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Tumore stomaco

Tumore allo stomaco

Cancro da amianto allo stomaco

Il tumore allo stomaco o cancro gastrointestinale (tumore gastrico) si sviluppa sul rivestimento dello stomaco. Dallo stomaco può diffondersi in altre parti del corpo, soprattutto al fegato, ai polmoni, alle ossa e ai linfonodi. Ogni anno sono registrati oltre 250.000 nuovi casi, con oltre 100.000 morti. Lo IARC (Agenzia Internazionale per la Ricerca sul Cancro) ha confermato che tra gli agenti eziologici del tumore alle ovaie vi è l’amianto.

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MEDICA STOMACO

Tumore allo stomaco sintomi

I primi sintomi del tumore allo stomaco comprendono sensazione di bruciore di stomaco, dolore all’addome superiore, nausea e perdita di appetito. Successivamente, si possono manifestare perdita di peso, ittero, vomito, difficoltà di deglutizione e sangue nelle feci.

Diagnosi tumore allo stomaco

Solitamente la diagnosi tumore allo stomaco avviene attraverso biopsia realizzata durante l’endoscopia. Possono essere poi effettuate indagini di imaging biomedico per determinarne la diffusione in altre parti del corpo. Una diagnosi precoce permette cure tempestive e più efficaci e, di conseguenza, maggiori chance di guarigione e sopravvivenza tumore allo stomaco.

I lavoratori esposti ad amianto dovrebbero sottoporsi a controlli sanitari periodici per una diagnosi tempestiva. La scarsità e genericità dei sintomi del cancro allo stomaco nella fase iniziale, infatti, ritarda notevolmente la diagnosi. Un ritardo diagnostico comporta un tasso di sopravvivenza a 5 anni inferiore al 10% dei casi.

Cura tumore allo stomaco

La terapia per il tumore allo stomaco include l’intervento chirurgico, la chemioterapia, la radioterapia e la terapia mirata. In caso di stadio avanzato, spesso si ricorre alle cure palliative.

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LEGALE STOMACOI diritti delle vittime di cancro allo stomaco

In caso di decesso, il risarcimento INAIL o rendita INAIL viene liquidata al coniuge superstite nella misura del 50% della prestazione spettante alla vittima (rendita di reversibilità) e ai figli nella misura del 20% per ognuno, a condizione che non superi l’iniziale 100%.

Riconoscimento INAIL

In Italia le malattie e i tumori da amianto sono riconosciuti ed indennizzati dall’INAIL. Le malattie professionali da amianto sono divise in 3 liste (liste malattie professionali INAIL). Il cancro allo stomaco è compreso nella Lista II (malattie causate dall’amianto la cui origine lavorativa è di limitata probabilità). Per questo motivo, la vittima deve dimostrare il nesso causale per ottenere le prestazioni (rendita e/o indennizzo INAIL, se il grado di invalidità riconosciuto è inferiore al 16%).

Monografia IARC: asbesto e tumore allo stomaco

Il tumore allo stomaco è una delle patologie asbesto correlate compresa nella tabella I INAIL, rispetto alla quale sussiste presunzione legale di origine.

La correlazione tra esposizione ad amianto e l’insorgenza del tumore allo stomaco è stata ampiamente trattata nella monografia dello IARC del 2010 “ASBESTOS (CHRYSOTILE, AMOSITE, CROCIDOLITE, TREMOLITE, ACTINOLITE, AND ANTHOPHYLLITE) ove si legge:

Cancer of the stomach

The Working Group reviewed 42 cohort studies and five population-based case–control studies that examined the association between asbestos and cancer of the stomach (See Table 2.6 online).

a) Cohort studies

Notable findings among the cohort studies are:

Selikof f et al. (1964) reported a nearly 3-fold excess mortality for cancer of the stomach (12 observed versus 4.3 expected) in a population of 632 insulation workers in New York and New Jersey occupationally exposed to asbestos dust. Further analysis within this cohort (Selikoff et al., 1979) found evidence of a dose–response relationship between duration of exposure to asbestos (in years), and risk of death from cancer of the stomach. The SMR for cancer of the stomach increased from 0.00 in workers exposed for < 20 years, to 4.00 (95%CI: 1.47 – 8.71)     in those exposed for 20 −35 years, and to 3.42 (95%CI:1.82 – 5.85) in those exposed for > 35 years.

Selikof f et al. (1967) found a modest, non- significant increase in risk of death for cancer of the stomach: 34 observed v. 29.4 expected, (SMR = 1.16;95%CI: 0.92 – 1.78) in a larger cohort study of 17800 insulation workers across the USA and Canada. No data on dose–response for cancer of the stomach were presented in this analysis.

Liddell et al. (1997) reported an overall SMR for cancer of the stomach of 1.24 (95%CI:1.07 −1.48) in a study of 10918 asbestos miners and millers exposed predominantly to chry- sotile asbestos, in Quebec, Canada. Within this cohort, a positive dose–response relationship was observed between cumulative exposure to asbestos dust (mcpf-year) and mortality for cancer of the stomach. Thus, for workers with cumulative dust exposure < 300, the SMR was 1.16; for workers with cumulative exposure of 300 – 400, the SMR was 1.29; for workers with cumulative exposure of 400 – 1000, the SMR was 1.21; and for workers in the highest exposure category, with cumulative exposure > 1000, the SMR was 3.21 (95%CI: 1.87 −5.14). An additional finding in this cohort was a modest interaction between cumulative asbestos exposure, ciga- rette smoking, and mortality from cancer of the stomach.

Musk et al. (2008) found an SMR for cancer of the stomach of 1.01 (95%CI: 0.71 – 1.40) in a cohort of 6943 asbestos miners and millers exposed predominantly to crocidolite asbestos in Wittenoom, Western Australia, followed through the end of 2000, and when all cohort members lost to follow-up were assumed to be alive. When the analysis was re-run censoring subjects at the date last known to be alive, the SMR was 1.71 (95%CI: 1.20–2.35).

Reid et al. (2004) conducted a nested case– control study within this same Australian cohort, and found a positive exposure-response relationship between cancer of the stomach and cumulative exposure to asbestos (test for trend, P = 0.057). No association was seen between cancer of the stomach and either time since first exposure or year of starting work with asbestos. Smoking status was associated with cancer of the stomach, but not significantly.

Meurman et al. (1974) found a non-signifi- cant increase in SMR for cancer of the stomach: SMR = 1.42 (95%CI: 0.76 – 2.43) in a cohort of 736 asbestos miners in Finland exposed to anthophyllite asbestos.

Berry et al. (2000) found a modest, non- significant increased risk for death from cancer of the stomach: 28 observed versus 23.1 expected (SMR, 1.21; 95%CI: 0.81–1.75) in a British study of factory workers producing asbestos insulation in the east end of London. Strongly positive dose–response associa- tions between cumulative asbestos response and cancer of the stomach were observed in two cohort studies of Chinese factory workers one in Beijing and the other in Qingdao; rela- tive risks for cancer of the stomach were 4.4 and 2.4, respectively (Zhu & Wang, 1993; Pang et al., 1997).

Raffn et al. (1989) observed 43 deaths from cancer of the stomach versus 30.09 expected (SMR, 1.43; 95%CI: 1.03 – 1.93) in a cohort of 7986 men employed from 1928–84 in the asbestos cement industry in Denmark.

Enterline et al. (1987) observed a SMR for cancer of the stomach of 1.80 (95%CI: 1.10–2.78) in a cohort of 1074 retired US asbestos workers.

Epidemiological studies of cohorts with asbestos-related diseases – asbestosis and benign pleural disease – have not found increased mortality for cancer of the stomach (Germani et al., 1999Karjalainen et al., 1999Szeszenia- Dabrowska et al., 2002).

b) Case–control studies

Case–control studies exploring the relation- ship between asbestos exposure and cancer of the stomach yield inconsistent results. The Working Group reviewed five case–control studies. Notable findings are these:

A study from Poland (Krstev et al., 2005) found an OR for cancer of the stomach of 1.5 (95%CI: 0.9−2.4) for workers ever exposed to asbestos, and of 1.2 (95%CI: 0.6–2.3) for workers with 10 or more years of exposure to asbestos.

The largest case–control study to examine the association between asbestos and cancer of the stomach (Cocco et al., 1994) reported an odds ratio of 0.7 (95%CI: 0.5–1.1) for workers ever exposed to asbestos, and of 1.4 (95%CI: 0.6−3.0) for those with 21+ years of exposure to asbestos. The most strongly positive case–control study linking asbestos to cancer of the stomach is the case–control study, cited above, nested within the Western Australia mining cohort (Reid et al.,2004).

c) Meta-analyses

Several meta-analyses have been undertaken of the association between asbestos exposure and cancer of the stomach.

A meta-analysis by Frumkin & Berlin (1988) stratified studies according to SMR for lung cancer and also according to percentage of deaths due to mesothelioma. Frumkin & Berlin found in cohorts where the SMR for lung cancer was < 2.00 that the SMR for cancer of the stomach was 0.91 (95%CI: 0.71–1.16). By contrast, when the SMR for lung cancer was > 2.00, the SMR for cancer of the stomach increased to 1.34 (95%CI: 1.07–1.67).

Gamble (2008) reported that point estimates for cancer of the stomach mortality tended towards 1.0 when the excess risk for lung cancer were less than 4-fold, but “tended to be somewhat elevated when lung cancer relative risks were 4-fold or greater.” Gamble observed further that “combined relative risks for cancer of the stomach stratified by lung cancer categories showed a suggestive trend, with a significant deficit (0.80) when lung cancer SMRs were <1.0 that increased monotonically to a significant 1.43-fold excess in the studies with lung cancer SMRs > 3.0.” Gamble observed no trend for increasing SMR for cancer of the stomach with increasing percentage of deaths from mesothelioma (Gamble, 2008).

The IOM (2006) conducted a meta-analysis of 42 cohort studies examining the association between asbestos exposure and cancer of the stomach. The IOM noted that the “majority of cohort relative risk estimates for cancer of the stomach exceed the null value (1.0), indicating excesses, although estimates varied considerably in strength.” In cohorts that compared “any” versus no exposure, the summary relative risk was 1.17 (95%CI: 1.07–1.28). The IOM notes that with respect to dose–response, the summary estimates were stable. Thus in the cohorts that compared “high” versus no exposure, the lower bound summary relative risk was 1.31 (95%CI: 0.97–1.76), and the higher bound summary rela- tive risk, 1.33 (95%CI: 0.98–1.79).

The IOM conducted a meta-analysis of the five case–control studies resulting in a combined rela- tive risk of 1.11 (95%CI: 0.76–1.64). The summary odds ratio increased when only extreme expo- sure was considered (OR, 1.42; 95%CI: 0.92–2.20) The Working Group developed a scatter plot comparing SMRs for lung cancer with SMRs for cancer of the stomach in the same cohorts. A positive trend was observed between the two, and the correlation coefficient (r2) = 0.66, see Fig. 2.1.

(i) Asbestos in drinking-water and cancer of the stomach.

Ecological correlational studies conducted from the 1960s into the early 1980s suggested an association between asbestos in drinking-water and cancer of the stomach. These studies corre- lated population exposure to asbestos in water supplies with population cancer rates. Levy et al. (1976) reported an excess in cancer of the stomach among persons in Duluth, MN, USA exposed to taconite asbestos in drinking-water. Wigle (1977) saw an excess of male cancer of the stomach among some exposed to asbestos in drinking-water in Quebec. Conforti et al. (1981) saw a similar association in the San Francisco Bay area, USA. Polissar et al. (1982) examined cancer incidence and mortality among residents of the Puget Sound area, USA, in relation to asbestos in regional drinking-water. They observed no asso- ciation between asbestos exposure and cancer of the stomach. A similarly negative study was observed in a study conducted in Woodstock, NY, USA (Howe et al., 1989). Kjærheim et al. (2005) examined cancer of the stomach incidence in Norwegian light-house keepers exposed to asbestos in drinking-water. They found an SIR for cancer of the stomach in the entire cohort of 1.6 (95%CI: 1.0–2.3). In the subcohort with “definite” exposure to asbestos, the SIR was 2.5 (95%CI: 0.9–5.5). In those members of the definite exposure subcohort followed for 20+ years, the SIR was 1.7 (95%CI: 1.1–2.7).

Cantor (1997) conducted a systematic review of the epidemiological literature on exposure to asbestos in drinking-water and cancer of the stomach, and concluded that the available data were inadequate to evaluate the cancer risk of asbestos in drinking-water.

Marsh (1983) conducted a critical analysis of 13 epidemiological studies of asbestos and drinking-water conducted in the USA and Canada, and found no consistent pattern of association.

Tumore allo stomaco è una malattia asbesto-correlata

Già in data 21 gennaio 1973, il New York Times ha pubblicato un articolo in cui denunciava la pericolosità dell’amianto per l’insorgenza dei tumori gastrici: “Amianto, il salvatore di vite ha anche un lato mortale” (Asbestos, the saver of lives, has a deadly side). Grazie agli studi del Prof. Irvin Selikoff, fin dagli anni ’60 risulta dimostrato che l’amianto è l’agente eziologico del cancro gastrico, oltre che diverse altre patologie: “instead of the normal nine or 10 deaths from cancer of the stomach, colon or rectum, there were 29—“not so unexpected,” as Selikoff points out, for “anybody who inhales dust also ingests it” (leggi l’intero articolo negli archivi del New York Times).

Altra letteratura scientifica conferma che il tumore allo stomaco è malattia asbesto-correlata:

Stomach Cancer Mortality Among Workers Exposed to Asbestos: A Meta-AnalysisThe relationship between asbestos and stomach cancer is not well understood because of small number of cases. This study aimed to determine the incidence and mortality of stomach cancer among workers exposed to asbestos based on a systematic review and meta-analysis approach.

Regulation of Gastric Carcinogenesis by Inflammatory CytokinesChronic inflammation caused by infection with Helicobacter pylori and autoimmune gastritis increases an individual’s risk of developing gastric cancer. More than 90% of gastric cancers are adenocarcinomas, which originate from epithelial cells in the chronically inflamed gastric mucosa. However, only a small subset of chronic gastritis patients develops gastric cancer, implying a role for genetic and environmental factors in cancer development. A number of DNA polymorphisms that increase gastric cancer risk have mapped to genes encoding cytokines. Many different cytokines secreted by immune cells and epithelial cells during chronic gastritis have been identified, but a better understanding of how cytokines regulate the severity of gastritis, epithelial cell changes, and neoplastic transformation is needed. This review summarizes studies in both human and mouse models, describing a number of different findings that implicate various cytokines in regulating the development of gastric cancer.

Tumore allo stomaco e radiazioni ionizzanti

Tra gli agenti cancerogeni responsabili dell’insorgenza del tumore dello stomaco, vi sono le radiazioni ionizzanti, fattore di rischio riconosciuto anche dall’AIRC. Le radiazioni ionizzanti sono in grado di indurre lo sviluppo di ogni forma di tumore, anche se tra l’esposizione alle radiazioni e l’insorgenza della malattia possono trascorrere molti anni, e varia da tumore a tumore.

Diversi studi hanno ormai confermato che anche bassi livelli di esposizione possono dare origine alle trasformazioni delle cellule che portano allo sviluppo del cancro. La quantificazione di questo rischio, tuttavia, è molto complessa.

In generale oggi è noto che:

  • il rischio di cancro aumenta al crescere della dose di radiazioni a cui si è esposti. Inoltre non è possibile determinare una dose al di sotto della quale l’aumento del rischio di sviluppare un tumore si azzeri;
  • i tumori solidi associati all’esposizione a radiazioni impiegano molto tempo per svilupparsi. Le leucemie sono il tipo di cancro che insorge più rapidamente (anche dopo pochi anni), mentre i tumori solidi impiegano diversi decenni;
  • il rischio di sviluppare una neoplasia come conseguenza dell’esposizione a radiazioni ionizzanti è diverso tra le leucemie e gli altri tumori del sistema emolinfopoietico (come alcuni linfomi) e quelli solidi.

Le radiazioni ionizzanti prodotte dall’uomo

Molte delle radiazioni ionizzanti responsabili dell’insorgenza di diverse patologie neoplastiche, sono prodotte dall’uomo. Gli impieghi principali sono la produzione di armi e di energia (centrali nucleari).

Anche se nell’immaginario collettivo il termine radiazioni ionizzanti rimanda direttamente alle armi nucleari utilizzate durante la Seconda Guerra Mondiale (Hiroshima e Nagasaki), l’utilizzo di quelle armi ha contribuito soltanto in minima parte alla produzione umana di radiazioni ionizzanti. Infatti, la maggior parte delle radiazioni disperse nell’ambiente dall’uomo, è rappresentata dai test sulle armi atomiche, specie quelli realizzati in atmosfera.

Fino al 1963, quando i test nucleari in atmosfera furono vietati (alcuni Stati hanno continuato però fino agli anni Ottanta), ne sono stati effettuati oltre 500. Ogni test nucleare ha disperso nell’atmosfera e poi al suolo (con quello che viene richiamato “fall-out” nucleare) consistenti quantità di materiali radioattivi che si sono diffusi su migliaia di chilometri quadrati. Si stima che ancora oggi in tutto il mondo la contaminazione radioattiva conseguente a quei test sia una fonte di esposizione per gli esseri umani a causa dei lunghi tempi di decadimento di alcuni elementi utilizzati. Gli effetti sulla salute delle popolazioni esposte sono difficilmente quantificabili.

ASS STOMACO 1

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