Hypothyroidism-Associated Gastric Dysfunction: A Case Study
Patient Profile: Mrs. A, a 55-year-old woman, presents to her primary care physician with complaints of persistent bloating, indigestion, and occasional nausea for the past six months. She reports a gradual onset of symptoms, which have worsened over time, despite dietary modifications and over-the-counter antacids. Mrs. A has a past medical history significant for hypothyroidism diagnosed five years ago, for which she takes levothyroxine 100 mcg daily. She denies any recent changes in her thyroid medication or dosing regimen.
Clinical Assessment: Upon physical examination, Mrs. A’s vital signs are within normal limits, and she appears well-nourished. Abdominal examination reveals mild distention and tenderness in the epigastric region without signs of peritoneal irritation. Laboratory investigations reveal normal complete blood count, electrolytes, liver function tests, and renal function tests. However, her thyroid function tests show elevated thyroid-stimulating hormone (TSH) levels (8.5 mIU/L; reference range: 0.4-4.0 mIU/L) with low free thyroxine (fT4) levels (0.8 ng/dL; reference range: 0.9-1.8 ng/dL), consistent with hypothyroidism.
Diagnostic Workup: Given Mrs. A’s clinical presentation and thyroid function abnormalities, further evaluation is warranted to assess for hypothyroidism-associated gastric dysfunction. Additional investigations include:
- Gastrin levels: Serum gastrin levels are found to be decreased (30 pg/mL; reference range: 40-120 pg/mL), suggestive of impaired gastrin secretion.
- Gastric emptying study: A gastric emptying study using scintigraphy reveals delayed gastric emptying, consistent with gastroparesis.
Discussion: Mrs. A’s presentation highlights the interplay between hypothyroidism and gastric dysfunction. Hypothyroidism-induced alterations in thyroid hormone levels disrupt normal gastric physiology, leading to impaired gastrin secretion and delayed gastric emptying. Gastrin, a peptide hormone essential for regulating gastric acid secretion and motility, is adversely affected by thyroid hormone deficiency, contributing to Mrs. A’s gastrointestinal symptoms.
Treatment and Management: Management of Mrs. A’s hypothyroidism-associated gastric dysfunction involves optimizing thyroid hormone replacement therapy and addressing gastrointestinal symptoms. The levothyroxine dose is adjusted based on her TSH and fT4 levels to achieve euthyroidism. Additionally, Mrs. A is prescribed prokinetic agents, dietary modifications (small, frequent meals with low-fat content), and lifestyle interventions (e.g., avoiding lying down after meals, regular physical activity) to alleviate her gastrointestinal symptoms and improve gastric motility.
Follow-up: Mrs. A is scheduled for regular follow-up appointments to monitor her thyroid function and symptomatology. Over the subsequent months, with optimized thyroid hormone replacement therapy and conservative management measures, her gastrointestinal symptoms gradually improve. Repeat thyroid function tests demonstrate normalization of TSH and fT4 levels, reflecting adequate thyroid hormone replacement. Gastrin levels show a modest increase within the reference range, indicating partial restoration of gastrin secretion.
Conclusion: This case illustrates the clinical manifestations, diagnostic evaluation, and management of hypothyroidism-associated gastric dysfunction. Recognition of the intricate relationship between thyroid hormones and gastric physiology is essential for effectively managing gastrointestinal symptoms in patients with hypothyroidism. A multidisciplinary approach, including thyroid function assessment, gastrointestinal evaluation, and tailored therapeutic interventions, is integral to optimizing patient outcomes in this context.