Statistics from Altmetric.com
A 75-year-old woman presented with an 8-hour history of severe, progressively worsening, abdominal pain. The pain was described as diffuse, burning in nature, and associated with nausea. The patient had been in her usual state of health prior to the onset of symptoms. She denied haematemesis, melaena, or haematochezia. The patient's medical history was significant for Parkinson's disease and depression. There was no history of peptic ulcer disease. On examination, her blood pressure was 123/52 mmHg, pulse rate 126 beats/min, temperature 36.5°C, and respiratory rate 24 breaths/min. The abdomen was soft, diffusely tender and moderately distended. Bowel sounds were hypoactive. Rebound and rigidity were absent. Rectal examination revealed guaiac negative, brown stool. The remainder of the examination was unremarkable. Laboratory data showed a white cell count of 25.8 × 109/l and haemoglobin 120 g/l. Coagulation studies, platelet count and routine chemistries were normal. Abdominal X-rays revealed free air under the diaphragm. An emergency, exploratory laparotomy was performed and showed a perforated ulcer, 5 mm in diameter, on the anterior aspect of the gastric fundus. It was repaired using the falciform ligament (Graham patch). Postoperatively, serum calcium levels were noted to vary from 2.4 to 2.9 mmol/l (normal range 2.1–2.5 mmol/l) over the next few days. The parathyroid hormone level was elevated to 1.5 times the upper limit of normal.
- What is the cause of the perforated gastric ulcer in the patient ?
- Describe the pathogenetic mechanism of peptic ulcer disease in the patient.
Primary hyperparathyroidism was the cause of our patient's perforated gastric ulcer. Primary hyperparathyroidism was reflected by abnormally elevated serum calcium and parathyroid hormone levels. An ultrasound of the neck revealed a nodule in the left parathyroid gland measuring 7 × 8 × 10 mm. A left parathyroidectomy was performed to remove the nodule. The histological evaluation of the resected nodule showed a parathyroid adenoma. The postoperative recovery was uneventful.
Hyperparathyroidism causes increased levels of calcium in the blood which leads to increased serum levels of gastrin and acetylcholine. These changes result in increased gastric acid secretions and peptic ulcer disease.1
The prevalence of peptic ulcer disease in patients with hyperparathyroidism varies from 10% to 25%.2 The incidence of hyperparathyroidism in patients with peptic ulcer disease is approximately 10 times higher than the general population.3
The association between primary hyperparathyroidism and peptic ulcer was first reported by Rogers in 1946.1 This association was most strikingly shown by the influence of the serum calcium level on gastric acid secretion.4 In a case of idiopathic hypoparathyroidism, Donegan and Spiro demonstrated the effects of serum calcium concentration on gastric acid secretion.4 The gastric acid was absent and the pepsin was low in the basal secretion of their patient. However, following infusion of calcium gluconate and injections of parathyroid hormone, the secretions were restored to normal levels. Gastric hypersecretion resulting from hypercalcaemia can be abolished by the administration of atropine and pentolinium. But atropine did not prevent the rise in serum gastrin due to hypercalcaemia. Thus, it was postulated that the calcium-induced gastric acid secretion resulted from calcium-induced hypergastrinaemia, and that vagal synergism with increased concentrations of serum gastrin levels is necessary to stimulate gastric acid secretion.5 Experiments by Passaro and Basso demonstrated gastric acid secretion following intravenous calcium infusion in patients who had undergone antrectomy and vagotomy.6 This was explained by calcium-induced gastrin secretion from extragastric sites.7
Peptic ulcers found in association with hyperparathyroidism (other than those in patients with multiple endocrine adenomas) differ in several ways from those in patients without hyperparathyroidism. A familial history of peptic ulcer is common, and the ulcers tend to be unusually severe. Hyperparathyroidism must be excluded before surgical treatment of refractory peptic ulcer disease is carried out to avoid the precipitation of a fatal acute hyperparathyroidism crisis, as reported by Rogers.1
hyperparathyroidism causes increased serum calcium levels which leads to increased serum levels of gastrin and acetylcholine. These changes result in stimulation of gastric acid secretion and peptic ulcer disease.
patients with refractory peptic ulcer disease should undergo screening for hyperparathyroidism. The cure of hyperparathyroidism is followed by healing of the ulcer in up to half of the patients
hyperparathyroidism must be excluded before surgical treatment of refractory peptic ulcer disease is carried out to avoid the precipitation of a fatal acute hyperparathyroidism crisis
In conclusion, the symptoms of peptic ulcer disease may precede those of complications of hyperparathyroidism (box). Therefore, if possible, screening of patients with peptic ulcer disease is necessary for the prompt diagnosis of hyperparathyroidism.1 The cure of hyperparathyroidism is followed by healing of the ulcer in about half of the patients.2
Perforated gastric ulcer as an initial manifestation of hyperparathyroidism.