Causality

In 1965, Sir Austin Bradford-Hill published his famous "postulates" in The Environment and Disease: Association or Causation [40], The nine Bradford-Hill's postulates (summarized in Table 6) give a mea sure of the degree in which evidence of causality between a factor and a disease could be established. The Bradford-Hill's postulates result particularly suitable to evaluate the degree in which an autoimmune rheumatic disease is conditioning a higher probability to develop a malignant neoplasm. Table 7 shows the degree of fulfilment of Bradford-Hill's postulates depending of the evidence reported in the medical literature. We can draw from the analysis presented in Table 7 that there is enough evidence of causality of an autoimmune rheumatic disease in association with a higher probability of developing a malignancy in four pathological entities: (i) RA in association with lymphoproliferative neoplasm; (ii) SS in association with lymphoproliferative neoplasm; (iii) dermato-myositis in association with solid tumors; and (iv) systemic sclerosis in association with lung cancer. For the above four autoimmune disease-cancer relationships the main Bradford-Hill's postulates are satisfied: strength, consistency and temporality of association, as well as plausibility, coherence and analogy. For other associations as that of SLE with solid tumor or with lymphoproliferative disorders, there is not enough evidence to establish causality. On the other hand, the absence of specificity, biological gradient, and experiment tells us that occurrence of cancer is not only conditioned by presence of the rheumatic disease. Also, there is no dose-response like gradient (e.g., more rheumatic disease vs. less rheumatic disease). Experiment on this could only be conducted in animal models.

Miettinen [41] distinguished two different types of causality: (i) descriptive, in which a parameter of occurrence is related to a determinant without any view to causal interpretation of the relationship; and (ii) causal, relevant to rational intervention (to influence the outcome through modification of the determinant). The latter is particularly relevant here considering the importance of establishing close surveillance in rheumatic patients on the probability that they develop a malignancy.

Vineis and Porta [42] comment on the current extended interpretation of the phenomenon: determination rather than causality. They suggest to use the word determinant of a disease as more appropriate in epidemiology. In this way, we can conclude of certain autoimmune rheumatic diseases as determinants of certain malignant neoplasms.

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