**Background:** Digital clubbing is enlargement of the distal phalanges of the hands or feet, most commonly associated with chronic pulmonary or cardiac disease. It can also occur in chronic gastrointestinal diseases such as inflammatory bowel disease, celiac disease, or cirrhosis, but GERD as a cause is rarely reported. The Herbst triad describes the combination of GERD, digital clubbing, anemia, and hypoalbuminemia due to protein-losing enteropathy. The pathophysiological mechanisms of clubbing remain unclear, though vascular endothelial growth factor (VEGF) is hypothesized to play a key role.
**Methods:** This is a single case report of a 6-year-old girl admitted for evaluation of 4 months of dysphagia, profuse salivation, abdominal pain, and anemia. Initial physical examination revealed clubbing of the fingers and toes and pale skin. Body weight was 19 kg (Z score –0.98) and height 118 cm (Z score –0.21). Laboratory findings showed microcytic anemia (Hb 74 g/L, MCV 57.0 fL) with low iron levels. Liver enzymes, blood urea nitrogen, and creatinine were normal. Cardiology and pulmonary evaluations were normal. Upper endoscopy revealed hyperemic esophageal mucosa with extensive erosions and fibrin deposits (esophagitis grade D per Los Angeles classification), a mild stenosis 22 cm from the tooth ridge, and a minor hiatal hernia. Histology showed inflammatory changes in the upper third of the esophagus and cardiac metaplasia with inflammatory infiltration of plasma cells and eosinophils (20–30 eosinophils per high-power field) in the middle and lower third, without intestinal metaplasia or dysplasia. Multichannel intraluminal impedance-pH monitoring confirmed an elevated number of reflux episodes: 368 total reflux episodes on impedance (121 acidic, 221 weakly acidic, 26 nonacidic). The 24-hour pH monitoring showed 93 acidic episodes, the longest lasting 11.2 minutes, and a reflux index of 6.5% (upper limit of normal). Other diagnostic tests (chest and abdominal x-ray, abdominal ultrasound, barium swallow, celiac serology, peripheral blood smear, hemoglobin electrophoresis, ECG, and echocardiogram) were normal.
**Key Results:** The patient was treated with esomeprazole 40 mg once daily (2 mg/kg/day), oral iron, and antireflux measures. Treatment reduced swallowing difficulties. Follow-up endoscopy at 2 months showed significant improvement: signs of inflammation remained but no erosions or stenosis were seen. Esophageal cardiac metaplasia persisted. Complete blood count normalized. An attempt to reduce PPI dosage led to symptom worsening, so the patient underwent Nissen fundoplication, which decreased symptoms. Notably, the patient did not have hypoalbuminemia, distinguishing this case from the classic Herbst triad.
**Clinical Implications:** This case demonstrates that GERD-related erosive esophagitis can cause digital clubbing and iron deficiency anemia even in the absence of hypoalbuminemia, suggesting that clubbing and anemia may precede protein-losing enteropathy. The authors speculate that the absence of hypoalbuminemia in this patient may be due to her ability to communicate symptoms early, before protein loss developed. Clinicians should consider gastrointestinal disorders, including GERD, in the differential diagnosis of digital clubbing, particularly in young children, patients with neurological impairment, and those who cannot easily communicate their symptoms. Early recognition and treatment of GERD in such patients may prevent progression to the full Herbst triad.