No abstract

Venlafaxine is a serotonin-norepinephrine reuptake inhibitor used as an antidepressant. Interindividual variability and herb-drug interactions can lead to drug-induced toxicity. We report the case of a 35-year-old female patient diagnosed with synchronous pneumonitis and acute cardiomyopathy attributed to venlafaxine. The patient sought medical attention due to dyspnea and dry cough that started three months after initiating treatment with venlafaxine for depression. The patient was concomitantly taking Centella asiatica and Fucus vesiculosus as phytotherapeutic agents. Chest CT angiography and chest X-ray revealed parenchymal lung disease (diffuse micronodules and focal ground-glass opacities) and simultaneous dilated cardiomyopathy. Ecocardiography revealed a left ventricular ejection fraction (LVEF) of 21%. A thorough investigation was carried out, including BAL, imaging studies, autoimmune testing, right heart catheterization, and myocardial biopsy. After excluding other etiologies and applying the Naranjo Adverse Drug Reaction Probability Scale, a diagnosis of synchronous pneumonitis/cardiomyopathy associated with venlafaxine was assumed. The herbal supplements taken by the patient have a known potential to inhibit cytochrome P450 enzyme complex, which is responsible for the metabolization of venlafaxine. After venlafaxine discontinuation, there was rapid improvement, with regression of the radiological abnormalities and normalization of the LVEF. This was an important case of drug-induced cardiopulmonary toxicity. The circumstantial intake of inhibitors of the CYP2D6 isoenzyme and the presence of a CYP2D6 slow metabolism phenotype might have resulted in the toxic accumulation of venlafaxine and the subsequent clinical manifestations. Here, we also discuss why macrophage-dominant phospholipidosis was the most likely mechanism of toxicity in this case.

Urinothorax most frequently develops in patients with excretory uropathy or blunt abdominal trauma, although other mechanisms have been reported. Traditionally, a pleural fluid to serum creatinine ratio higher than one is a hallmark of this condition. In certain settings, taking this diagnosis into account at an early stage might be crucial for a good outcome.

Nitrofurantoin-induced diffuse lung toxicity is well documented in the literature but is often misdiagnosed. We describe an 82-year-old female medicated with nitrofurantoin for the previous 2 years who was admitted for dyspnoea, dry cough and fatigue for 4 months. She was febrile and tachypnoeic and she presented with bilateral basal crackles, hypoxaemic respiratory failure and slightly elevated C-reactive protein levels. A chest radiograph showed bilateral air-space consolidation and interstitial infiltrates and the high-resolution computed tomography scan was evocative of a perilobular pattern of organising pneumonia (OP). Due to the clinical–radiological context, she was diagnosed with a presumable nitrofurantoin-induced OP. She was started on prednisolone 60 mg daily with a progressive improvement. It is important that clinicians are aware of the spectrum of side effects associated with nitrofurantoin so as to monitor patients.LEARNING POINTSIt is crucial to ensure that a thorough medical history with a systems review and a complete drug history are carried out.Chronic pulmonary toxicity due to nitrofurantoin is rare and it occurs primarily in older women who have been prescribed relatively small doses of nitrofurantoin for UTI prevention.The cessation of nitrofurantoin is the basis of the treatment and may be sufficient for clinical and radiological improvement.

Case report of a male patient with a five-decade follow-up history in a tertiary care hospital distinguished for malabsorption syndrome, failure-to-thrive, meningitis and recurrent bacterial, fungal and mycobacterial pulmonary infections. Additionally, he developed epidermodysplasia verruciformis, several in situ spinocellular carcinomas and an uncharacteristic parenchymal lung disease. Surgical lung biopsy suggested pulmonary alveolar proteinosis with fibrotic change. Retrospectively, severe monocytopenia had been overlooked in the past, as well as low B and NK cell blood counts. Flow cytometry confirmed the absence of the previous cell subsets along with an undetectable population of dendritic blood cells. Dendritic cell, monocyte, B and NK lymphoid Human Deficiency Syndrome (DCMLS) is a novel rare immunodeficiency described in 2010, linked to GATA-2 mutation. This syndrome should be highlighted as a rare cause of acquired PAP, with a radiological pattern encompassing potential fibrotic change. Failure to recognize monocytopenia may impede the chance to diagnose.