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Clin Exp Emerg Med > Volume 11(3); 2024 > Article
Wusterbarth, Pederson, and Gottlieb: Diffuse incidental dural calcifications
A 30-year-old woman presented with severe headache and left flank pain after a motor vehicle collision. On examination, she had moderate tenderness to palpation to her left flank but an otherwise unremarkable examination with no focal neurologic deficits. Complete blood count, complete metabolic panel, and lipase were unremarkable (Table 1). She had a normal computed tomography (CT) of the abdomen/pelvis. A noncontrast CT of the head was also obtained (Fig. 1).
The CT of the head demonstrated dense calcifications of the dura along the bilateral cerebral convexities, falx, and tentorial leaflets concerning for hyperparathyroidism. Excess secretion of parathyroid hormone leads to hypercalcemia through increased bone resorption, increased intestinal absorption, and decreased urinary excretion of calcium. It is frequently diagnosed after the fifth decade of life by asymptomatic lab abnormality with common clinical manifestations being renal stones and decreased bone mineral density [1]. The presence of cerebral calcifications as a sequela of hyperparathyroidism is rare. The differential diagnosis includes vitamin D intoxication, Gorlin syndrome (nevoid basal cell carcinoma syndrome), hypertelorism, Maroteaux type brachyolmia, myotonic dystrophy, renal failure, and malignancy [2]. This patient’s age also raised suspicion for Gorlin syndrome as 90% of patients have ectopic calcification by age of 30 years [3].
Based upon the CT, we sent a parathyroid hormone level, which was 214 pg/mL (normal range, 10–55 pg/mL). She had no history of basal cell carcinoma, so Gorlin syndrome was deemed less likely. She was diagnosed with hyperparathyroidism and referred to endocrinology for further management with a plan for parathyroidectomy. This case highlights the importance of clinicians’ awareness of diffuse dural calcifications as an incidental finding that requires referral for endocrinologic evaluation.

Ethics statement

Informed consent for publication of the research details and clinical images was obtained from the patient.

NOTES

Conflicts of interest
The authors have no conflicts of interest to declare.
Funding
The authors received no financial support for this study.
Data availability
Data sharing is not applicable as no new data were created or analyzed in this study.
Author contributions
Conceptualization: MG; Investigation: all authors; Project administration: all authors; Supervision: MG; Visualization: all authors; Writing–original draft: all authors; Writing–review & editing: all authors. All authors read and approved the final manuscript.

REFERENCES

1. Pyram R, Mahajan G, Gliwa A. Primary hyperparathyroidism: skeletal and non-skeletal effects, diagnosis and management. Maturitas 2011; 70:246-55.
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2. Debnath J, Satija L, George RA, Vaidya A, Sen D. Computed tomographic demonstration of unusual ossification of the falx cerebri: a case report. Surg Radiol Anat 2009; 31:211-3.
crossref pmid pdf
3. Evans DG, Oudit D, Smith MJ, et al. First evidence of genotype-phenotype correlations in Gorlin syndrome. J Med Genet 2017; 54:530-6.
crossref pmid

Fig. 1.
(A–C) Computed tomography scans of the head with calcifications (arrows) of the dura along the bilateral cerebral convexities, falx, and tentorial leaflets.
ceem-24-234f1.jpg
Table 1.
Patient laboratory values from complete metabolic panel
Laboratory test Value
Sodium (mmol/L) 138
Potassium (mmol/L) 3.5
Chloride (mmol/L) 107
Bicarbonate (mmol/L) 25
Blood urea nitrogen (mg/dL) 11
Creatinine (mg/dL) 1.09
Glucose (mg/dL) 98
Albumin (g/dL) 3.7
Calcium (mg/dL) 9.3
Magnesium (mg/dL) 2.1
Phosphorus (mg/dL) 3.7
Total protein (g/dL) 8.2
Total bilirubin (mg/dL) 0.7
Alkaline phosphatase (U/L) 103
Aspartate transaminase (U/L) 10
Alanine transaminase (U/L) 16
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