High Procalcitonin Does Not Always Indicate a Bacterial Infection.

Abstract

Procalcitonin (PCT) has become essential for differentiating bacterial infections from viral infections and noninfectious causes of inflammation, as most inflammatory markers rise with inflammation without indicating a specific etiology. The significance of PCT was underscored during the COVID-19 pandemic, when many patients exhibited elevated inflammatory markers, complicating decisions regarding antibacterial therapy without PCT levels. However, a rise in PCT cannot always be attributed to a bacterial infection, as it is also a precursor of calcitonin produced in the thyroid gland. We present a case of a 77-year-old female patient with a history of medullary thyroid cancer, which she underwent surgical resection and radiotherapy for in 1980. She also experienced right vocal cord palsy as a side effect of radiotherapy and had stable liver metastases. Her past medical history included hypothyroidism, trigeminal neuralgia, gastroesophageal reflux disease, prediabetes, meningioma, vertebral fracture, osteoporosis, depression, and chronic kidney disease stage 4. The patient had recurrent episodes of aspiration pneumonia and poor swallowing. She presented with progressive dysphagia, and her chest X-ray revealed consolidation, with positive Mycoplasma IgM. At the end of her antibiotic course, there were no residual infective symptoms. Prior to admission, a CT scan of the thorax, abdomen, and pelvis showed bilateral upper zone medial fibrotic changes related to radiation, with no sinister lung lesions. It also revealed a few non-united fractures involving the left-sided ribs posteriorly, while biliary distension and liver and bone disease appeared stable. Interestingly, her PCT levels remained consistently elevated at >100 ng/L throughout her admission, despite normal CRP and white blood cell counts. This case was extensively discussed with the infectious diseases team, who suggested that the elevated PCT levels were likely related to thyroid cancer metastases, which can synthesize PCT. Consequently, PCT would be functionally increased in such circumstances and would be an unreliable marker for infection. Further analysis indicated that the PCT elevation resulted from her stable medullary thyroid cancer liver metastases, which were dormant and not affecting liver function but were secreting PCT. This case illustrates that a patient with medullary thyroid cancer metastases to the liver, who was treated for pneumonia, exhibited persistently high PCT levels despite completing the treatment. Calcitonin levels, checked on one occasion, were also elevated, reinforcing that the rise in PCT was attributed to production from medullary cancer metastatic cells rather than an inflammatory response. In bacterial septicemia, PCT is produced through alternate pathways, either directly or indirectly, and is therefore not related to the rise in calcitonin. Consequently, persistently high PCT levels in the absence of other infection markers should prompt further investigation.