Objective Pneumonia is a morbid complication of stroke, but evidence-based strategies for its prevention are lacking. Acid-suppressive medications have been associated with increased risk for nosocomial pneumonia in hospitalized patients. It is unclear whether these results can be extrapolated to stroke patients, where other factors strongly modulate pneumonia risk. We investigated the association between acid-suppressive medication and hospital-acquired pneumonia in patients with acute stroke. Methods All patients hospitalized with acute ischemic stroke or intracerebral hemorrhage in a large, urban academic medical center in Boston, Massachusetts from 6/2000 – 6/2010, ≥ 18 years of age and hospitalized for ≥ 2 days were eligible for inclusion. Acid-suppressive medication use was defined as any pharmacy charge for a proton-pump inhibitor or histamine-2 receptor antagonist. Multivariable logistic regression was used to control for confounders. The main outcome measure was hospital-acquired pneumonia, defined via ICD-9-CM codes. Results The cohort comprised 1,676 admissions. Acid-suppressive medication was ordered in 1,340 (80%) and hospital-acquired pneumonia occurred in 289 (17.2%). The unadjusted incidence of hospital-acquired pneumonia was higher in the group exposed to acid-suppressive medication compared to unexposed (20.7% versus 3.6%, OR=7.0, 95% CI 3.9–12.7). After adjustment, the OR of hospital-acquired pneumonia in the exposed group was 2.3 (95% CI 1.2–4.6). The association was significant for proton-pump inhibitors (OR=2.7, 95% CI 1.4–5.4), but not for histamine-2 receptor antagonists (OR=1.6, 95% CI 0.8–3.4). Interpretation In this large hospital-based cohort of patients presenting with acute stroke, acid-suppressive medication use was associated with increased odds of hospital-acquired pneumonia.

Hypersensitivity reactions to dihydropyridine calcium channel blockers (CCB) are exceedingly rare, although sporadic reports of isolated angioedema seem to be gradually increasing in frequency. We present a case of angioedema likely triggered by amlodipine.

This protocol for rapid desensitization to intravenous radiographic contrast material (RCM) improves the strategy first reported by Uppal et al. Desensitization is a validated preventative measure for medical emergencies, such as cardiac catheterization, when patients present with histories of anaphylactoid reactions to the allergen of concern. The patient required another catheterization that was modified to repeat the final dosage of 320 mg/mL of Visipaque®, accommodating cardiac catheterization postponement, contrary to readministration of doses 4 (0.625 mg/mL) and 8 (10 mg/mL) as reported in Uppal et al. Our risk score calculations suggested that the patient was at low risk of contrast-induced nephropathy (CIN) that did not necessitate reduced dosage. No complications were reported following catheterization. We propose repetition of the final RCM dosage as a more effective and efficient desensitization strategy, as long as the scoring system does not indicate high risk for CIN.

The increasing availability of genetic testing for modern immunologists in the evaluation of immune diseases could provide a definite diagnosis in elusive cases. A 27-year-old white male patient presented to the clinic with recurrent sinopulmonary and cutaneous infections since childhood. The patient’s mother had seronegative polyarthritis, and one of two sisters of the patient had chronic sinopulmonary infections. Serum immunoglobulins, immunoglobulin G (IgG) subclasses, lymphocyte subset markers, mannose-binding lectin, mitogen and antigen stimulation, bacteriophage study, and Streptococcus pneumoniae titers to 23 serotypes were all normal. B-cell phenotyping revealed a decrease in both nonswitched memory B cells (CD19+CD27+IgD+) and switched memory B-cells (CD19+CD27+IgD−). Genetic testing and the improvement of clinical symptoms after IgG replacement led to the final diagnosis.

Introduction The coronavirus disease 2019 (COVID-19) pandemic due to the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes worldwide devastation. We describe the course of a patient with COVID-19 in the setting of an acquired humoral deficiency as a result of chemotherapeutic treatment for rheumatologic conditions. Case Report A 49-year-old Caucasian male presented with non-relieving fever, hypoxemia, and persistent diarrhea after seven days following a positive SARS-CoV-2 polymerase chain reaction (PCR) assay. The patient’s past medical history was significant for mixed connective tissue disease, rheumatoid arthritis, and systemic lupus erythematosus treated with methotrexate and rituximab since 2008. He was diagnosed with acquired humoral deficiency in 2017 managed by intravenous immunoglobulin (IVIG) infusion every three weeks. The patient’s course of hospitalization was complicated by acute respiratory distress which necessitated intensive unit care and required up to 20 L/min oxygen supplementation via a humidified high flow generator. He was treated with hydroxychloroquine and azithromycin and received an IVIG transfusion. The patient was discharged to home after forty-two days of hospitalization with oxygen supplementation only during ambulation and a complete resolution of diarrhea. Discussion According to current limited data, patients with immunodeficiency have longer length of hospitalization compared to immunocompetent individuals. Our patient demonstrated a form of immunodeficiency as the result of a chemotherapeutic agent, and his clinical course appeared to be more severe. Conclusion More studies are necessary to shed light on the immunological response to SARS-CoV-2 and its impact on immunocompromised and immunocompetent and individuals. We describe the course of a patient with COVID-19 in the setting of an acquired humoral deficiency.