or left ventricular dP/dt at 50 mmHg after prostaglandin E1. These results indicate that exogenously administered prostaglandin E1 causes active vasodilatation of the pulmonary vascular bed and has no inotropic action on the cardiac muscle.Though the effect of exogenously administered prostaglandin E (PGE) on the pulmonary circulation has been studied both in various species of animal and in healthy man (Bergstrom et al., 1959(Bergstrom et al., , 1965Hauge et al., 1967;Carlson et al., 1969;Hyman, 1969;Sobel and Robinson, 1969;Anderson et al., 1971;Koss et al., 1973;Kadowitz et al., 1974), the part it plays in the regulation of the pulmonary circulation in disease has not yet been analysed. It has been assumed that PGE, which is liberated and metabolised in the lungs, fulfils the role of a local mediator influencing the pulmonary circulation in hypoxaemia or in anaphylactic reactions (Bergofsky, 1974).The effect of exogenous PGE on the pulmonary vascular bed can be usefully studied in patients with mitral stenosis, in whom pulmonary vasoconstriction resulting from chronic hypoxaemia plays an important part in the development of pulmonary hypertension (Bergofsky, 1974). Subjects and methodsThe effect of prostaglandin E1 (PGE1) was studied in 20 patients, 4 men and 16 women, ranging Received for publication 13 March 1978 in age from 19 to 59 years (average 36-7 years). Mitral stenosis was present in all with mitral regurgitation also in 2 patients. The diagnosis was established by clinical examination and haemodynamic study, and was confirmed at operation in all cases. Heart failure was grade 2 and was found in 4 cases, grade 3 in 11, and grade 4 in 5, according to the NYHA classification. All the patients had pulmonary arterial hypertension: the mean value of the mean pulmonary arterial pressure was 38-5 + 15-2 mmHg, and the total pulmonary resistance was 808-2 + 387 dynes s cm-5 (10.1 ± 4-8 units). The majority of patients were receiving a digitalis preparation and a thiazide diuretic, but for 2 weeks before the investigation non-steroidal anti-inflammatory drugs were not given.A prostaglandin solution was prepared immediately before the injection by dissolving PGE1 (Upjohn Co. Ltd) in a 95 per cent ethanol solution.The appropriate dose of this solution was then diluted in 120 ml of 0 9 per cent saline. The preparation was administered by continuous intravenous infusion, using a Unipan peristaltic pump, in doses of [0][1]

We describe a rare case of Pneumocystis jirovecii pneumonia (PCP) in a heterosexual man with a pertinent medical history of well-controlled human immunodeficiency virus (HIV) on highly active antiretroviral therapy (HAART) and PCP prophylaxis with atovaquone. The patient presented with recurrent shortness of breath, worsening malaise, and fever, following treatment for hypersensitivity pneumonitis one month prior, including a twenty-four-day course of 40 milligrams daily glucocorticoid with taper. However, transbronchial biopsies, lavage, and cytology from prior admission were inconclusive. The patient refused video-assisted thoracic surgery (VATS) at that time. Upon readmission, bronchoscopy with right VATS and lung biopsy were performed. Grocott’s methenamine silver stain of right lung biopsy was positive for Pneumocystis jirovecii. This case is a rare example of PCP in a patient with a normal CD4 count (>487 cells/μL) and a low viral load (<20 copies/mL) despite PCP prophylactic antibiotics in the setting of recent iatrogenic immunosuppression.

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