aspiration of tumours harmless? Lancet 1989;1:620. 11. Sonoda T, Kanematsu T, Takenaka K, Sugimachi K. Ruptured hepatocellular carcinoma evokes risk of implanted metastases. J Surg OncoI1989;41:183-6.
Upper gastrointestinal injury caused by diquat To the Editor: Diquat (1,1' -ethylene-2,2' -bipyridynium dibromide) is a widely used broad-spectrum bipyridynium herbicide. This compound is quite similar to paraquat (1,1' -dimethyl-4,4'bipyridynium dichloride), in its chemical, herbicidal, and biochemical effects. 1• 2 However, while several reports are present in the literature on the serious systemic toxic effects of paraquat, diquat poisoning is commonly considered less frequent and is rarely investigated. Moreover, as yet there are no data on any toxic effects these compounds may have on the upper gastrointestinal tract. We report here a case of severe upper gastrointestinal tract involvement in a factory worker accidentally exposed to diquat herbicide. A 24-year-old man was admitted to our department for continuous vomiting, diffuse abdominal pain, and diarrhea. He worked in the production of substances known to be toxic, such as synthetic resins and adhesive products, but did not incur any direct contact with any of them. On careful questioning, it was found the patient had been briefly exposed to a diquat-based herbicide while using it in his garden. He believed the contact with diquat might have happened accidentally when he licked his lips after rubbing them with a rubber glove he was wearing. On admission, routine biochemical tests revealed neutrophilic leukocytosis (WBC 16,000, N 91 %), mild hypokalemia (3.4 mmol/liter), hyperazotemia (11.4 mmol/liter; range, 2.5 to 7.5), hyperglycemia (13.3 mmol/liter, range, 3.6 to 6.0), and glomerular selective proteinuria (4 g/liter); microscopy of centrifuged urine showed hyaline cylinders. Upper gastrointestinal endoscopy showed severe pan-esophagitis and a localized area of erosive hemorrhagic gastritis at the fundus. Moreover, a large zone of dysepithelization of tongue mucosa appeared a few days later. The patient was treated by forcing diuresis which resulted in a prompt recovery of tubular renal status. Blood and urine samples were collected to test for the presence of paraquat, which has more severe toxic effects, and can derive from diquat chemical synthesis as a collateral product. However, no traces were detected. For the upper gastrointestinal tract changes, the patient was given anti-secretory (ranitidine, 300 mg/day) and cytoprotective therapy (sucralfate, 4 g/day). An endoscopic examination performed 10 days after diagnosis revealed a slight inflammation of the lower onethird of the esophagus and a linear ulcer of the fundus. The tongue lesion had already disappeared. An endoscopic examination, made 1 month later, showed that the lesions had healed. The clinical and pathological features of poisoning after paraquat inhalation, mainly consisting of fatal progressive lung damage and acute renal failure, have been reported in several articles. 3 Experimental and clinical studies demonstrated that the degree of pulmonary damage as well as the clinical effects of exposure to paraquat are dose dependent. 4 Diquat also induces lung fibrosis after intratracheal admin204
istration, but this effect is less toxic and not dose dependent. 5 There are no reports on upper gastrointestinal tract lesions induced by either paraquat or diquat in humans. This report demonstrates the extreme upper gastrointestinal tract and renal toxicity of diquat, since minimal amounts of the substance were apparently ingested by the patient. This report also supports the need for upper gastrointestinal tract examination in all patients suffering from diquat and paraquat poisoning, since small amounts may be introduced by swallowing saliva even when the compounds are only inhaled. Flavia Valiante, Fabio Farinati, Pierluigi Oal Santo, Bastianello Germana, Francesco Oi Mario, Remo Naccarato,
MO MO MO MO MO MO
Divisione Di Gastroenterologia "R. Farini" Policlinico Universitario Padova, Italy
REFERENCES 1. Dodge AD, Harris N, Baldwin BC. The mode of action of paraquat and diquat. Biochem J 1970;118:43-5. 2. Baldwin RC, Pasi A, Mac Gregor JT, Hine CH. The rate of radical formation from the bipyridynium herbicides paraquat, diquat and morfamquat in homogenates of rat lung, kidney and liver: an inhibitory effect of carbon monoxide. Toxicol Appl Pharmacol 1975;32:298-300. 3. Fisher KH, Humpries M, Bails R. Paraquat poisoning. Recovery from renal and pulmonary damage. Ann Intern Med 1971;75: 731-6. 4. Levin PJ, Klaff LJ, Rose AG, Ferguson AD. Pulmonary effects of contact exposure to paraquat: a clinical and experimental study. Thorax 1979;34:150-60. 5. Manabe J, Ogata T. Lung fibrosis induced by diquat after intratracheal administration. Arch ToxicoI1987;60:427-9.
Adequacy of resection and histological preparation of pedunculated colon polyps To the Editor: The ability to completely remove adenomatous polyps via the colonoscope 1 coupled with the widespread view that nearly all carcinomas of the colon arise within pre-existing adenomas 2 has led most gastroenterologists to adopt a strategy to identify and remove adenomatous polyps in an effort to lessen colon cancer. Approximately 1 to 3% of such polyps contain cancer that has invaded beyond the muscularis mucosa. To determine whether the polyp removal is curative of the cancer, the relationship of the resection line to the nearest approach of cancer cells must be determined from histological examination. 3 •4 To gain the maximum benefit of polyp removal, all of the neoplastic tissue must be removed. To maximize histological interpretation, the sections must be cut such that the relation of the tumor to the stalk and the resection lines are clear. A recent review of our group of 49 invasive cancers encountered in colonoscopically removed polyps pointed out possible problems in both resection of the polyps and in sectioning and mounting them. This prompted a review of routine polyp removal at Hines Veterans Administration Hospital. The endoscopic database, as developed by the American GASTROINTESTINAL ENDOSCOPY
Upper gastrointestinal injury caused by diquat To the Editor: Diquat (1,1' -ethylene-2,2' -bipyridynium dibromide) is a widely used broad-spectrum bipyridynium herbicide. This compound is quite similar to paraquat (1,1' -dimethyl-4,4'bipyridynium dichloride), in its chemical, herbicidal, and biochemical effects. 1• 2 However, while several reports are present in the literature on the serious systemic toxic effects of paraquat, diquat poisoning is commonly considered less frequent and is rarely investigated. Moreover, as yet there are no data on any toxic effects these compounds may have on the upper gastrointestinal tract. We report here a case of severe upper gastrointestinal tract involvement in a factory worker accidentally exposed to diquat herbicide. A 24-year-old man was admitted to our department for continuous vomiting, diffuse abdominal pain, and diarrhea. He worked in the production of substances known to be toxic, such as synthetic resins and adhesive products, but did not incur any direct contact with any of them. On careful questioning, it was found the patient had been briefly exposed to a diquat-based herbicide while using it in his garden. He believed the contact with diquat might have happened accidentally when he licked his lips after rubbing them with a rubber glove he was wearing. On admission, routine biochemical tests revealed neutrophilic leukocytosis (WBC 16,000, N 91 %), mild hypokalemia (3.4 mmol/liter), hyperazotemia (11.4 mmol/liter; range, 2.5 to 7.5), hyperglycemia (13.3 mmol/liter, range, 3.6 to 6.0), and glomerular selective proteinuria (4 g/liter); microscopy of centrifuged urine showed hyaline cylinders. Upper gastrointestinal endoscopy showed severe pan-esophagitis and a localized area of erosive hemorrhagic gastritis at the fundus. Moreover, a large zone of dysepithelization of tongue mucosa appeared a few days later. The patient was treated by forcing diuresis which resulted in a prompt recovery of tubular renal status. Blood and urine samples were collected to test for the presence of paraquat, which has more severe toxic effects, and can derive from diquat chemical synthesis as a collateral product. However, no traces were detected. For the upper gastrointestinal tract changes, the patient was given anti-secretory (ranitidine, 300 mg/day) and cytoprotective therapy (sucralfate, 4 g/day). An endoscopic examination performed 10 days after diagnosis revealed a slight inflammation of the lower onethird of the esophagus and a linear ulcer of the fundus. The tongue lesion had already disappeared. An endoscopic examination, made 1 month later, showed that the lesions had healed. The clinical and pathological features of poisoning after paraquat inhalation, mainly consisting of fatal progressive lung damage and acute renal failure, have been reported in several articles. 3 Experimental and clinical studies demonstrated that the degree of pulmonary damage as well as the clinical effects of exposure to paraquat are dose dependent. 4 Diquat also induces lung fibrosis after intratracheal admin204
istration, but this effect is less toxic and not dose dependent. 5 There are no reports on upper gastrointestinal tract lesions induced by either paraquat or diquat in humans. This report demonstrates the extreme upper gastrointestinal tract and renal toxicity of diquat, since minimal amounts of the substance were apparently ingested by the patient. This report also supports the need for upper gastrointestinal tract examination in all patients suffering from diquat and paraquat poisoning, since small amounts may be introduced by swallowing saliva even when the compounds are only inhaled. Flavia Valiante, Fabio Farinati, Pierluigi Oal Santo, Bastianello Germana, Francesco Oi Mario, Remo Naccarato,
MO MO MO MO MO MO
Divisione Di Gastroenterologia "R. Farini" Policlinico Universitario Padova, Italy
REFERENCES 1. Dodge AD, Harris N, Baldwin BC. The mode of action of paraquat and diquat. Biochem J 1970;118:43-5. 2. Baldwin RC, Pasi A, Mac Gregor JT, Hine CH. The rate of radical formation from the bipyridynium herbicides paraquat, diquat and morfamquat in homogenates of rat lung, kidney and liver: an inhibitory effect of carbon monoxide. Toxicol Appl Pharmacol 1975;32:298-300. 3. Fisher KH, Humpries M, Bails R. Paraquat poisoning. Recovery from renal and pulmonary damage. Ann Intern Med 1971;75: 731-6. 4. Levin PJ, Klaff LJ, Rose AG, Ferguson AD. Pulmonary effects of contact exposure to paraquat: a clinical and experimental study. Thorax 1979;34:150-60. 5. Manabe J, Ogata T. Lung fibrosis induced by diquat after intratracheal administration. Arch ToxicoI1987;60:427-9.
Adequacy of resection and histological preparation of pedunculated colon polyps To the Editor: The ability to completely remove adenomatous polyps via the colonoscope 1 coupled with the widespread view that nearly all carcinomas of the colon arise within pre-existing adenomas 2 has led most gastroenterologists to adopt a strategy to identify and remove adenomatous polyps in an effort to lessen colon cancer. Approximately 1 to 3% of such polyps contain cancer that has invaded beyond the muscularis mucosa. To determine whether the polyp removal is curative of the cancer, the relationship of the resection line to the nearest approach of cancer cells must be determined from histological examination. 3 •4 To gain the maximum benefit of polyp removal, all of the neoplastic tissue must be removed. To maximize histological interpretation, the sections must be cut such that the relation of the tumor to the stalk and the resection lines are clear. A recent review of our group of 49 invasive cancers encountered in colonoscopically removed polyps pointed out possible problems in both resection of the polyps and in sectioning and mounting them. This prompted a review of routine polyp removal at Hines Veterans Administration Hospital. The endoscopic database, as developed by the American GASTROINTESTINAL ENDOSCOPY
