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Hypothyroidism in primary hyperoxaluria type 1

Y Frishberg1, S Feinstein, C Rinat

  • 1Division of Pediatric Nephrology, Shaare Zedek Medical Center and Hebrew University, Haddasah Medical School, Jerusalem, Israel.

The Journal of Pediatrics
|February 5, 2000
PubMed

Insights

Severe hypothyroidism in patients with primary hyperoxaluria type 1 (PH1) and oxalosis may stem from calcium oxalate deposits. Thyroid hormone replacement therapy proved effective, highlighting the need for thyroid monitoring in PH1 patients.

Area of Science:

  • Nephrology
  • Endocrinology
  • Metabolic Disorders

Background:

  • Primary hyperoxaluria type 1 (PH1) is a rare genetic disorder leading to excessive oxalate production and deposition.
  • End-stage renal disease (ESRD) is a common complication of PH1 due to kidney damage from calcium oxalate crystals.
  • Oxalosis, the systemic deposition of calcium oxalate in various tissues, can cause multi-organ dysfunction.

Observation:

  • This study reports on four patients with PH1 and ESRD who presented with severe, symptomatic hypothyroidism.
  • Patients ranged in age from 3 months to 23 years.
  • All patients exhibited diffuse calcium oxalate deposition in kidneys, skeleton, eyes, and heart.

Findings:

  • Hypothyroidism in these patients was responsive to thyroid hormone replacement therapy.
  • The hypothyroidism is hypothesized to result from thyroid tissue damage caused by extensive calcium oxalate accumulation.
  • This suggests a direct link between oxalosis and endocrine dysfunction in PH1.

Implications:

  • Thyroid function should be routinely monitored in patients diagnosed with PH1 and oxalosis.
  • Early detection and management of hypothyroidism may improve outcomes for PH1 patients.
  • Understanding the impact of oxalosis on endocrine organs is crucial for comprehensive patient care.

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