Alcohol-induced pancreatitis triggers aHUS in man: Case report
His condition improved without the need for complement inhibitors
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Acute inflammation of the pancreas, or pancreatitis, induced by alcohol abuse triggered atypical hemolytic uremic syndrome (aHUS) in a 43-year-old man, a team of U.S. researchers reported.
The man, with a history of alcohol abuse, sought medical attention due to abdominal pain and nausea and was found to have pancreatitis. He later developed signs of aHUS, including destruction of red blood cells, low platelet levels, and acute kidney injury.
His condition improved with supportive treatment for pancreatitis, without the need of complement inhibitors.
“The extremely rare occurrence of aHUS in the setting of alcohol-induced acute pancreatitis highlights the clinical significance of this case, as well as the importance of having [thrombotic microangiopathy] on the differential in patients with pancreatitis,” researchers wrote. Thrombotic microangiopathy (TMA) refers to a group of diseases, including aHUS, characterized by the formation of blood clots in small blood vessels.
The case was described in “A Unique Case of Atypical Hemolytic Uremic Syndrome Secondary to Alcohol-Induced Acute Pancreatitis,” published in The Cureus Journal of Medical Science.
Triggering event typically required in aHUS
Abnormal activity of the complement cascade, a part of the immune system, causes aHUS. This leads to blood clotting in small blood vessels, or TMA, which causes damage to several organs, including the kidneys. While most people with aHUS have genetic mutations that impair the regulation of the complement cascade, a triggering event, such as an infection, is typically needed.
In their report, researchers describe the case of a man who developed aHUS secondary to alcohol-induced acute pancreatitis.
He sought medical attention for generalized abdominal pain and nausea. He reported having similar episodes every few months, and a medical history of gastroesophageal reflux disease, commonly called heartburn, hypertension (high blood pressure), and alcohol use disorder.
Physical examination showed normal heart, breathing, and bowel sounds. He did not have skin changes and was alert and oriented.
Laboratory tests revealed elevated levels of lipase, an enzyme produced by the pancreas to help digest fats, indicating pancreatic injury. He also had elevated levels of liver enzymes and bilirubin, indicative of liver damage and hemolysis, or destruction of red blood cells, respectively. A CT scan revealed the presence of acute pancreatitis.
The patient was admitted for acute pancreatitis secondary to alcohol abuse and was initially managed with fluids delivered directly into the bloodstream and medication for pain and nausea. But by the end of the second day in the hospital, his platelet levels dropped.
As patient’s pancreatitis eased, platelet levels normalized
Further laboratory analysis revealed the man also had hemolytic anemia — low haptoglobin and elevated lactate dehydrogenase and bilirubin — and high levels of creatinine and urea nitrogen, indicative of acute kidney injury. At this point, the patient was suspected of having aHUS.
During the first two days of admission, he also developed respiratory failure and systemic inflammatory response syndrome — elevated levels of white blood cells, fast heart rate, and fever — secondary to pneumonia as seen on chest X-ray. He began a treatment with antibiotics and inhaled corticosteroids.
As the patient’s pancreatitis eased, platelet levels and other blood parameters normalized, and kidney function quickly improved. Ten days after hospital admission, his respiratory symptoms resolved, and he was discharged on the next day.
Overall, this case supports the idea that when “aHUS arises from an identifiable trigger, management should primarily focus on treating the underlying condition,” the researchers wrote.
In the medical literature, “there are cases of aHUS associated with acute pancreatitis, including alcohol-induced pancreatitis specifically, that have demonstrated clinical resolution with therapies focused on controlling pancreatic inflammation and systemic illness rather than complement inhibition,” they added.
The team further noted the lack of genetic testing as a limitation of this study.
