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  Table of Contents    
LETTER TO EDITOR  
Year : 2021  |  Volume : 64  |  Issue : 4  |  Page : 859-861
COVID-19 induced acute pancreatitis


1 Department of Pathology, MGUMST, Jaipur, Rajasthan, India
2 Department of Medicine, MGUMST, Jaipur, Rajasthan, India
3 Department of Radiology, MGUMST, Jaipur, Rajasthan, India
4 Department of Community Medicine, MGUMST, Jaipur, Rajasthan, India

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Date of Submission28-Jan-2021
Date of Decision14-Jul-2021
Date of Acceptance15-Jul-2021
Date of Web Publication20-Oct-2021
 

How to cite this article:
Sharma R, Jaiswal RM, Rijwani P, Choudhary J, Sharma CK. COVID-19 induced acute pancreatitis. Indian J Pathol Microbiol 2021;64:859-61

How to cite this URL:
Sharma R, Jaiswal RM, Rijwani P, Choudhary J, Sharma CK. COVID-19 induced acute pancreatitis. Indian J Pathol Microbiol [serial online] 2021 [cited 2021 Nov 28];64:859-61. Available from: https://www.ijpmonline.org/text.asp?2021/64/4/859/328514




Dear Editor,

Coronavirus (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) leading to increased mortality worldwide. Initially, it started as an epidemic in China, and eventually, the WHO declared this medical emergency a global pandemic.[1] The infection primarily affects the respiratory tract but gastrointestinal involvement has also been reported in an increasing number of patients.[2]

However, COVID-induced pancreatic involvement is rarely reported. Gallstones and alcohol abuse are the most common causes of acute pancreatitis; however, viral-induced acute pancreatitis has also been described.[3] The pathophysiology of COVID-19-induced pancreatitis includes the direct cytopathic effects or indirect systemic inflammatory and immune-mediated cellular responses, resulting in organ damage or secondary enzyme abnormalities.[4]

A 25-year-old female with no medical history presented with complaints of headache, fever with chills, and sore throat for 1 day. The patient was tested positive for COVID-19. The initial evaluation revealed a temperature of 101–102°F, a blood pressure of 110/80 mmHg, a heart rate of 90 beats per min, a respiratory rate of 20 per min, and oxygen saturation of 99–100% on room air. The patient was home quarantined and was started on doxycycline, favipiravir, ivermectin, montek LC, multivitamins, zinc, and limcee.

She remained clinically stable with remission of fever and improvement of her symptoms. On the 8th day after the onset of symptoms, she experienced excruciating epigastric pain which was radiating to the back with one episode of vomiting. The pain got relieved on taking medication but after a few hours, she again developed epigastric pain with three to four episodes of vomiting. The patient was admitted to a tertiary care hospital. Both the symptoms and clinical signs suggested a high index of suspicion for acute pancreatitis. Therefore, the following investigations were suggested including complete blood count, C-reactive protein, liver function test, serum creatinine, serum urea, serum electrolytes, serum lipase, serum amylase, d-dimer, and Computed Tomography (CT) scan of the abdomen. Finally, she was diagnosed as a case of acute pancreatitis on the basis of high serum lipase (11920.7 U/L), serum amylase (1814.6 U/L), and abdomen Contrast-enhanced computed tomography (CECT) scan (acute interstitial pancreatitis with mild ascites, modified Computed tomography severity index (CTSI)-6) [Figure 1] and [Figure 2]. The clinical examination revealed epigastric tenderness with the presence of bowel sound and raised blood pressure. She has, of note, no history of alcohol use, recent abdominal surgery, abdominal trauma, or use of any known offending drugs that may cause acute pancreatitis. The patient was kept nil by mouth and was started on IV fluids (3–4 L/day), remdesivir, enoxaparin, intravenous multivitamins, IV paracetamol, ondansetron, metronidazole, piperacillin and tazobactam, and pantoprazole. And the levels of serum amylase and serum lipase were monitored. On the 10th day, oxygen saturation of the patient started falling to 65–70% on room air and was maintained to 93% on 12 L/min oxygen through venturi mask. So, the patient was shifted to the COVID ICU for further management and High- resolution computed tomography (HRCT) was done which showed patchy ground-glass opacities on the left lung, COVID-19 Reporting and Data System (CO-RADS) 6, and bilateral pleural effusion (left > right). Then Inj ulinastatin, Inj frusemide, and Inj methylprednisolone were started. And Inj piperacillin was replaced with Inj imipenem. And from the 12th day onward, the condition of the patient started improving with oxygen saturation coming back to 90% on room air. On the 13th day, the patient was COVID negative and was shifted to the general ward. And from the 15th day onward, the patient was started on a liquid and semisolid diet with the continuation of IV fluids (1 L/day). The patient was discharged on the 18th day and oral medication was prescribed [Table 1] and [Table 2].
Figure 1: CECT Abdomen showing diffusely bulky pancreas with poor enhancement. Soft-tissue stranding in peripancreatic fat

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Figure 2 : CECT Abdomen showing diffusely bulky pancreas with poor enhancement. Soft-tissue stranding in peripancreatic fat

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Table 1: Comprehensive laboratory panel on the first day of admission

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Table 2: Comprehensive laboratory panel on the last day of admission

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The mechanism behind pancreatitis in COVID-19 is due to the expression of angiotensin-converting enzyme 2 (ACE2) receptors in the pancreatic cells. Glycosylated-spike (S) protein is a prime inducer of the host immune response and is one of the structural proteins which are encoded by the coronavirus genome. This protein mediates the host cell invasion by binding to the ACE2 receptor protein located on the host cell surface membrane.[5]

The most common reported causes of acute pancreatitis are gallstones and alcohol abuse, however, in approximately 10% of the cases, infectious agents such as mumps, cytomegalovirus, and influenza were found to be responsible. Therefore, it is likely to consider SARS-COV-2 as a potential cause of pancreatitis.[3]

According to the Atlanta classification, acute pancreatitis can be diagnosed by the presence of two of the following three criterias: (1) upper abdominal pain consistent with the disease activity (acute onset, epigastric, and usually radiating to back); (2) serum lipase or amylase level >3x the upper limit of normal; (3) distinctive acute pancreatitis findings on imaging modalities (such as ultrasonography, abdominal CT, or Magnetic resonance imaging (MRI)). The symptomatic management is done in acute pancreatitis including supportive care with fluids and analgesia, and nutritional support with enteral nutrition.

The patient was healthy previously and had no history of alcohol or drug abuse. Similarly, the abdominal ultrasonography revealed no evidence of gallstones. Furthermore, hypertriglyceridemia as a possible trigger was not considered due to the serum triglycerides level of 97.4 mg/dL (normal value <150 mg/dL) shown on the lipid panel. Her improvement with conservative management confirmed acute pancreatitis attributable to COVID-19.

Due to the involvement of the Gastrointestinal (GI) system, especially the pancreas, the COVID-19 infection has become a pressing concern. Clinicians should be aware that a COVID-19 patient even with mild gastrointestinal symptoms requires pancreatic enzymes evaluation and abdomen imaging to diagnose pancreatitis. This diagnosis is important for adequate treatment and better management of systemic repercussions in the COVID-19 patients.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Kumaran NK, Karmakar BK, Taylor OM. Coronavirus disease-19 (COVID-19) associated with acute necrotising pancreatitis (ANP). BMJ Case Rep 2020;13:e237903.  Back to cited text no. 1
    
2.
Alves AM, Yvamoto EY, Marzinotto MA, de Sá Teixeira AC, Carrilho FJ. SARS-CoV-2 leading to acute pancreatitis: An unusual presentation. Braz J Infect Dis 2020;24:561-4.  Back to cited text no. 2
    
3.
Kataria S, Sharif A, Rehman AU, Ahmed Z, Hanan A, et al. COVID-19 induced acute pancreatitis: A case report and literature review. Cureus 2020;12:e9169.  Back to cited text no. 3
    
4.
Patel KP, Patel PA, Vunnam RR, Hewlett AT, Jain R, Jing R, et al. Gastrointestinal, hepatobiliary, and pancreatic manifestations of COVID-19. J Clin Virol 2020;128:104386.  Back to cited text no. 4
    
5.
Zhu N, Zhang D, Wang W, Li X, Yang B, Song J, et al. China novel coronavirus investigating and research team. A novel coronavirus from patients with pneumonia in China, 2019. N Engl J Med 2020;382:727-33.  Back to cited text no. 5
    

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Correspondence Address:
Richa Sharma
Department of Pathology, Mahatma Gandhi Medical College and Hospital, Jaipur, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijpm.ijpm_105_21

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    Figures

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    Tables

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