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Sep 20, 2018 · CLL in Blood Cancers & Disorders

During imbruvica treatment my white count peaked in the low 40 Ks, absolute lymphocyte count 30 K plus, Prior to my first treatment, with Rituxan, lympocytes were over 150,000, lymphatic involvement very extensive, spleen enlarged with symptoms of ischemia. It was a question of treating the CLL or removing the spleen. After rituxan, lymphocyte count bottomed out at 1K, and rose to about 10K when I started imbruvica. On 2 occasions when I had clonal and total lymphocyte counts, at time of diagnosis and shortly after relapse (prior to imbruvica), the difference was about 1K per microliter, presumably consisting of normal b-lymphocytes plus T-cells, with T-cells predominating as they should. That would be a low T-cell count and a low count for normal b-cells. CLL is known to suppress T-cell counts as well as counts of normal b-cells. I've had serious problems with infections since about 6 weeks after starting imbruvica. However, I am resistant to starting IVIG again and want to see how things go at a reduced dose before re-visiting the issue of starting IVIG. I got very little benefit from IVIG when I was previously getting it for about 2 years. Imbruvica is a serious immune suppressant that is FDA approved treatment of chronic Graft Versus Host Disease. I am hoping that a dose reduction provides adequate relief from the immune suppressant features of imbruvica without rendering it ineffective as a CLL treatment.

Sep 20, 2018 · CLL in Blood Cancers & Disorders

I had a partial remission for less than 6 months following a couple rounds of rituxan in 2016. I had to cut back my work schedule to 24 hours per week, 3 shifts per week in a corporate group home for patients with respiratory depression, mostly vent patients, early in 2013. For about 4 months in 2016 I was scheduled to work 24 hours per week at a nursing home as charge nurse (also administered all medications and treatments). The 8 hours shifts usually turned into 9 to 10 hour shifts with no rest breaks. I had to quit that job for the same health reasons that compelled me to cut my hours in 2013. Most of the time, my shifts at the group home were just as demanding, or more so, than the nursing home job in 2016.

I drove taxi for over a year in 2010 to 2011 and then for a few months in 2014. I could tolerate working up to 60 hours per week, in 12 hour shifts as a taxi driver in 2010-2011, but could tolerate only 3 shifts per week for a total of 36 hours in 2014. My average earnings after job expenses (lease and gas) worked out to $5 per hour in 2010-2011 and less than that in 2014.

Then I got a restaurant delivery job that lasted about 18 months until I landed the nursing home job in 2016. I tolerated working about 20-24 hours per week pretty well as a delivery driver, and I was never offered more hours than that with the first job. At the second restaurant delivery job in 2016, I ended up working about 30 hours per week and was noticing some adverse effects from that. Then I was involved in collision with another car on Jan 1, 2017. I had moderate to severe rotator cuff tears in both shoulders and had to quit driving and work with restrictions compatible with "light duty" jobs. I worked an inside job, making pizza and all other tasks assigned to non-supervisory workers until I took a medical leave for a surgical repair of the most damaged tendons.

I was seldom offered more than 20-24 hours of work per week doing inside work at the restaurant . My earnings in 2017 were too low to meet the criteria for "substantial, gainful employment," which means that I passed the earnings test to get a claim approved for social security disability benefits. Because of the quickly relapsed CLL and plans to start Imbruvica, I also met medical severity criteria under the non-hodkins lymphoma listing. At that point I finalized an application for disability benefits and a favorable determination was made within two months. Payment was delayed because of a pending work comp claim related to the auto accident. A settlement or hearing on the work comp claim is still pending. I started collecting benefits in February. I have been working 4 hour shifts as a pharmacy tech since January 2018. I started out at 20 hours per week, but had to cut back to no more than 12 on a regular basis due to complications of fatigue and activity intolerance.

I started Imbruvica on 4 October 2017. After 6 weeks, I began to have frequent, hard to treatment infections, seriously high blood pressure and worsening activity tolerance and fatigue. As a result, I had to reduce the number of hours that I was working and cancel surgery scheduled for repair of tendons in the shoulder than was less badly damaged in August 2018. When I started having serious side effects from Imbruvica, it was not yet clear to me how much the imbruvica could be implicated and hoped that the side effects would become much less severe within 6 months to a year. I was disappointed. The approach advocated by my CLL specialist was to throw medications at the problem, e.g. blood pressure medication and IVIG. I got started on a blood pressure medication, but refused the IVIG. I was on IVIG in 2014 to 2016, and it helped a little, but not enough. I met criteria for CLL treatment per IW guidelines for diagnosis and treatment of CLL, but was offer no treatment until I had symptoms of spleen ischemia in 2016 that could not be attributed to anything else. The spleen symptoms improved and went away while I was in remission, then resurfaced since the relapse. My b-grade symptoms and low immune globulin levels were originally attributed to Common Immune Variable Disorder and that treatment of the CLL wouldn't help. However, I am not aware that the diagnosis of Common Immune Variable Disorder was ever confirmed. However, I was told that the b-grade symptoms could not be caused by CLL because b-grade symptoms don't happen in "early stage" CLL. Yet I stopped the IVIG and was infection free for almost 6 months following the CLL treatment. Other b-grade symptoms also disappeared for a good while overlapping with the vacation from antibiotics. I think that the diagnosis of Common Immune Variable Disorder is not supported by the evidence, it is just wrong and it was used to justify not treating the CLL.

There are some things that I recently learned about imbruvica that I did not know when I started it. Imbruvica was initially investigated as an immuno suppressant to treat autoimmune disorders and is FDA approved as an immuno suppressant to treat chronic Graft Versus Host Disease. The targeted molecule, Bruton's Tyrosine Kinase is one of about 540 kinases found in humans, and it is expressed in all cells originating as a pleuripotent hemopoetic stem cells, except T-lymphocytes. BTK allows CLL cells to live long and proliferate. However, BTK also plays an important role in the maturation of cells that express it. If BTK receptors are fully saturated by imbruvica, it is not just the CLL cells that are impacted. So it is not entirely coincidential that bone marrow suppression and high rates of infection are associated with Imbruvica. Imbruvica is designed to function as an immuno suppressant. The manufacturer never got baseline data on infections for its clinical trials, and thus cannot confirm a causal link and can even claim that there is no evidence of a link thanks to the absence of baseline data. We do know that the intensity of at least some side effects from imbruvica dose related. Lowest absorption and bio availability occurs with taking it under fasting conditions. More than double the absorption and bio availability taken with or soon after a meal. One is simply instructed to take it consistently at about the same time of day. Can a dose greater than necessary to fully saturate BTK sites augment its anti-CLL effect? My guess is that it doesn't. Why is it that when Imbruvica is abruptedly stopped there is a rebound effect: CLL clones strive and multiple very quickly for a while. Why? Could that have anything to do with lingering immuno suppressant effects? Imbruvica irreversibly binds to BTK receptors. The immunosuppressant effect will endure for a while after Imbruvica is discontinued. Immune factors that keep CLL in check are weakened by imbruvica. Is full saturation of BTK receptors necessary or desirable when treating CLL? What portion of the BTK receptors must be occupied for CLL to have its optimum effect? One must consider both the direct effect on CLL and immune functions that keep CLL in check. There is no commercially available test for BTK occupancy and I've gotten the impression that the optimal degree of saturation of BTK receptors has yet to be determined. In Clinical practice, the optimal dose can only be determined through a process of trial and error, of adjusting dosage by theraputic response and side effects. Infections are not a problem for some CLL patients who take imbruvica, yet a big problem for others. Dosing is likely a factor, and someone who already has a fairly compromised immune system and history of frequent infections will be even more susceptible to have increased problems with infections while on imbruvica. I want to see if a dose reduction of imbruvica helps with side effects and remains effective in treating the CLL before considering going back on IVIG. In fact, if infections are bad enough for me to resort to restarting IVIG, I would rather try another treatment. As bad as imbruvica is, I suspect that chemo plus rituxan would be worse. Venetaclax plus rituxan looks promising, particularly because it is reportedly more effective than Bendamustine plus rituxan. I assume that that means that is not necessarily a forever regime. Venetaclax has immune suppressant actions similar to imbruvica, but hopefully less severe. If I switch to that regime, I will not be content to "wait and see" if serious side effects eventually go away on their own, as I have done with imbruvica. Maybe imbruvica will work just fine at the current dose, and I will stick with it.

Jan 9, 2018 · New confused diabetic in Diabetes/Endocrine System

In nursing school near the end of 1989 I went from a high fat, low carb diet to a high carb, low fat diet recommended in a nutrition class. I gained 20 pounds in a matter of months, and the next year gained weight faster than my wife when she was pregnant. I didn’t question authority. But my weight went from 180 to as much as 270 pounds. My blood glucose levels got quite high by 1992, and I had the sense to cut out processed sugars and starches, which caused my weight to drop 20 pounds in a month and get blood glucose levels to the normal range. But I was still trying to follow the low fats dietary advice. I tried out the south beach diet and later took the trouble to read Dr. Atkins Diet Revolution. I started a low carb diet in late 2003 and got my weight down to 190 pounds by 2009.

I recommend writings by Gary Taube, a science writer who got interested in the high carb vs. low carb when investigating low sodium diets recommended by doctors for hypertension. Unless someone renal function was impaired, the low sodium diet had no impact. Sodium levels are hormonally regulated, and one hormone with an impact was insulin. That led to looking into how diet can impact insulin and the role of insulin in fat accumulation. It has long been known that insulin is necessary for fat accumulation. The hypothesis that dietary fat makes you fat, advance by Ansel Keyes of the University of MN, was initially disputed by the AMA, later endorsed. What was know about insulin as a hormone that promotes fat accumulation has been forgotten.

I have consulted with many endocrinologists, and most recommend a high carb, low fat, low calorie diet. I lost my respect for that profession, at least in the US, but not only because of dodgy dietary advice I had received. I had documented thyroid storms beginning in 1979. T4 and T4 levels were high, then dropped to borderline low, then rose and plateaued, then another storm, and so forth. The high and low end reading were falling. The effect left me disable within several years. Consults with endocrinologists were pointless. No one offered any treatment. I hunted through the card catalog at the U of MN medical library in search of journal articles concerning treatment of thyroiditis, and eventually found one by a doctor who had newly diagnosed patients take a 325 mg tablet of Aspirin daily, and saw symptomatic improvement. Patients referred to psychiatry were weaned successfully from psych medications. He then had many patient who had long been disabled try the daily aspirin regime, and most of the saw huge improvements. Most patients on psych medications were successfully weaned from those medications. I tried it out, and within a few month the chronic low grade fever and fatigue went away. I went back to school, studied practical nursing and started working in that field

In 1989, one the eve of starting nursing school, I consulted an endocrinologist who was trained in Germany. She didn’t only answer questions, but volunteered some information and encouraged me to educate myself. She did a thorough work up and looked at recorded thyroid labs and expected that I would need thyroid replacement therapy in about 5 years. She was right, but had moved to Florida (which I didn’t know until many years later) I could not find an endocrinologist or any doctor willing to treat because my TSH wasn’t high enough. By 1997 I had extraordinarily dry skin, very thick, deeply fissured callouses on my heels, and frequent external auditory ear canal infections. An Eye Nose Throat doctor said that this was an endocrine problem, and endocrinologist saw no problem.

By early 2000 I had to cut back to part time work because of fatigue and episodes of high blood pressure if I tried to work more than 3 days per week. By 2003 I was beginning to see myxedema, which began fairly severe by the end of the year. While on a coronary care unit because of a hypertensive episode a resident dismissed my concern about hypothyroidism, and told me that there is no such thing as myxedema, though “myxedema coma” is a valid medical term. I had read about myxedema in medical reference books and medical and nursing textbooks from the 1950s when I worked at a nursing home as a nursing assistant in the 1970s. I saw examples of myxedema, including severe myxedema in a patient who was not being treated for severe hypothyroidism because of insurance and prescribing rules. The idea behind deleting myxedema as well as hypothyroid heart disease (or Hypothyroid Heart Failure) was that doctors would never see it because of a cheap, commercially available test for serum thyroxin levels. Hypothyroidism would be treated early and effectively, and late stage symptoms would never emerge, except in rare cases where the thyroid gland was damaged and surgically removed, and in those cases the myxedema would be quickly reversed. I finally got treated in February 2004, not because severe myxedema and cardiovascular symptoms, but because I saw a primary care doctor who was aware that guidelines for the diagnosis and treatment of hypothyroidism allowed treatment in the presence of symptoms and if TSH was above 2.5. My level was about about 3.0. The doctor refused to order baseline T4 and T3 levels and until pretty well into the therapy, and they were borderline low at that point.

More recently, changes in guidance for doctors allowed my primary doctor to shift from thyroxine to liothyronine replacement because of peripheral neuropathy and signs of hypothyroidism apparently related to poor peripheral conversion of T4 to T3. I recently saw a endocrinologist for another issue, and he did not approve of using cytomel. Thyroxine is the standard, etc. I told him that I don’t want an endocrinologist in charge of thyroid replacement therapy or anything else, if I can help it.

For the foregoing reasons, I don’t trust endocrinologists, except maybe one who was trained in Germany. Based on what I have read on Mayo Clinic web site, I wouldn’t expect to see anything radically different at Mayo than I have seen elsewhere. For example, the term myxedema is used to connote myxedema coma and not the edema one sees in late stage hypothyroidism. Doctors see a lot of myxedmea in women over 50, but have no idea what it is. Hypothyroidism is often not diagnosed until it is late stage because of misplaced confidence in blood tests to diagnose and treat hypothyroidism. I have also seen obesity described as a consequence of overeating and under-exercise and not as the result of a hormonally regulated process of fat accumulation. In my opinion, diet and exercise have effects on hormones that regulate fat accumulation, and what you eat is more important than how much you eat.

Dec 24, 2017 · CLL - newly diagnosed in Blood Cancers & Disorders

Warning: I present the information below without citing any authority and it should not be considered authoritative, although I am sure it is fairly accurate.

Diagnostic criteria for CLL and SLL per International Workshop guidelines changed almost a decade ago with updates in 2007 or 2008. An absolute lymphocyte count of 5,000 per micro-liter was the cut-off between CLL and SLL or monoclonal lymphocytosis. If above 5K at time of diagnosis it was CLL. If below 5K it was SLL (with adenopathy) or monoclonal lymphocytosis (without adenopathy). The term adenopathy refers to enlarged lymph nodes or spleen. Now the threshold for CLL diagnosis is a clonal population of 5K, which is determined by flow cytometry. The absolute lymphocyte count is arrived at with a Complete Blood Count with differential, which is a much cheaper test. The absolute lymphocyte count is the sum of the clonal population plus normal lymphocytes. The threshold has been effectively raised, and fewer newly diagnosed patients will be classified as having CLL, and more will be classified as having SLL or Mono Clonal Lymphocytosis.

SLL is essentially the same malignancy as CLL, but it is staged differently. The Ann Arbor staging system for indolent lymphomas is used. The Ann Arbor system is based on the extent of adenopathy, with stage 1 involving fewer than 3 lymph nodes or clusters above or below the diaphragm. Stage 2 is 3 or more enlarged lymph nodes above or below the diaphragm. Stage 3 more is 3 or more lymph nodes above and below the diaphragm. And stage 4 has the stage 3 criteria plus involvement of the spleen and / or liver. A PET scan is sometimes used to verify the presence of cancer in a lymph node and to select a node for biopsy.

SLL is rarely caught at an early stage, when it is confined to no more than a couple lymph nodes or node clusters. It can usually be cured at that point, much like some other forms of indolent lymphoma when caught very early. You might not have detectable amounts of the cancer in your blood stream in stage one. By stage 3 or 4 it is likely going to be detectable in the blood stream and probably getting established in the bone marrow. If there are grade B symptoms, the letter B is added to the number. B grade symptoms include frequent infection, mouth sores and drenching night sweats. So a stage 3 with B-grade symptoms would be stage 3B. The presence of B grade symptoms is an indication for treatment, and the goal of treatment is to eliminate the B grade symptoms. Stage 4 SLL isn’t necessarily treated unless there are b-grade symptoms.

In SLL, a malignant B lymphocyte arrives at a germinal site in a lymph node (perhaps other clones were destroyed in the bone marrow and blood or it simply didn’t start clonal reproduction until it arrived at a germinal site outside of the bone marrow.) It is also hypothesized that genetic defects characteristic of CLL do occur after the cell has arrived at a germinal site outside of the bone marrow.

In CLL, the clonal population is established in the marrow of a bone, gets into the blood stream and spreads to other bones and to lymph nodes, spleen, liver and just about anywhere the blood will carry it. Lymphocytes are produced by Pleuripotent Hemopoetic stem cells which produce all types of bloods cells: red, white and platelets. CLL is not caused by stem cells churning out viable CLL cells. The stem cells sometimes push out cells that have defects or acquire defects that characterize a CLL/SLL cell. CLL almost always starts out with a single cell that the immune system fails to destroy and fails to keep in check forever. For every person who develops CLL or SLL, there are probably ten persons who have CLL/SLL cells and are never diagnosed with CLL/SLL.

CLL in rai stage 2 can involve the same degree of adenopathy as stage 4 SLL. Of those diagnosed with CLL stage 0,1 or 2, about 10% to 15% have B grade symptoms before they advance to stage 3. Ordinarily CLL is not treated before old Rai stage 3 except when b-grade symptoms are present. The original or old Rai staging went from stages zero to 4 and is still widely used in the US. The new Rai staging system is about the same as the Binet, which is used more in Europe, with stages 1, 2 and 3; early, middle and late stage. The goal of treatment of CLL with B grade symptoms is the same as SLL with B grade symptoms: to eliminate or reduce the symptoms to below b-grade thresholds.

Current treatment protocols are still based on risk / benefit analysis of traditional chemotherapy. Chemo agents such as Chlorambucil, Bendamustine, Fludaribine, and Cyclophosfomide, are less effective and more toxic than some of the targeted treatments that are commercially available. Generally, chemo given early does more harm than good. Until a short term regime is developed that cures CLL/SLL, there isn’t much point to treating someone who has no symptoms. But current treatment criteria may be too restrictive given treatment options that are much less toxic than standard chemo. The next step for clinical trials is to determine if there is a benefit to treating when symptoms are present but do not yet meet b-grade criteria or when blood chemistries suggest CLL/SLL will soon progress to the point where treatment will be indicated under current guidelines.

Cost of the newer treatment options is a reason that chemotherapy is favored for some patients. Moreover, the combination of Benamustine and Rituximab and Fludaribine, Cyclophosphomide and Rituxin have produced deep and long lasting remissions in many patients. On the other hand, Ibrutinib and Veneticlax are given indefinitely as single agents. There are clinical trials underway to find out if a combination of these newer agents can be administered on a short term basis and, like standard chemo plus rituxan, produce deep, long-lasting remissions. Short term combinations of newer agents could reduce overall costs of treatment compared to a single agent given indefinitely. It is to be hoped that eventually the cost of the new wonder drugs will come down and will not be so much a factor limiting access.

Dec 20, 2017 · CLL - newly diagnosed in Blood Cancers & Disorders

The White and lymphocyte reference ranges in the US are about the same. 10^9/L is a microliter, which is the same volume of blood used in reporting blood cell counts in the US. The diagnosis of CLL requires a clonal lymphocyte cell count of at least 5K per microliter, and the total lymphocyte count will be higher than that. If lower, and there is no adenopathy (enlarged lymph nodes) it will be classified as monoclonal lymphocytosis, and with adenopathy, SLL (small cell lymphocytic Leukemia).

CLL involves the same kind of malignant lymphocytes as SLL and is therefore essentially the same disease. CLL usually starts with a clonal population in the bone marrow, SLL with a clonal population in a lymph node or in the spleen. CLL spreads to the lymph nodes and spleen, and SLL will migrate to other lymph nodes and then into the blood stream and bone marrow. In most cases, CLL more closely resembles other forms of leukemia than lymphoma in early stages and leads to bone marrow suppression earlier than SLL. But some cases of CLL can look like an advanced lymphoma (SLL) in early Rai stage (old rai stages 0-2).

Given all of the subtypes of CLL/SLL and individual variation in their presentation, there is no such thing as a “typical” case of CLL/SLL. I have a lot more confidence that I will get competent treatment from a CLL specialist than a oncology / hematology generalist. CLL specialists are far more likely to follow standards of care, such as the International Workshop Guidelines for Diagnosis and Treatment of CLL. Some general oncology / hematology practices will not treat early rai stage CLL in the presence of b-grade symptoms, which are an indication for treatment per the IW guidelines and per 2 other widely recognized standards-setting organizations.

There is a big CLL support group on facebook in which I participate that members of this forum who are dealing with CLL/SLL might want to check out. It is called “CLL Support Group”

Dec 18, 2017 · Newly diagnosed in Blood Cancers & Disorders

I met criteria for CLL treatment for about 2 years before I got any treatment. During that time I was taking a big dose of Green Tea extract in the AM and a large dose of a curcuminoid extract in the evening. I was on and off the regime for periods of time to figure out if it made a difference. I think that it did, but the benefit was not huge. No problem tolerating the supplements. But they are not a good substitute for medications like rituxan and ibrutinib, in my opinion.

I was symptomatic at time of diagnosis and for two year of watch and wait, and the supplement regimes had little effect on the symptoms. I had drenching night sweats, bacterial infections requiring long courses of a combination of high dose levaquin and cefdinir about once per month. I was on antibiotics more of the time than off. And I was getting IVIG infusions every 3 weeks.

I was seen by cancer generalists at Health Partners in the Twin Cities who treated CLL patients but consciously ignored and didn’t agree with the International Workshop guidelines for diagnosis and treatment of CLL. I was rai stage 2 and symptomatic, but CLL was not treated before stage 3 by Onc-hemes who I saw, and I saw most of them. However, an exception was made for me very reluctantly because of symptoms of spleen ischemia for which no alternative hypothesis could be supported with CTs and lab tests.

I had two set of rituxan infusions in 2016. The spleen symptoms improved a lot with the first set of infusions, and blood work normalized. After the second set of infusions I had almost 6 months without night sweats, bacterial infections and antibiotics, and without IVIG. I did have a brief flair up of spleen symptoms plus pleuritis about 6 weeks after each infusion, but then those symptoms subsided. So I was happy with the rituxan.

When my lymphoma and spleen symptoms came back this year I was being followed at the Mayo Clinic by Dr. Tim Call, who offered some treatment options, and I have been on ibrutinib since 4 Oct 2017. I had a localized, allergic rash (beat red with hives) that came and went in a few days and a few infections which the ibrutinib may or may not have contributed to. Night sweats are far fewer and milder now compared to Sept and Oct. I take two capsules daily instead of 3. Palpable lymph nodes shrunk to normal size. Lymphocyte count went from 10K to 32K and just registered at 29K.

Prior to my first rituxan treatment the absolute lymphocyte count was over 150K per uL. The Rituxan then ibrutinib sequence seems to work well for me. I have a CLL subtype that is supposed be “good,” mutated variable region and 13q deletion. Since I am only 61 and apparently healthy, I was offered chemo + rituxan. But I said “no thanks” to that. The CLL has done a great deal of damage all by itself, and I have other chronic illness. I don’t think I am as fit as my doctors assume. I can’t understand the allure of chemotherapy when less toxic regimens are available.

Dec 6, 2017 · CLL - newly diagnosed in Blood Cancers & Disorders

I started imbruvica on Oct 4, 2017. I had rituxan infusions, 2 sets of 4, in 2016 because of symptoms of spleen ischemia (I also had lymphoma symptoms, including night sweats and frequent bacterial infections until late in 2016). My lymphocyte count dropped below 2K at one point and was at 10K when I started imbruvica because of worsening lymphoma symptoms. At two weeks after starting imbruvica my lymphocyte count had risen to 20K and to 30K 6 weeks after starting imbruvica. There was notable reduction in palpable lymph node sizes at both the first and second check ups, and milder and less frequent night sweat (which I note on my calendar). I am taking only 2 capsules daily. I had a transient localized allergic rash soon after starting imbruvica that might have been caused by Imbruvica. But otherwise, no apparent side effect, e.g., no bleeding problems.

Dec 6, 2017 · CLL - newly diagnosed in Blood Cancers & Disorders

Have you consulted a CLL specialist? I encountered non-specialists who were either ignorant of or disregarded guidelines for diagnosis and treatment of CLL issued by the International Workshop for CLL. I met criteria for treatment based on lymphoma symptoms, but the doctors wouldn’t consider treatment prior to late rai stage. If you are having serious ENT problems secondary to enlarged lymph nodes, maybe it is time to consider CLL treatment, such as with Imbruvica.