- Email: [email protected]
Prevention of rubella
THE LANCET
azide/phosphate buffered saline for 8 min. Expressions of CD44v3 and CD44v6 on epithelium were semiquantified. Increased expression of CD44v3 and CD44v6 were found in the colonic epithelium of UC patients, compared with controls or those with Crohn’s disease (table) (CD44v3, p<0·05%; UC vs normal, UC vs CD, CD44v6, p<0·05%; UC vs CD; non-parametric analysis). Using frozen sections fixed with PLP, the results we have obtained were similar to those reported by the Rosenberg group.1
3
4 5
Panax: economic and medicinal plant research. London: Academic Press Inc, 1985; 1: 218–84. Soldati F, Sticher O. HPLC separation and quantitative determination of ginsenosides from Panax ginseng, Panax quinquefolium and from Ginseng drug preparations. Planta Medica 1980; 39: 348–57. Ries CA, Sahud MA. Agranulocytosis caused by Chinese herbal medicines. JAMA 1975; 231: 352–55. Scaglione F, Cogo R, Cucuzza C, Arcidacono M, Beretta A. Immunomodulatory effects of Panax ginseng C.A. Meyer (G115) on alveolar macrophages from patients suffering with chronic bronchitis. Int J Immunother 1994; 10: 21–24.
Atsuo Kitano, *Nobuhide Oshitani, Takayuki Matsumoto, Kenzo Kobayashi
Authors’ reply
*Third Department of Internal Medicine, Osaka City University Medical School, Osaka 545, Japan; and Department of Internal Medicine, Juso Municipal Hospital of Osaka
SIR—Because SJS and toxic epidermal necrolysis (TEN) are related to toxic administration,1 mainly of a drug, we postulated that ginseng could be responsible for the illness. The patient stopped aspirin, local antibiotics (amylmetacresol, tyrochricin), and vitamin C 6 days before the onset of SJS. These drugs have short plasma half-lives or are not absorbed by the intestine;2 therefore, they could not be present at the time of SJS. Indeed, ginseng was the sole drug taken at that time. The patient’s girlfriend still had four capsules of ginseng which was bought in the Chinese area of Paris. We thus postulated that it was Panax ginseng, the Chinese or Korean ginseng. We did toxicological analysis (FPIA, TDX, Abbott) which did not shown NSAIDs, salicylates, or antiepileptics, the most frequent drugs implicated in SJS and TEN. However, the composition of the active vegetable compound could not be assessed. The coating of the capsules was gelatine. These results cannot eliminate the putative role of ginseng, since more than 100 drugs have been implicated as causes of SJS or TEN.1 Moreover, ginseng has been suspected of various non-cutaneous side-effects, such as mind-altering effects or cerebral arteritis.3 Undoubtedly, the need for a careful quality control of ginseng and herbal products is necessary.
1
2
Rosenberg WMC, Prince C, Kaklamanis L, et al. Increased expression of CD44v6 and CD44v3 in ulcerative colitis but not colonic Crohn’s disease. Lancet 1995; 345: 1205–09. Papadoginnakis N, Gad A, Chenard MP, Bellocq JP, Duclos B. Expression of CD44 variants in differential diagnosis of ulcerative colitis and Crohn’s disease. Lancet 1996; 347: 1413–14.
Ginseng as cause of Stevens-Johnson syndrome? SIR—Dega and co-workers (May 11, p 1344),1 report a probable association of Stevens-Johnson syndrome (SJS) with ginseng. The relation between the diagnosed syndrome and the ingestion of ginseng cannot, however, be established beyond doubt. It is imperative to assess which species of ginseng the patient has used. In addition to various types available on the market, such as Panax ginseng, Panax notoginseng, or Panax quinquefolius, other plant species are also marketed under the name ginseng. Such herbs, however, are taxonomically not related to the medicinal plant Panax ginseng C A Meyer. Panax ginseng is monographed as a medicinal plant in the pharmacopoeias of several countries such as Austria, China, France, Germany, Russia, Switzerland, and Japan. Panax ginseng does not exert anti-inflammatory activities, nor does it contain non-steroidal anti-inflammatory substances.2 On the other hand, non-standardised pseudoginseng products are available. Such products do not guarantee a uniform content of active substances and have undergone no toxicological or clinical tests.3 In addition, some marketed products, in particular originating from Asian countries, are known to be adulterated with undeclared substances. Some patients are reported to have developed agranulocytosis after taking Chinese herbal medicines for relief of arthritis and back pain. Such medicines, however, proved to contain substantial amounts of undeclared aminopyrine and phenylbutazone, drugs that are known to cause agranulocytosis.4 Toxicological and clinical studies on products containing the standardised Panax ginseng extract G115, which we produce and which is registered as a medicine in more than 50 countries, have, on the other hand, clearly demonstrated its safety and efficacy.5 We therefore would re-emphasise the need for a careful quality control of ginseng products, as is currently done for the high-quality herbal products. *Ricardo Faleni, Fabio Soldati Medical Department, R&D, Pharmaton SA, 6903 Lugano, Switzerland
1 2
Chosidow O, Dega H, Laporte J-L, Francès C, Herson S. Ginseng as a cause for Stevens-Johnson syndrome? Lancet 1996; 347: 1344. Shibata S, Tanaka O, Shoji J, Saito H. Chemistry and pharmacology of
Vol 348 • July 27, 1996
*Olivier Chosidow, Hervé Dega, Gilles Peytavin *Department of Internal Medicine, Groupe Hospitalier Pitié-Salpêtrière, 75651 Paris, France; and Department of Clinical Pharmacy, Groupe Hospitalier Bichat-Claude Bernard, Paris
1
2
3
Roujeau JC, Kelly JP, Naldi L, et al. Medication use and risk of Stevens-Johnson syndrome or toxic epidermal necrolysis. N Engl J Med 1995; 333: 1600–07. Becq-Giraudon B. Polypeptides cycliques. In: Giroud JP, Mathé G, Meyniel G, eds. Pharmacologie clinique. Bases de la Thérapeutique. Paris: Expansion Scientifique Française, 1988: 1500–11. Ryu SJ, Chien YY. Ginseng-associated cerebral arteritis. Neurology 1995; 45: 829–30.
Prevention of rubella SIR—Rushworth and colleagues (May 4, p 1262)1 report that despite rubella vaccination of schoolgirls (started in 1971 and continuing to the present) and of male adolescents (started in 1994), congenital rubella continues to occur in New South Wales, Australia. They state that the “eradication of congenital rubella is realisable only when protective levels of rubella immunity are maintained among women of reproductive age”, apparently in support of the strategy of selective rubella vaccination of adolescents. However, this strategy does not affect the transmission dynamics of rubella virus infection in children. With continuing circulation of rubella virus there is persistent risk of infection in susceptible (non-immune) pregnant women, even when only 2–3% of pregnant women are non-immune.2 This conundrum is illustrated in their findings of increasing proportions of mothers remaining non-immune as age increased, and by the continued occurrence of congenital rubella.1 Thus,
267
THE LANCET
congenital rubella will not be eliminated by the strategy of selective vaccination. The alternate strategy is to reduce the circulation of rubella virus in the community to such low levels that nonimmune women of reproductive age are at no or very low risk of infection. This reduction is accomplished by offering vaccination to young children and by achieving high coverage. Indeed, both selective and childhood rubella vaccination strategies could be combined, because they are complementary to each other. Of 22 countries in the WHO American region using rubella vaccine, 13 follow the childhood vaccination strategy and nine the combined strategy.3 Of 11 countries in the WHO European region using rubella vaccine, seven follow the childhood strategy and four the combined strategy.4 Countries planning to newly introduce rubella vaccination should learn from the experience of others. The combined strategy requires a two-dose schedule of rubella vaccination of all children, first at 12–15 months of age and later at a convenient time between 5 and 15 years. When high (>90%) coverage is achieved for both doses congenital rubella will most probably be eliminated. Eradication of only one manifestation (congenital rubella) of a prevalent virus infection (rubella) is not a realistic goal. To eliminate congenital rubella, virus transmission should be interrupted. We believe that interruption of rubella transmission is feasible; in other words, rubella is eradicable.
oesophagus. Histology showed low-grade B-cell MALT lymphoma in specimens from all masses. Endoscopic ultrasonography showed thickening of mucosal and submucosal layers but intact muscularis propria with no evidence of extramural extension or adenopathy. The patient was referred for chemotherapy. MALT lymphomas tend to appear in patients with chronic inflammatory disorders. Normal gastric mucosa contains no organised lymphoid tissue, but H pylori infection has been associated with MALT lymphoma.4 Scattered lymphocytes are usually present in oesophageal mucosa which may be affected by many chronic inflammatory conditions, although MALT lymphoma has not been described in the oesophagus. The spectrum of gastrointestinal MALT lymphomas should be expanded to involve the oesophagus. Assaad M Soweid, *Paul E Z achary Jr Division of Gastroenterology and Hepatology, St Louis University Health Sciences Center, 3635 Vista Avenue, St Louis, MO 63110, USA
1
2 3
4
*Reuben Samuel, T Jacob John
Radeszkiewicz T, Dragosics B, Bauer P. Gastrointestinal malignant lymphomas of the mucosa-associated lymphoid tissue: factors relevant to prognosis. Gastroenterology 1992; 102: 1628–38. Isaacson PG, Spencer J. Malignant lymphoma of mucosa-associated lymphoid tissue. Histopathology 1987; 11: 445–62. Hussell T, Isaacson PG, Crabtree JE, Spencer J. The response of cells from low-grade B-cell gastric lymphomas of mucosa-associated lymphoid tissue to Helicobacter pylori. Lancet 1993; 342: 571–74. Stolte M, Eidt S. Healing gastric MALT lymphomas by eradicating H pylori? Lancet 1993; 342: 568.
Department of Clinical Virology, Christian Medical College and Hospital, Vellore 832 004, India
1 2 3
4
Rushworth RL, Bell SM, Morrel S, Robertson PW. Rubella in mothers. Lancet 1996; 347: 1262. Galazka A. Rubella in Europe. Epidemiol Infect 1991; 107: 43–54. Anon. Expanded programme on immunization: immunization schedules in the WHO region of the Americas. Wkly Epidemiol Rec 1985; 70: 153–60. Anon. Expanded programme on immunization: immunization schedules in the WHO European region, 1995. Wkly Epidemiol Rec 1995; 70: 221–28.
Mucosa-associated lymphoid tissue lymphoma of the oesophagus SIR—Primary lymphomas of the gastrointestinal tract probably originate from mucosal lymphocytes and represent the largest group of all extranodal lymphomas.1 They originate in the stomach in 24% of cases, in the small bowel in 10%, in the colon and rectum in 7%, and in Waldeyer’s ring in 11%.1 Mucosa-associated lymphoid tissue (MALT) lymphoma, is a subtype of lymphoma.1–3 Gastric MALT lymphoma has been causally linked to mucosal Helicobacter pylori infection. MALT lymphomas have been reported in other parts of the gastrointestinal tract, such as the duodenum, ileum, and colon. We report MALT lymphoma involving the oesophagus. A 61-year-old man had an episode of upper gastrointestinal bleeding from a gastric antral ulcer. He had evidence of H pylori infection and was treated with metronidazole, tetracycline, and bismuth subsalicylate in addition to ranitidine. Repeat upper gastrointestinal endoscopy showed a nodular antral mass. Biopsies indicated MALT lymphoma. No evidence of H pylori infection was found. He was started on clarithromycin and lansoprazole and referred to us for further evaluation. Endoscopy showed an antral nodular mass (2⫻2 cm), fundic polypoid mass (2⫻3 cm), and two linear raised lesions (1⫻2 cm) with apparently normal overlying mucosa in the proximal
268
Regression of salivary gland MALT lymphoma after treatment for Helicobacter pylori SIR—A 62-year-old Asian woman with a previous history of Sjögren’s syndrome presented with a right cheek mass of recent onset. On examination, she was found to have a 2 cm mass in the right periparotid region and no other abnormality. A biopsy specimen of the mass showed total replacement of the parotid gland by sheets of centrocyte-like cells and plasmacytoid lymphocytes, with areas showing prominence of monocytoid lymphocytes (upper figure). Occasional residual germinal centres and focal lymphoepithelial lesions (lower figure) were present. No Helicobacter pylori organisms were identified. Immunohistochemistry showed expression of CD45 (LCA), CD20 (L-26), CD43 (Leu-22), and kappa light chain restriction by the lymphocyte population. Polymerase chain amplification with FR3A and Jh consensus primers confirmed the presence of a monoclonal B-lymphocyte population.1 The lesion was classified as primary low-grade lymphoma of mucosaassociated lymphoid tissue (MALT) arising from a salivary gland. Magnetic resonance imaging (MRI) showed multifocal lesions confined to the right parotid gland, periglandular tissues, and bilateral submandibular masses. Serological studies revealed antibodies against H pylori, Sjögren’s antibodies, and antinuclear antibody with a speckled pattern. A single endoscopic evaluation with gastric biopsy showed chronic gastritis with H pylori organisms identified, but no histological evidence of lymphoma. Because the patient refused conventional lymphoma therapy, only antibacterial therapy for H pylori infection, consisting of doxocycline 100 mg, metronidazole 500 mg, omeprazole 20 mg, and bismuth 100 mg, all given three times a day for 2 weeks. Following this therapy, the patient’s parotid gland and submaxillary masses disappeared. Clinical follow-up, including repeat MRI study, for 22 months after treatment has shown no evidence of recurrence. An association between H pylori infection and MALT
Vol 348 • July 27, 1996
azide/phosphate buffered saline for 8 min. Expressions of CD44v3 and CD44v6 on epithelium were semiquantified. Increased expression of CD44v3 and CD44v6 were found in the colonic epithelium of UC patients, compared with controls or those with Crohn’s disease (table) (CD44v3, p<0·05%; UC vs normal, UC vs CD, CD44v6, p<0·05%; UC vs CD; non-parametric analysis). Using frozen sections fixed with PLP, the results we have obtained were similar to those reported by the Rosenberg group.1
3
4 5
Panax: economic and medicinal plant research. London: Academic Press Inc, 1985; 1: 218–84. Soldati F, Sticher O. HPLC separation and quantitative determination of ginsenosides from Panax ginseng, Panax quinquefolium and from Ginseng drug preparations. Planta Medica 1980; 39: 348–57. Ries CA, Sahud MA. Agranulocytosis caused by Chinese herbal medicines. JAMA 1975; 231: 352–55. Scaglione F, Cogo R, Cucuzza C, Arcidacono M, Beretta A. Immunomodulatory effects of Panax ginseng C.A. Meyer (G115) on alveolar macrophages from patients suffering with chronic bronchitis. Int J Immunother 1994; 10: 21–24.
Atsuo Kitano, *Nobuhide Oshitani, Takayuki Matsumoto, Kenzo Kobayashi
Authors’ reply
*Third Department of Internal Medicine, Osaka City University Medical School, Osaka 545, Japan; and Department of Internal Medicine, Juso Municipal Hospital of Osaka
SIR—Because SJS and toxic epidermal necrolysis (TEN) are related to toxic administration,1 mainly of a drug, we postulated that ginseng could be responsible for the illness. The patient stopped aspirin, local antibiotics (amylmetacresol, tyrochricin), and vitamin C 6 days before the onset of SJS. These drugs have short plasma half-lives or are not absorbed by the intestine;2 therefore, they could not be present at the time of SJS. Indeed, ginseng was the sole drug taken at that time. The patient’s girlfriend still had four capsules of ginseng which was bought in the Chinese area of Paris. We thus postulated that it was Panax ginseng, the Chinese or Korean ginseng. We did toxicological analysis (FPIA, TDX, Abbott) which did not shown NSAIDs, salicylates, or antiepileptics, the most frequent drugs implicated in SJS and TEN. However, the composition of the active vegetable compound could not be assessed. The coating of the capsules was gelatine. These results cannot eliminate the putative role of ginseng, since more than 100 drugs have been implicated as causes of SJS or TEN.1 Moreover, ginseng has been suspected of various non-cutaneous side-effects, such as mind-altering effects or cerebral arteritis.3 Undoubtedly, the need for a careful quality control of ginseng and herbal products is necessary.
1
2
Rosenberg WMC, Prince C, Kaklamanis L, et al. Increased expression of CD44v6 and CD44v3 in ulcerative colitis but not colonic Crohn’s disease. Lancet 1995; 345: 1205–09. Papadoginnakis N, Gad A, Chenard MP, Bellocq JP, Duclos B. Expression of CD44 variants in differential diagnosis of ulcerative colitis and Crohn’s disease. Lancet 1996; 347: 1413–14.
Ginseng as cause of Stevens-Johnson syndrome? SIR—Dega and co-workers (May 11, p 1344),1 report a probable association of Stevens-Johnson syndrome (SJS) with ginseng. The relation between the diagnosed syndrome and the ingestion of ginseng cannot, however, be established beyond doubt. It is imperative to assess which species of ginseng the patient has used. In addition to various types available on the market, such as Panax ginseng, Panax notoginseng, or Panax quinquefolius, other plant species are also marketed under the name ginseng. Such herbs, however, are taxonomically not related to the medicinal plant Panax ginseng C A Meyer. Panax ginseng is monographed as a medicinal plant in the pharmacopoeias of several countries such as Austria, China, France, Germany, Russia, Switzerland, and Japan. Panax ginseng does not exert anti-inflammatory activities, nor does it contain non-steroidal anti-inflammatory substances.2 On the other hand, non-standardised pseudoginseng products are available. Such products do not guarantee a uniform content of active substances and have undergone no toxicological or clinical tests.3 In addition, some marketed products, in particular originating from Asian countries, are known to be adulterated with undeclared substances. Some patients are reported to have developed agranulocytosis after taking Chinese herbal medicines for relief of arthritis and back pain. Such medicines, however, proved to contain substantial amounts of undeclared aminopyrine and phenylbutazone, drugs that are known to cause agranulocytosis.4 Toxicological and clinical studies on products containing the standardised Panax ginseng extract G115, which we produce and which is registered as a medicine in more than 50 countries, have, on the other hand, clearly demonstrated its safety and efficacy.5 We therefore would re-emphasise the need for a careful quality control of ginseng products, as is currently done for the high-quality herbal products. *Ricardo Faleni, Fabio Soldati Medical Department, R&D, Pharmaton SA, 6903 Lugano, Switzerland
1 2
Chosidow O, Dega H, Laporte J-L, Francès C, Herson S. Ginseng as a cause for Stevens-Johnson syndrome? Lancet 1996; 347: 1344. Shibata S, Tanaka O, Shoji J, Saito H. Chemistry and pharmacology of
Vol 348 • July 27, 1996
*Olivier Chosidow, Hervé Dega, Gilles Peytavin *Department of Internal Medicine, Groupe Hospitalier Pitié-Salpêtrière, 75651 Paris, France; and Department of Clinical Pharmacy, Groupe Hospitalier Bichat-Claude Bernard, Paris
1
2
3
Roujeau JC, Kelly JP, Naldi L, et al. Medication use and risk of Stevens-Johnson syndrome or toxic epidermal necrolysis. N Engl J Med 1995; 333: 1600–07. Becq-Giraudon B. Polypeptides cycliques. In: Giroud JP, Mathé G, Meyniel G, eds. Pharmacologie clinique. Bases de la Thérapeutique. Paris: Expansion Scientifique Française, 1988: 1500–11. Ryu SJ, Chien YY. Ginseng-associated cerebral arteritis. Neurology 1995; 45: 829–30.
Prevention of rubella SIR—Rushworth and colleagues (May 4, p 1262)1 report that despite rubella vaccination of schoolgirls (started in 1971 and continuing to the present) and of male adolescents (started in 1994), congenital rubella continues to occur in New South Wales, Australia. They state that the “eradication of congenital rubella is realisable only when protective levels of rubella immunity are maintained among women of reproductive age”, apparently in support of the strategy of selective rubella vaccination of adolescents. However, this strategy does not affect the transmission dynamics of rubella virus infection in children. With continuing circulation of rubella virus there is persistent risk of infection in susceptible (non-immune) pregnant women, even when only 2–3% of pregnant women are non-immune.2 This conundrum is illustrated in their findings of increasing proportions of mothers remaining non-immune as age increased, and by the continued occurrence of congenital rubella.1 Thus,
267
THE LANCET
congenital rubella will not be eliminated by the strategy of selective vaccination. The alternate strategy is to reduce the circulation of rubella virus in the community to such low levels that nonimmune women of reproductive age are at no or very low risk of infection. This reduction is accomplished by offering vaccination to young children and by achieving high coverage. Indeed, both selective and childhood rubella vaccination strategies could be combined, because they are complementary to each other. Of 22 countries in the WHO American region using rubella vaccine, 13 follow the childhood vaccination strategy and nine the combined strategy.3 Of 11 countries in the WHO European region using rubella vaccine, seven follow the childhood strategy and four the combined strategy.4 Countries planning to newly introduce rubella vaccination should learn from the experience of others. The combined strategy requires a two-dose schedule of rubella vaccination of all children, first at 12–15 months of age and later at a convenient time between 5 and 15 years. When high (>90%) coverage is achieved for both doses congenital rubella will most probably be eliminated. Eradication of only one manifestation (congenital rubella) of a prevalent virus infection (rubella) is not a realistic goal. To eliminate congenital rubella, virus transmission should be interrupted. We believe that interruption of rubella transmission is feasible; in other words, rubella is eradicable.
oesophagus. Histology showed low-grade B-cell MALT lymphoma in specimens from all masses. Endoscopic ultrasonography showed thickening of mucosal and submucosal layers but intact muscularis propria with no evidence of extramural extension or adenopathy. The patient was referred for chemotherapy. MALT lymphomas tend to appear in patients with chronic inflammatory disorders. Normal gastric mucosa contains no organised lymphoid tissue, but H pylori infection has been associated with MALT lymphoma.4 Scattered lymphocytes are usually present in oesophageal mucosa which may be affected by many chronic inflammatory conditions, although MALT lymphoma has not been described in the oesophagus. The spectrum of gastrointestinal MALT lymphomas should be expanded to involve the oesophagus. Assaad M Soweid, *Paul E Z achary Jr Division of Gastroenterology and Hepatology, St Louis University Health Sciences Center, 3635 Vista Avenue, St Louis, MO 63110, USA
1
2 3
4
*Reuben Samuel, T Jacob John
Radeszkiewicz T, Dragosics B, Bauer P. Gastrointestinal malignant lymphomas of the mucosa-associated lymphoid tissue: factors relevant to prognosis. Gastroenterology 1992; 102: 1628–38. Isaacson PG, Spencer J. Malignant lymphoma of mucosa-associated lymphoid tissue. Histopathology 1987; 11: 445–62. Hussell T, Isaacson PG, Crabtree JE, Spencer J. The response of cells from low-grade B-cell gastric lymphomas of mucosa-associated lymphoid tissue to Helicobacter pylori. Lancet 1993; 342: 571–74. Stolte M, Eidt S. Healing gastric MALT lymphomas by eradicating H pylori? Lancet 1993; 342: 568.
Department of Clinical Virology, Christian Medical College and Hospital, Vellore 832 004, India
1 2 3
4
Rushworth RL, Bell SM, Morrel S, Robertson PW. Rubella in mothers. Lancet 1996; 347: 1262. Galazka A. Rubella in Europe. Epidemiol Infect 1991; 107: 43–54. Anon. Expanded programme on immunization: immunization schedules in the WHO region of the Americas. Wkly Epidemiol Rec 1985; 70: 153–60. Anon. Expanded programme on immunization: immunization schedules in the WHO European region, 1995. Wkly Epidemiol Rec 1995; 70: 221–28.
Mucosa-associated lymphoid tissue lymphoma of the oesophagus SIR—Primary lymphomas of the gastrointestinal tract probably originate from mucosal lymphocytes and represent the largest group of all extranodal lymphomas.1 They originate in the stomach in 24% of cases, in the small bowel in 10%, in the colon and rectum in 7%, and in Waldeyer’s ring in 11%.1 Mucosa-associated lymphoid tissue (MALT) lymphoma, is a subtype of lymphoma.1–3 Gastric MALT lymphoma has been causally linked to mucosal Helicobacter pylori infection. MALT lymphomas have been reported in other parts of the gastrointestinal tract, such as the duodenum, ileum, and colon. We report MALT lymphoma involving the oesophagus. A 61-year-old man had an episode of upper gastrointestinal bleeding from a gastric antral ulcer. He had evidence of H pylori infection and was treated with metronidazole, tetracycline, and bismuth subsalicylate in addition to ranitidine. Repeat upper gastrointestinal endoscopy showed a nodular antral mass. Biopsies indicated MALT lymphoma. No evidence of H pylori infection was found. He was started on clarithromycin and lansoprazole and referred to us for further evaluation. Endoscopy showed an antral nodular mass (2⫻2 cm), fundic polypoid mass (2⫻3 cm), and two linear raised lesions (1⫻2 cm) with apparently normal overlying mucosa in the proximal
268
Regression of salivary gland MALT lymphoma after treatment for Helicobacter pylori SIR—A 62-year-old Asian woman with a previous history of Sjögren’s syndrome presented with a right cheek mass of recent onset. On examination, she was found to have a 2 cm mass in the right periparotid region and no other abnormality. A biopsy specimen of the mass showed total replacement of the parotid gland by sheets of centrocyte-like cells and plasmacytoid lymphocytes, with areas showing prominence of monocytoid lymphocytes (upper figure). Occasional residual germinal centres and focal lymphoepithelial lesions (lower figure) were present. No Helicobacter pylori organisms were identified. Immunohistochemistry showed expression of CD45 (LCA), CD20 (L-26), CD43 (Leu-22), and kappa light chain restriction by the lymphocyte population. Polymerase chain amplification with FR3A and Jh consensus primers confirmed the presence of a monoclonal B-lymphocyte population.1 The lesion was classified as primary low-grade lymphoma of mucosaassociated lymphoid tissue (MALT) arising from a salivary gland. Magnetic resonance imaging (MRI) showed multifocal lesions confined to the right parotid gland, periglandular tissues, and bilateral submandibular masses. Serological studies revealed antibodies against H pylori, Sjögren’s antibodies, and antinuclear antibody with a speckled pattern. A single endoscopic evaluation with gastric biopsy showed chronic gastritis with H pylori organisms identified, but no histological evidence of lymphoma. Because the patient refused conventional lymphoma therapy, only antibacterial therapy for H pylori infection, consisting of doxocycline 100 mg, metronidazole 500 mg, omeprazole 20 mg, and bismuth 100 mg, all given three times a day for 2 weeks. Following this therapy, the patient’s parotid gland and submaxillary masses disappeared. Clinical follow-up, including repeat MRI study, for 22 months after treatment has shown no evidence of recurrence. An association between H pylori infection and MALT
Vol 348 • July 27, 1996