SAT-824 - Toothpaste Toxicity: A Case of Normocalcemic Hyperparathyroidism and Sclerotic Bone Lesions with Excessive Fluoride Ingestion

Introduction:
Normocalcemic hyperparathyroidism is often linked to vitamin D deficiency. However, when laboratory and imaging findings—such as markedly elevated parathyroid hormone (PTH) and diffuse sclerotic bone lesions—are atypical, alternative diagnoses should be explored.

Case:
A 57-year-old man with no significant past medical history presented to the hospital with upper gastrointestinal bleeding due to chronic NSAID use. CT scan incidentally revealed diffuse sclerotic bone lesions. Laboratory studies showed elevated parathyroid hormone (PTH; 109 pg/mL), elevated alkaline phosphatase (ALP; 825 U/L, peak 1035 U/L), elevated bone specific alkaline phosphatase (290 ug/L), normal gamma-glutamyl transferase (GGT; 32 U/L), undetectable vitamin D ( < 6 ng/mL), normal corrected calcium (9.1 mg/dL). A bone scan demonstrated diffuse uniform tracer uptake. No evidence of metastatic disease. He was diagnosed with hyperparathyroidism secondary to severe vitamin D deficiency and discharged on high-dose vitamin D supplementation.

At his two-month follow-up, vitamin D improved to 29 ng/mL and ALP decreased to 306 U/L, but PTH further increased to 236 pg/mL. Repeat bone survey showed diffusely increased sclerosis. Dual-energy X-ray absorptiometry revealed AP spine T-score +6.7, Z-score + 7.2, and left femur T-score +5.5, Z-score +6.5. Due to the high PTH, persistent sclerosis, and elevated bone mass, skeletal fluorosis was considered. Fluoride testing revealed elevated serum fluoride (0.18 mg/L).

On further questioning, the patient reported regularly ingesting toothpaste due to its taste, suggesting a behavioral source of fluoride exposure. He was advised to discontinue this habit. Six months after cessation of toothpaste ingestion, follow-up labs showed normalization of PTH to 47.0 pg/mL, ALP improvement to 141 U/L, vitamin D to 39.5 ng/mL, and undetectable serum fluoride. Repeat X-ray bone survey demonstrated reduced sclerosis and density of osseous structures.

Discussion:
This case highlights the importance of considering fluoride ingestion on the differential diagnosis of hyperparathyroidism with sclerotic bone findings. Though vitamin D deficiency certainly contributed to this patient’s hyperparathyroidism, it did not explain the degree of PTH and ALP elevation nor the diffuse bone findings. Skeletal fluorosis, though rare in non-endemic regions, can result from chronic ingestion or inhalation of fluoride-containing substances such as contaminated water, black tea, inhalants like difluoroethane, and—as in this case—fluoride-containing toothpaste. After addressing common causes like low dietary intake of calcium, vitamin D deficiency, chronic kidney disease, and malabsorption syndromes, careful history-taking and fluoride testing may be considered in patients with unexplained hyperparathyroidism especially with osteosclerosis.

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