Tuesday, February 19, 2019

Babesia confusion

Babesia is a protozoan, a higher life form than bacteria. Both are single cell organisms.  The primary difference is protozoa have an organized nucleus containing DNA. It is a member of the phylum Apicomplexa.  This is a relatively small group of organisms. Its closest relative is Malaria; only Babesia and Malaria (Plasmodium spp.) are intraerythrocytic, meaning live inside red blood cells. Because of this, many therapies against malaria are also effective against Babesia.  Mainstream medicine offers two therapies only: quinine/clindamycin and Zithromax/Mepron (atovaquone). These approaches frequently fail and additional approaches are required. 
Historically, Babesia was first described in the 1950s as a cattle disease.  The first human cases, B. microti were described around Nantucket Island in the 1960s.  Many physicians have stubbornly, erroneously clung to the belief that human babesiosis on the east coast, is virtually always caused by B. microti.  Although B. duncani was first described on the West Coast, it currently accounts for the majority of speciated cases diagnosed on the East Coast as well.  More often than not the diagnosis is made without speciation. (the species of Babesia causing the illness is not identified).  There are more than 100 species of Babesia known.  Other species, MO1, CA1 are recognized human pathogens in the US.  B. divergens, a bovine species, is known to have jumped species, cow to human.
Most Lyme doctors make the diagnosis empirically, based on symptoms.  Underused diagnostic tools include Giemsa stains and FISH tests.  Many Babesia symptoms are nonspecific.  In my practice I especially pay attention to a triad:  night sweats +/- feeling feverish, air hunger and change in emotional state – especially random bouts of tearfulness. 
For many patients the two “standard” therapies, as stated above, proves ineffective or only partially effective.  Other therapies may be effective and medically necessary.  Therapies must be science based and rational. The term evidence based refers to mainstream treatment vetted through a peer reviewed process and frequently, not always FDA approved.  Second tier drugs and therapies are used when “evidence based” treatments have failed.  Science based approaches require biological plausibility, e.g. med works well against malaria and/or their use is supported by body of empirical evidence, e.g. traditional herb has been used for a century to treat malaria.  Doctors prescribing these therapies need to be knowledgeable about the disease.  
One approach/theory must be debunked.  This is the idea that 4 months of treatment is all that is required.  The basis for this thinking is that red blood cells only live 120 days. Therefore, after 4 months every infected red blood cell will have been replaced. It may sound plausible, but the reasoning is not sound. Every red blood cell (RBC) has a different birthday and at a different point in its lifecycle.  Cells are destroyed and made every day.  Infected senescent cells may transfer merozoites (infecting stage of parasite) to new born cells on any given day.  There is no specific duration that will always be effective. A short course of therapy, e.g. 3 weeks of quinine/clindamycin could at times achieve compete remission. 
Antimalaria drugs make work well but not all antiprotozoal drugs kill Babesia. This seems to be a common misconception.  Some drugs used to treat toxoplasmosis (like Mepron) may be effective against Babesia.  Drugs active against, Giardia, Amoeba, Leishmaniasis and other protozoans will likely not be effective.  Flagyl is a broad-spectrum drug with activity against Giardia and Amoeba. It is also an effective anti-Lyme drug. It has no activity against Babesia. 
Anti-worm drugs, such as ivermectin, is active against microfilaria, and has no antibabesia properties.  If the drug provides relief of symptoms it is doing something else.
Unless you are a scientist -- reading about complex cellular biology, biochemistry, etc. is likely only to confuse. A patient copied and pasted something from the internet which claims that Babesia infection suppresses the production of nitric oxide.  The truth is that Babesia infection activates macrophages and stimulates the production of nitric oxide (NO).  Nitric oxide is an extremely complex signaling molecule and an entire science journal is dedicated to this one compound. Reading about cytokines and metabolic pathways, killer T cells, Th1, Th2 etc. and trying to apply it to your illness is an example of how a little knowledge can be dangerous.
The Mepron/ Zithromax combinations is the most widely used initial approach.  The higher dose, Zithromax 500-600 mg and Mepron 2 tsp twice daily is more likely to be effective.  Medication doses are within FDA recommended levels.  This is generally the best place to start. 
Quinine/clindamycin is too toxic for most to tolerate but is very effective. 
Malarone has been used in lieu of Mepron but the dose of the active ingredient, atovaquone is quite low. 
The traditional herb artemisinin has a long track record and is a very helpful adjunct to treatment.  Combining active artemisinin with the whole plant (artemisia) may enhance adsorption and bioavailability.
The FDA approved Coartem contains artemether, a more active derivative of artemisinin and is very effective. 
Liposomal artemisinin available through a compounding pharmacy is a potent alternative. 
Artesunate is another artemisinin derivate, available in other countries; it may also be highly active.  An oral version of the agent is also available through TCM (Traditional Chinese Medicine) sources. 
There are many traditional herbs, this is a partial list.   Cryptolepis can be very effective at times, sold as a single agent through a compounding pharmacy.  
Herbal combination therapy, described by Buhner: cryptolepis, sida acuta and alchornea may be an effective option. 
Daraprim (with leucovorin) folic acid antagonist, a drug typically used to treat toxoplasmosis and has some anti-Babesia properties.  It may be helpful adjunctively. 
Larium, related to quinine (with doxycycline) is very effective but its use has been limited because the side effect depression. 
Antibiotics, generally not effective as single agents.  IV clindamycin can be effective in stubborn cases. 
Bactrim touted to have anti-babesia properties is typically ineffective. 
Other, novel approaches have been used in patients with very resistant disease.  For example, the anticoagulant heparin coats merozoites and inhibits RBC penetration. (works in mice, some human data).

Babesia can be associated with numerous symptoms: fever, feeling flulike, malaise, fatigue, chills, sweats, headache, air hunger, cough, joint pain, muscle pain, cough, abdominal pain, nausea, depression, changes in emotional state and many others.

Clinically, Babesia is usually seen as a coinfection with Lyme and other tickborne pathogens and symptoms may be more confused.  Babesia is the second most common tickborne infection after Lyme. Long term remission is attainable in the vast majority of patients, time frame unpredictable.

Wednesday, February 13, 2019

Lyme ADD

Attention deficit disorder, ADD/ADHD brains operate in much the same way.  For purposes of this piece I will only discuss ADD. ADD is common, perhaps much more than appreciated. It may affect 20% of the general population. Symptoms vary tremendously in degree  and severity from one person to the next. 

ADD is closely associated with “executive function” disorder. Brain housekeeping functions controlled by the frontal lobe are askew.  Patients have problems with focus, attention and staying on task.  Minds wander. Patients are impatient and interrupt. They don’t follow conversations; their minds are elsewhere. Their memories are full of holes. They lose their keys, wallets and misplace important papers. They forget where they parked their car at the mall. Routine tasks don’t get done, like washing dishes or filing tax forms. If something interests the ADD brain the person may hyper-focus: play a video game for hours on end, stay up all night reading a book despite predictable exhaustion the next day.  It is not all bad. People with ADD can be extremely creative, interpret the world in unique ways.  For example, only an ADD Einstein could imagine what it is like to travel next to a beam of light and discover relativity.  The same Einstein never learned to drive a car, he lacked the required focus. (Einstein’s brain was unique in other ways as well). ADD people are risk takers, which may be good or bad. They have other unique personality traits/quirks. 
These are the symptoms I hear every day from Lyme patients. They have ADD. Adult ADD. Or do they?
Adult ADD is a misnomer.  ADD is a genetic brain glitch. You are born with it. Symptoms should be present in elementary school or before.  Preexisting ADD may be discovered at any age.  Once it was believed that ADD, a pediatric disorder resolved over time. Perhaps the hyperactivity component resolves in many cases; the important frontal lobe executive dysfunction does not. 
The important question for a Lyme patients is: were you like that before?  If the answer is: no, I was precise, organized and orderly. Then the diagnosis is not ADD.  It is Lyme masquerading as ADD, or “Lyme ADD.”  Findings on functional brain scans, like SPECT may be similar to those seen with ADD.  Patients with preexisting ADD are afflicted the most. They experience ADD on steroids. 
Of course, Lyme, Lyme brain, Lyme encephalopathy, neuroborreliosis (synonyms) are treated with antibiotics etc.  But “Lyme ADD” patients can also be effectively treated, if only temporarily with classic ADD drugs and experience much improvement. 
Stimulants tend to be the most effective agents and may be multipurpose since most patients are suffering with severe fatigue as well.  Drugs like Nuvigil work only for wakefulness, not for ADD.  The principal drugs are Ritalin and Adderall and there are multiple variants. 
Proper dosing, side effect are other clinical details are outside the scope of this discussion. 

Appropriate treatment may drastically improve quality of life for many suffering with "Lyme brain."

Thursday, February 7, 2019

Lyme and Hashimoto's.

It has been reported by “Lyme doctors” that Lyme infection is associated with endocrinopathies (disorders of the endocrine system). The most frequent is thyroid disease, generally autoimmune hypothyroidism AKA Hashimoto’s disease.  When looking at Lyme associated endocrine disorders, we need to take them one at a time.  A patient I saw today gained 70 pounds and was first diagnosed with hypothyroidism prior to Lyme. Thyroid supplementation helped him loose the weight. Thyroid disease, particularly autoimmune Hashimoto’s disease is very common. Lyme is very common. But do Lyme patients have hypothyroidism more frequently than would be expected on the basis of chance? Is there is a causal relationship? Hypothyroidism is almost entirely autoimmune. Anti-TPO and other anti-thyroid autoantibodies are invariably present. First off, we know that Hashimoto’s is a familiar disorder, e.g. mom and 2 daughters all suffer with it.  It has been well established that there is genetic predisposition, i.e. HLA DR3, DR5 mutations. 
Autoimmune disease likely is caused by several different mechanisms, one is called molecular mimicry. It has been reported that Bb shares certain amino acid sequences with thyroid proteins.  Antibodies directed against Lyme, in genetically predisposed individuals, may precipitate the productions of self-directed antibodies.  In other words, Lyme antibodies accidentally trigger anti-thyroid antibodies in some cases. 
It appears there may be a causal relationship.  I don’t think there is anything published confirming this suspicion. 
Most endocrine disorders are not autoimmune, including: hypothalamic, pituitary, adrenal disorders, sex hormones and (? POTS -- angiotensin 1 receptor).  If relationships exist, other factors are in play. 
All of my Lyme patients, who invariably complain of fatigue, have their thyroid functions checked.  Most doctors just screen with TSH.  T3 and T4 may be helpful but anti-thyroid antibodies are essential.  If these antibodies are present the patient will need thyroid supplementation sooner or later. If they have exhaustion – sooner, irrespective of the other numbers (except with hyperthyroidism or Grave’s disease).

Thursday, January 31, 2019

Lyme disease and Sherlock Holmes: facts precede theory

Lyme patients, suffering with chronic fatigue, chronic pain, cognitive difficulties seek medical care through “the system.” Where else would you go?  
More often than not, the doctors, the healers? dismiss patient symptoms and concerns, the tears and misery,  not looking up from the omnipresent computer screen saying it’s all in their head, without emotion, without a single iota of compassion or empathy.  
Patients seek validation, but it is not to be found as the physician scribbles a referral for a psych eval as he calls "nurse" and moves to the next exam room. 
The healer is gone, replace by an evidenced-based robotic technician.
A 30-year-old former military officer complains of: severe fatigue, generalized pain, weakness, brain fog, “strange symptoms,” and bouts of presyncope (almost passing out) leading to ER visits was told by one doctor he suffers with a psychosomatic disorder. He lives in a wooded area; favorite activities including running through the woods with his 3 dogs (none treated for ticks), hiking, camping and running. He trained in Quantico VA, crawling through tall grasses and wooded areas 7 years ago.  Doctor after doctor after doctor found nothing wrong, and all reassured him that he did not have Lyme -- because the standard test was negative. 
A 62-year-old female has been diagnosed with longstanding, severe fibromyalgia. She is plagued by allodynia (touching skin excruciating) and she exhibits diffuse, paired tender spots: neck, trapezius, interscapular, paraspinal, SI, chest wall, anterior shoulders, above elbows and knees, anserine bursa area, ankles, heels, shins and other. There is no evidence of joint inflammation, swelling, warmth or redness. (Classic findings of fibromyalgia). Her rheumatologist diagnosed post-Lyme arthritis and wants to prescribe Zeljanz. The patient didn’t even know the drug is an immune suppressing biological until I told her.  In this case a rural rheumatologist accepted a non-CDC interpretation of a Lyme test.  
Sherlock Holmes was a very smart guy (physician author, Arthur Conan Doyle). Paraphrased, he said:  you must collect all the data before formulating a theory; if you start with theory you will twist the facts, to comport with your theory. The theory (therefore conclusions) will be severely biased. Roughly what he said. 
If you start with theory, the foregone conclusion really that Lyme is rare, presents classically doesn’t persist etc. (IDSA theory), you dismiss, distort or spin the facts, crucial facts -- like crawling through grass and woods surrounding Quantico VA, camping, hiking and hunting. If you start with an open mind, collect the facts and process them, a different theory clearly emerges: patient one is suffering with manifestations of Lyme. 
The theories or hypotheses must fit the facts. Doctors must start with a reasonable fund of knowledge. I think patient 2 was diagnosed with posttreatment Lyme disease syndrome.  OK. Maybe.  However, the diagnosis of post-Lyme arthritis and the recommendation of Zeljanz can only come from a place of creative ignorance.  Perhaps attractive drug reps are leaving samples. The dangerous drug goes for more than 2000.00 dollars a month. 
Lyme disease complex -- our understanding of the disease nascent, a work in progress. Different practitioners are finding different ways of understanding the disease guided by differing philosophies, belief systems and so on.  A work in progress. 
Chronic Lyme disease is what I have been chasing all these years. 

How do I define chronic Lyme disease:
Lyme disease is a chronic, complex, (usually) multisystem disorder characterized by an intense inflammatory response causing a wide spectrum of symptoms and syndromes, associated with persistence of the causative microorganisms (Borrelia species), frequently in conjunction with other opportunistic microbes (co-infections) which also tend to persist.  Something like that. 
How do we define posttreatment Lyme disease syndrome?
Perhaps we need to return to the wisdom of the late 19th century detective.  It has the same definition. It is really the same thing except the afflicted patient has treated with a formulaic course of antibiotics which proved ineffective.  Bending over backwards, to compromise with the Lyme deniers may admittedly be destined to fail.  Is it a workable bridge or a bridge to nowhere?  The designation of PTLDS may have a dark side if used as a justification for prescription of dangerous biologicals. The facts are the facts.  Facts must precede theory. Evidenced based guidelines (IDSA) start with entrenched theories; facts are twisted to the breaking point in support of deeply flawed beliefs which are severely biased – at the very least.  It is elementary my dear…

Tuesday, January 22, 2019

Why do 40 doctors still get it wrong? Isn't the science clear?

A 50-year male, an academic, a PhD in biology came to see me, somewhat reluctantly. I was a last resort, an afterthought. He was suffering with a disabling mix of symptoms: headaches, joint pain, pins and needles, overall weakness, fatigue, fevers, night sweats and trouble thinking clearly. He still worked 5 days a week, thankfully a government job, something he knew inside and out. He still struggled to get through the day crashing on the sofa the moment he got home. The guy lives in a wooded area of Prince George’s County MD around the DC beltway. Deer camp in his back yard. He  previously prided himself in his athletic prowess, doing motor cross and competitive downhill skiing. He spent hours in the back yard, gardening and clearing brush. Chopping wood for the fireplace. Sports were a distant memory now. He had seen by 40 or so doctors, some of the best he thought. University professors and the like. No diagnosis could be made. It was suggested it was psychosomatic and he needed to see a psychiatrist.  Sure, he felt depressed and considered the diagnosis, but he knew that wasn’t it. He admits to epic tick exposure, 25 ticks on his body yearly for more than 10 years. He found a few attached ticks but thought he always remove them early. He had no history of a bull’s eye rash or other known Lyme symptom – he thought, at least that is what the books and reliable sources said.  His doctors said he most certainly did not have Lyme disease. 
To my way of thinking the likelihood of tickborne illness approached 100%.  Maybe he removed most ticks, but it is almost certain he missed some.  Larval and nymph forms are stealthy and sometimes impossible to find.  And – what else could cause that particular mix of symptoms? 
His Lyme tests were negative.  I repeated his Western Blot; it was clearly negative.  Tickborne testing was negative except the blood Giemsa slide which showed parasites inside his red blood cells. 
There is much talk about how long ticks need to be attached to transmit Lyme. Its an open question. I haven’t heard any discussion about how long it takes to transmit Babesia. Nonetheless, I thought it was unlikely that Babesia was responsible for most of his symptoms.  Lyme must be there as well and perhaps other coinfections. 
Doctors today are not taught to think and solve complex clinical problems and may worse, risk penalty if they dare do so. Docs are taught cookbook guidelines. “Medicine for Dummies.” Dogma states: Lyme patients always get rashes and are positive by the ELISA/Western Blot. Science informs that many patients do not get rashes, and many are “seronegative.” Undisputed fact. Why are doctors fed bad facts? ID doctors clearly have an agenda when it comes to Lyme disease. 
Guidelines are specialty driven.  ID doctors think about germs, cardiologist hearts, nephrologists kidneys and so on. Medicine is divided into various narrowly focused specialties. 
Primary care doctors should be the ones to put things together, integrate all the reports and data. But they are too busy or scared.  This is crazy.  
I am speaking from an allopathic perspective, fact based, and science based (my perspective).  An integrative, holistic approach must look at the interplay of genetic, environmental and psychosocial factors and the complex interplay amongst the various organ systems and “virtual” organ systems, the most important of which is the immune system. Germs are now and always have been the most important environmental factor associated with human disease. 
Infection has an established role in cardiovascular disease and cancer. Infection plays a role in autoimmune disease and perhaps much more. 
Science describes new and emerging multisystem diseases:  dysautonomia, mast cell activation syndromes and others for which there is scientific understanding.  Their existence is settled science. 
Elusive syndromes such as fibromyalgia, CFS, migraines are partially understood scientifically. There existence settled science. 
And posttreatment Lyme disease syndrome, a valid, across the board accepted diagnosis, of which a lot has been written is settled science diagnosis. 
From a mainstream medical perspective, the most likely diagnosis should be posttreatment Lyme disease syndrome. The cause of the disease (PTLDS), according to authorities is not understood. 
Why isn’t Lyme the most likely diagnosis?
Come on. 
Politics? Willful misdirection on the part of the mentors and supposed experts? IDSA?
There are likely many conflicts of interests and the fog of a paradigm war clouds the truth – not to mention hubris with reputations and careers on the line. 
The academic world, no matter the field, is fraught with politics and political correctness. In medicine lives are on the line. The culture of guru – ism is outdated and dangerous. 
The ID agenda must be exposed and squelched. 
When you open the door to PTLDS you open the door to chronic Lyme disease. (Cause unknown). The spirochetes persist in test tubes and animals – and humans. If this is true (it is), perhaps the persistence of coinfection is also true. The science suggests a reasonable theory is persistent infection plays a significant role in the perpetuation of  PTLDS.   Lyme is a multisystem, immune suppressing disease. An understanding of immune mechanisms further supports the hypothesis. Opportunistic infection makes sense. 
Empiric evidence should not be ignored.  Empiricism is a time honored source of data in medicine. 
Physicians are allowed discretion. Yes, they are. Evidence based medicine as described in UpToDate admits to biases and limitations and allows for discretionary use of its findings and recommendations.  The IDSA admits only 20% of their guidelines are based on high level evidence; their guidelines in general are largely opinion driven. The IDSA states guidelines are recommendations only and do not dictate gospel. How did these guidelines become gospel, the word of God?
There is a turf issue at play.  Specialists want to maintain control over their slice of the pie. But specialists are unable to look at the whole pie.  Only thoughtful generalists (or others with that perspective) can take in the depth and breadth of the entire pie can do so.  The pie only gets larger and more complex with each passing year. 
An allopathic, fact based, common sense based, and science-based understanding of Lyme and related infections ultimately leads to an ILADS’s -type understanding of the illness. It is inevitable. All roads lead to Rome. The logic and science are unassailable. 
It shouldn’t have taken over 40 doctors. Hundreds of tick bites? Specialty driven biases blocked the obvious answer at every step. A system of checks and balances is absent. 
The diagnosis may not be 100% clear or certain. A working diagnosis is a place to start. 
The outstanding question should relate to appropriate therapy. How do you treat chronic Lyme and coinfections, or specifically, how do you treat this patient?
The best place to look for answers is doctors like me who have been treating the disease for years and decades. 

Monday, January 14, 2019

Treating Lyme, 2019, a brief overview: The more things change the more things remain the same ( Plus ça change, plus c'est la même chose)

Things are changing slowly.

My paradigm for treating Lyme is in constant flux.  Lyme is in general, a systemic, multisystem disorder characterized by widespread inflammation. I try to understand the underlying cause of inflammation. Inflammation is due to an immune response which may be appropriate, inappropriate and/or autoimmune.  Mast cell activation (MCAS), for example, is an example of inappropriate immune response/inflammation which may be triggered by infection.  Germ persistence is a key factor. But related autoimmunity is important. For example, Lyme may trigger rheumatoid arthritis – or something that looks like it.  We know that other factors that incite systemic autoimmune responses, for example, gluten in susceptible patients may exacerbate symptoms of Lyme.. A variety of other autoimmune manifestations need be considered, for example, PANS (PANDAS) causing autoimmune encephalitis. Consider POTS, another multisystem disorder which can look like Lyme. Underlying genetic, somatic disorders may contribute to symptoms, for example, Ehlers Danlos syndrome, a connective tissue disorder. 
Following “Sutton’s Law” I try to go where the money is.  I treat symptoms, like disturbed sleep and fatigue. Increasing functionality is key to restoring quality of life. I focus on: Lyme, coinfections, inflammation, genetic disorders and symptoms. Nutritional issues are important.  I put aside: viral infection, heavy metal toxicity, mold toxins and other confounding issues that seem popular. (Antiviral meds can be very helpful). I put aside “adrenal fatigue.” Universally, chronically ill patients and Lyme patients develop adrenal dysfunction. This will usually fix itself when the underlying disease is treated, and treatment can backfire. Thyroid disease/dysfunction is another matter and must be treated. The role of epigenetics is unclear and not something I focus on early in treatment.  The notion that antibiotics alone will fix everything is incorrect. 
The antibiotics, antimicrobials mentioned are examples and not recommendations. Only a treating physician can decide what might be appropriate. Choice of antibiotics is driven by symptoms.  Lyme” coverage” is always present, if at a lower intensity.  If Lyme is the main driver of symptoms a cocktail of 3 drugs may be used.  Doxycycline, Rifampin and Tindamax is an example of a 3-drug cocktail – there are many others.  When rifampin is used Bartonella Herxheimer reactions may appear and may be severe.  If Bartonella is the primary target a cocktail of Zithromax or Biaxin, doxycycline and Rifampin may be used – and others.  If Babesia is the main issue a Cocktail of Zithromax, Mepron and doxycycline and others may be considered. Depending on the patient, one drug may be added, incrementally, every 3-4 days. The meds listed are exemplary.  Details including dosages and management of Herxheimer reactions is beyond the scope of this brief post. Transition from one therapy to another also not discussed here.  In some situations, for example, acute Lyme encephalopathy, IV Rocephin is used out of the gate. Rocephin remains the first line of intravenous therapy. I use continuous rather than pulse therapy. When a patient improves, I transition to pulse therapy and fewer antibiotics. Drugs like Dapsone may have a role impacted Babesia and Lyme. There are many other antibiotics and antibiotic combinations not mentioned here. 

Every patient is different and requires a unique treatment plan.  There are no "protocols."
Co-morbidities (other diseases, syndromes) are addressed.  Antibiotics don’t fix everything. 
Insomnia is treated with a variety of agents, e.g.: doxepin, Restoril, Seroquel, etc – whatever it takes. I routinely order sleep studies.  Sleep disorders including sleep apnea are common accompaniments of Lyme. I am frequently surprised to meet patients with 10 years or more of chronic fatigue who have never had a sleep study. 
Fatigue can frequently be effectively treated with drugs such as Nuvigil and others. 
Depression and pain must be treated.  I put the two together because some of the therapies dovetail.  Patients may tolerate various antidepressants in a way I cannot predict.  Some patients are on SSRI, e.g. Lexapro. The patient may not tolerate Cymbalta which is effective for pain. A very low dose of amitriptyline, e.g. 10 mg 1-3 daily can confer to the SSRI the pain modulating properties of Cymbalta without amitriptyline side effects. Gabapentin is indispensable. Muscle relaxers like Zanaflex or Flexeril, when dosed properly can be very effective.  Ketamine, effective for pain and depression is the drug of the future, already in use. There are numerous other approaches. 
Brain fog, cognitive impairment can be treated in part with supplements and prescription drugs like Namenda. 
Inflammation can be treated with supplements like curcumin e.g Theracurmin and Wobenzym, etc.  Rarely short courses of steroids and/or other immune modulators like Plaquenil and biologics may be considered. 
Adjunctive therapies may be very helpful, e.g. hyperbaric oxygen therapy, saunas, and perhaps EMF therapy. 
Ultimately, graded exercise is important. 
Treatment must be paced.  Herxheimer reactions must be heeded.   
We must exclude: immune deficiency disorders, e.g. low IgG and subclasses (IVIG may be very helpful); mast cell disorders; nutritional disorders; autoimmune disorders, e.g. thyroid disease and pernicious anemia and many other medical disorders.  A problem list is created for each symptom.  A differential diagnosis list is attached to each symptom to be revisited if needed.
When a therapy doesn’t work as expected the treatment and/or diagnosis must be reconsidered. 
To summarize:  Aggressive, frequently 3 agent therapy required. Treat other syndromes which may be present. Treat symptoms. Increase function and quality of life.  Address the most likely causes of illness. 

I do things differently from some of my colleagues.  I incorporate many mainstream medical therapies, practices (baby and bathwater).  This treatment approach has been very effective.

The approach is science based, allopathic but translational, incorporating new ideas, theories and clinical therapies. I try to keep things focused and simple (it is obviously quite complicated). 
The above represents opinions of the author, presented for educational purposes only and not intended for any clinical purposes, including the diagnosis or treatment of any patient.

Monday, December 17, 2018

Dapsone, wonder drug? Not just about killing germs

People have been excited about trying Dapsone for PTLDS.  Horowitz has had good clinical results. Then Zhang did the test tube trials and it was a bust. It’s a sulfa drug and I have not been impressed using sulfa drugs treating Lyme.  Dapsone is used for leprosy, skin conditions including acne and dermatitis herpetiformis – the skin condition associated with celiac disease. With this portfolio I wouldn't have thought Lyme.  Dapsone may be a true wonder drug, one off the radar since it has been around forever (since 1937, predating penicillin, first synthetized in 1908) and there is no money in it for pharmaceutical companies. But what a drug! 

There are many ways the drugs may be repurposed and it is not just about killing germs, at least not directly.
Dapsone has tremendous anti-inflammatory properties with widespread effects on immune function. It positively impacts:  effector cells, cytokines, adhesion molecules, prostaglandins, leukotrienes, interleukins, tumor necrosis factor, leukocyte activation, ROS (reactive oxygen species), folate antagonist (this I knew) and a lot more. 
It is active against bacteria and protozoa, including malaria (Babesia?). 
It is bacteriostatic, not bactericidal and suppresses: strep, staph, pneumococcus, mycobacteria and more. 

I has been successfully used in rheumatoid arthritis with efficacy comparable to more toxic drugs.
It has steroid sparing effects which may make it useful in a wide variety of inflammatory and autoimmune disorders
It prevents UV associated photosensitivity (think doxy during the summer). 
It is well adsorbed into all tissues, including the brain. It may have neuroprotective effects (human stroke study). ?Brain fog in Lyme patients. 
It may have anti-cancer effects, even against brain tumors. 
It might be effective for life extension (works in a worm).  We are not worms.  
It may help kill Lyme through non-antibiotic effects. For example, it improves immune function and generates ROS which have natural antibiotic properties. 
There is much more.
It has potential toxicity and side effects which must be monitored.  

It sounds too good to be true, so I include the reference.

Archives of Dermatology (2014) 306:103-124, Wozel, Blasum (University of Dresden, Germany)
Open access with extensive references.