See editorial on page 36. See editorial on page 36. In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, and it has rapidly spread throughout China.1Mo P. et al.Clin Infect Dis. 2020; (ciaa270)PubMed Google Scholar Recent studies have focused mainly on the epidemiologic and clinical characteristics of patients with confirmed infection.1Mo P. et al.Clin Infect Dis. 2020; (ciaa270)PubMed Google Scholar, 2Wang D. et al.JAMA. 2020; 323: 1061-1069Crossref PubMed Scopus (16387) Google Scholar, 3Chen H. et al.Lancet. 2020; 395: 809-815Abstract Full Text Full Text PDF PubMed Scopus (2655) Google Scholar Little attention has been paid to the pancreatic injury caused by SARS-CoV-2 infection. Fifty-two patients with coronavirus disease 2019 (COVID-19) pneumonia were admitted to Zhongnan Hospital of Wuhan University from January 20 to February 28, 2020. The disease was confirmed by detecting SARS-CoV-2 nucleic acid in throat swab samples by using the reverse-transcription polymerase chain reaction assay method. On admission, all patients had a comprehensive laboratory examination, including blood cytology, biochemistry, and inflammatory indicators. Pancreatic injury was defined as any abnormality in amylase (normal range, 0–90 U/L) or lipase (normal range, 0–70 U/L). Serious illness was defined if at least 1 of the following items was present: (1) breathing rate, ≥30/min; (2) pulse oximeter oxygen saturation, ≤93% at rest; or (3) ration of partial pressure of arterial oxygen to fraction of inspired oxygen, ≤300 mm Hg (1 mm Hg = 0.133 kPa). During the hospitalization, each patient had a swab virus test every other day. Negative conversion time of SARS-CoV-2 was defined as the interval between symptom onset and the first of 2 consecutive negative virus test results. Categorical data are described as percentages and continuous data as mean with standard deviation (SD). Pearson correlation analysis was used to compare variables between the patients with COVID-19 with and without pancreatic injury. A 2-sided P < .05 was considered statistically significant. Among the 52 patients with COVID-19 pneumonia, the incidence was 33% for heart injury (abnormal lactate dehydrogenase or creatine kinase levels), 29% for liver injury (any abnormality in aspartate aminotransferase, alanine aminotransferase, γ-glutamyltransferase, or alkaline phosphatase levels), 17% for pancreatic injury, 8% for renal injury (abnormal creatinine level), and 2% for diarrhea. The 9 patients with pancreatic injury had an average age of 55 years, ranging from 25 to 71 years (Table 1). Five patients had underlying diseases such as hypertension, diabetes, and heart disease. The most common chief complaints were fever and respiratory symptoms. Four patients were categorized as having serious illness on admission. In laboratory tests, these patients had a decrease in lymphocytes and the lymphocyte subsets as well as an increase in hepatic and myocardial enzymes and inflammatory indicators. Seven patients received corticosteroid therapy, and 1 received mechanical ventilation. The median time of SARS-CoV-2 negative conversion was 22 days from symptom onset.Table 1Characteristics of Patients With COVID-19 Pneumonia With Pancreatic InjuryVariablePatients with COVID-19 with pancreatic injuryPatients with COVID-19 without pancreatic injury (N = 43)P valuePatient 1Patient 2Patient 3Patient 4Patient 5Patient 6Patient 7Patient 8Patient 9OverallAge, y, mean ± SD25556265667136566255 ± 1552 ± 18.633Male, n (%)YYYYYYNNN6 (67)18 (42).181Comorbidities, n (%) HypertensionNYYNYNNNN3 (33)7 (16).246 DiabetesYNYNYNNNN3 (33)7 (16).246 HeartNNNNNNNNY1 (11)2 (5).460 CerebrovascularNNNNNNNNN0 (0)2 (5).519 RespiratoryNNNNNNNNN0 (0)1 (2).652Chief complaints on admission, n (%) FeverYYYYYYYYN8 (89)26 (60).107 Chest distress/breath shortnessYNYYYNNNN4 (44)7 (16).062 CoughNNNNYYNNY3 (33)10 (23).535 FatigueNNNYNNNNN1 (11)9 (21).506 AnorexiaNNNNNNNYN1 (11)0 (0).027 DiarrheaNNNYNNNNN1 (11)0 (0).027 HeadacheNNNNNNNNN0 (0)1 (2).652Severe illness on admission, n (%)YNYYYNNNN4 (44)6 (14).035Blood cytology Leukocytes (3.5∼9.5 × 109/L)5.316.294.868.0310.74.944.118.542.776.17 ± 2.485.21 ± 3.33.421 Neutrophils (1.8∼6.3 × 109/L)4.344.613.867.2410.163.813.416.821.585.09 ± 2.563.76 ± 3.38.276 Monocytes (0.1∼0.6 × 109/L)0.340.790.280.380.250.370.100.760.260.39 ± 0.230.41 ± 0.17.841 Platelets (125∼350 × 109/L)21924811227917974209220134186 ± 67198 ± 87.701 Lymphocytes (1.1∼3.2 × 109/L)0.620.870.710.380.290.760.590.950.900.67 ± 0.230.94 ± 0.49.119CD3+ T cell (805–4459/μL)300—292—184562362129542339 ± 165948 ± 686.027CD4+ T cell (345∼2350/μL)108—114—8630410381236147 ± 87503 ± 367.016CD8+ T cell (345∼2350/μL)189—170—9623922345277177 ± 82397 ± 380.138CD4/CD8 ratio (0.96∼2.05)0.57—0.67—0.901.270.461.780.850.93 ± 0.461.68 ± 1.07.078CD19+ B cell (240∼1317/μL)154—79—1463888495186 ± 47147 ± 85.078CD16+CD56+ NK cell (210∼1514/μL)322—609—136142240812210 ± 209210 ± 148.994Blood biochemistry, mean ± SD ALT (9∼50 U/L)175544748551313112349 ± 5130 ± 32.167 AST (15∼40 U/L)90698255712919163352 ± 2829 ± 15.001 ALB (40∼55 g/L)43.93738.936.634.436.14329.432.536.9 ± 4.636.7 ± 5.0.943 GLB (20∼30 g/L)32.135.337.636.328.829.029.727.328.731.6 ± 3.830.0 ± 6.9.499 GGT (8∼57 U/L)1546375123515413132063 ± 4931 ± 19.003 ALP (30∼120 U/L)748476106855263876577 ± 1674 ± 30.794 Creatinine (64∼104 μmol/L)89.3130.9158.7106.473.768.959.0109.257.894.9 ± 34.561.6 ± 17.6.000 Glucose (3.9∼6.1 mmol/L)15.266.909.498.4213.785.448.854.915.638.74 ± 3.6611.11 ± 24.81.779 LDH (125∼243 U/L)29243564694533186207192281318 ± 182219 ± 81.019 Creatinine kinase (<171 U/L)4722972536541951916920125253 ± 201120 ± 206.093 D-dimer (0∼500 ng/mL)233261410382633395147—251339 ± 150889 ± 1757.385 Amylase (0∼90 U/L)8410711310914913610015186115 ± 2552 ± 18.001 Lipase (0∼70 U/L)8347451121242145857771 ± 3431 ± 13.001Blood inflammatory indicators, mean ± SD CRP (0∼10 mg/L)10.098.0137.3161.1104.511.420.02.315.062.2 ± 62.635.5 ± 47.0.162 ESR (0∼15 mm/h)893568262—34—1951 ± 3225 ± 23.016 IL-6 (0.1∼2.9 pg/mL)18.89—21.44—19.9054.682.547.0635.0322.79 ± 17.5619.76 ± 24.07.756Hospitalized treatment, n (%) CorticosteroidYNYYYYYYN7 (78)18 (42).051 Mechanical ventilationNNNYNNNNN1 (11)3 (7).679Virus negative conversion time, d, mean ± SDaThe interval between symptom onset and the first of 2 consecutive negative virus test results.40201317212519211822 ± 817 ± 8.090ALB, albumin; ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; GGT, γ-glutamyltranspeptidase; GLB, globulin; IL, interleukin; LDH, lactate dehydrogenase; N, no; NK, natural killer; SD, standard error; Y, yes.a The interval between symptom onset and the first of 2 consecutive negative virus test results. Open table in a new tab ALB, albumin; ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; GGT, γ-glutamyltranspeptidase; GLB, globulin; IL, interleukin; LDH, lactate dehydrogenase; N, no; NK, natural killer; SD, standard error; Y, yes. Compared with the patients without pancreatic injury, those with pancreatic injury had a higher incidence of loss of appetite and diarrhea; more severe illness on admission; lower levels of CD3+ and CD4+ T cells; and higher levels of aspartate aminotransferase, γ-glutamyltransferase, creatinine, lactate dehydrogenase, and erythrocyte sedimentation rate. The 2 groups showed no significant difference in corticosteroid treatment, mechanical ventilation, or virus negative conversion time. In this study, we found that the incidence of pancreatic injury was not very low in patients with COVID-19 pneumonia. In the previous pneumonia caused by SARS-CoV infection (2003), the virus was detected not only in the tissues of the lung, liver, kidney, and intestine but also of the pancreas, indicating the pancreas as a potential coronaviral target.4Ding Y. et al.J Pathol. 2004; 203: 622-630Crossref PubMed Scopus (841) Google Scholar Moreover, the SARS-CoV receptor of angiotensin-converting enzyme 2 was highly expressed in pancreas islets, and SARS-CoV infection caused damage of the islets and subsequent acute diabetes.5Yang J.K. et al.Acta Diabetol. 2010; 47: 193-199Crossref PubMed Scopus (752) Google Scholar In our study of 9 patients with COVID-19 with pancreatic injury, 6 patients were found to have abnormal blood glucose levels. These findings suggest that the pancreatic injury in COVID-19 might be caused directly by the cytopathic effect mediated by local SARS-CoV-2 replication. On the other hand, the pancreatic injury might be caused indirectly by systemic responses to respiratory failure or the harmful immune response induced by SARS-CoV-2 infection, which also led to damage in multiple organs. In this study, heart, liver, and renal injuries were detected simultaneously. In addition, most patients took antipyretics before admission, which could also cause drug-related pancreatic injury. In conclusion, these results show potential mild pancreatic injury patterns in patients with COVID-19 pneumonia, and these may be related to direct viral involvement of the pancreas or from secondary enzyme abnormalities in the context of severe illness without substantial pancreatic injury. They do not show clinically severe pancreatitis as a common manifestation. Further research and larger series are warranted to evaluate whether a subset of patients have clinical pancreatitis as a presenting or concomitant disease entity. This retrospective study was approved by the ethics committee of Zhongnan Hospital of Wuhan University (no. 2020011). Fan Wang, MD (Conceptualization: Lead; Formal analysis: Lead; Writing–original draft: Lead; Writing–review & editing: Lead). Haizhou Wang, MD (Conceptualization: Equal; Formal analysis: Equal; Writing–original draft: Lead). Junli Fan, MD (Data curation: Lead; Formal analysis: Equal; Methodology: Lead). Yongxi Zhang, MD (Conceptualization: Lead; Data curation: Lead). Hongling Wang, Professor (Conceptualization: Lead; Writing–review & editing: Lead). Qiu Zhao, MD (Conceptualization: Lead; Writing–review & editing: Lead). Mild Pancreatic Enzyme Elevations in COVID-19 Pneumonia: Synonymous With Injury or Noise?GastroenterologyVol. 160Issue 5PreviewWe read the article1 by Dr Wang and colleagues with interest. They suggest that pancreatic enzyme elevations signify pancreatic injury due to cytotoxic effects of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. Although preliminary data2 suggest that the transmembrane protease serine 2 (TMPRSS2) and angiotensin-converting enzyme 2 (ACE2), which mediate cellular entry of SARS-CoV-2, are found on pancreatic ductal cells, the pathologic consequences of this are not clear at the current time. Full-Text PDF Increased Amylase and Lipase in Patients With COVID-19 Pneumonia: Don't Blame the Pancreas Just Yet!GastroenterologyVol. 160Issue 5PreviewWe have read with interest the article entitled "Pancreatic injury patterns in patients with COVID-19 pneumonia" by Dr Wang and colleagues.1 This was a retrospective study involving 52 patients with Coronavirus Disease 2019 (COVID-19) admitted to the Zhongnan Hospital of Wuhan University, China. It aimed to describe the incidence of pancreatic injury in patients with COVID-19, defined as any abnormality in amylase or lipase. Based on this, 17% of patients with COVID-19 met criteria for pancreatic injury. Full-Text PDF Coronavirus Disease-19 Has Come Home to Roost in GastroenterologyGastroenterologyVol. 159Issue 1PreviewThe greatest current threat to global health involves the pandemic outbreak of the novel coronavirus (CoV) that is structurally related to the virus that causes severe acute respiratory syndrome (SARS-CoV) or Middle East respiratory syndrome, and is known as SARS-CoV-2.1 Human infection with SARS-CoV-2 was initially recognized in December 2019 in Wuhan, China, and has since been named coronavirus disease 2019 (COVID-19).2,3 SARS-CoV-2 is highly contagious and containment has been a challenge given its high rate of transmissibility through respiratory droplets. Full-Text PDF