Doing the Numbers

Cancer is a numbers game.

This can be both good or bad.  The good news is that everything cancer is studied and published and this information is now available to all.  The bad news it that as a patient sometimes you just feel like a number.

The reality is that we are all just numbers, and this can work against the patient who is seeking the best outcome - in other words, it's not always in the best interest of "the numbers" to stray from the standard protocols.

After "failing" first line treatment, and with no response to Brentuximab,  I started "doing the numbers" on the recommendation for a stem cell transplant.  And the numbers are telling me that I'm going to have to work really hard to beat the odds.


According to Hodgkin lymphoma: 2016 update on diagnosis, risk-stratification, and management.

Management of relapsed/refractory disease: High-dose chemotherapy (HDCT) followed by an autologous stem cell transplant (ASCT) is the standard of care for most patients who relapse following initial therapy. For patients who fail HDCT with ASCT, brentuximab vedotin, PD-1 blockade, nonmyeloablative allogeneic transplant or participation in a clinical trial should be considered.

SEOM clinical guidelines for the treatment of Hodgkin's lymphoma.

In general, the new "immunotherapy" drugs are reserved for those who fail stem cell transplant (ASCT)

According to the journal article, Salvage Therapy in Hodgkin's Lymphoma:

The majority of patients with Hodgkin's lymphoma (HL) are cured with first-line therapy; however, approximately 15%–20% of patients with stage I–II HL and 35%–40% of patients with stage III–IV HL and risk factors relapse after first-line therapy

The current standard of care for patients with relapsed or refractory HL results in cure approximately 50% of the time. 

Multiple single-arm studies incorporating both relapsed and refractory HL patients have demonstrated that a salvage approach incorporating HDCT/ASCT results in durable PFS and OS rates in the range of 40%–50% and 50%–60%, respectively [3, 6, 23–26]. Importantly, patients with refractory disease generally do worse, with durable PFS and OS rates in the range of 15%–32% and 26%–36%, respectively [7, 8, 23, 27, 28].

In addition to refractoriness to initial chemotherapy, several other factors have been identified in the relapsed/refractory HL setting that predict a worse prognosis. 

Brice et al. [31] used two adverse prognostic factors (end-of-treatment to relapse interval ≤12 months and extranodal relapse) to predict outcome in a French population of patients receiving ASCT. Patients with zero, one, or two of these factors had 4-year OS rates of 93%, 59%, and 43%, respectively.
In a prospective study, Moskowitz et al. [15] demonstrated that B symptoms, extranodal disease, and time to relapse <12 months influenced outcome after ASCT. Patients with none or one of these factors had a 43-month EFS rate of 83%, compared with 27% and 10% for patients with two or three factors, respectively.

These studies demonstrate that it is possible to use distinct clinical features at relapse to make general predictions about the likelihood of success with HDCT/ASCT.

Patients with refractory disease or poor-risk relapse are unlikely to do well with this modality and should be considered for other options.  

Relapse after ASCT generally portends a poor prognosis, with a median survival duration in the range of 24 months



This data suggests that in my case, with immediate relapse/refractory disease, advanced stage with B symptoms, bone marrow involvement, and extra nodal disease (spleen, etc) I am unlikely to do well with autologous stem cell transplant.


More research suggests that; Patients with classical Hodgkin lymphoma experiencing disease progression after treatment with brentuximab vedotin have poor outcomes.

Optimal management of patients with HL requires an accurate diagnosis and careful staging of the disease. Identification of poor prognostic features then allows for risk-adapted therapy to potentially increase the likelihood of cure and minimize toxicity. Future directions to further improve the outcome of patients with HL will include incorporating into frontline therapy those agents that are effective in the relapsed setting.




A recent article in the New York Times provides some hope.


For decades, he explained, oncologists had treated relapsed Hodgkin’s lymphoma in a standard manner. “There were limited options,” O’Connor said. “We gave some patients more chemotherapy, with higher doses and more toxic drugs, hoping for a response. For some, we tried to cure the disease using bone-marrow transplantation.” But the failure rate was high: About 30 percent of patients didn’t respond, and half of them died.

Then a year or two ago, he tried something new. He began to use immunological therapy to treat relapsed, refractory Hodgkin’s lymphoma. Immunological therapies come in various forms. There are antibodies: missile-like proteins, made by our own immune systems, that are designed to attack and destroy foreign microbes (antibodies can also be made artificially through genetic engineering, armed with toxins and used as “drugs” to kill cancer cells). And there are drugs that incite a patient’s own immune system to recognize and kill tumor cells, a mode of treatment that lay fallow for decades before being revived. O’Connor used both therapies and found that they worked in patients with Hodgkin’s disease. “We began to see spectacular responses,” he said.

Doing the numbers, and asking the questions…

Seeking a second opinion, and hoping to find a Dr that able to step out of the box and apply a "risk-adapted therapy to potentially increase the likelihood of cure and minimize toxicity."

Otherwise, I'm going to end up a number...




References:

Hodgkin lymphoma: 2016 update on diagnosis, risk-stratification, and management.

SEOM clinical guidelines for the treatment of Hodgkin's lymphoma.

 Salvage Therapy in Hodgkin's Lymphoma
    Jason H. Mendler and Jonathan W. Friedberg, James P. Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, USA. First published online in THE ONCOLOGIST Express on April 2, 2009.
 
Patients with classical Hodgkin lymphoma experiencing disease progression after treatment with brentuximab vedotin have poor outcomes.


 The Improvisational Oncologist, New York Times magazine, May 15, 2015

…or False Hope?

Seems the power of positive thought does not always work…  This is the latest PET scan, 6 month followup to first line treatment for Hodgkins lymphoma.  The spot in my chest has grown and new spots have emerged, signifying recurrence.

Unfortunately this means I will need more treatment to try to cure this "most curable" cancer.  We visited City of Hope last week, and the doctor seems good - she actually gave me options!

I was not ready to accept the standard protocol, ICE, which requires three day inpatient administration over 4 months with many side effects. This dr has offered a couple of trials on newer therapies.

The new drugs she offered are immuno type therapies, and listed on the website http://www.cancerresearch.org/cancer-immunotherapy/impacting-all-cancers/lymphoma

The targeted drug brentuximab vedotin (Adcetris®)—a monoclonal antibody linked to a chemotherapy drug—is approved to treat Hodgkin lymphoma in patients whose disease has failed to respond to other treatment and, as of August 2015, to prevent relapse following a stem cell transplant. 

Nivolumab (Opdivo®) is an anti-PD-1 antibody made by Bristol-Myers Squibb (BMS). Nivolumab was granted FDA “Breakthrough Therapy” designation status for Hodgkin lymphoma based on a cohort of patients in a phase Ib trial testing nivolumab alone or with ipilimumab (see below) for blood cancers (NCT01592370). In that trial, 87% (20/23) of Hodgkin lymphoma patients responded to the treatment. - 

so salvage chemo will be either Brentuximab or a combo of the two, either way much less side effects than ICE and much easier to administer (IV drip, no port)

unfortunately stem cell transplant is 3 weeks in the hospital and seems daunting - but I guess people get through it.

--------

So let's consider the past 6 months a brief "vacation" from this little adventure.  I will try to post some of the great things I have been able to do during this "vacation," with big hopes for more in the future...


---------

More on Brentuximab:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3646316/

The ADC brentuximab vedotin was associated with manageable toxicity and induced objective responses in 75% of patients with relapsed or refractory HL after auto-SCT. Durable CRs approaching 2 years were observed, supporting study in earlier lines of therapy.

The ORR was 75% with complete remission (CR) in 34% of patients. The median progression-free survival time for all patients was 5.6 months, and the median duration of response for those in CR was 20.5 months. After a median observation time of more than 1.5 years, 31 patients were alive and free of documented progressive disease. The most common treatment-related adverse events were peripheral sensory neuropathy, nausea, fatigue, neutropenia, and diarrhea.

More on Hodgkins lymphoma treatment:  http://patient.info/doctor/hodgkins-lymphoma-pro

Primary resistant and relapsed classical Hodgkin's lymphoma^[7]

• Repeat biopsy is recommended for patients thought to have relapsed, and should be considered in those who have residual lesions after treatment. PET/CT is the preferred restaging modality after salvage therapy (high-dose chemotherapy).
• Autologous stem cell transplantation (ASCT) is the standard treatment for patients with primary resistant disease or with relapsed disease who achieve an adequate response to salvage chemotherapy. ASCT is not recommended in those failing to achieve an adequate response.
• The choice of a first-line salvage regime in patients eligible for ASCT should be based on individual patient factors. Regimens containing stem cell toxic agents (eg, carmustine and melphalan) should be avoided if possible until stem cells have been successfully collected and cryopreserved if ASCT is planned.

False Positive on PET scan?

Last week I had the followup CT/PET scan. This was technically 5 weeks after the conclusion of the 6th cycle of chemotherapy. (yes, I made it though 6 months of treatment!)

Given the encouraging results from the interim PET scan after 2 cycles, we were expecting a clear scan.  Unfortunately the Dr revealed that there is a "spot" in my chest that is of concern.  He did not say much more about what it may or may not be… of course leaving us fearing the worst.

Aug 19, 2015: PET scan shows bright "spot" in chest

First of all, one of the risks following chemotherapy is a "second cancer," and if this happens the prognosis is much worse than that for the original Hodgkin's lymphoma.

More than 80% of patients with Hodgkin’s disease can be cured with first-line treatment, depending on their risk factor profile. Long-term survivors are at risk for second malignancy, which are often fatal. Solid tumors, leukemia and non-Hodgkin’s lymphoma (NHL) have all been reported.   [1]


However;

PET scans are imperfect with many false-negative and false-positive results. The reasons for false-negative PET scans include technical problems, uncontrolled diabetes, and variability of FDG avidity among lymphoma subtypes. The lengthy list of causes of false positives, which may occur in one quarter of patients, includes inflammation, infection, tumor necrosis, and scanning too soon after chemotherapy or radiotherapy…

Only one third of patients with an inconclusive PET had a suspicious CT scan with a biopsy-proven 33% false-positive rate. For patients with a positive PET and a negative CT, the false-positive rate was 42%. FDG-PET identified unsuspected early relapse in only 10% of patients with Hodgkin's lymphoma, which was assisted by clinical risk and CT findings.  [2]


The CT looked clear, so it would seem that the odds of a "false positive" are there…

Digging further, I learned about;

...a phenomenon called thymic rebound (also called benign thymic hyperplasia), which is defined as thymic regrowth 50% greater than baseline volume. Benign thymic hyperplasia occurs mainly after treatment with chemotherapy, but infrequent case reports describe its occurrence after periods of stress in cancer patients off chemotherapy as well. Chemotherapy causes thymic atrophy and a decrease in average volume of 33%, and regrowth occurs after treatment completion.

The literature in adults is scarce, but it may occur in about 25% of adult chemotherapy patients. Benign thymic hyperplasia in adults has been documented in early stage breast cancer, lymphoma and uterine leiomyosarcoma. It usually occurs within the first year after chemotherapy, but it can present as many as five years later. In one case series, 31 of 134 PET scans (23.1%) for lymphoma showing focal flurodeoxyglucose uptake were diagnosed as nontumoral radiotracer uptake. Five of the 31 false-positive PET scans were related to thymic hyperplasia.   [3]

The "spot" on my scan is in the area of the thymus, slightly above and in front of the heart. Given the published information I feel a lot better about things.

The thymus gland, despite containing glandular tissue and producing several hormones, is much more closely associated with the immune system than with the endocrine system. The thymus serves a vital role in the training and development of T-lymphocytes or T cells, an extremely important type of white blood cell. T cells defend the body from potentially deadly pathogens such as bacteria, viruses, and fungi.

The thymus is a soft, roughly triangular organ located in the mediastinum of the thoracic cavity anterior and superior to the heart and posterior to the sternum…. The function of the thymus is to receive immature T cells that are produced in the red bone marrow and train them into functional, mature T cells that attack only foreign cells. T cells first reside within the cortex of the thymus where they come in contact with epithelial cells presenting various antigens. The immature T cells that respond to the antigens corresponding to foreign cells are selected to survive, mature, and migrate to the medulla while the rest die via apoptosis and are cleaned up by macrophages. This process is known as positive selection.

Several hormones produced by the thymus promote the maturation of the T cells prior to their release into the bloodstream. The now mature T cells circulate through the body where they recognize and kill pathogens, activate B cells to produce antibodies, and store the memory of past infections.

Unlike most organs that grow until the age of maturity, the thymus enlarges throughout childhood but slowly shrinks from the onset of puberty and throughout adulthood. As the thymus shrinks, its tissues are replaced by adipose tissue. The shrinking is due to the reduced role of the thyroid in adulthood – the immune system produces most of its T cells during childhood and requires very few new T cells after puberty. [4]



Is this a case of thymic rebound, thus a "false positive?"

I have been referred to a specialist, so we will learn more…


Update:

On Sept 1 we travelled down to City of Hope in Pasadena.  After much paperwork, bloodwork, and hard work getting a CD of my scans, the Dr more or less confirmed my theory.  In our conversation she mentioned the Thymus and confirmed that this could be what we are seeing.  Multiple spots would be more of a concern.  She also said I probably wouldn't be feeling so good, so while nothing is certain, I consider it a positive prognosis.

Next Steps: port removal and re-scan in 90 days.  Biopsy to follow if needed.


REFERENCES:

1. A positive PET/CT after treatment for Hodgkin’s lymphoma, Carrie Wasserman, MD; Munir Ghesani, MD;  HemOnc Today, July 10, 2008.

2. The Case Against Heavy PETing, Bruce Cheson, American Society of Clinical Oncology, 2009.

3. Enlarging mediastinum on PET/CT after treatment for Hodgkin’s lymphoma,  Carrie Wasserman, MD; Frank Colella, MD; Munir Ghesani, MD;  HemOnc Today, May 10, 2008.

4. Thymus Gland - Anatomy Pictures and Information, Innerbody.com

the Cost of Lyme Disease

A recent headline states,

 A 'hidden epidemic' in the US has ballooned into a public-health fiasco — and no solutions are in sight.

According to Business Insider,
             "A recent study goes beyond human suffering inflicted by Lyme disease to estimate the monetary cost of this "hidden epidemic," as some call it. Researchers sifted through the health-insurance claims of 47 million people and discovered a staggering financial burden incurred by tens of thousands treated for Lyme disease — possibly more than $1 billion a year in the US alone."

These costs could potentially be avoided by public education and, when presented with a tick bite, proper first treatment of at least 3-4 weeks of antibiotics. Unfortunately, most medical doctors in Ventura County will fiercely state that there is no Lyme Disease here and, when presented with a potential lyme case will, at best, prescribe a minimum antibiotic protocol of 2 weeks.  This may be due to the fact that the minimal tick testing done by the Public Health Department did not find Lyme spirochetes.

I spent a lot of money out of pocket while treating Lyme.  Insurance also spent a lot…  I haven't tried to add it up, but antibiotic prescriptions, a total of 5 different antibiotics over a nine month period, must have totaled many thousands of dollars.  And then the costs of diagnosing, treating, and tracking cancer for the rest of my life…  hundreds of thousands of dollars!

Lyme disease is now the most common vector born disease in the United States and Europe, with AT LEAST 300,000 new cases in the US each year.    Adding the lost productivity of those who are misdiagnosed and untreated for this debilitating infection, the societal costs of this disease are astronomical!

Can chemotherapy kill Lyme?

Of course, as I prepare to complete the ABVD chemotherapy for Hodgkins, the question that remains is

Can chemotherapy kill Lyme?

If so, I may be "lucky" to have found a cure for my Lyme infection.  Or, as they say, "Killing two birds with one stone."

Coincidentally I was sent an article today titled "Researchers' discovery may explain difficulty in treating Lyme disease." In the paper published in the Journal of the American Society for Microbiology, the researchers note that an anti-cancer drug completely eradicated lyme "persister cells" in a single dose.  It is these persister cells that has made antibiotics, even combination treatments, ineffective against the lyme bacteria.

So perhaps there's hope that coming out of this I shall be both cancer-free and lyme-free…

Reference:

Borrelia burgdorferi, the causative agent of Lyme disease, forms drug-tolerant persister cells. Bijaya Sharma1, Autumn V. Brown1, Nicole E. Matluck1, Linden T. Hu2 and Kim Lewis1*
1 Department of Biology, Northeastern University, Boston, Massachusetts, USA;
2 Department of Medicine, Division of Geographic Medicine and Infectious Diseases,
Tufts Medical Center, Boston, Massachusetts, USA.

Lyme to Lymphoma?

Many people, upon hearing my cancer diagnosis, have said, "Oh, so you never had Lyme?"  Indeed, I was so sick for so long it's hard to imagine that a tick bite could do that…

And of course, I think it's common for those diagnosed with cancer to wonder how it happened.  In general there are so many factors that each individual is exposed to in a lifetime it's hard to point at a single cause.  But this all started with a little tick bite!

So with that I felt compelled to ask the question,

Can Lyme disease cause cancer?

On this, opinions start to fly.  The one thing I know for sure is I got bit by a tick and ended up on chemotherapy.  Perfectly healthy one day, almost dead a year and a half later.

There are only 3 possible answers to this question:

1)  Coincidence - the tick bite happened at the same time as cancer, the two are not related
2)  Infection triggered cancer - in my case the lymph was involved from the start
3)  Disabled immune response allowed the cancer to grow

1) Coincidence 

Really?  I suppose bad luck happens, but twice at the same time? I see this as an easy out for an oncologist who specializes in treating cancer but has no need to understand what causes it…  or those who don't believe in Lyme disease.

2) Infection triggered cancer

a. In my case the Lyme infection entered the lymphatic system right from the start.  Almost three months after the initial bite and 2 weeks of antibiotics, I felt a swollen lymph gland under my arm. This is consistent with recent research that reveals that the bacteria that cause Lyme disease appear to hide out in the lymph nodes.  Although I was unknowingly having progressive neurological symptoms, this was the first sign that something was wrong. Then, following the first 6 months of the triple antibiotic treatment, the lymph nodes in my neck became visibly enlarged. The nodes continued to grow (along with severe weight loss) until my lymphoma diagnosis 9 months later.

b. Scientists know that certain viruses can trigger cancers.  But can a bacterial infection trigger cancer?  It turns out that there are at least two examples of Bacteria that can lead to cancer:

• Helicobacter pylori         =>   Stomach cancer 
• Chlamydia trachomatis   =>   Cervical cancer

In the latter example,"studies have not shown that chlamydia itself causes cancer, but it might work with HPV in a way that promotes cancer growth."  

3) Disabled immune response

"Having a compromised immune system, such as from HIV/AIDS or from having an organ transplant requiring medications to suppress the immune response, increases the risk of Hodgkin's lymphoma."

- Mayo Clinic 

Throughout my illness it was clear that my immune and digestive systems were compromised. This is common in Lyme patients and happens for two reasons:

a. Lyme specifically acts to disable the immune system. This often results in autoimmune conditions such as chronic fatigue, fibromyalgia, and often leading to other more serious conditions like MS.

A recent study from UC Davis reveals how Lyme disease subverts the immune system;

The bacteria initially trigger a strong immune response in an infected animal, but findings from this study indicate that the bacteria soon cause structural abnormalities in “germinal centers” — sites in lymph nodes and other lymph tissues that are key to producing a long-term protective immune response.  The researchers found that following Borrelia burgdorferi infection, this process even prevented induction of strong immune responses to an influenza infection. 

b. Lyme treatment usually involves long-term antibiotic therapy - this may compound the Lyme's impact on immune function by killing off the "good bugs" in the digestive tract.  Emerging science is showing that the gut "microbiome" is critical to a healthy immune system.   (More on this later)

Examples of immune disorder and cancer

A good place to look for the connections between immune deficiency and cancer is HIV/AIDS.  According to cancer.org:

"...some types of cancer occur so often in people with AIDS that they are considered AIDS-defining conditions – that is, their presence in a person infected with HIV is a clear sign that full-blown AIDS has developed."

The cancers that define a person with HIV as having AIDS include:

• Kaposi sarcoma
• Non-Hodgkin lymphoma (especially primary central nervous system lymphoma)
• Invasive cervical cancer

"Some other cancers are also more common in people with HIV or AIDS than people who are not infected, but the reasons for the increased risk aren’t clear. It may be that some of these cancers are able to develop and grow more quickly because of a weakened immune system brought on by the infection itself."

Hodgkins lymphoma is among those other cancers listed as more likely to develop in people with HIV than in people who are not infected. In these cases:

Some of these cancers have been linked to infections with different viruses. These viruses can cause cancer in people with and without HIV, but the risk might be higher in people with HIV because their immune systems are less able to control the viral growth. For example, anal cancer and some mouth and throat cancers are linked to infection with HPV, the same virus that causes cervical cancer. Liver cancer is known to be more common in people infected with the hepatitis B or C viruses. Some types of lymphoma have been linked with viral infections as well.

Hmm.  In my case, tests revealed that I may have a past infection with Epstein-Barr virus (EBV) (mononucleosis)  that has been linked to Hodgkins.

Documented links between Lyme and cancer

It turns out there are medical references discussing possible links between Lyme disease and various cancers.  According to cancer.org, primary cutaneous marginal-zone B-cell lymphoma is sometimes linked to an infection with Borrelia, the germ that causes Lyme disease.  And several medical references are listed on lymeneteurope.org linking Lyme Disease and Various Forms of Lymphoma.  More medical references are listed below.

Conclusions

So while all this information does not "prove" anything, there are several factors that could lead to the conclusion that a tick bite ultimately led to my cancer.  Lyme disease, immune suppression, antibiotics, Epstein-barr virus, and other documented cases...

It is possible that I had Hodgkins disease lurking in my system, and my healthy body was keeping it at bay.  Or the Lyme infection somehow triggered a malignancy in the lymphatic system. Or the Lyme infection re-activated EBVvirus and triggered Hodgkins that took advantage of a compromised immune system.  Certainly more research is warranted, as Lyme has become an epidemic around the world and in many cases can be life threatening.

I am not a doctor, nor am I qualified to make medical conclusions, but the evidence seems fairly clear.  Although I know coincidences can happen,

in this case I'm going with a combination of (2) and (3) above…

Yes, Lyme disease can result in cancer.

References:

From American Cancer Society website, cancer.org:

• Bacteria that can lead to cancer
• How are HIV and AIDS related to cancer?
• Types of lymphoma of the skin

From lymeneteurope:

• Lyme Disease and Various Forms of Lymphoma

From Mayo Clinic:

•  Hodgkins Risk Factors

From UC Davis:

Lyme disease subverts immune system, prevents future protection

Lyme disease bacteria take cover in lymph nodes

Reference: Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection
Rebecca A. Elsner, Christine J. Hastey, Kimberly J. Olsen, Nicole Baumgarth  Published: July 2, 2015DOI: 10.1371/journal.ppat.1004976


From PubMed: National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM):

1.	Borrelia and subsequent risk of solid tumors and hematologic malignancies in Sweden.
	Chang CM, Landgren O, Koshiol J, Björkholm M, Löve TJ, Kristinsson SY.
	Int J Cancer. 2012 Nov 1;131(9):2208-9. doi: 10.1002/ijc.27483. Epub 2012 Mar 15. No abstract available.
	PMID: 22322900 [PubMed - indexed for MEDLINE]
	Related citations

2.	Risk of malignancy associated with Lyme disease: still up in the air.
	Stricker RB, Johnson L.
	Int J Cancer. 2012 Dec 1;131(11):2717; author reply 2718. doi: 10.1002/ijc.27559. Epub 2012 Apr 16. No abstract available.
	PMID: 22461012 [PubMed - indexed for MEDLINE]
	Related citations

3.	Neuroborreliosis and CNS lymphoma: what is the nexus?
	Saggese CE, Cecotti L, Lazzarino de Lorenzo LG.
	Neurol Sci. 2013 Dec;34(12):2253-4. doi: 10.1007/s10072-013-1492-8. Epub 2013 Aug 10. No abstract available.
	PMID: 23934519 [PubMed - indexed for MEDLINE]
	Related citations

4.	Borrelia infection and risk of non-Hodgkin lymphoma.
	Schöllkopf C, Melbye M, Munksgaard L, Smedby KE, Rostgaard K, Glimelius B, Chang ET, Roos G, Hansen M, Adami HO, Hjalgrim H.
	Blood. 2008 Jun 15;111(12):5524-9. doi: 10.1182/blood-2007-08-109611. Epub 2008 Apr 18.
	PMID: 18424667 [PubMed - indexed for MEDLINE] Free PMC Article
	Related citations

5.	Borrelia burgdorferi-associated primary cutaneous marginal-zone B-cell lymphoma: a case report.
	Monari P, Farisoglio C, Calzavara Pinton PG.
	Dermatology. 2007;215(3):229-32.
	PMID: 17823520 [PubMed - indexed for MEDLINE]
	Related citations

6.	Lyme neuroborreliosis mimicking primary CNS lymphoma.
	Walther EU, Seelos K, Bise K, Mayer M, Straube A.
	Eur Neurol. 2004;51(1):43-5. Epub 2003 Nov 21. No abstract available.
	PMID: 14639029 [PubMed - indexed for MEDLINE]
	Related citations

7.	Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells.
	Hulínská D, Roubalová K, Schramlová J.
	Folia Biol (Praha). 2003;49(1):40-8.
	PMID: 12630667 [PubMed - indexed for MEDLINE]
	Related citations

8.	[Infectious causes of non-Hodgkin lymphomas].
	Munksgaard L, Hjalgrim H, Melbye M.
	Ugeskr Laeger. 2002 Dec 9;164(50):5927-32. Review. Danish.
	PMID: 12553112 [PubMed - indexed for MEDLINE]
	Related citations

9.	[Occurrence of angioimmunoblastic T-cell lymphoma six months after onset of Lyme disease].
	Hatanaka K, Miyagishima T, Kamata T, Nakagawa M, Miura Y, Arai S, Kishimoto A, Kamishima Y, Shibata M, Choi GH, Kudo M, Okabe M, Tsukamoto T, Miyamoto K.
	Rinsho Ketsueki. 2000 Dec;41(12):1273-6. Japanese.
	PMID: 11201153 [PubMed - indexed for MEDLINE]
	Related citations

10.	Exploring the causes of cutaneous B-cell lymphoma: we should learn from the Lyme disease experience.
	Naldi L, Minelli C.
	Dermatology. 2000;201(4):353-5.
	PMID: 11146350 [PubMed - indexed for MEDLINE]
	Related citations

11.	Incidence patterns of lyme disease and cutaneous B-cell non-Hodgkin's lymphoma in the United States.
	Munksgaard L, Frisch M, Melbye M, Hjalgrim H.
	Dermatology. 2000;201(4):351-2.
	PMID: 11146349 [PubMed - indexed for MEDLINE]
	Related citations

12.	Borrelia burgdorferi-associated cutaneous marginal zone lymphoma: a clinicopathological study of two cases illustrating the temporal progression of B. burgdorferi-associated B-cell proliferation in the skin.
	Goodlad JR, Davidson MM, Hollowood K, Batstone P, Ho-Yen DO.
	Histopathology. 2000 Dec;37(6):501-8.
	PMID: 11122431 [PubMed - indexed for MEDLINE]
	Related citations

13.	Positive serology for Lyme disease borrelias in primary cutaneous B-cell lymphoma: a study in 22 patients; is it a fortuitous finding?
	Jelić S, Filipović-Ljesković I.
	Hematol Oncol. 1999 Sep;17(3):107-16.
	PMID: 10641031 [PubMed - indexed for MEDLINE]
	Related citations

14.	Borrelial lymphocytoma--a historical case.
	Sonck CE, Viljanen M, Hirsimäki P, Söderström KO, Ekfors TO.
	APMIS. 1998 Oct;106(10):947-52.
	PMID: 9833696 [PubMed - indexed for MEDLINE]
	Related citations

15.	Borrelia burgdorferi-associated cutaneous B cell lymphoma: clinical and immunohistologic characterization of four cases.
	Garbe C, Stein H, Dienemann D, Orfanos CE.
	J Am Acad Dermatol. 1991 Apr;24(4):584-90.
	PMID: 2033136 [PubMed - indexed for MEDLINE]
	Related citations

… but chemo sucks

I couldn't get up on Sunday.  The overwhelming "chemo" feeling made me roll over and go back to sleep.  A few times.  Just hoping that I could "sleep it off."

As the imagery shows, chemotherapy for my Hodgkins lymphoma works…

        ...but chemo sucks.

I can say that, I am in the middle of treatment.  This is not "negative," just dealing with the reality.  And working through it all.

The reality is I can count on feeling really bad at least 10 days a month, and feeling pretty good only about 4 to 6 days a month.  The rest of the time is a crapshoot. I'm often surprised when I think I'm feeling better, but then I unexpectedly have to just go lay down and check out…  (Or go surfing, catch one wave, and wash up on the beach with almost-disabling vertigo!)

It's the up and downs that make it tough. It's a mental game as much as anything.  Since I'm on a 2 week regimen, I'm actually feeling pretty darn good by day 12 and 13.  Weak as hell, but feeling good.  Just in time to go back in and start all over again. "Do I really have to, Doc?"

What does this feel like?

For me, initially after treatment, I feel like someone drugged me and kicked me really hard in the stomach.  Dizzy, nauseous, spacey… blah.  And knowing that my gut flora (those friendly bacteria that make digestion possible) is being nuked once again, and it will take at least a week to work through the constipation, gas and bloating.

I am figuring it out, but it seems every time is a bit different.

What helps?

• Acupuncture
• Colonics
• Cannabis
• Diet & supplements
• Rest and time outside

That last one is important.  Outside, fresh air, freedom...

But every other Thursday it's right back to the beginning again.

Sometimes I feel like I just have to pay my dues.  Complete my sentence. As if I'm playing a game and I landed on

              "Get Bit by a Tick: Do to 6 months of Chemo."

But this is real, and there is no "Get Out of Jail Free" card.  And there is no "Just Sleep it Off."

Even so, I am grateful to be living in a time when we have access to something that works.  Otherwise I would not be here to write this.  There is such a bright light at the end of this tunnel, and it's getting closer every day.  Ready for July!