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A previously healthy 38-year-old man presents to an emergency department in Patchogue, New York. He has a fever and is suffering from severe stomach pain, accompanied by nausea and vomiting. He explains that his symptoms have come on quite suddenly, and he has not experienced any similar symptoms in the past. However, he reports that one week ago, he attended a local testing center and tested positive for SARS-CoV-2.

On further questioning, he tells clinicians he has no respiratory symptoms, nor does he have diarrhea, and there is no evidence of blood in his vomit. His medical, surgical, and social history are unremarkable.

Laboratory test results

Notable findings include a white blood cell count of 12.53×10⁹/L and lipase level of 10,255 ukat/L. Calcium, triglyceride, bilirubin, and liver function test results are all within normal limits. An abdominal ultrasound reveals no evidence of gallstones or inflammation of the gall bladder, and his bile ducts appear normal.

Clinicians admit the patient for acute pancreatitis of unclear etiology, and he is put on airborne and droplet isolation to prevent SARS-CoV-2 transmission. His condition improves with conservative management, including aggressive intravenous fluid and pain control, and he is discharged to home with instructions to self-isolate.

One week later

The patient returns to the ED, suffering again from recurrent sharp abdominal pain radiating to his back, along with nausea and vomiting. He has no fever or cough, and notes that his pain is not related to food intake. He denies any use of alcohol or medications, and says he has not suffered any recent injury or had surgery.

Clinicians review his medical records, note his recent positive test for SARS-CoV-2 infection, and place the patient on airborne isolation.

Initial vital signs are normal. On physical examination, the patient has moderate tenderness to light palpation in the epigastric region, and Murphy's sign is negative.

Laboratory test results

Test findings are similar to those of the previous week, except for greater elevations of his white blood cell count to 14.82×10⁹/L and lipase level, which is almost doubled at 20,320 ukat/L. As before, his other test results are unremarkable. Abdominal ultrasound shows the patient's gallbladder is normal, with no gallstones, and no biliary ductal dilation. Abdominal CT scan reveals acute pancreatitis with no signs suggesting chronic pancreatitis.

Clinicians diagnose the patient with recurrent idiopathic acute pancreatitis. He is admitted and managed with IV fluid, complete bowel rest, and pain control. He is tested again for SARS-CoV-2 viral nucleic acid with a nasopharyngeal specimen using a system authorized by the FDA; results are positive.

Clinicians order further investigations with magnetic resonance cholangiopancreatography and MRI of the abdomen. Test results indicate acute pancreatitis, normal gallbladder, and no evidence of intra- or extrahepatic biliary pathology. Hepatitis serology and serum immunoglobulin testing rule out possible autoimmune etiology of his pancreatitis. Once the patient's clinical status is stable, he is discharged to home with instructions to return if his symptoms return.

Discussion

Clinicians reporting this of recurring acute pancreatitis in a patient with recent SARS-CoV-2 infection urge other physicians to consider this potential etiology of acute pancreatitis: they add that cases of idiopathic pancreatitis warrant further testing for SARS-CoV-2, even in the absence of respiratory symptoms. Furthermore, they suggest testing pancreatic enzymes in COVID-19 patients who present with gastrointestinal symptoms, to rule out potential unrecognized pancreatic involvement in this population.

A growing body of evidence suggests that a wide range of complications may result from SARS-CoV-2 infection. The virus is well-known to cause pneumonia, and can also cause damage to other organ systems, including the gastrointestinal tract. According to a small of pancreatic injury patterns in 52 patients admitted to the hospital in Wuhan, China, with COVID-19 pneumonia, the incidence of organ injury 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, defined as any abnormality in amylase (normal range, 0–90 U/L) or lipase (normal range, 0–70 U/L), 8% for renal injury (abnormal creatinine level), and 2% for diarrhea.

Case authors note that in patients with gastrointestinal conditions, the possibility of SARS-CoV-2 infection should not be overlooked. Elevations in pancreatic enzymes have been increasingly reported in COVID-19 patients, they note, citing several case studies describing patients presenting with idiopathic acute pancreatitis. They point to a report of 2 first-degree relatives found to have severe idiopathic acute pancreatitis after being admitted to an Intensive Care Unit for SARS-CoV-2 infection, which suggests a casual association between idiopathic acute pancreatitis and COVID-19. They add that patients with COVID-19 whose respiratory symptoms improve may still test positive for SARS-CoV-2, and remain at risk for developing acute pancreatitis.

According to a recent of almost 77,000 hospitalized COVID-19 patients, the estimated pooled prevalence of underlying disorders was as follows:

• Hypertension: 16.37% (95% CI 10.15%-23.65%)
• Cardiovascular disease: 12.11% (95% CI 4.40%-22.75%)
• Smoking history: 7.63% (95% CI 3.83%-12.43%)
• Diabetes: 7.87% (95% CI 6.57%-9.28%)

As an acute inflammatory process of the pancreas, acute pancreatitis has the potential to cause significant morbidity.

Diagnosis of acute pancreatitis requires two of the following three criteria:

• Characteristic acute epigastric pain
• Elevation of serum amylase or lipase more than 3 times the upper limit of normal
• Evidence of acute pancreatitis on diagnostic imaging

More than 80% of all cases of acute pancreatitis are attributed to gallstones and alcohol use, case authors note. However, acute pancreatitis may also be caused by hypertriglyceridemia, hypercalcemia, medications, and trauma. About 10% of cases of AP are thought to be caused by infectious microorganisms, including viruses (e.g., mumps, Coxsackie B, and hepatitis), bacteria (e.g., Mycoplasma pneumoniae and leptospirosis), and parasites (e.g., Ascaris lumbricoides, Fasciola hepatica, and hydatid disease). Clues to the infectious nature of pancreatitis may be found in the characteristic signs and symptoms associated with the particular infectious agent, case authors note.

While the observed association between idiopathic pancreatitis and COVID-19 is interesting, case authors note that the prevalence and the pathogenesis of acute pancreatitis in SARS-CoV-2 infection remains poorly understood. Studies suggest that angiotensin-converting enzyme 2 receptors (ACE2) have a role in the pathogenesis of COVID-19, and these transmembrane proteins are highly expressed in pancreatic cells, case authors add.

They cite a recent that suggests that ACE2 expression in the pancreas may cause pancreatic damage after COVID-19 infection. Those researchers note that some data suggest that approximately 40% of COVID‐19 patients present with gastrointestinal symptoms, including abdominal pain. As well, among patients with severe SARS-CoV-2 infection, up to 16% have raised serum amylase and lipase, and 7% show evidence of significant pancreatic changes on CT.

However, it remains to be determined whether acute pancreatitis in the setting of COVID-19 infection is directly related to the cytopathic effect of local viral replications, or indirectly caused by a harmful immune response generated by the virus, case authors write.

The recent diagnosis of COVID-19 and the presentation of recurring acute pancreatitis in this patient with no known precipitating factors of pancreatitis raise the suspicion that there is a causal relationship between this novel virus and acute pancreatitis, case authors conclude.

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