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“Golf ball liver”: a cause of chronic hepatitis ?
  2. G McCUSKER,
  1. Craigavon Area Hospital Group HSS Trust,
  2. 68 Lurgan Road,
  3. Portadown,
  4. Craigavon BT63 5QQ, UK
  1. C M BURKE
  1. C O’KEANE
  1. J S DOYLE
  1. Division of Pulmonary & Critical Care Medicine,
  2. Stanford University Medical Center,
  3. Stanford, CA 94305, USA
  4. Department of Respiratory Medicine,
  5. James Connolly Memorial Hospital,
  6. Dublin 15, Ireland
  7. Department of Histopathology,
  8. Mater Misericordiae Hospital,
  9. Eccles Street, Dublin, Ireland
  10. Professor of Medicine – Emeritus,
  11. Beaumont Hospital,
  12. Dublin, Ireland

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Editor,—A 23 year old man was referred to the outpatient clinic in view of persistently abnormal liver function tests for five years. In 1992, he had a gastrointestinal illness manifest by abdominal pain, diarrhoea and vomiting which lasted intermittently for one month. At that time, investigations by his general practitioner revealed that his liver function tests were abnormal: alkaline phosphatase (ALP) 408 U/l, aspartate aminotransferase (AST) 383 IU/l, alanine aminotransferase (ALT) 922 U/l, γ-glutamyl transferase (GGT) 147 IU/l. Viral serology for hepatitis A and B and a Paul–Bunnell test were negative. His symptoms resolved, but his liver function tests did not return to normal.

He was referred to the medical outpatient clinic in 1997 because of the development of further symptoms: episodic abdominal pain, diarrhoea, itch, and fatigue. His urine was noted to be dark and his faeces was pale. Alcohol consumption was moderate and confined to social occasions. He had no history of recent foreign travel, substance or drug misuse. He had no contacts with jaundice and no previous blood transfusions. Liver function tests were persistently abnormal at that time: ALP 622 U/l, AST 86 IU/l, ALT 193 U/l, GGT 555 IU/l. Other investigations including full blood analysis, erythrocyte sedimentation rate, coagulation screen, urea and electrolytes, serum ferritin, serum copper, and alpha-1-antitrypsin were normal. Analysis of plasma proteins revealed albumin 45 g/l, globulin 37 g/l, total protein 82 g/l. IgG (30.3 g/l) and IgM (4.65 g/l) were raised. Titres of antinuclear antibody (IgG 1:20) and anti-smooth muscle antibody (IgG 1:40) were low. Viral serology for hepatitis A, B and C and Epstein–Barr and cytomegalovirus were negative. Abdominal ultrasound revealed an enlarged spleen, which was not palpable, and normal liver architecture.

Percutaneous liver biopsy revealed nodules separated by fibrous bands and a moderately dense mononuclear cell infiltrate within the portal tracts and fibrous bands, composed mainly of lymphocytes. The bile ducts were well preserved. There was moderately active lymphocytic piecemeal necrosis. Stains for Wilson’s disease and alpha-1-antitrypsin deficiency were carried out and were negative. The appearances suggested chronic hepatitis progressing to cirrhosis.

This young man has been a very keen amateur golfer for many years and licks his golf balls during every round. All investigations as indicated above have failed to reveal a specific cause for his chronic hepatitis and cirrhosis. In view of the recent case report (Gut 1997;40:687–8) relating acute hepatitis to inadvertent ingestion of 2,4-D, it is proposed that ingestion of this substance by golfers may also lead to chronic hepatitis and even cirrhosis as in the case of this young man with no other apparent cause for his liver disease. The results of abstention from licking his golf balls are eagerly anticipated.


Editor,—We were interested to read the letter by Johnston et al, further to our report in the July issue, which appears to document a case of chronic active hepatitis possibly caused by the patient’s habit of licking his golf balls. It appears that the habit of golf ball licking is certainly not confined to Ireland and appears, at least anecdotally, to be a relatively common practice. Given this widespread practice and the now documented ability of 2,4-D to cause an acute hepatitis, it is certainly within the realms of possibility that a chronic hepatitis may also result from chronic exposure to 2,4-D.

However, the case reported by Johnston et al requires some clarification. It would be helpful to know whether any eosinophils were seen on the liver biopsy sample, and if not readily seen on straightforward stains then possibly monoclonal markers such as EG1 or EG2 could be used. This is of importance as if chronic golf ball liver exists then it raises the question of whether it is a toxic phenomenon or a chronic allergic/hypersensitivity process.

It would also be of interest to know whether the authors documented that 2,4-D was actually being spread on the patient’s golf course. How long had the patient been licking his golf balls prior to the intial illness in 1992, and had the chemicals used on the patient’s golf course changed in or around this time. Was there any temporal relation between the patient’s symptoms and the times of heaviest concentration of 2,4-D on the golf course or the frequency of this patient’s golfing excursions? We await with interest any further developments.