Pfizer-BioNTech (BNT162b2), Moderna (mRNA-1273) COVID-19 mRNA vaccines and hypersensitivity reactions.

The SARS-CoV-2 Virus (COVID-19) is responsible for over 239 million cases and 4.8 million deaths globally (Data source WHO COVID-19 Dashboard accessed on October 14, 2021). It continues to surge and ravage countries, leaving healthcare systems in constant struggle and uncertainty. A variety of vaccines were developed to combat the spread of the COVID-19 Virus. Reports of possible allergic reactions with COVID-19 vaccines are a significant cause of public concern, especially among those with a known history of a severe allergic reaction (e.g., anaphylaxis). Here we review articles relevant to COVID-19 vaccines and their excipients (especially PEG (Polyethylene glycol) and hypersensitivity reactions associated with COVID-19 vaccines (including clinical features, pathophysiology, special populations receiving COVID-19 vaccinations, potential diagnostic tests, and preventive measures that can be taken to minimize the risks of hypersensitivity reactions with COVID-19 vaccines).

Negative pressure pulmonary oedema due to rigors and chills associated with liver abscess.

A 61-year-old male presented with progressive generalized weakness, myalgia, diaphoresis, fever, episodic chills and rigors that had started 4 days previously. Chest x-ray (CXR) showed overlying curvilinear radio-opacities. Abdominal computed tomography revealed liver and bilateral adrenal lesions. Empiric 7-day intravenous Piperacillin / Tazobactam (Zosyn) was initiated, and he was admitted for sepsis. After an episode of rigors on Day 2, he developed acute hypoxic respiratory failure with inspiratory stridor. CXR revealed new, bilateral airspace disease. Racemic Epinephrine, Solumedrol, Ketorolac (Toradol) and Diphenhydramine were given, and he was transferred to the intensive care unit with presumptive diagnosis of foreign body aspiration or allergic reaction. With each subsequent episode of rigor and chills, he continued developing hypoxic respiratory failure with stridor and an incremental increase in pulmonary oedema on imaging. Pulmonologist concluded it likely secondary to negative pressure pulmonary oedema caused by transient laryngeal dyskinesia induced by the increased work of breathing associated with rigors. Symptoms resolved after the complete course of antibiotics along with supportive therapy.

Effect of Triple Therapy with Budesonide-Formoterol-Tiotropium Versus Placebo-Tiotropium on Sleep Quality in Patients with Chronic Obstructive Pulmonary Disease.

BACKGROUND: Factors responsible for poor sleep quality in patients with chronic obstructive pulmonary disease (COPD) includes the effects of medications. This study evaluates the effect of the inhaled triple therapy of budesonide-formoterol-tiotropium versus placebo-tiotropium on sleep quality in COPD patients. METHODS: Twenty-three patients (11 [48%] males; age 55 [51-60, 48--5] years; body mass index [BMI] 25 [22-30, 18-40] kg/m2; forced expiratory volume in 1 second [FEV1]1.10 [0.80 -1.90, 0.60-2.80] L, 42 [31-62, 24-75] % predicted) were studied. Ten patients were randomized to budesonide-formoterol-tiotropium and 13 patients to placebo-tiotropium. At baseline and after 28 days, patients completed spirometry, polysomnography, an Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), COPD-specific St George's Respiratory Questionnaire (SGRQ-C) and short form 36 (SF 36). RESULTS: After 28 days, there was a significant 29% increase in the bedtime FEV1 in the budesonide-formoterol-tiotropium group (from 0.75 [0.55-1.30, 0.50-2.40] L to 1.00 [0.75-1.55, 0.50-3.00] L, p=0.031), with no change in the placebo-tiotropium group (from 1.20 [0.80-1.50, 0.60-1.90] L to 1.15 [0.75-1.55, 0.50-1.80] L, p=0.91). No significant change was found post treatment in sleep efficiency or total sleep time in both the budesonide-formoterol-tiotropium group (from 78 [72-92, 62-98]% to 88 [77-92, 40-98]%, p=0.70 and 290 [268-358, 252-382] min to 342 [303-358, 157-372] min, p=0.77, respectively) and the placebo-tiotropium group (from 82 [75-88, 46-93]% to 84 [77-87, 62-94]%, p=0.96 and 320 [292-350, 180-378] min to 339 [303-349, 241-366] min, p=0.79, respectively). While there was no significant change in the arousal index in the budesonide-formoterol-tiotropium group (9 [5-16, 0-48] arousals/hour to 14 [9-17, 2-36] arousals/hour, p=0.43), a significant increase was seen in the placebo-tiotropium group (11 [4-13, 3--2] arousals/hour to 17 [11-21, 2-33] arousals/hour, p=0.027). Similarly, there was no change in the ESS in the budesonide-formoterol-tiotropium group (6 [3-8, 0-11] to 6 [5-8, 0-1]), p=0.44), but a marginally significant increase in the placebo-tiotropium group (8 [5-12, 2-18] to 10 [7-13, 5-18], p=0.07), with a significant difference in the ESS 28 days post treatment between the 2 groups (6 [5-8, 0-11] versus 10 [7-13, 5-18], p=0.043). There was no significant change in nocturnal oxygenation, sleep architecture, PSQI, SGRQ-C, or SF 36 in both groups. CONCLUSION: In patients with COPD, inhaled triple therapy with budesonide-formoterol-tiotropium as compared to placebo-tiotropium improves pulmonary function while preserving sleep quality and architecture.