Quite a few interesting studies in the April 1 issue of “Blood.” One of them (see abstract: http://tinyurl.com/2sshyj) examines the risk that white and black male U.S. vets with prior autoimmune, infectious, inflammatory and allergic disorders have of developing multiple myeloma or MGUS. The researchers looked at the computerized discharge records of more than four and a half MILLION vets (between 1969 and 1996). They found 4641 patients who were discharged with a diagnosis of myeloma, and 2046 with MGUS. They looked only at the above-mentioned type of patient (some patients, such as women, were excluded due to small percentages; furthermore, those who had cancer at admission or developed cancer or died within the fist year were not included). You can read some of the results in the abstract, so let me have a look at the full study, for which I am indebted as usual to Sherlock.
Benign, asymptomatic MGUS is thought to be the first pathogenetic step in the development of most, if not all MM; however, the specific trigger that initiates the progression from MGUS to MM is unknown.
Skipping the usual dire statistics, let’s go to a more interesting part: Several studies have investigated the hypothesis that repeated or chronic stimulation of the immune system may lead to MM. Some studies have observed elevated risks for categories of immune-stimulating medical conditions (eg, autoimmune conditions, infections, and allergies) or for specific immune-stimulating medical conditions (eg, rheumatoid arthritis and eczema); however, results have generally been inconsistent. This has been a recurrent topic on the myeloma patient lists: is it a good thing to take immune system stimulators (medicinal mushrooms, e.g.) when our immune systems are already over-stimulated? I confess I haven’t come up with a satisfactory answer yet (although I have a gut feeling about it ), and would be glad to read any and all opinions.
Study results: patients with previous autoimmune diseases had an elevated risk of developing myeloma. Statistically elevated risks were also observed for the following specific autoimmune diseases: polymyositis/dermatomyositis, systemicsclerosis, autoimmune hemolytic anemia, pernicious anemia, and ankylosing spondylitis. Where numbers allowed comparison, risks were generally similar for white and black men.
And read this: Risks were also significantly elevated for both races combined for prior infectious disorders, specifically pneumonia, hepatitis, meningitis, septicemia, herpes zoster, and poliomyelitis Risk of influenza was significantly elevated for white men, but not for both races combined. The flu, a possible trigger? Yep, the relative risk is 1.18.
As for inflammatory ailments and allergies, There was a statistically increased risk of 18% associated with inflammatory disorders, largely due to significantly elevated risks for osteoarthritis (the most commonly reported disorder in our dataset) glomerulonephritis, and nephrotic syndrome. There were no significant elevations in risk for allergies overall or for any specific allergies for both races combined. For the five patients with celiac disease, the relative risk was 2.07. That’s quite high, actually. Compare that to the 34 patients with psoriasis, whose relative risk was 0.86. Ailments of the respiratory system were also considered, from sinusitis (RR: 1.17) to pneumonia (RR: 1.54).
Asthma, which I have (guess what? I’m allergic to CATS, no kidding! In order have cats in my life, I must use a cortisone inhaler once a day and Ventolin whenever necessary, although matters have vastly improved since I began taking curcumin), is also mentioned (RR: 0.98). Heck, even having urticaria puts you somewhat at risk!
Interesting titbit in the Discussion part: There is also the possibility that treatment for certain conditions rather than the condition itself may increase susceptibility to MM. For example, we previously reported an increased risk of MM among Connecticut women following use of steroids. Hmmm, so the risk of developing myeloma is due in some cases more to the treatment (prednisone, as the study suggests) than the disease itself. How about that?
Another good one: Our observation of an association between MM/MGUS and specific prior bacterial or viral infections suggest that these infectious conditions may be a potential trigger for MM/MGUS development or a manifestation of underlying immune disturbances due to undetected MM or late-stage MGUS. Recurrent infections largely of bacterial origin (septicemia, meningitis, and pneumonia) are often part of the natural history of MM. This study and a previous Danish one found that patients with a history of pneumonia had a more elevated risk of developing MGUS, which suggests that pneumonia could be a precipitating event for the development of MGUS.
The biggest drawback of this study, apart from the focus on a certain population (don’t you just love this sentence: The exclusion of women might limit the generalizability of our results. Just “might,” huh? ), was the fact that the researchers didn’t have access to any medical records. Theirs was a computerized study, period. But I found it interesting, and besides, it gave me a break from another study that is driving me up the wall (I am spending heaps of time looking up the meaning of about a zillion acronyms and medical terms that I do not recognize; sigh, why can’t studies be written in plain English…or Italian?).
I would like to add that I am only moderately curious as to how I developed cancer. I have it, I am trying to DO something about it, and life goes on. Only time will tell if what I am doing will keep me stable. But sometimes I wonder: if I could figure out what triggered it…well, could that possibly help me fight the cancer now? (I have excluded a few possible triggers already, such as H. pylori.) Was it triggered by a general weakening of my immune system caused by allergies or by the case of Epstein Barr I had in grad school? Or were these “underlying causes” (see below)? I suppose one could really go berserk thinking about possible triggers blablabla. Therefore, I am just going to forget about the issue. I have better things to do.
Study conclusion (RA is rheumatoid arthritis, by the way): In summary, we found significantly elevated risks of MM/MGUS associated with broad categories of autoimmune, infectious, and inflammatory disorders, but not with allergic conditions or RA. We also observed significantly elevated risks for a number of specific autoimmune disorders. Some of these disorders may be a potential trigger for MM/MGUS development, while others may represent underlying conditions due to undetected MM or late-stage MGUS. These results highlight the need to explore the pathologic mechanisms underlying the association of these diseases with MM/MGUS and to consider the diagnosis of MM/MGUS in patients presenting with these conditions.