An update on acalabrutinib to treat chronic lymphocytic leukemia.

Acalabrutinib was approved by the U.S. Food and Drug Administration (FDA) for treatment-naive (TN) and relapsed/refractory (R/R) use for patients with chronic lymphocytic leukemia (CLL) in November 2019 following the phase III ASCEND and ELEVATE-TN registration trials. Acalabrutinib is a second-generation Bruton tyrosine kinase inhibitor (BTKi) that was developed after ibrutinib, the first-in-class BTKi. Ibrutinib is usually well tolerated and provides durable remissions; however, some patients experience toxicities from the off-target effects that lead to treatment discontinuation. A recent press release of the phase III ELEVATE-RR trial comparing acalabrutinib to ibrutinib in relapsed high-risk CLL reported noninferior progression-free survival and statistically significantly lower rates of atrial fibrillation; however, publication of this data is pending. There is currently 53 months of follow-up for patients receiving acalabrutinib compared with 8 years for those on ibrutinib. Acalabrutinib is approved as monotherapy in the R/R or TN setting, and in the TN setting can be combined with the anti-CD20 monoclonal antibody obinutuzumab. The data for acalabrutinib development and clinical use are discussed in this review.

Laryngeal tuberculosis.

Since the introduction of antituberculous medications, the incidence of laryngeal tuberculosis (TB) has decreased and remains stable. However, with the incidence of TB increasing, mainly caused by the acquired immunodeficiency syndrome epidemic, the incidence of laryngeal involvement may be on the rise. The main presenting symptom of laryngeal TB is dysphonia. The diagnosis is confirmed with the identification of granulomatous inflammation, caseating granulomas, and acid-fast bacilli on histopathologic examination of biopsied laryngeal tissue. However, making the diagnosis difficult can be the presence of pseudoepitheliomatous hyperplasia, which mimics squamous cell carcinoma. Treatment is primarily with antituberculous medications with surgery reserved for those cases of airway compromise. Laryngeal complications can occur; thus, long-term follow-up is recommended. We report a case of laryngeal TB in a human immunodeficiency virus-negative patient and review the literature.

Effect of dehydration on cardiovascular responses and electrolytes after hypertonic saline/dextran treatment for moderate hemorrhage.

STUDY OBJECTIVE: To determine if hypertonic saline/dextran (HSD) is effective in treating hemorrhage in the presence of dehydration. DESIGN: After surgical preparation, swine were euhydrated or dehydrated for 24 or 48 hours. Animals were bled 25 mL/kg over 60 minutes and treated with HSD. SETTING: Laboratory. PARTICIPANTS: Seventeen immature Yorkshire pigs. INTERVENTIONS: 4 mL/kg HSD (7.5% NaCl in 6% dextran-70) administered over one minute. MEASUREMENTS AND MAIN RESULTS: All euhydrated animals survived; 100% of the pigs survived 180 minutes after treatment. Two animals dehydrated for 24 hours and three animals dehydrated for 48 hours died within three hours of HSD treatment. In all groups, plasma potassium was reduced significantly and equally; cardiac output was increased; mean arterial pressure rose rapidly within first five minutes, but was sustained only in euhydrated animals; hematocrit, hemoglobin, and plasma total protein levels were reduced; and plasma glucose increased with persistent between-group differences. RESULTS: HSD immediately rectified the decreases in mean arterial pressure and cardiac output incurred during hemorrhage; over time, however, the improvement in pressure was not sustained in dehydrated pigs. Parallel increases in plasma osmolality and sodium concentrations were offset by the initial group differences resulting from dehydration. CONCLUSION: Dehydration does not compromise the efficacy of HSD as a resuscitation treatment for hemorrhagic shock.

Removal of bacteria from blood by charcoal hemoperfusion.

E. coli bacteria were successfully removed from contaminated RBC/plasma by using a special matrix of micro-encapsulated albumin activated charcoal (ACAC). Efficacy of removing the bacteria was directly related to the amount of time the contaminated blood was in contact with the charcoal. The data indicated that the bacteria adhered to the ACAC, but that the charcoal was not bactericidal.