Domoic Acid Poisoning - Europe PMC

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to 70-year-old men without known prostate problems suggest a sensitivity of about 67%, a specificity of about. 82%, and a positive predictive value of about 43%.

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to 70-year-old men without known prostate problems suggest a sensitivity of about 67%, a specificity of about 82%, and a positive predictive value of about 43%. These values are higher than those found for digital rectal examination in the same study. This would generally be considered inadequate accuracy for a screening test. When both the digital rectal examination and PSA assay reveal abnormalities, specificity is increased but sensitivity falls to 33%, and the positive predictive value is only slightly increased (49%). Screening of only symptomatic men produces higher sensitivity but lower specificity. Strategies to make the test both more sensitive and more specific have been elusive. General screening with the PSA assay is thus likely to be expensive (in evaluating false-positive results) while still missing many cancers. While detecting and curing some cancers that would have been fatal, the balance of cost and benefit in such screening is unclear. One analysis suggests it would cost $12.7 billion a year to screen (with PSA tests), evaluate, and treat all American men aged 50 to 75 for prostate cancer. The cost per cancer death prevented would be four times that for mammographic screening. Despite the American Cancer Society's conclusion that optimal cancer detection should include annual PSA testing for men older than 50, many others have urged caution in its routine use, and the United States Food and Drug Administration has approved PSA assays for use only in observing patients after diagnosis. Clinicians may achieve more efficient diagnostic aid from this imperfect but valuable test by using it selectively when specific symptoms, rectal examination findings, family history, or African-American ethnicity predict an increased risk. Preliminary data suggest that consistent annual increments in the PSA level (velocity), rather than a single elevated value, may provide a more physiologic and cost-effective criterion for pursuing the possibility of cancer. The only current certainty is that the PSA controversy will challenge physicians' skill in interpreting the ambiguities of science to newspaper-reading patients and to cost-conscious payers. DAVID A. McKAY, MD, MPH San Jose, California

REFERENCES Babaian RJ, Mettlin C, Kane R, et al: The relationship of prostate-specific antigen to digital rectal examination and transrectal ultrasonography-Findings of the American Cancer Society National Prostate Cancer Detection Project. Cancer 1992; 69:1195-2000 Crawford ED, DeAntoni EP: PSA as a screening test for prostate cancer. Urologic Clinics North Am 1993; 20:637-646 Dorr VJ, Williamson SK, Stephens RL: An evaluation of prostate-specific antigen as a screening test for prostate cancer. Arch Intem Med 1993; 153:2529-2537 Kramer BS, Brown ML, Prorok PC, Potosky AL, Gohagan JK: Prostate cancer screening: What we know and what we need to know. Ann Intem Med 1993; 119:914-923

Domoic Acid Poisoning DOMOIC ACID POISONING is the newest threat to the seafood-consuming public. This bizarre syndrome is caused by the neurotoxin domoic acid, which may be concentrated by finfish or filter-feeding shellfish as they consume the unicellular algae that produces the toxin. Domoic acid poisoning was first recognized in No-

vember 1987, after an outbreak of gastrointestinal and neurologic illness in Canadians who had eaten cultivated mussels from Prince Edward Island in eastern Canada. In this outbreak, more than 100 persons became ill with a syndrome characterized by nausea, vomiting, abdominal cramps, diarrhea, severe headache, confusion, loss of short-term memory, and a number of less common symptoms. In most cases, symptoms lasted a few days to a few weeks. The memory impairment was severe and in some cases permanent, and thus, the syndrome was originally called amnestic shellfish poisoning. The source of domoic acid in the mussels was determined to be an intense bloom of the diatom Nitzchia pungens the month before. Domoic acid is a tricarboxylic amino acid that is classified as an excitatory amino acid (along with the dicarboxylic amino acids glutamic acid and aspartic acid). It acts through the inotropic non-NMDA receptor and especially affects the hippocampus and amygdala of the brain. The time from ingestion to intoxication can range from minutes to hours. Since the original Canadian outbreak of domoic acid poisoning, public health monitoring data and some published studies have shown that domoic acid can be found in various other North American coastal waters. Domoic acid is of particular concern to the Pacific Coast states. The only method to determine if domoic acid poisoning is present is to test the shellfish. In September 1991, an epidemic of domoic acid poisoning killed hundreds of brown pelicans and cormorants in Monterey Bay, California. No human illnesses were reported in this incident, but it was especially notable because it was the first documentation of domoic acid poisoning occurring outside of Atlantic Canada and the first documentation of domoic acid being found in herbivorous finfish (anchovies) and being produced by the phytoplankton Pseudonitzschia australis. Three species of Pseudonitzschia are now known to produce domoic acid. In October and November 1991, an outbreak of domoic acid poisoning occurred in Washington State, affecting about two dozen people who had consumed razor clams. Shellfish testing determined that razor clams were contaminated at several locations along both the Oregon and Washington coasts, although mussels were almost entirely free of the toxin. It was later determined that Dungeness crabs from all along the Pacific Coast also were contaminated with domoic acid. In the past two years, considerable sampling and other work has been done in an effort to define the biology and ecology of the phytoplanktons of concern, the extent of domoic acid contamination of West Coast shellfish, the ecologic determinants of domoic acid-producing diatom blooms, and the toxic effects of domoic acid, among other things. Many questions remain, but it is now clear that domoic acid may be found in a number of edible marine species all along the Pacific Coast of North America, as well as in eastern Canadian Atlantic waters and the Gulf of Mexico. Clinicians should be alert to the occurrence of this new syndrome and notify public health authorities imme-

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diately about the occurrence of any suspect cases. Of note, there is no antidote and treatment is supportive. Likewise, public health, food safety, and fishery agencies need to continue monitoring programs aimed at detecting contamination of fish or shellfish before the fish get into the channels of trade or are harvested by sport fishers. KENNETH W. KIZER, MD, MPH Davis, Califomia

REFERENCES California Department of Health Services: Domoic acid intoxication. Calif Morbidity, May 1, 1992, Nos. 17 and 18 Dickey RW, Fryxell GA, Granade HR, Roelke D: Detection of the marine toxins okadaic acid and domoic acid in shellfish and phytoplankton in the Gulf of Mexico. Toxicon 1992; 30:355-359 Perl TM, Bedard L, Kosatsky T, Hockin JC, Todd ECW, Remis RS: An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. N Engl J Med 1990; 322:1775-1780 Teitelbaum J, Zatorre RJ, Carpenter S, et al: Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. N Engl J Med 1990; 322:1781-1787

Gastric Adenocarcinoma and Helicobacter pylori Infection GASTRIC ADENOCARCINOMA is the second most common cause of cancer death in the world. In the United States, however, where socioeconomic and hygienic factors have improved dramatically over the past half century, the incidence of gastric cancer has plummeted. From being the most common form of cancer in the 1930s, gastric cancer is now the ninth most common malignant neoplasm, affecting fewer than 10 per 100,000 persons per year. Studies of immigrant populations have provided clues to the events leading to the decline in the gastric cancer incidence. Persons who move from high-risk to lower-risk regions lessen their cancer risk only moderately, even if they immigrate at a young age. Second-generation immigrants, however, adopt a gastric cancer risk much closer to that of their new country. It has thus been inferred that an environmental factor is important in causing cancer and that this factor exerts its influence in childhood. Furthermore, it has been concluded that this risk factor is somehow related to socioeconomic conditions. Recent data suggest that infection with a bacterium, Helicobacter pylori is a critical environmental factor in gastric carcinogenesis. Helicobacterpylori is a gram-negative rod that causes both gastritis and peptic ulcer disease. The organism, which had remained uncharacterized until the early 1980s, lives in a neutral pH niche between the mucous layer of the stomach and the gastric epithelium. There it produces large quantities of urease, cleaving urea into ammonia and protecting the organism from surrounding acid with a base cloud. Helicobacter pylori is never found remote from gastric epithelium and does not invade tissue. It is extremely common, infecting about 40% of the United States population. Infection rates increase with age and with low socioeconomic status. Once a person is infected, the organism remains in the stomach and is not eliminated without complicated antibiotic therapy. Long before the "discovery" of H pylori, it was known that the stomach undergoes a sequence of histopathologic

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changes before cancer occurs. In chronologic progression, these "preneoplastic" conditions are superficial gastritis, atrophic gastritis, intestinal metaplasia, dysplasia, and finally cancer. Because H pylori is the clear causal agent in superficial gastritis, it is intuitive to suspect it would be linked to cancer. This pathologic association has been confirmed in numerous studies, including ecologic studies, case-control studies of cancer patients, and nested case-control studies within large cohort populations. The combination of studies provides convincing evidence that gastric cancer occurs in regions of high H pylori prevalence, that H pylori is more common in cancer patients than in controls, and that Hpylori infection precedes the onset of cancer by many years. In prospective studies, infection increases the risk for cancer between threefold and sixfold. From this it has been calculated that 40% to 60% of gastric cancers would not occur if Hpylori did not exist. Despite these powerful data, however, it must be recognized that infection with Hpylori is common in all populations and that the overwhelming majority of infections will not result in cancer. Both the age at which infection begins (persons infected during childhood are at worst risk) and the site of infection within the stomach (corporal involvement is probably worse than antral infection only) may determine the degree of risk. Moreover, in many people, infection alone may not be sufficient to cause cancer unless combined with other cofactors, such as dietary nitrates or salt. About 30% of cancers worldwide are now thought to be attributable, at least in part, to infectious agents such as schistosomes, Clonorchis sinensis, papillomavirus, hepatitis viruses, or Epstein-Barr virus. Helicobacter pylori is the first bacterium among these infectious pathogens to be associated with carcinoma. Although there are plausible mechanisms for Hpylori-related carcinogenesis, final confirmation of a causal association awaits trials showing that curative antibiotics against H pylori prevent the development of cancer. Until then, the routine treatment of asymptomatic carriers to prevent cancer cannot be recommended. JULIE PARSONNET, MD Stanford, California

REFERENCES Correa P: Human gastric carcinogenesis: A multistep and multifactorial process-First American Cancer Society Award lecture on Cancer Epidemiology and Prevention. Cancer Res 1992; 52:6735-6740 Forman D: The etiology of gastric cancer, In O'Neill IK, Chen J, Bartsch H (Eds): Relevance to Human Cancer of N-Nitroso Compounds, Tobacco, and Mycotoxins. Lyon, France, International Agency for Research on Cancer, 1991, pp 22-32 Parsonnet J, Friedman GD, Vandersteen DP, et al: Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med 1991; 325:1127-1131 Taylor DN, Blaser MJ: The epidemiology of Helicobacter pylori infection. Epidemiol Rev 1991; 13:42-59

Domestic Violence DOMESTIC VIOLENCE, spousal abuse, and battering are terms that refer to controlling behaviors between people in past or present intimate relationships. Children also often suffer physical and emotional trauma through domestic violence. Research has focused on the violence