Guselkumab-Associated Pulmonary Disease and Diffuse Alveolar Hemorrhage with Drug Rash with Eosinophilia and Systemic Symptoms.

Psoriasis is a common skin condition worldwide. Moderate-to-severe disease is treated with biologic or non-biologic disease-modifying anti-rheumatic drugs. These include tumor necrosis factor (TNF)-a inhibitors, interleukin (IL)-17 inhibitors, and IL-23 inhibitors. Case reports of inhibitors of TNF-a and IL-12p40 subunits causing interstitial pneumonia (IP) have been published in the literature, but no case of anti-IL-23p19 subunit biologics causing IP and acute respiratory distress syndrome (ARDS) has been reported before. We report a case of a patient with restrictive lung disease secondary to a body mass index of 36.54 kg/m2, obstructive sleep apnea, and psoriasis, who developed IP and ARDS presumed to be secondary to guselkumab, an anti-IL-23p19 subunit monoclonal antibody. He was on ustekinumab, an anti-IL-12/23p40 for the treatment of psoriasis, but was switched to guselkumab eight months before the presentation, and since then he had been complaining of progressive shortness of breath. He initially presented to the hospital after having drug reaction with eosinophilia and systemic symptoms (DRESS) after being started on amoxicillin for a tooth infection. He was treated with high-dose intravenous steroids but developed progressive shortness of breath. Broad-spectrum antibiotics were added. An extensive infectious, autoimmune, and hypersensitivity work-up was undertaken, which returned negative. A bronchoscopy with bronchoalveolar lavage was performed, which revealed diffuse alveolar hemorrhage (DAH). His lung imaging and oxygenation progressively got worse; hence, no lung biopsy was taken. He was intubated and required inhaled nitric oxide, but due to the lack of improvement, the family elected for comfort measures, and the patient was extubated and passed away. To our knowledge, this is the first case of an association between guselkumab, IP, ARDS, and DAH. Rare instances of DAH with DRESS have been reported before. Whether it was DRESS or guselkumab that caused DAH was uncertain in our patient. Clinicians should monitor for DAH and shortness of breath in patients on guselkumab so that more data can be obtained and studied in the future.

Acute Respiratory Distress Syndrome Secondary to Enterovirus-Human-Rhinovirus Infection in an Adult

Enterovirus-human-rhinovirus (EV-HRV) are small RNA viruses that are airborne and can spread by direct contact or fomites and usually cause the common cold, asthma and chronic obstructive pulmonary disease exacerbation. EV-HRV-associated acute respiratory distress syndrome (ARDS) is common in children but is a rare cause of ARDS in adults. ARDS is defined according to the Berlin criteria and can be mild, moderate or severe depending on the PaO2 to FiO2 ratio. We report a case of a 70-year-old female with cardiac comorbidities, emphysema, second-hand smoking of 25 years, on methotrexate for rheumatoid arthritis presenting with ARDS secondary to EV-HRV infection. Despite initial treatment with appropriate antibiotics, steroids, low tidal volume mechanical ventilation, rescue maneuvers such as ventilation in prone positioning, paralyses, and inhaled nitric oxide, she passed away. EV-HRV causes upper respiratory tract infections but causes cytokine releases such as IL-1, IL-6, and IL-8 in the lower respiratory tract and in the blood which can cause ARDS. Very few cases of EV-HRV ARDS in immunocompetent adults are reported in the literature. Female sex is also associated with EV-HRV ARDS. No antiviral therapy exists for patients critically ill with EV-HRV;however, one case of successful treatment with high-dose intravenous vitamin C (HIVC) is reported in the literature. EV-HRV is one of the most common viruses identified in patients admitted with viral pneumonia in the intensive care unit. It should not be forgotten as a cause of ARDS.

A rare case of rectal bleeding and Fusobacterium mortiferum sepsis due to solitary fibrous tumour originating from the mesentery.

Solitary fibrous tumours (SFTs) are rare mesenchymal tumours that are mostly seen in the pleura. Lately, they have also been described in other locations. Recent discovery of the NAB2-STAT6 fusion gene which is specific for SFTs has led to an accurate diagnosis of SFTs. The occurrence of SFTs in the mesentery is very rarely reported in the literature. We report a case of a 63-year-old female who presented with abdominal pain, rectal bleeding and Fusobacterium bacteraemia, who was ultimately found to have a mesenteric SFT.

Hantavirus Cardiopulmonary Syndrome and Diffuse Alveolar Hemorrhage in the Era of COVID-19.

Hantavirus Cardiopulmonary Syndrome (HCPS) can occur after infection with Hantavirus which can occur by inhaling aerosolized rodent urine, feces, and saliva contaminated with the virus. It presents with the rapid development of pulmonary edema, respiratory failure, and cardiogenic shock with the hallmark being microvascular leakage. We report a patient with a history of alcohol abuse and recent exposure to mice and sick kittens who presented with cough with sputum production, shortness of breath, orthopnea, and new-onset lower extremity edema. Imaging revealed bilateral infiltrates more common on the left with an unremarkable echocardiogram. Testing for COVID-19, Human Immunodeficiency Virus (HIV), influenza, bacterial pneumonia including tuberculosis and methicillin-resistant Staphylococcus aureus (MRSA), aspergillosis, histoplasmosis, Blastomyces, and Coccidiodes was negative. Bronchoscopy and bronchoalveolar lavage revealed diffuse alveolar hemorrhage (DAH) and were negative for acid-fast bacilli and Nocardia cultures. He was further tested for Hantavirus, Q fever, leptospirosis, toxoplasmosis, and empiric treatment with doxycycline initiated. His Hantavirus IgM antibody came back positive. Human Hantavirus infection occurs after inhalation of infected rodent excreta; fortunately, human-to-human transmission has not been documented. HCPS most commonly occurs due to the Sin Nombre virus (SNV), has a case fatality rate of 50%, and is a notifiable disease in the United States. It has 3 distinct phases, prodromal, cardiopulmonary, and convalescent/recovery. The cardiopulmonary phase occurs from increased permeability of pulmonary capillaries and in severe cases can progress to cardiogenic shock. Diagnosis is based on the presence of IgM and IgG Hantavirus antibodies. Treatment is mainly supportive; however, patients are usually treated with broad-spectrum antibiotics while workup is underway. In animal models, ribavirin and favipiravir are only effective when administered in the prodromal phase. If suspicion of Hantavirus infection exists, early mobilization to the intensive care unit for treatment is recommended. Extracorporeal membrane oxygenation (ECMO) has been suggested to improve outcomes in severe HCPS with refractory shock.