The Life and Times of Michael C. McGoodwin
Non-Hodgkin's Lymphoma ("Lem")

The entire economy of the Western world is built on things that cause cancer.
(attributed to the 1985 movie "Bliss")



Michael and Lem just prior to starting chemotherapy February 2005
Michael and Lem
 just prior to starting chemotherapy February 2005


Topics Discussed On This Page

 

 

This page deals solely with my experience directly related to Non-Hodgkin's Lymphoma, and would probably be of interest only to close family members and to other lymphoma patients.  Although the separation may be artificial or even conceptually incorrect, I have discussed my experiences with CFS, UAS, and other medical disorders on another page.

Please note the following:

Medical Disclaimer: Although I will always be a physician with an M.D. degree (and as of 2012 am still licensed to practice medicine in the State of Washington), I have not been in active medical practice as a radiologist since 1994, and have not practiced general medicine since 1972, nor do I carry malpractice insurance.  I am not in a position to give or imply any direct or specific medical advice about diagnosing or treating any medical illness or condition, including CFS, UAS, and lymphoma.  If you are a patient with a seemingly similar or related condition, you must be individually assessed by your own physician(s), and your treatment should be based on your specific circumstances and needs as well as on newer medical concepts, testing, and therapies that undoubtedly will come along after I was evaluated and treated.  I am not recommending any specific treatments for you as a patient, only mentioning what did and did not seem to work for me in my own possibly unique circumstances and at the time I was treated.

Possible Early Symptoms and Signs of Lymphoma (Prior to 2004)

Left Upper Quadrant Abdominal Pain: I saw my rheumatologist Dr. Mease and subsequently a gastroenterologist Dr. D for unexplained pain in the left upper quadrant of the abdomen and temporary colonic blockage in December 1999 and January 2000.  Blood tests including amylase (for the pancreas) were normal, as was an abdominal ultrasound, colonoscopy, and barium studies of the upper GI tract and small intestine.  A CT of the abdomen on January 7, 2000 was read as normal.  However, in retrospect (and comparing to the later CTs of the abdomen dated November 30, 2004 and January 13, 2005), it already demonstrated a wisp of unexpected tissue-density material in the mesenteric fat.  This was non-calcified, and was accompanied by somewhat prominent regional lymph nodes, consistent with very early manifestations of lymphoma.  The diagnosis in 2000 was uncertain but Dr. D concluded I probably had a "splenic flexure syndrome".  The symptoms essentially resolved after a few days.  

I had earlier developed gastroesophageal reflux (by 1998), but this did not seem to be related. 

After 2000, I continued to experience occasional unexplained sharp pains in the left upper quadrant of the abdomen, but we did not further pursue this prior to my surgery.

Epigastric Abdominal Pain: I returned to the gastroenterologist Dr. D in 2002 with a complaint of burning upper mid-abdominal (epigastric) pain at night, which seemed to be like peptic ulcer pain and which seemed to respond well to oral antacids.  He placed me on Nexium 40 mg/day.  Nexium is a "proton pump inhibitor" or PPI, a drug which blocks the secretion of gastric acid.  This was prescribed partly for the possible ulcer symptoms and partly because of my ongoing gastroesophageal reflux, which can lead to reflux esophagitis.  I did not have further episodes of ulcer-like or epigastric pain, but remained on the Nexium until 2009.  I tried going off Nexium in 2009 but developed mild epigastric and lower thoracic pain consistent with mild reflux esophagitis.  I therefore elected to resume taking a PPI, namely pantoprazole 20 mg daily (a PPI reputed to have fewer drug interactions).

Right Posterior Chest Mass: A pleural and parenchymal partially calcified mass or thickening in the posterior right lung base was noted as an incidental finding on electron beam tomography of the heart in November 2002.  (This exam was intended to screen for coronary artery disease by displaying and quantitating the amount of calcium in the coronary arteries.)  The lesion was further evaluated by CT of the thorax in December 2002 and by a PET (positron emission tomography) scan in January 2003.  It was concluded that the lesion did not take up enough glucose to suggest an active tumor, and was therefore likely to be a scar (perhaps from my previous TB, or exposure to the common fungus histoplasmosis while growing up in Texas).  In my opinion, the precise nature of this lesion remained uncertain, but it has remained quite stable in appearance through 2009.

Left Mid-Abdominal Lesion on PET: However, the PET in 2003 also showed an incidental finding of focally increased uptake in the left mid-abdomen.  At the time, this was considered merely normal tracer uptake in bowel, but some other cause could not be excluded.  This seemed at the time to be a "red herring" since our interest was in the chest, and it was not further pursued at the time.  (In retrospect, the uptake was clearly caused by the lymphoma, which became more apparent the following year.)

Small Bowel Obstruction and Diagnosis of Follicular Lymphoma

I developed rapid onset of abdominal pain on the night of November 28, 2004, and later loose stools and vomiting.  By 2 AM of November 29, I was writhing in severe pain and Becky took me in to our nearest major hospital, the ER of the UW Medical Center (formerly called the University Hospital).  The following day, I underwent CT scan of the abdomen and pelvis.  In addition to signs of obvious obstruction of the small intestine, it showed a lobulated dominant abdominal tumor mass measuring 7.2 x 3.2 cm, located in the left small bowel mesentery, and exhibiting heterogeneous dense calcification.  There were also multiple regional enlarged mesenteric lymph nodes (lymphadenopathy) consistent (in retrospect) with additional foci of tumor in these nodes.  My attending internist, Dr. Paul Sutton, advised me that the previous abdominal CT scan in 2000 also showed lymphadenopathy, though much less prominent, so that the tumor foci were likely slow-growing and present for at least 4 years (and quite possibly longer).  The then current 2004 CT, read by old friends and colleagues Drs. Patrick Freeny and William Bush, also showed a small 1 cm calcific mass in the right mesentery area and some regional distortion & retraction in the mesentery apparently due to inflammatory changes related to the lymphoma.  Clearly, this tumor was not confined to a single focus even in the abdomen. The dominant mass was unusual in appearance, and it was initially suspected to be a carcinoid tumor prior to the surgery.

Tests for carcinoid tumor and for pancreatitis were normal.  My surgeon, Dr. Brant Oelschlager, tried a trial of conservative therapy with nasogastric suction to seek spontaneous resolution of the obstruction, but this failed to help.  I was taken to surgery on December 1, the third hospital day, at which time Dr. Oelschlager and assistants found several adhesive bands in the lower right abdomen causing the small bowel obstruction, far removed from the dominant left-sided tumor mass.  The dominant mass in the mesentery was felt to be unresectable (i.e., it could not safely be removed due to its position), and was merely biopsied and cultured.  The mesentery was thickened apparently from regional inflammation and edema.  (It was later suggested that the retraction, caused by the tumor inflammation and fibrosis, combined with the pre-existing adhesions, tipped the delicate balance in favor of obstruction—therefore the tumor and the small bowel obstruction were indeed related though by force-at-a-distance.)

During the hospitalization, I intermittently developed PAF, more frequently than my usual.  My hospital cardiologists Drs. S. and R. were at odds with me during this admission, refused to believe that I had earlier been in normal rhythm or could reliably tell the difference, refused to contact my much respected outside cardiologist Dr. D, and in my opinion made some unwise decisions regarding use of medications.  Postoperatively, I developed atrial fibrillation or flutter with a rapid ventricular response, a worrisome arrhythmia.  Various medication adjustments were made, and at one point the cardiologists tried Ativan 2 mg ostensibly to calm my heart down, but this induced a bizarre state of delirium and hallucinations—I had to be watched continuously through a long and restless night by an attendant.

I was slow to be able to resume eating, and other hospital complications ensued, including a wound hematoma that became infected and required opening the wound, as well as septicemia caused by a multiple-drug-resistant staphylococcus ("MRSA") possibly related to an infected IV catheter—this  was treated with IV Vancomycin and later oral Bactrim.  Echocardiogram fortunately showed no endocarditis. 

The preliminary pathology report from the biopsies was of a low-grade follicular lymphoma, a type of non-Hodgkin's lymphoma (NHL), presumably present at least since the abdominal CT in December 2000.  Flow cytometry (on a lymph node) was reported as showing a clonal B-cell population comprising 81% of leukocytes, and expressing CD45, CD10, CD19, CD38, and CD20 with kappa light chain restriction without significant CD5. The immunophenotype suggested a follicular center origin consistent with follicular lymphoma.  The final pathology report was a mesenteric mass and mesenteric lymph node both showing Malignant B-cell lymphoma, follicular center type, grade I (a type of non-Hodgkin's lymphoma).  Cultures from the mass grew out no bacterial of fungal organisms.

No specific therapy was initiated for this slow-growing tumor while I was in the hospital, though future treatment options were discussed.  I was anticoagulated for the recurring PAF, and, when I could take pills by mouth, restarted on sotalol and digoxin along with the diltiazem for the atrial fibrillation.

I was finally discharged December 14 on hospital day 16, lighter ultimately by 20 pounds and very weak and traumatized from the protracted hospital experience including the complications, worried about my future (including a new paucity of available veins), but glad to have survived what, without surgery, would surely have been a fatal attack of bowel obstruction.  I was grateful for the generally excellent care I had been given by the nurses, housestaff, and most of the attending physicians during this admission, though I wish I had been spared the postoperative MRSA infection.  I was also pleased to have become better acquainted with the many improvements in my alma mater, the UW Medical Center.  I was especially pleased to have provided an opportunity for my daughter Wendy, by then a mature first year resident in internal medicine, to display her growing professionalism and equanimity in helping me interface with the myriad health care providers during a most difficult and drug-clouded period.  In fact, my wife, who selflessly stayed with me night and day, and both daughters were extremely helpful to me throughout this admission, and I will always be most grateful for their loving attention.  

Ironically, my hospitalization and new cancer diagnosis provided other silver linings.  I was visited in the hospital or soon after discharge by many caring old friends, some of whom I had not seen in many moons, and my new circumstances also seemed to improve my relations with a long-estranged close relative.  I was also gratified to find that some persons, including a number of former physician colleagues—who a few years earlier had seemed to withdraw from my life (perhaps because I was under a cloud of doubt and skepticism pertaining to my chronic illness CFS / UAS)—now seemed to find me more respectable and acceptable in their eyes. 

Risk Factors for Non-Hodgkin's Lymphoma (NHL)

It is reasonable to wonder, what causes a lymphoma such as I have?  Although the etiology of lymphoma is not known, and many patients have no apparent explanation, there are a number of conditions which have been mentioned in the medical literature as possibly being linked to or predisposing to NHL (some of the items listed below predispose to a more specific type of NHL).  The following list of risk factors, compiled in 2005 from various sources, is probably not complete, and I do not know how well established each item is as a risk factor for NHL:

In my own case, it would appear that the category of systemic autoimmune disorder and particularly Sjögren's Syndrome is most likely related to my NHL.  As an idle speculation to tuck away pending more definitive medical knowledge, I have wondered if immune disorders that appeared in some of my close family members might have had some indirect relationship to my immune system disorders UAS and lymphoma—these consisted of autoimmune iridocyclits (1990), neurodermatis (1991), and even feline lymphoma/leukemia (in our cat in 1991, though this infection is currently thought to not be non-transmissible to humans). 

Chemotherapy and Attitude Adjustment in 2005

My recovery out of the hospital was rather slow, and it took several months for me to regain the twenty pounds I had lost (perhaps I should have kept them off) as well as most of my former strength.  I was grateful to have the early support of several friends, some with past experiences with lymphoma—either personally as patients or as a treating physician.  I continued with anticoagulation on Coumadin or warfarin, which acquainted me with the excellent clinical pharmacists running the Anticoagulation Clinic at the UW's Roosevelt Clinic (and caused a severe bleeding complication in December 2006).

My main hospital attending physician, Dr. Sutton, agreed to continue on as my primary care physician, and I saw him several times after the hospitalization.  My rheumatologist Dr. Overman, who kindly visited me in the hospital, was very supportive upon my discharge, at a time when I was quite anxious about what to do, and I used him to help me plan my future actions.  I considered continuing my care with a medical oncologist Dr. G at the Seattle Cancer Care Alliance and met with him in late December 2004.  However, there was a snafu on scheduling this visit, and in addition he informed me that he would be available to see me only on two half-days per week.  I wanted to have greater continuity than this, and to be cared for by the most smoothly oiled oncology machine possible.  With the invaluable counsel and facilitation of my cardiologist Dr. D, I therefore arranged to be cared for at the Swedish Cancer Institute by Dr. Henry G. "Hank" Kaplan MD, a decision I have not regretted.

After consulting with my surgeon and getting a second opinion from his own pathologists, as well as repeating the CT and PET, Dr. Kaplan was able to satisfy himself that the tumor was truly as billed, and that it probably did have something to do with the bowel obstruction.  The positive findings on the January 2005 CT/PET were:

My only clearly tumor-related symptoms were occasional twinges of left upper quadrant and mid-abdominal pain, which I had experienced for several years.  Dr. Kaplan advised me that prognosis with this tumor is quite variable and hard to predict, though it seemed to me that the central abdominal location and inability to use radiation therapy were worrisome.  One article (cited below) placed me in the "Intermediate risk group" (assuming Stage III and age > 60) and set mine at a probability of about 78% for 5-year survival and 50% for 10-year survival from the time of diagnosis (based on standard therapies available during the time these statistics were gathered). 

Dr. Kaplan discussed the many available treatment options (reflecting the uncertainty in 2005 on what was the best course of action).  He finally recommended and I consented to an "induction" series of IV treatments with Rituximab (a synthetic monoclonal antibody which is billed at about $16,000 per dose), Cytoxan (Cyclophosphamide), Vincristine (Oncovin), and oral Decadron (which was substituted for Prednisone)—this regimen goes by the acronym "CVP-R" or "R-CVP".

I received the first full R-CVP treatment on February 10 (after loading doses of Rituximab on February 2 and February 9).  However, this treatment produced such severe weakness in me that we feared we were seeing the well-known but infrequent neurological toxicity of Vincristine, and Vincristine was not further given.  I went on to have 5 more cycles in 2005 of Rituximab, Cytoxan, and Decadron ("R-CP"), the last being June 29, 2005.  Thanks to the benefit of the newer-generation antinausea drug Kytril, I had dysphoria (an unpleasant feeling) and some discomfort but little nausea on the days of infusion.  However, this multi-drug regimen continued to produce: (1) marked exacerbations of my CFS-like fatigue and weakness, lasting from about day 4 to about day 14 post-infusion; (2) sores and pain in the corners of my mouth (cheilosis) and inside the mouth (oral mucositis, which Dr. Kaplan treated with oral L-glutamine); (3) a flareup of foot pain (possibly gout, gradually resolved); (4) leg and foot edema (possibly related to diltiazem); (5) reduction of the white blood cell count especially the lymphocytes (which are targeted by Rituximab); and some other side effects.  I seemed to verify what Dr. Kaplan had warned me about, that CFS patients often do not tolerate the treatments as well as other patients (and certainly I never improved in my CFS symptoms while receiving Rituximab).  Fortunately, my hair loss in 2005 was incomplete, and as there was plenty to start with, I did not end up bald.  My hair gradually grew back over several months after ceasing combined chemotherapy.  Though I did not become bald, I came to greatly admire the private and public persons who have helped to reduce the stigma and embarrassment of chemotherapy-induced baldness.

After completing the "induction" phase of these six toxic treatments, Dr. Kaplan repeated the CT scans of the chest, abdomen, and pelvis in July 2005.  Compared to the pretreatment CT in January 2005, the dominant left-sided tumor mass had shrunk a little, the other presumably tumor-laden enlarged mesenteric lymph nodes appeared slightly less prominent, and some of the inflammatory changes in the mesenteric fat appeared diminished.  However, I also had a CT scan in April 2005 after receiving three treatments, and there had been little further improvement between April and July.  (Selected images comparing some of the images from several of these CT and PET scans in 2005 and 2006 may be seen here.)  Dr. Kaplan, influenced as well by the substantial side effects I was experiencing, concluded that we had reached "the point of diminishing returns" for the full treatments with R-CP, and he advised that I switch to a "maintenance" program consisting solely of IV Rituximab given once every 8 weeks.  I had the first maintenance infusion solely of Rituximab on September 7, 2005.

Throughout this process, my loving wife stayed by my side to help me through what many persons find to be a terribly stressful and anxiety-provoking experience.  The staff at the Swedish Cancer Institute and Dr. Kaplan have all been great to deal with, and I have been quite satisfied with my care.  I regret that my tumor was not found to be amenable to radiation therapy or surgical resection, and that it did not more dramatically shrink in size under treatment, but at least it did not obviously grow further in 2005.  I continued in 2005 to have occasional abdominal pains which seemed to be tumor-related, and which diminished during the induction phase of intensive chemotherapy.  

The bounty of our great Mother Earth September 2005
The bounty of our great Mother Earth
September 2005

Facing such a daunting tumor experience, including the process of chemotherapy and all that attends it, took a lot of my time and available energy, and required me to draw on my deepest resources of strength and fortitude.  As my physician friend Bill Warren told me, undergoing cancer treatment can be a full-time job, and indeed, in the first year of chemotherapy (2005) I seemed to accomplish less in other spheres than I used to. 

I personified my worthy adversary, naming him "Lem the lymphoma", or just Lem for short.  He is very much like an uninvited guest who refuses to leave, and in fact I am advised that he will be with me for the rest of my life.  I have also tried to find humor where I can, to avoid unnecessary stress (including needlessly stressful people), to keep as physically and intellectually active as possible, to keep my attitude upbeat and positive, and to continue working as diligently as I can on a variety of satisfying projects such as tending our P-Patch vegetable garden, nurturing my family members, and writing these memoirs.

Progress in 2006 – 2012

Despite the mild state of immunosuppression from chemotherapy, I managed at the end of December 2005 to undergo arthroscopic knee surgery for a torn cartilage (meniscus) with a rapid and incident-free recovery.  

I continued in 2006 to receive Rituximab maintenance chemotherapy IV infusions at 8 week intervals, again without significant side effects, and found this a tolerable if tedious experience involving long days at the clinic.  I suspect that the immunosuppression caused by Rituximab contributed to an eruption of suspected scalp shingles (herpes zoster) in 2006, and a right leg infection in 2007.  The last dose of Rituximab that I have so far received was administered in April 2007.  My abdominal pain symptoms, such as might be caused by the underlying tumor, were mostly transient and rather modest in 2006, and these symptoms essentially resolved by 2007 or 2008.

A follow-up CT scan in February 2006 showed no further decrease in the size of the dominant left-sided abdominal tumor or "satellite" nodes, but certainly no enlargement since treatment began in 2005.  The right thorax lesion may have shrunk a little following therapy, comparing with pre-treatment images in early 2005, increasing the chances that this was lymphoma all along (despite the low uptake of glucose on PET scans found in January 2003 and January 2005).  If so, this would simply help to confirm that the PET scan is not immune to false negatives.  As I understand things, my prognosis is only a little worse if the chest lesion is lymphoma, compared to having lymphoma confined solely to the abdomen. 

Writing now in 2014, I have survived more than 9 years post-diagnosis, and 13 years since the first CT evidence of abdominal tumor that can in retrospect be identified.  It remains a little disappointing and disconcerting that, on annual follow-up CT scans up to the most recent in January 2010, Lem has not further shrunk in size.  Instead he just sits there, "sulking" as I say, or "indolent" as Dr. Kaplan describes him.  But looking on the bright side, Lem has not grown since treatment began in 2005.  Perhaps I should just declare victory—as George Aiken advocated for the Vietnam War—and stop worrying about it.

Acknowledgements

I have already sung my praise for family and friends above.  But let me say again how deeply grateful I am for the many family members, friends, neighbors, and medical professionals who have been supportive to me as I have faced this challenge, and who have helped me to continue to cherish the precious gift of life. 

References

(1) P Solal-Céligny, et al.  "Follicular Lymphoma International Prognostic Index."  Blood 104:1258, 1 September 2004.