February 2007. A 46 year old female walked into my office for a "Lyme consult." I did not know at of our meeting-- she had recently been found in the middle of a road trying to end her life. Luckily, she was picked up by a police cruiser and subsequently admitted to a psychiatric facility. I did not know, until today, that a past treating physician, a rheumatologist, had called her an "f...ing moron." This patient/human being, has had a long and bumpy ride, but no longer entertains thoughts of suicide. She was sick of being sick. She had been sick for one half of her life, since age 24. She had suffered with total body pain. She had been diagnosed with "seronegative" rheumatoid arthritis. Gold shots, prednisone and other "remedies" offered no respite from her misery. She had swollen lymph node. Her joints and muscles hurt--really hurt. She was told she had "a weak immune system." She had numerous neurological complaints. There was progressive loss of memory and global cognitive function for over 15 years. Most troubling of all was severe, unrelenting abdominal pain. This was her worst symptom. Numerous specialist had been unable to identify the source of the trouble.
Prioritising, the first thing I did was examine her belly. She had right upper quadrant tenderness and a positive Murphy's sign. Gastroenterologists and surgeons insisted there was nothing wrong with her gallbladder. Sonograms and HIDA scans had been abnormal. I sent her for another HIDA CCK test: normal. I told her she had a bad gallbladder--I didn't care what the tests said. Two surgeons refused to operate. A third ( a close friend) reluctantly agreed. Her gallbladder was bad--chronically infected. Her pain was gone! Now she thought I was a genius. No. I have just seen chronic cholecystitis in many Lyme patients. And her physical exam was classic for cholecystitis. I followed a rule one of mentors taught me back in medical school: treat the patient not the lab. I quess most doctors today had a different mentor.
She was seropositive for Babesia at the outset. The Labcorp Western Blot showed no bands. Her Igenex test negative although IgM bands were "inderterminate" at the 39, 41 and 93 positions.
Treat the patient. Rocephin. She Herxed. We went around the block--numerous times. Gradually, after much Mepron, a mix of oral antibiotics and two courses of Rocephin she was significantly better.
We(she) struggled with serious nicotine addiction: 3 packs per day. She ended up with a severe lung infection. I prescribed Levaquin and Cleocin. The Herx brought her to the hospital. It looked like a cavitary mass or abscess. This was February 2009. The surgeons were sure she had a tumor. The biopsies showed no cancer and no microbes would grow in the lab. Faint colonies were seen only to disappear. The surgeons still wanted to operate. Two PET scans later-- no cancer. She had a miracle response to Ivanz. I have written about this before. The pulmonologist gave her months to live(she tells me), severe COPD. I don't think so. She is not short of breath even with moderate excertion. Maybe he is just trying to scare her.
Today I saw her. She is depressed because she retired from her job (voluntarily). She cleans houses part-time! Her pain is mangaged with modest help from "our friends". Good days and bad days. The bad ones aren't that bad. She is nervous: another PET scan. She wants to quit smoking--just can't do it.
I never knew about the suicide attempt--until today.
Tuesday, November 10, 2009
Monday, November 9, 2009
What do those lab tests mean?
The CD57 test (only from Labcorp) measures a subset of NKT cells. These are Natural Killer T Cells. These T cells are actors in the innate immune response. In other words, these cells automatically attack what our immune system sees as foreign invaders. Our immune systems are naturally smart (anthropomorphically). They have pattern recognition cells which can determine tissues/cells that belong in our bodies from things (like bacteria) that do not belong in our bodies. The second part of the immune system, the acquired immune system relates to a complex set of reactions by which the immune system learns to make specific antibodies to attack the foreign invader. In some situations only the innate immune system is in play. Primarily this occurs when the "invaders" are intracellular. The acquired responses just don't work here. In the case of Lyme disease it is the intracellula- L-forms which are attacked by the NKT cells. When the CD57 count is low it would appear these cells are busy combating the L-forms of Lyme. Unfortunately, the innate immune system is never 100% effective in eliminating the bacteria. This is one of the mechanisms by which Lyme is able to persist in the face of antibiotics and immune responses.
C3a and C4a (Labcorp) are products of the complement system, cleaved from C3 and C4. These proteins are mobilized by the immune system as part of its acquired and to a lesser extent innate immune responses. These proteins can attach to unwanted bacteria and target them for destruction. These tests are sensitive indicators of a busy immune system attacking unwanted proteins or germs. These markers can provide a general sense of immune activation in the face of infection or inflammation.
C3d (Quest only) is a test for circulating immune complexes (CIC). These antibody/antigen complexes are not supposed to be present in our blood. The presence of these CICs indicates infection or inflammation and can be used as another indicator of disease activity.
C-reactive protein (CRP) is a naturally occurring protein found in blood circulation. It is one of two proteins which activate the complement system associated with immune activation. This is another marker which can help assess disease activity. This marker is elevated in many diseases and is not specific for Lyme disease. When used here, the clincially useful cut-off points may be much lower than the "normal" reported by the lab.
There are many other labs/markers of infection/inflammation. But here a few that seem to confuse many patients (and doctors).
C3a and C4a (Labcorp) are products of the complement system, cleaved from C3 and C4. These proteins are mobilized by the immune system as part of its acquired and to a lesser extent innate immune responses. These proteins can attach to unwanted bacteria and target them for destruction. These tests are sensitive indicators of a busy immune system attacking unwanted proteins or germs. These markers can provide a general sense of immune activation in the face of infection or inflammation.
C3d (Quest only) is a test for circulating immune complexes (CIC). These antibody/antigen complexes are not supposed to be present in our blood. The presence of these CICs indicates infection or inflammation and can be used as another indicator of disease activity.
C-reactive protein (CRP) is a naturally occurring protein found in blood circulation. It is one of two proteins which activate the complement system associated with immune activation. This is another marker which can help assess disease activity. This marker is elevated in many diseases and is not specific for Lyme disease. When used here, the clincially useful cut-off points may be much lower than the "normal" reported by the lab.
There are many other labs/markers of infection/inflammation. But here a few that seem to confuse many patients (and doctors).
Friday, November 6, 2009
Musings with a patient today
Biaxin and Plaquenil? We have been taught that Plaquenil makes the intracellular environment more alkaline so Biaxin works better. Is this true? I don't know. I have also read that Plaquenil is anti-cyst. Sapi has now shown that Plaquenil induces cysts. You are on so many meds: let's drop the Plaquenil for now. The Malarone seems to be making the sweats go away. You are not sure, could the the sweats are hormonally induced? Possibly. My guess is that we are fighting Babesia: you tested positive. The low dose anti-malarial drug seems to work. Other patients require much higher doses.Biaxin decreases the Atovaquone by up to 40%. Many doctors switch to Zithromax for Babesia; Biaxin is a much better Lyme drug. We are covering more territory. The Bactrim you are taking for Bartonella also has some anti-Babesia effects; perhaps that is why you are doing so well. Patients seem to do better in the long run when anti-cyst drugs are added. Tindamax is the best--but that is for later.
How long do we treat Babesia for? Good question. Until the symptoms go away. There is no magic number. It has been said treat for 5 months because red blood cells have a 4 month life span. The only problem is that Babesia can also hide in the bone marrow, liver and spleen. The IDSA claims that it only resides in red blood cells--not true.
You followed all of that? You are doing better than you think!
How long do we treat Babesia for? Good question. Until the symptoms go away. There is no magic number. It has been said treat for 5 months because red blood cells have a 4 month life span. The only problem is that Babesia can also hide in the bone marrow, liver and spleen. The IDSA claims that it only resides in red blood cells--not true.
You followed all of that? You are doing better than you think!
Bartonella: brief report
A patient with documented chronic Lyme disease had further testing for Bartonella.
A test performed at Fry labs reported abnormally shaped red blood cells without bacteria.
A wet mount at Clongen showed scarce round motile bacteria.
A PCR at Clongen for "Bartonella species," was positive.
In general, PCR testing for Bartonella is not performed because of a low yield.
These results, albeit in a single patient, suggest that: 1) wet mount exams may be more accurate than stained whole blood samples for the identification of these bacteria and 2) these small round organisms seen in patient's blood do in fact suggest ongoing infection with Bartonella species.
A test performed at Fry labs reported abnormally shaped red blood cells without bacteria.
A wet mount at Clongen showed scarce round motile bacteria.
A PCR at Clongen for "Bartonella species," was positive.
In general, PCR testing for Bartonella is not performed because of a low yield.
These results, albeit in a single patient, suggest that: 1) wet mount exams may be more accurate than stained whole blood samples for the identification of these bacteria and 2) these small round organisms seen in patient's blood do in fact suggest ongoing infection with Bartonella species.
Friday, October 30, 2009
Odds and ends and ILADS
Patients treated for Bartonella seem to experience of lot of itching which may be associated with rashes, bumps or normal skin. It seems to be some sort of Herx reaction.
Eva Sapi's research: very revealing. Lyme in the test tube quickly convert to cyst form when doxycyline is added to the cultures. Plaquenil also increases cyst formation (some Lyme literature claims that Plaquenil is an anti-cyst drug). Three drugs were shown to reduce the cyst load. In order of increasing potency: albendazole, metronidazole (Flagyl) and tinidazole (Tindamax). Of course this is in a test tube or culture medium. There are no cells. L-form transformation cannot be observed.
The ILADS' conference was great this year. Presentations were scientific and evidenced based.
Sessions discussing therapeutic options were great as well. I started my first patient on tigacyline, a drug much favored by Dr. Burasanno.
I have liked the layering approach for very ill patients. Start with IV Rocephin, add IV Zithromax and then add IV Flagyl. Dr. Martz agrees with my approach. We have both found this to be very effective. Other physicians recommend pulsing antibiotics in very high doses, primarily with Rocephin. Dr. Burasanno and Dr. Horowitz were animated and informative. "There is no one right way to treat Lyme."---Dr. Burascanno.
Eva Sapi's research: very revealing. Lyme in the test tube quickly convert to cyst form when doxycyline is added to the cultures. Plaquenil also increases cyst formation (some Lyme literature claims that Plaquenil is an anti-cyst drug). Three drugs were shown to reduce the cyst load. In order of increasing potency: albendazole, metronidazole (Flagyl) and tinidazole (Tindamax). Of course this is in a test tube or culture medium. There are no cells. L-form transformation cannot be observed.
The ILADS' conference was great this year. Presentations were scientific and evidenced based.
Sessions discussing therapeutic options were great as well. I started my first patient on tigacyline, a drug much favored by Dr. Burasanno.
I have liked the layering approach for very ill patients. Start with IV Rocephin, add IV Zithromax and then add IV Flagyl. Dr. Martz agrees with my approach. We have both found this to be very effective. Other physicians recommend pulsing antibiotics in very high doses, primarily with Rocephin. Dr. Burasanno and Dr. Horowitz were animated and informative. "There is no one right way to treat Lyme."---Dr. Burascanno.
Tuesday, October 27, 2009
A second opinion
A 36 year woman recently requested a second opinion after a recent diagnosis of MS.
She reported a history of tick bite. A Lyme WB from Labcorp revealed positive bands: IgG 41 and IgM 23. She was told her test results excluded Lyme in the differential.
One month prior to our visit she complained of numbness in her left upper and lower extremities. She also reported some stiffness in her neck.
Other symptoms were discounted: flu like symptoms with sweats and low grade fevers, swollen glands, joint swelling and pain and fatigue. Additional history revealed Bell's Palsy 15 years ago, heart palpitations and irritability. She initially denied all cognitive symptoms, only after further questioning she did admit to some progressive memory loss of the preceding two years.
An MRI revealed 4 white matter lesions in the brain and one in the cervical spinal cord.
The radiology report: "....demyelination due to multiple sclerosis or Lyme disease." This report was not from a radiology source which is familiar with my work.
As part of the MS work up the neurologist did an LP (spinal tap). I asked her to send a specimen to Clongen for PCR.
A report came to my desk amongst the usual pile of of daily lab reports and various requests.
This one caught my eye. Her spinal fluid was PCR positive for Lyme.
I called back to the office right away.
Her lab result and her appearance were incongruent. She sat across from me smiling, in no distress, appearing healthy in a casual glance.
This patient had Lyme in her spinal fluid. She had lesions in her brain.
She felt minimally ill and looked remarkably well. Of course I started IV Rocephin immediately.
During our most recent visit she told me she had seen "Under Our Skin."
She asked me: "How comes I am not sick like those people with Lyme?"
She reported a history of tick bite. A Lyme WB from Labcorp revealed positive bands: IgG 41 and IgM 23. She was told her test results excluded Lyme in the differential.
One month prior to our visit she complained of numbness in her left upper and lower extremities. She also reported some stiffness in her neck.
Other symptoms were discounted: flu like symptoms with sweats and low grade fevers, swollen glands, joint swelling and pain and fatigue. Additional history revealed Bell's Palsy 15 years ago, heart palpitations and irritability. She initially denied all cognitive symptoms, only after further questioning she did admit to some progressive memory loss of the preceding two years.
An MRI revealed 4 white matter lesions in the brain and one in the cervical spinal cord.
The radiology report: "....demyelination due to multiple sclerosis or Lyme disease." This report was not from a radiology source which is familiar with my work.
As part of the MS work up the neurologist did an LP (spinal tap). I asked her to send a specimen to Clongen for PCR.
A report came to my desk amongst the usual pile of of daily lab reports and various requests.
This one caught my eye. Her spinal fluid was PCR positive for Lyme.
I called back to the office right away.
Her lab result and her appearance were incongruent. She sat across from me smiling, in no distress, appearing healthy in a casual glance.
This patient had Lyme in her spinal fluid. She had lesions in her brain.
She felt minimally ill and looked remarkably well. Of course I started IV Rocephin immediately.
During our most recent visit she told me she had seen "Under Our Skin."
She asked me: "How comes I am not sick like those people with Lyme?"
Monday, October 19, 2009
Thoughts on psych drugs for Lyme patients
These are my opinions based on my reading and clinical experiences.
Most of the patients I treat with significant chronic Lyme disease suffer with a variety of neuro-psychiatric symptoms. Patients have recently commented to me about the post on Klonopin.
Patients with Lyme-Brain seem to have poor tolerance for SSRIs: drugs which increase serotonin levels in brain synapses. Perhaps the injured brain is sensitive to these drugs. Many patients come to me already taking drugs with a strong affinity for serotonin receptors in the brain such as Lexapro or Cymbalta. These drugs may cause increased brain fog, irritability and a paradoxical increase in depression.
Other anti-depressants act primarily on the brain chemical norepinephrine. Patients seem to tolerate these drugs better. These includes the anti-depressant Wellbutrin and ADD medicines which also effect dopamine. Charts in pharma books show the relative affinity of anti-depressants for serotonin and norepinephrine. If the ratio favors norepinephrine the patients may tolerate this drug better. This includes drugs such as Desipramine, an old TCA antidepressant. These meds are best tolerated in low doses.
Drugs used for ADD can be quite helpful. These drugs target the neuro-transmitter dopamine as
well as norepinephrine. These drugs increase wakefulness and energy and may correct some frontal lobe dysfunction seen in many Lyme patients. My favorite drug here is Ritalin which comes in a variety of doses and can be carefully titrated.
Mood stabilizers can be very helpful as well. These drugs are anti-convulsants which stabilize abnormal chemical/electrical imbalances in the brain. I like Lamictal because it has antidepressant effects and mild glutamate inhibition. This drug has significant toxicity and should only be prescribed by physicians familiar with its side effects. Glutamate toxicity is thought to be a major problem in the injured brain. The best drug for glutamate toxicity may be the anti-Alzheimer's drug Namenda, which frequently improves cognitive dysfunction.(Rocephin also works by this mechanism).
Klonopin binds to the neuro-transmitter GABA, which is a major inhibitory neuro-transmitter.
Lyme patients can suffer with excessive expression of excitatory neurochemical in the brain. Most of this is mediated by serotonin, the "work horse of the brain." This dovetails with my comments about the potential harmful effects of serotonergic drugs.
Other commonly used GABA drugs are Neurontin and Lyrica which may be well tolerated. In my experience, benzodizapines like Klonopin work better. This may be due their increased anti-anxiety effects.
Anti-psychotic medicines, like Seroqel, are certainly helpful for patients experiencing psychotic symptoms such as hallucinations. They may help in other ways. Although they inhibit dopamine, they bind to different receptors, deep in the brain, unlike ADD medications which stimulate dopamine pathways in the cortex of the brain.
Many Lyme patients have sleep disorders. The activating neuro-chemicals, serotonin and norepinephrine are prominent during waking hours. This is counteracted by a predominance of acetlycholine effects which occur during sleep. Restful sleep is important. When a "sleeper" is needed I prefer Restoril which produces a good night's sleep and promotes normal sleep architecture. Lunesta may be a good alternative.
Most of the patients I treat with significant chronic Lyme disease suffer with a variety of neuro-psychiatric symptoms. Patients have recently commented to me about the post on Klonopin.
Patients with Lyme-Brain seem to have poor tolerance for SSRIs: drugs which increase serotonin levels in brain synapses. Perhaps the injured brain is sensitive to these drugs. Many patients come to me already taking drugs with a strong affinity for serotonin receptors in the brain such as Lexapro or Cymbalta. These drugs may cause increased brain fog, irritability and a paradoxical increase in depression.
Other anti-depressants act primarily on the brain chemical norepinephrine. Patients seem to tolerate these drugs better. These includes the anti-depressant Wellbutrin and ADD medicines which also effect dopamine. Charts in pharma books show the relative affinity of anti-depressants for serotonin and norepinephrine. If the ratio favors norepinephrine the patients may tolerate this drug better. This includes drugs such as Desipramine, an old TCA antidepressant. These meds are best tolerated in low doses.
Drugs used for ADD can be quite helpful. These drugs target the neuro-transmitter dopamine as
well as norepinephrine. These drugs increase wakefulness and energy and may correct some frontal lobe dysfunction seen in many Lyme patients. My favorite drug here is Ritalin which comes in a variety of doses and can be carefully titrated.
Mood stabilizers can be very helpful as well. These drugs are anti-convulsants which stabilize abnormal chemical/electrical imbalances in the brain. I like Lamictal because it has antidepressant effects and mild glutamate inhibition. This drug has significant toxicity and should only be prescribed by physicians familiar with its side effects. Glutamate toxicity is thought to be a major problem in the injured brain. The best drug for glutamate toxicity may be the anti-Alzheimer's drug Namenda, which frequently improves cognitive dysfunction.(Rocephin also works by this mechanism).
Klonopin binds to the neuro-transmitter GABA, which is a major inhibitory neuro-transmitter.
Lyme patients can suffer with excessive expression of excitatory neurochemical in the brain. Most of this is mediated by serotonin, the "work horse of the brain." This dovetails with my comments about the potential harmful effects of serotonergic drugs.
Other commonly used GABA drugs are Neurontin and Lyrica which may be well tolerated. In my experience, benzodizapines like Klonopin work better. This may be due their increased anti-anxiety effects.
Anti-psychotic medicines, like Seroqel, are certainly helpful for patients experiencing psychotic symptoms such as hallucinations. They may help in other ways. Although they inhibit dopamine, they bind to different receptors, deep in the brain, unlike ADD medications which stimulate dopamine pathways in the cortex of the brain.
Many Lyme patients have sleep disorders. The activating neuro-chemicals, serotonin and norepinephrine are prominent during waking hours. This is counteracted by a predominance of acetlycholine effects which occur during sleep. Restful sleep is important. When a "sleeper" is needed I prefer Restoril which produces a good night's sleep and promotes normal sleep architecture. Lunesta may be a good alternative.
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