Dear Dr. Roach: My 72-year-old husband was diagnosed with multiple myeloma recently, and we have been told that he will need chemo treatments. He also has anemia, which I think is probably normal. He had a back injury in early February and a kyphoplasty in May, with a bone biopsy done routinely. After tests, we now have the diagnosis of multiple myeloma. What can be expected from this diagnosis? I understand that he has elevated kappa light chains.
I.F.
Multiple myeloma is a type of blood cancer coming from plasma cells, the cells that make antibodies. As in any cancer, the cells reproduce uncontrollably. Damage from the cancer can come from what cancer cells produce, or by the fact that they take up necessary space and nutrition from the organs they occupy. In the case of multiple myeloma, the myeloma cells usually secrete immunoglobulins (antibodies, or parts of antibodies). Kappa chains are a component of antibodies (so are lambda chains, the other type of 鈥渓ight鈥� chain protein). High amounts of myeloma protein can damage the kidneys.
Unfortunately, these antibodies aren鈥檛 helpful in fighting off infection, despite the fact that antibodies are an important part of the immune system. In fact, the myeloma cells can grow so much in the bone marrow that they can push aside the cells that normally grow there, including red blood cells (which is why anemia is a common sign), other white blood cells (making infection more likely) and platelets (bleeding can become a problem).
Like many cancers, myeloma can progress from a more benign condition 鈥� in this case, monoclonal gammopathy of uncertain significance. Not all people with MGUS progress to myeloma, but the condition needs to be carefully watched.
Once it becomes myeloma, treatment, usually chemotherapy, is recommended. Multiple myeloma is a highly variable disease, and its prognosis depends on many factors; some come from blood testing, some from the bone marrow biopsy, and some are based on your husband鈥檚 overall health. Your husband鈥檚 hematologist/oncologist can give a better estimate of his prognosis based on these factors.
听
Dear Dr. Roach: My doctor ordered a hemochromatosis gene test because I had a borderline-high iron level.
Here鈥檚 the result: 鈥淭his person has inherited two defective copies of the HFE gene 鈥� one from each parent. Each defective copy has the H63D mutation. Homozygous H63D genotypes (H63D/H63D) rarely show symptoms of hemochromatosis. There is a 100 per cent chance that this patient will pass a copy of the defective HFE gene to the next generation.鈥� Is there anything to worry about here? I have been donating blood every four to six months, and my ferritin is now between 50 and 100.
A.N.
Hemochromatosis is a condition of iron overload. It can be caused by a genetic defect that prevents the body from being able to regulate iron absorption (primary or hereditary hemochromatosis), or it can be caused by excess blood transfusions (secondary hemochromatosis), especially in someone with sickle cell disease or another condition that requires frequent transfusions. 听
The body has no way to get rid of excess iron normally, and donating blood is one way of doing so. This is obviously not possible for people who need transfusions, so chelation of iron is the only treatment for secondary hemochromatosis.
Several different genes are involved in hereditary hemochromatosis. The gene you have is a low-risk gene. Only about one per cent of men and 0.5 per cent of women with this gene will develop iron overload. Giving blood at regular intervals will reduce the risk to zero, while benefitting others.
I鈥檓 surprised you didn鈥檛 meet with a genetic counsellor, who has expertise in providing and interpreting this kind of information.
