Asparaginase‐induced acute parotitis: An uncommon and self‐limiting complication

Chan, Godfrey Chi-Fung; Chiang, Alan Kwok Shing; Ha, Shau Yin; Lau, Yu Lung; Ong, Jeannie B; Lee, Acw

doi:10.1002/mpo.10068

Cited by 6 publications

(6 citation statements)

References 4 publications

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“…The heightened ER stress response presumably is protective in the context of the unique translational nature of the pancreatic acinar cells, and it is consistent with reports that these cells possess high basal autophagy 37 . Our finding of high ASNS expression in the parotid gland, albeit lower than in the pancreas, is consistent with the histologic similarity of both exocrine glands 15 and the clinical observation that ASNase occasionally is associated with the complication of parotitis 38 …”

Section: Discussionsupporting

confidence: 91%

Asparagine Synthetase Is Highly Expressed at Baseline in the Pancreas Through Heightened PERK Signaling

Mukherjee

Ahmed

Rose

et al. 2020

Cellular and Molecular Gastroenterology and Hepatology

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Asparaginase (ASNase) causes pancreatitis in approximately 10% of leukemia patients, and the mechanisms underlying this painful complication are not known. ASNase primarily depletes circulating asparagine, and the endogenously expressed enzyme, asparagine synthetase (ASNS), replenishes asparagine. ASNS was suggested previously to be highly expressed in the pancreas. In this study, we determined the expression pattern of ASNS in the pancreas and the mechanism for increased pancreatic ASNS abundance. Compared with other organs, ASNS was highly expressed in both the human and mouse pancreas, and, within the pancreas, ASNS was present primarily in the acinar cells. The high baseline pancreatic ASNS was associated with higher baseline activation of protein kinase R-like endoplasmic reticulum kinase (PERK) signaling in the pancreas, and inhibition of PERK in acinar cells lessened ASNS expression. ASNase exposure, but not the common pancreatitis triggers, uniquely up-regulated ASNS expression, indicating that the increase is mediated by nutrient stress. The up-regulation of acinar ASNS with ASNase exposure was owing to increased transcriptional rather than delayed degradation. Knockdown of ASNS in the 266-6 acinar cells provoked acinar cell injury and worsened ASNase-induced injury, whereas ASNS overexpression protected against ASNase-induced injury. In summary, ASNS is highly expressed in the pancreatic acinar cells through heightened basal activation of PERK, and ASNS appears to be crucial to maintaining acinar cell integrity. The implications are that ASNS is especially hardwired in the pancreas to protect against both baseline perturbations and nutrient deprivation stressors, such as during ASNase exposure.

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Section: Discussionsupporting

confidence: 91%

Asparagine Synthetase Is Highly Expressed at Baseline in the Pancreas Through Heightened PERK Signaling

Mukherjee

Ahmed

Rose

et al. 2020

Cellular and Molecular Gastroenterology and Hepatology

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“…A review of drug-induced parotitis identified cases involving L-asparaginase (7 cases in 4 reports), clozapine (13 case reports) and phenylbutazone (13 cases) (2). Nine cases of L-asparaginase-induced parotitis, including another case report and the present case, are summarized in Table (3)(4)(5)(6)(7). Each of these nine cases developed parotitis during induction chemotherapy for ALL.…”

Section: Discussionmentioning

confidence: 94%

L-asparaginase-induced Parotitis in an Elderly Patient with Acute Lymphoblastic Leukemia

et al. 2020

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A 67-year-old woman received induction chemotherapy comprising vincristine, daunorubicin, cyclophosphamide, L-asparaginase and prednisolone for acute lymphoblastic leukemia with a common B-cell phenotype. The administration of L-asparaginase at 3,000 U/m 2 for 6 days was planned. Before the fourth administration on day 16, left parotid swelling was identified along with increased serum amylase (991 U/L; 94% derived from salivary glands). An enlarged left parotid gland was apparent on computed tomography. The symptoms resolved after cessation of L-asparaginase, with serum amylase normalizing by day 20. This rare adverse event should be recognized as improving within a week after ceasing L-asparaginase.

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“…However, in mumps-related acute sialadenitis, the viral etiology was shown to be consisting of Epstein-Barr virus (EBV), adenovirus, enteroviruses (coxsackieviruses, echovirus), influenza A and B viruses, parvovirus, and parainfluenza viruses. 7,8 Davidkin et al 7 reported that the 3 most frequent agents of nonmumps acute parotitis were EBV, parainfluenza type 1, and adenovirus, respectively. Elbadawi et al 8 documented that influenza viruses and herpes viruses should be suspected in patients who have acute parotitis or other sialadenitis, without encountering mumps cases or outbreaks.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 Davidkin et al 7 reported that the 3 most frequent agents of nonmumps acute parotitis were EBV, parainfluenza type 1, and adenovirus, respectively. Elbadawi et al 8 documented that influenza viruses and herpes viruses should be suspected in patients who have acute parotitis or other sialadenitis, without encountering mumps cases or outbreaks.…”

Section: Discussionmentioning

confidence: 99%

Acute Sialadenitis in Children With Acute Leukemia During Chemotherapy: A Case Series Study

Töret

Aksakal

Kar

et al. 2021

Pediatric Infectious Disease Journal

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Asparaginase‐induced acute parotitis: An uncommon and self‐limiting complication

Cited by 6 publications

References 4 publications

Asparagine Synthetase Is Highly Expressed at Baseline in the Pancreas Through Heightened PERK Signaling

Asparagine Synthetase Is Highly Expressed at Baseline in the Pancreas Through Heightened PERK Signaling

L-asparaginase-induced Parotitis in an Elderly Patient with Acute Lymphoblastic Leukemia

Acute Sialadenitis in Children With Acute Leukemia During Chemotherapy: A Case Series Study

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