Archive for the ‘Treatment’ Category

Mast Cell Activation Syndrome & Lyme/MSIDS

The path to health leads many Lyme/MSIDS patients down numerous rabbit holes.  A pathogen invasion of various bacteria, funguses, viruses, and nematodes depletes the body of many important things.  We are literally being feasted upon, and patients find that they need to supplement their deprived bodies of many things after becoming infected.

Pathogen invasion also causes autoimmunity, where the body attacks itself. Cytokine cascades are continually being set off and the body is in a state of immunoconfusion with a pro-inflammatory response.  The immune system can no longer identify bad guys from good guys.  For many, getting the immune system straightened out is at least half the battle.

Mast Cell Activation Syndrome (MCAS) can cause these things as well.

Dr. Lawrence Afrin, M.D. wrote about MCAS in his book, Never Bet Against Occam.  In reading the book, it becomes clear there are as many nuances with MCAS as there are with Lyme/MSIDS.  Every patient is truly, uniquely different. In treatment, there is much trial and error, with each patient responding to differing things.

Our personal experience with MCAS stems from my daughter who developed allergy-type symptoms over years which came to a head when she developed severe Epstein Bar Virus (EBV).  Prior to that she would frequently have to stop running or walking due to severe itching (exercise induced urticardia).  http://www.mayoclinicproceedings.org/article/S0025-6196(11)63475-7/fulltext  Our LLMD uses LDA/LDI for those with immunoconfusion with success.  Although, she thankfully doesn’t present with Lyme/MSIDS, she definitely struggles with a confused immune system and EBV.  Read here for more on LDA/LDI:  https://madisonarealymesupportgroup.com/2016/05/30/new-kids-on-the-block-ldaldi/  In her case, she reacted strongly to the LDA.  The injections are  somewhat separated so you can visibly see what your issues are.  She developed a facial rash which was deep and painful.  Within a day of her shot it resolved completely, showing how skin symptoms can definitely be caused by allergens and immunoconfusion.

IMG_0475

https://www.linkedin.com/pulse/mast-cell-activation-syndrome-mcas-when-histamine-carnahan-md?trk=v-feed&lipi=urn%3Ali%3Apage%3Ap_flagship3_search_srp_content%3BH0Gf8FqaKVxrspeojT9VVA%3D%3D

Mast Cell Activation Syndrome (MCAS): When Histamine Goes Haywire…

Published on October 31, 2016
Jill C. Carnahan, MD – Used with permission
Founder, Medical Director, Flatiron Functional Medicine

Mast cells are present in most tissues throughout the human body, especially connective tissue, skin, intestinal lining cardiovascular system, nervous system, and reproductive organs. They are part of the allergic response designed to protect us from threat and injury. When the body is exposed to a perceived threat, the mast cells secrete chemical mediators, such as histamine, interleukins, prostaglandins, cytokines, chemokine and various other chemicals stored in the cytoplasm of the cell. These chemical messengers produce both local and systemic effects, such as increased permeability of blood vessels (inflammation and swelling), contraction of smooth muscle (stomach cramps and heart palpitations), and increase mucous production (congestion, sneezing, etc). Historically, we thought of mast cells only in relation to an allergic or anaphylactic response. We now know they play a profound role in immune activation, development of autoimmunity and many other disorders, such as POTS (postural orthostatic hypotension). Sadly we are seeing a large increase in patients presenting with mast cell disorders and MCAS. I believe it is in part do to the onslaught of more pervasive environmental toxins, molds and chemicals.

Without mast cells, we would not be able to heal from a wound. They protect us from injury and help the body to heal. Unfortunately, overactive mast cells can cause a variety of serious symptoms.

Symptoms of overactive mast cells may include:

skin rashes/hives
swelling/edema
flushing
itching
abdominal pain
nausea/vomiting
diarrhea
wheezing
shortness of breath
heart palpitations
anxiety, difficulty concentrating
headaches
brain fog
low blood pressure
fatigue

Mast cell activation syndrome (MCAS) is a condition symptoms involving the skin, gastrointestinal, cardiovascular, respiratory, and neurologic systems. It can be classified into primary (clonal proliferation or mastocytosis), secondary (due to a specific stimulus), and idiopathic (no identifiable cause). Proposed criteria for the diagnosis of MCAS included episodic symptoms consistent with mast cell mediator release affecting two or more organ systems with hives, swelling, flushing, nausea, vomiting, diarrhea, abdominal pain, low blood pressure, fainting, heart palpitations, wheezing, red eyes, itching, and/or nasal congestion.

Triggers may be medications, foods, supplements, hormones, opioids, stressors (physical or emotional), cold temperature, heat, pressure, noxious odors, chemicals, insect bites, trauma or environmental toxins.

We commonly see mast cell activation syndromes associated with CIRS (chronic inflammatory response syndrome) in response to biotoxins, such as mold, inflammagens, and lyme-related toxins.

Low MSH and Mast Cell Disorders?

As mentioned above, we frequently see histamine intolerance and MCAS in patients with mold-related CIRS (chronic inflammatory response syndrome). It is interesting to note that a common finding in CIRS is low MSH. According to this study in the Journal of Investigative Dermatology, alpha-MSH plays an immunomodulatory role during inflammatory and allergic reactions of the skin. In addition, there is evidence that MSH induces mast-cell apoptosis (cell death).

Definition of Mast Cell Activation Syndrome (MCAS)

Typical clinical symptoms as listed above
Increase in serum tryptase level or an increase in other mast cell derived mediators, such as histamine or prostaglandins (PGD2), or their urinary metabolites,
Response of symptoms to treatment

Diseases Associated with Mast Cell Activation Syndrome (MCAS)

Allergies and Asthma
Autism
Autoimmune diseases (Hashimoto’s thyroiditis, systemic lupus, multiple sclerosis, bullous pemphigoid, rheumatoid arthritis and others.                                            Eczema
Celiac Disease
Chronic Fatigue Syndrome
CIRS (chronic inflammatory response syndrome)
Eosinophilic Esophagitis
Fibromyalgia
Food Allergy and Intolerances
Gastroesophageal reflux (GERD)
Infertility (mast cells in endometrium may contribute to endometriosis)
Interstitial Cystitis
Irritable Bowel Syndrome (IBS)
Migraine Headaches
Mood disorders – anxiety, depression, and insomnia
Multiple Chemical Sensitivities
POTS (postural orthostatic hypotension)

Mast cells are known to be the primary responders in allergic reactions, orchestrating strong responses to minute amounts of allergens. Several recent observations indicate that they may also have a key role in coordinating the early phases of autoimmune diseases, particularly those involving auto-antibodies.

Lab tests specific to mast cell activation for suspected MCAS may include:

Serum tryptase (most famous mast cell mediator)
Serum chromogranin A
Plasma histamine
Plasma PGD2 (chilled)
Plasma heparin (chilled)
Urine for PGD2 (chilled)
PGF2a
N-methylhistamine

Tryptase is the most famous mast cell mediator. Serum tryptase value is usually normal in MCAS patients, but sometimes it is elevated. Tryptase values that show an increase of 20% + 2 ng/ml above the baseline level are considered diagnostic for MCAS.
Chromogranin A is a heat-stable mast cell mediator. High levels can suggest MCAS, but other sources must first be ruled out, such as heart failure, renal insufficiency, neuroendocrine tumors and proton pump inhibitor (PPI) use.
Heparin is a very sensitive and specific marker of mast cell activation. However, due to its quick metabolism in the body, it is very difficult to measure reliably.
N-methylhistamine is usually measured in a 24 hour urine test to account for the variability in release over the course of the day.
Prostaglandin D2 is produced by several other cell types, but mast cell release is responsible for the dominant amount found in the body. PGD2 is less stable than histamine and metabolized completely in 30 minutes.
Other less specific mast cell mediators that are sometimes abnormal in MCAS patients include Factor VIII, plasma free norepinephrine, tumor necrosis factor alpha, and interleukin-6.

Treatments to reduce MCAS symptoms and lower histamine

H1 Blockers – hydroxyzine, doxepine, diphenhydramine, cetirizine, loratadine, fexofenadine
H2 Blockers Famotidine (Pepcid, Pepcid AC), Cimetidine (Tagamet, Tagamet HB) Ranitidine (Zantac)
Leukotriene inhibitors: Montelukast (Singulair), Zafirlukast (Accolate)
Mast cell stabilizers -Cromolyn, Ketotifen
Tyrosine kinase inhibitors – imatinib
Natural anti-histamines and mast-cell stabilizers
Ascorbic Acid
Quercetin
Vitamin B6 (pyridoxal-5-phosphate)
Omega-3 fatty acids (fish oil, krill oil)
Alpha Lipoic Acid
N-acetylcysteine (NAC)
Methylation donors (SAMe, B12, methyl-folate, riboflavin)
Certain probiotics decrease histamine productionLactobacillus rhamnosus and bifidobacter species
DAO Enzymes with meals – Xymogen HistDAO or Histamine
Decrease consumption of high histamine foods (more on histamine-restricted diet)
Avoid alcoholic beverages
Avoid raw and cured sausage products such as salami.
Avoid processed or smoked fish products. Use freshly caught seafood instead.
Avoid pickles
Avoid citrus fruits.
Avoid chocolate
Avoid nuts
Avoid products made with yeast and yeast extracts
Avoid soy sauce and fermented soy products
Avoid black tea and instant coffee
Avoid aged cheese
Avoid spinach in large quantities
Avoid tomatoes, ketchup and tomato sauces
Avoid artificial food colorings & preservatives
Avoid certain spices: cinnamon, chili powder, cloves, anise, nutmeg, curry powder, cayenne pepper

Specific Symptom Treatment in MCAS

(Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options)

Headache⇒ paracetamol; metamizole; flupirtine
Diarrhea⇒ colestyramine; nystatin; montelukast; ondansetron
Colicky abdominal pain ⇒ metamizole; butylscopolamine
Nausea⇒ metoclopramide; dimenhydrinate; 5-HT3 receptor inhibitors; icatibant
Respiratory symptoms (mainly increased production of viscous mucus and obstruction with compulsive throat clearing) ⇒ montelukast; acute: short-acting albuterol
Gastric complaints⇒ proton pump inhibitors
Osteoporosis, bone pain⇒ biphosphonates, Vitamin D plus calcium
Non-cardiac chest pain⇒ H2-histamine receptor antagonist; proton pump inhibitors
Tachycardia⇒ verapamil; AT1-receptor antagonists; ivabradin
Neuropathies ⇒ a-lipoic acid
Interstitial cystitis⇒ pentosan, amphetamines
Sleep-onset insomnia/sleep-maintenance insomnia⇒ triazolam/oxazepam
Conjunctivitis⇒ preservative-free eye drops with glucocorticoids for brief course
Elevated prostaglandin levels, persistant flushing⇒ incremental doses of acetylsalicylic acid (50-350 mg/day; extreme caution because of the possibility to induce mast cell degranulation)

For more on MCAS, Lyme/MSIDS, and parasites:  https://madisonarealymesupportgroup.com/2017/03/23/rebecca-keith-on-mcas-parasites-lymemsids/

References

Mast Cell Activation Syndrome, A Review http://www.jillcarnahan.com/downloads/MCASReview.pdf
Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options  http://jhoonline.biomedcentral.com/articles/10.1186/1756-8722-4-10
Presentation, Diagnosis and Management of Mast Cell Activation Syndrome by Dr. Afrin  http://www.jillcarnahan.com/downloads/MCAS-Afrin.pdf
Histamine and Gut Immune Mucosal Regulation  http://www.jillcarnahan.com/downloads/Histamine-gut.pdf
Dr. Theoharides presents “Mast Cell Disorders”  https://www.youtube.com/watch?v=92nrFwcNSwc&feature=youtu.be
Diagram of Histamine Symptoms  https://mastcellblog.files.wordpress.com/2013/11/mast-cell-symptoms.jpg
Mast Cell Aware  http://www.mastcellaware.com
A Tale of Two Syndromes  http://www.dysautonomiainternational.org/blog/wordpress/a-tale-of-two-syndromes-pots-and-mcas/
Mold Histamine Connection  https://healinghistamine.com/the-mold-histamine-link/

Category:

Lyme, Treatment, Viruses

Ocular Bartonellosis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318637/
J Trop Med. 2017; 2017: 7946123.
Published online 2017 Feb 7. doi:  10.1155/2017/7946123
PMCID: PMC5318637

Clinical Profile and Visual Outcome of Ocular Bartonellosis in Malaysia
Chai Lee Tan, Lai Chan Fhun,  Evelyn Li Min Tai, Nor Hasnida Abdul Gani, Julieana Muhammed, Tengku Norina Tuan Jaafar, Liza Sharmini Ahmad Tajudin, and Wan-Hazabbah Wan Hitam 

Abstract

Background. Ocular bartonellosis can present in various ways, with variable visual outcome. There is limited data on ocular bartonellosis in Malaysia. Objective. We aim to describe the clinical presentation and visual outcome of ocular bartonellosis in Malaysia. Materials and Methods. This was a retrospective review of patients treated for ocular bartonellosis in two ophthalmology centers in Malaysia between January 2013 and December 2015. The diagnosis was based on clinical features, supported by a positive Bartonella spp. serology. Results. Of the 19 patients in our series, females were predominant (63.2%). The mean age was 29.3 years. The majority (63.2%) had unilateral involvement. Five patients (26.3%) had a history of contact with cats. Neuroretinitis was the most common presentation (62.5%). Azithromycin was the antibiotic of choice (42.1%). Concurrent systemic corticosteroids were used in approximately 60% of cases. The presenting visual acuity was worse than 6/18 in approximately 60% of eyes; on final review, 76.9% of eyes had a visual acuity better than 6/18. Conclusion. Ocular bartonellosis tends to present with neuroretinitis. Azithromycin is a viable option for treatment. Systemic corticosteroids may be considered in those with poor visual acuity on presentation.

In the results section we learn that 19 patients with ocular bartonellosis were followed from 3-68 weeks. Neuroretinitis is an inflammation of the neural retina and optic nerve which can be caused by viruses, autoimmune disease, or bacteria including: syphilis, Rocky Mountain Spotted Fever, toxoplasmosis, toxocariasis, histoplasmosis, leptospirosis, and Lyme Disease. Tuberculosis and Tularemia can also present similarly. The most common ocular complaint was blurred vision with around 60% reporting headaches as their initial symptom.

We also learn that the treatment of choice was Azithromycin followed by Doxycyline, ciprofloxacin, ceftazidime, and cotrimoxazole, with 60% receiving systemic corticosteroid therapy. The discussion section states that the treatment of Bartonellosis is still controversial and that they had to resort of isolated case reports for information.

http://webeye.ophth.uiowa.edu/eyeforum/cases/36-CatScratchBartonella.htm In this case study a 44 year old woman had non-specific blurriness of vision in her left eye. After they went through about every other possibility, they asked about pets at which she showed multiple cat scratches on her arms.

Laboratory results showed:
*White blood cell count: 18,200 with left shift (12,194 segmented neutrophils and 3276 bands)
*Bartonella Henselae IgG 1:1024 (strongly positive)

According to this study, a literature review suggested that a one month course of doxycycline or erythromycin (with or without rifampin) is adequate to treat the organism and hasten recovery. They chose a one month course of doxycycline 100 mg twice daily. The patient returned for follow-up appointments one and two months after this initial diagnosis. Vision improved to 20/60 in the affected eye, improving visual fields, decreased optic disc edema, and resolving sub-retinal fluid.

The case study also states that diagnosis officially requires 3 out of 4 criteria:
• Lymphadenopathy in the absence of other reason (can be missed because it is not present yet or subclinical)
• Positive Bartonella H. titer or skin test
• Known cat contact, preferably with pustule or papule at the site
• Lymph node biopsy with bacilli present, necrosis

They admit this woman met only 2 of the criteria. They also state it is well documented patients will almost always get better on their own but that hundreds of reports give various treatment regimens including doxycycline, erythromycin, rifampin, azithromycin, ciprofloxacin, later addition of steroid drop, and many others.

The unfortunate thing about both of these reports is they make Bartonellosis out to be a benign pathogen, which for Lyme/MSIDS patients couldn’t be further from the truth.

As to the criteria to diagnose:

Thankfully, this woman didn’t present with swollen lymph nodes so they had to find a reason and state it was either subclinical or hadn’t presented yet.

*Hardly anyone I know with Bartonella has swollen lymph nodes.

*The testing for Lyme and every coinfection, including Bartonella, is abysmal.

*They emphasize the cat’s role but don’t even mention ticks, mites, biting flies, other arachnids, sand flies, mosquitoes, fleas and flea feces, the human body louse, potentially from needles and syringes in the drug addicted, as well as bites and scratches from other reservoir hosts.

*As to node biopsy, even this NIH study shows a lack of specificity and lack of typical micro abscesses in almost half of the cases and may mimic other lymphadenopathies.
https://www.ncbi.nlm.nih.gov/pubmed/26551620

*https://wwwnc.cdc.gov/eid/article/22/3/15-0269_article This CDC article states that Bartonella spp. may be the cause of unclear and undiagnosed chronic illness in humans previously bitten by ticks.

*They also fail to mention there are 15 species and counting of Bartonella known to infect humans and that Dr. Ricardo Maggi states, “This case reinforces the hypothesis that any Bartonella species can cause human infection.”
http://townsendletter.com/July2015/bartonellosis0715_3.html  Besides the cat (including bobcats, mountain lions, and other large cats), rats, dogs, rabbits, deer, cattle, small woodland animals, rodents, coyotes, foxes, and elk were found to harbor Bart.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88941/ The question really should be, “What doesn’t carry Bartonella?”

https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/  Here, Dr. Mozayeni states about 60% of Lyme patients tested positive for Bartonella and that it is one of the major coinfections. This link also has treatments, explanation of Bartonella including what it does and how it can present, along with a link for a checklist you can print out and take to your doctor to discuss.

I appreciate Dr. Breitschwert’s and Dorsey Kordick’s comment in the concluding remarks,

“Not too long ago, many were taught during microbiology courses (or medical school training) that blood is generally a sterile medium. Increasingly, this assertion must be qualified with regard to Bartonella spp. as well as other intracellular pathogens that have coevolved with humans and animals to persist in circulating blood cells such as erythrocytes or macrophages for months to years and perhaps longer.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88941/

I wish more researchers were this transparent, then perhaps patients would be taken more seriously.   And, don’t kid yourself, Bartonella is a formidable foe to the immunocompromised.

Category:

Bartonella, Lyme, mosquitoes, research, Ticks, Transmission, Treatment

Kelly Osbourne on Lyme

http://www.usmagazine.com/celebrity-news/news/kelly-osbournes-book-details-lyme-disease-battle-excerpt-w474949

Kelly Osbourne bought a reindeer sanctuary for Ozzy’s birthday which led to a tick bite she burned off with a match. Doctors diagnosed her with epilepsy, and the next ten years were marked with traveling pain until she finally had a seizure.

She was familiar with Philip Battiade at Infusio, an alternative medicine practitioner, who treated her brother for MS, and made an appointment and flew to Germany for two weeks to start stem cell therapy.  http://www.infusio.org/medical/lyme-disease/

Osbourne kept quiet about Lyme disease for fear of pharmaceutical companies coming after her for going to Germany for alternative treatment.

She’s written the book, There Is No F*cking Secret, to be published on April 25, 2017.

 

Category:

Activism, Lyme, Treatment

Sulfa Drugs Against Stationary Phase Bb in Vitro

http://www.mdpi.com/2079-6382/6/1/10

Jie Feng, Shuo Zhang, Wanliang Shi and Ying Zhang *
Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA
Academic Editor: Christopher C. Butler
Received: 19 January 2017 / Revised: 7 March 2017 / Accepted: 14 March 2017 / Published: 22 March 2017

Abstract

Lyme disease is a most common vector-borne disease in the US. Although the majority of Lyme patients can be cured with the standard two- to four-week antibiotic treatment, at least 10%–20% of patients continue to suffer from prolonged post-treatment Lyme disease syndrome (PTLDS). While the cause for this is unclear, one possibility is that persisting organisms are not killed by current Lyme antibiotics.

In our previous studies, we screened an FDA drug library and an NCI compound library on B. burgdorferi and found some drug hits including sulfa drugs as having good activity against B. burgdorferi stationary phase cells. In this study, we evaluated the relative activity of three commonly used sulfa drugs, sulfamethoxazole (Smx), dapsone (Dps), sulfachlorpyridazine (Scp), and also trimethoprim (Tmp), and assessed their combinations with the commonly prescribed Lyme antibiotics for activities against B. burgdorferi stationary phase cells.

Using the same molarity concentration, dapsone, sulfachlorpyridazine and trimethoprim showed very similar activity against stationary phase B. burgdorferi enriched in persisters; however, sulfamethoxazole was the least active drug among the three sulfa drugs tested. Interestingly, contrary to other bacterial systems, Tmp did not show synergy in drug combinations with the three sulfa drugs at their clinically relevant serum concentrations against B. burgdorferi.

We found that sulfa drugs combined with other antibiotics were more active than their respective single drugs and that four-drug combinations were more active than three-drug combinations. Four-drug combinations dapsone + minocycline + cefuroxime + azithromycin and dapsone + minocycline + cefuroxime + rifampin showed the best activity against stationary phase B. burgdorferi in these sulfa drug combinations.

However, these four-sulfa-drug–containing combinations still had considerably less activity against B. burgdorferi stationary phase cells than the Daptomycin + cefuroxime + doxycycline used as a positive control which completely eradicated B. burgdorferi stationary phase cells. Future studies are needed to evaluate and optimize the sulfa drug combinations in vitro and also in animal models.

Category:

Lyme, research, Treatment

One Pill of Doxy Only Reduces Prevalence of Rash, Not Lyme Disease

https://www.lymedisease.org/single-dose-doxy-tick-bite-prevents-rash-not-lyme-disease/  This link shows that Daniel J. Cameron, MD MPH, states there has only been one study (Nadelman et al) on the effectiveness of 1 pill of doxycycline and only found a reduction in the number of erythema migraines (EM) rashes compared to the placebo group.  According to him, the IDSA 1 pill of doxy approach started in 2006 despite the fact that three previous prophylactic antibiotic trials for a tick bite had failed.

http://www.jem-journal.com/article/S0736-4679(17)30026-4/abstract  However, the authors of this recent study in the Journal of Emergency Medicine support the 1 pill of doxy approach.  It fails to mention the ILADS approach where Lyme literate doctors with much experience treating Lyme/MSIDS advise against 1 pill of doxy and the reasons stated above by Cameron.

He also states that the evidence is easily accessible in open access, peer-reviewed journals in PubMed and the National Guideline Clearing House.

Cameron states:

“ILADS 2014 guidelines used the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system to conclude that the evidence for a single, 200 mg dose of doxycycline was “sparse, coming from a single study with few events, and, thus, imprecise.” 

 

According to Cameron Nadelman’s study had several other limitations:

“It was not designed to detect Lyme disease if the rash were absent.
The six-week observation period was not designed to detect chronic or late manifestations of Lyme disease.
It was not designed to assess whether a single dose of doxycycline might be effective for preventing other tick-borne illnesses such as Ehrlichia, Anaplasmosis, or Borrelia miyamotoi.”

Please spread the word and tell doctors.

 

 

Category:

Lyme, Treatment