Minocycline-Associated Pancreatitis

Gabriel, Joseph; Bhogal, Sukhdeep; Kapila, Aaysha

doi:10.1097/mjt.0000000000000635

Cited by 6 publications

(4 citation statements)

References 11 publications

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“…Pancreatitis has been found to be associated with both tetracycline 22 and minocycline 23 . Tetracycline‐induced AP with no known history of liver disease has occurred in the range of 4 months to 2 years with an average total daily dose of 1083‐1353 mg/d 24 .…”

Section: Discussionmentioning

confidence: 99%

Analysis of clinical characteristics of tigecycline‐induced acute pancreatitis

2020

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What is known and Objective The purpose of this study is to explore the clinical characteristics of tigecycline‐induced acute pancreatitis. Methods We searched the PubMed/Medline, Web of Knowledge, OVID, Elsevier, Springer Link, Embase, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang Data, and Chinese VIP databases from 2005 and identified 19 studies of tigecycline‐induced acute pancreatitis involving a total of 22 patients for inclusion in a retrospective analysis. Results and Discussion The median (range) age of 22 patients with acute pancreatitis was 58 years (range 9‐83). Overall, the median (range) time of symptom onset was 6.5 days (range 2‐28), or 6 days (range 2‐14) and 6 days (range 3‐28) in patients with or without a loading dose of tigecycline, respectively. Symptoms included nausea, vomiting and abdominal distension (73%) and abdominal pain (73%); 90% (18/20) of patients developed mild acute pancreatitis (MAP), and 10% (2/20) developed severe acute pancreatitis (SAP). Computed tomography (CT) scans showed oedematous infiltrate in 56% (10/18) of cases and acute pancreatitis in 28% (5/18) of cases. The median (range) level of lipase and amylase was 936U/L (range 382‐4089) and 588U/L (range 312‐1166), respectively. The median (range) time to recovery of symptoms was 4 days (range 1‐10), and the time for recovery of pancreatic enzymes to the normal range was 5 days (range 1‐30) after the withdrawal of tigecycline in all patients. What is new and Conclusion Clinicians should be particularly mindful of clinical signs and symptoms, the level of serum pancreatic enzymes and abdominal CT images in order to monitor the development of pancreatitis when using tigecycline.

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Section: Discussionmentioning

confidence: 99%

Analysis of clinical characteristics of tigecycline‐induced acute pancreatitis

2020

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“…However, as antibiotics, tetracycline derivatives have the common side effects of all antibiotics. In particular, gastrointestinal disorders induced by tetracycline derivatives are particularly severe (Gabriel et al, 2018); and the irreversible hyperpigmentation characteristically induced by tetracycline derivatives is particularly unacceptable psychosocially (Voets et al, 2016). Therefore, further study is necessary to identify the endogenous ligands and receptors that cause asthmatic activation of brainstem microglia, so that specific antagonists can be developed.…”

Section: Discussionmentioning

confidence: 99%

Asthmatic Airway Vagal Hypertonia Involves Chloride Dyshomeostasis of Preganglionic Neurons in Rats

Chen

Zeng

et al. 2020

Front. Neurosci.

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Airway vagal hypertonia is closely related to the severity of asthma; however, the mechanisms of its genesis are unclear. This study aims to prove that asthmatic airway vagal hypertonia involves neuronal Cl − dyshomeostasis. The experimental airway allergy model was prepared with ovalbumin in male adult Sprague-Dawley rats. Plethysmography was used to evaluate airway vagal response to intracisternally injected γ-aminobutyric acid (GABA). Immunofluorescent staining and Western-blot assay were used to examine the expression of microglia-specific proteins, Na +-K +-2Cl − co-transporter 1 (NKCC1), K +-Cl − co-transporter 2 (KCC2) and brain-derived nerve growth factor (BDNF) in airway vagal centers. Pulmonary inflammatory changes were examined with hematoxylin and eosin staining of lung sections and ELISA assay of ovalbumin-specific IgE in bronchoalveolar lavage fluid (BALF). The results showed that histochemically, experimental airway allergy activated microglia, upregulated NKCC1, downregulated KCC2, and increased the content of BDNF in airway vagal centers. Functionally, experimental airway allergy augmented the excitatory airway vagal response to intracisternally injected GABA, which was attenuated by intracisternally preinjected NKCC1 inhibitor bumetanide. All of the changes induced by experimental airway allergy were prevented or mitigated by chronic intracerebroventricular or intraperitoneal injection of minocycline, an inhibitor of microglia activation. These results demonstrate that experimental airway allergy augments the excitatory response of airway vagal centers to GABA, which might be the result of neuronal Cl − dyshomeostasis subsequent to microglia activation, increased BDNF release and altered expression of Cl − transporters. Cl − dyshomeostasis in airway vagal centers might contribute to the genesis of airway vagal hypertonia in asthma. Keywords: Na +-K +-2Cl − co-transporter 1/K +-Cl − co-transporter 2, asthma, microglia, bumetanide, airway vagal preganglionic neuron, minocycline Abbreviations: ACSF, artificial cerebral spinal fluid; AVPNs, airway vagal preganglionic neurons; BALF, bronchoalveolar lavage fluid; BDNF, brain-derived neurotrophic factor; C dyn , dynamic compliance of the lungs; CNS, central nervous system; CSF, cerebral spinal fluid; eNA, the external formation of the nucleus ambiguus; GABA, γ-aminobutyric acid; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IA-AVPNs, inspiratory-activated airway vagal preganglionic neurons; II-AVPNs, inspiratory-inhibited airway vagal preganglionic neurons; KCC2, K +-Cl − co-transporter 2; NA, nucleus ambiguus; NKCC1, Na +-K +-2Cl − co-transporter 1; NTS, nucleus tractus solitarius; OVA, ovalbumin; PEF, peak expiratory flow; PIF, peak inspiratory flow; R e , expiratory resistance of the airway; R i , inspiratory resistance of the airway.

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“…In these 2 cases, neither re-challenge nor consistent latency were existing and accordingly minocycline is specified as class III drug in Badalov classification for druginduced acute pancreatitis [14]. A newer two cases of minocycline-induced pancreatitis in non-cystic fibrosis patients had been recently published [15]. In both cases, all other etiologies of acute pancreatitis have been excluded and resolution of the condition was achieved few days after minocycline discontinuation [15].…”

Section: Antibioticsmentioning

confidence: 99%

“…A newer two cases of minocycline-induced pancreatitis in non-cystic fibrosis patients had been recently published [15]. In both cases, all other etiologies of acute pancreatitis have been excluded and resolution of the condition was achieved few days after minocycline discontinuation [15]. Drug idiosyncrasy could explain minocycline pancreatitis in non-cystic fibrosis cases paralleling the explanation of minocycline-induced hepatotoxicity.…”

Section: Antibioticsmentioning

confidence: 99%

Updates in drug-induced acute pancreatitis

Alhaddad

Elsabaawy

Elfauomy

et al. 2020

Egypt Liver Journal

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Background Being infrequent, drug-induced acute pancreatitis (DIP) is an overlooked clinical entity that can be serious with significant morbidity and mortality. Main body A renovative review of drugs incriminated in acute pancreatitis had been presented with all relevant data and case presentations. Antibiotics, antidiabetics, antihypertensive agents, H2 blockers (H2B) and proton pump inhibitors (PPIs), anticancer therapies, and the new direct-acting antiviral therapies (DAAs) of hepatitis C virus (HCV) were discussed pertinently to DIP. Conclusions DIP should be suspected as a potential adverse event to every newly emerged drug. Herein, an updated review of drugs recently alleged to be implicated in DIP.

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Minocycline-Associated Pancreatitis

Cited by 6 publications

References 11 publications

Analysis of clinical characteristics of tigecycline‐induced acute pancreatitis

Analysis of clinical characteristics of tigecycline‐induced acute pancreatitis

Asthmatic Airway Vagal Hypertonia Involves Chloride Dyshomeostasis of Preganglionic Neurons in Rats

Updates in drug-induced acute pancreatitis

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