Archive for the ‘research’ Category

Bartonella & Sudden-Onset Adolescent Schizophrenia a Case Study

https://news.ncsu.edu/2019/03/bartonella-schizophrenia/

Case Study: Bartonella and Sudden-Onset Adolescent Schizophrenia

March 18, 2019
Alumni Gateway near sunset.

In a new case study, researchers at North Carolina State University describe an adolescent human patient diagnosed with rapid onset schizophrenia who was found instead to have a Bartonella henselae infection. This study adds to the growing body of evidence that Bartonella infection can mimic a host of chronic illnesses, including mental illness, and could open up new avenues of research into bacterial or microbial causes of mental disorders.

Bartonella is a bacteria most commonly associated with cat scratch disease, which until recently was thought to be a short-lived (or self-limiting) infection. There are at least 30 different known species of Bartonella, and 13 of those have been found to infect human beings. The ability to find and diagnose Bartonella infection in animals and humans – it is notorious for “hiding” in the linings of blood vessels – has led to its identification in patients with a host of chronic illnesses ranging from migraines to seizures to rheumatoid illnesses that the medical community previously hadn’t been able to attribute to a specific cause.

In a case study published in the Journal of Central Nervous Disease, an adolescent with sudden onset psychotic behavior – diagnosed as schizophrenia – was seen and treated by numerous specialists and therapists over an 18-month period. All conventional treatments for both psychosis and autoimmune disorders failed. Finally a physician recognized lesions on the patient’s skin that are often associated with Bartonella, and the patient tested positive for the infection. Combination antimicrobial chemotherapy led to full recovery.

“This case is interesting for a number of reasons,” says Dr. Ed Breitschwerdt, Melanie S. Steele Distinguished Professor of Internal Medicine at NC State and lead author of the case report. “Beyond suggesting that Bartonella infection itself could contribute to progressive neuropsychiatric disorders like schizophrenia, it raises the question of how often infection may be involved with psychiatric disorders generally.

“Researchers are starting to look at things like infection’s role in Alzheimer’s disease, for example. Beyond this one case, there’s a lot of movement in trying to understand the potential role of viral and bacterial infections in these medically complex diseases. This case gives us proof that there can be a connection, and offers an opportunity for future investigations.”

Co-authors of the study include NC State research associate professor Ricardo Maggi and research technician Julie Bradley, psychiatrist Dr. Rosalie Greenberg, rheumatologist Dr. Robert Mozayeni, and pediatrician Dr. Allen Lewis. Funding was provided by the College of Veterinary Medicine Bartonella/Vector Borne Disease Research Fund.

“Bartonella henselae Bloodstream Infection in a Boy With Pediatric Acute-Onset Neuropsychiatric Syndrome”

DOI: 10.1177/1179573519832014

Authors: Ed Breitschwerdt, Ricardo Maggi, Julie Bradley, North Carolina State University; Rosalie Greenberg, Medical Arts Psychotherapy Associates; Robert Mozayeni, Translational Medicine Group; Allen Lewis, Sancta Familia Center for Integrative Medicine

Published: Journal of Central Nervous System Disease

Abstract:
Background: With the advent of more sensitive culture and molecular diagnostic testing modalities, Bartonella spp. infections have been documented in blood and/or cerebrospinal fluid specimens from patients with diverse neurological symptoms. Pediatric acute-onset neuropsychiatric syndrome (PANS) is characterized by an unusually abrupt onset of cognitive, behavioral, or neurological symptoms. Between October 2015 and January 2017, a 14-year-old boy underwent evaluation by multiple specialists for sudden-onset psychotic behavior (hallucinations, delusions, suicidal and homicidal ideation).
Methods: In March 2017, Bartonella spp. serology (indirect fluorescent antibody assays) and polymerase chain reaction (PCR) amplification, DNA sequencing, and Bartonella enrichment blood culture were used on a research basis to assess Bartonella spp. exposure and bloodstream infection, respectively. PCR assays targeting other vector-borne infections were performed to assess potential co-infections.
Results: For 18 months, the boy remained psychotic despite 4 hospitalizations, therapeutic trials involving multiple psychiatric medication combinations, and immunosuppressive treatment for autoimmune encephalitis. Neurobartonellosis was diagnosed after cutaneous lesions developed. Subsequently, despite nearly 2 consecutive months of doxycycline administration, Bartonella henselae DNA was PCR amplified and sequenced from the patient’s blood, and from Bartonellaalphaproteobacteria growth medium enrichment blood cultures. B. henselaeserology was negative. During treatment with combination antimicrobial chemotherapy, he experienced a gradual progressive decrease in neuropsychiatric symptoms, cessation of psychiatric drugs, resolution ofBartonella-associated cutaneous lesions, and a return to all preillness activities.
Conclusions: This case report suggests that B. henselae bloodstream infection may contribute to progressive, recalcitrant neuropsychiatric symptoms consistent with PANS in a subset of patients.

_______________

**Comment**

Pandora’s Box is just beginning to be opened.  Expect to hear a lot more about Bartonella….

https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/

https://madisonarealymesupportgroup.com/2018/11/10/neurological-presentations-of-bartonella-henselae-infection/

https://madisonarealymesupportgroup.com/2017/08/02/neurological-and-immunological-dysfunction-in-two-patients-with-bartonella-henselae-bacteremia/

https://madisonarealymesupportgroup.com/2018/04/03/encephalopathy-in-adult-with-cat-scratch-disease/

https://madisonarealymesupportgroup.com/2016/11/29/bartonella-seizures/

https://madisonarealymesupportgroup.com/2018/05/07/fox-news-bartonella-is-the-new-lyme-disease/

 

 

Category:

Bartonella, Psychological Aspects, research

How Do Hormones Affect the Heart?

https://www.womensinternational.com/how-do-hormones-affect-the-heart/

How Do Hormones Affect the Heart?

Written by Michelle Violi, PharmD – Women’s International Pharmacy

“How does hormone supplementation affect the heart?” This is a question that our pharmacists hear regularly. Much like the poor, maligned egg in the cardio-healthy diet, hormones have fallen in and out of favor with regard to their effect on the cardiovascular system over the years.

Although a number of studies examine hormonal effects on the cardiovascular system, these studies rarely distinguish between bioidentical and synthetic hormones. However, one study by Dr. Ferdinand Roefsena, Rebecca J. Yang, and Dr. Johannes Veldhuis looked specifically at the bioidentical hormones, estradiol, and progesterone, publishing their results in the Journal of the Endocrine Society. Let’s see what they found!

How Was the Study Designed?

Forty healthy postmenopausal women, ages 50-80, participated in the study. The women were divided into four treatment groups:

  1. Bioidentical estradiol (injection) and bioidentical progesterone (by mouth)
  2. Bioidentical estradiol (injection) and no bioidentical progesterone
  3. Bioidentical progesterone (by mouth) and no bioidentical estradiol
  4. No bioidentical estradiol and no bioidentical progesterone

After 23 days of using these therapies, the women’s blood was drawn and the researchers measured various markers.

What Did the Study Look At?

Because the study was only 23 days long, Dr. Roefsena et al. were unable to evaluate primary endpoints,such as heart attacks or strokes. Instead, they looked at various markers in the blood that have been associated with physical outcomes such as heart disease, stroke, and diabetes. The researchers looked at many significant markers, including:

  1. Total cholesterol
  2. Low-density lipoprotein cholesterol (LDL-C) (referred to as “bad” cholesterol by the American Heart Association)
  3. High-density lipoprotein cholesterol (HDL-C) (referred to as “good” cholesterol by the American Heart Association)
  4. Apolipoprotein B (Apo B)
  5. High sensitivity C-reactive protein (hsCRP)
  6. Adiponectin

With the exception of HDL-C and adiponectin, for which higher levels appear beneficial, decreased levels of the other markers listed above are generally considered favorable, according to the American Heart Association.

What Did the Study Find?

When compared to women who weren’t using any hormone therapies:

  1. Women who used bioidentical estradiol alone had lower levels of total cholesterol, LDL-C, and Apo B. They also had higher levels of HDL-C, which are considered beneficial differences. The researchers had expected this result, based on previous studies as described in the article The Bioidentical Hormone Debate: Are Bioidentical Hormones (Estradiol, Estriol, and Progesterone) Safer or More Efficacious than Commonly Used Synthetic Versions in Hormone Replacement Therapy? by Dr. Kent Holtorf.
  2. Women who used bioidentical progesterone alone had decreased adiponectin, but they were still well within the average reference range (below which would indicate risk).
  3. Women who used bioidentical estradiol and bioidentical progesterone together had lower levels of total cholesterol, LDL-C, Apo B, and HDL-C. While the reduced HDL-C levels are not considered beneficial, other studies, as discussed in Dr. Holtorf’s article, indicate that when synthetic progestins are used instead of bioidentical progesterone, the cholesterol and LDL-C-lowering effect of bioidentical estradiol is also blocked. Bioidentical progesterone did not block this effect!
  4. hsCRP levels were higher in women using bioidentical estradiol and bioidentical progesterone, but still well below the value above which indicates increased risk.

In Summary:

As the researchers expected, the women using bioidentical estradiol exhibited improved cholesterol levels (including decreased LDL-C and increased HDL-C). Even though the bioidentical progesterone was associated with reduced HDL-C levels, it allowed the positive effects of bioidentical estradiol on the other cholesterol levels to remain. Synthetic progestins have been seen to reduce the positive effects of bioidentical estradiol on cholesterol levels, as evidenced by the studies discussed in Holtorf’s article. These findings suggest that bioidentical hormones may be preferable to synthetic.

This study is not without its flaws, such as its short length and small group size. Its short length made it necessary to evaluate markers rather than primary endpoints, and the data was further limited by comparing the groups to each rather than evaluating the differences between the beginning and ending measurements. The patients in the bioidentical estradiol groups were treated with injectable bioidentical estradiol—a form which is rarely used in clinical practice—and used two doses ten days apart as opposed to the usual two- to four-week intervals.

Despite this study’s shortcomings, when we combine its results with information obtained in other studies, we see that bioidentical progesterone doesn’t appear to interfere with the positive effects estrogen has on cholesterol levels. By contrast, other studies have suggested that synthetic progestins do negate these effects. And this makes perfect sense! Why would we assume that a molecule that is similar, but not identical to what the body makes, should have the same effect in the body as a molecule that is identical to what the body makes?

Due to our differences as individuals, no study is perfect. Therefore, the question of whether hormones are good for your heart may never be answered definitively because the answer may differ from person to person. Through studies like that by Dr. Roefsena et al. and others, however, one thing is becoming clear: the difference between bioidentical and synthetic hormones may prove a significant factor in whether hormones are beneficial to the heart.

Additional Resources:

Women’s International Pharmacy has several other articles focused on how hormones affect heart health. Check them out at our Heart Health Resources page!

© 2019 Women’s International Pharmacy

Reviewed by Carol Petersen, RPh, CNP; Women’s International Pharmacy

Category:

Heart Issues, research, Supplements

Lyme Disease Study Raises Possibility of Mother-to-Baby Transmission

https://www.thechronicleherald.ca/news/local/lyme-disease-can-cause-pregnancy-complications-study-292577/

Lyme disease study raises possibility of mother-to-baby transmission

Andrew Rankin (arankin@herald.ca)

Published: Mar 15 at 8:23 p.m.

A female blacklegged tick is embedded in a human arm. A new study says that a developing fetus can be harmed if the mother has Lyme disease. - Public Health Agency of Canada
A female blacklegged tick is embedded in a human arm. A new study says that a developing fetus can be harmed if the mother has Lyme disease. – Public Health Agency of Canada

A scientist who co-authored a recent Public Health Agency of Canada study on the impact of Lyme disease during pregnancy says the illness can have fatal consequences for a developing fetus if the mother goes untreated.

“Miscarriage, newborn death, and newborns with respiratory problems or jaundice have been found to occur,” said American epidemiologist Alison Hinckley.

But the Centers for Disease Control and Prevention scientist says more research is needed to show a definitive link between Lyme disease and pregnancy complications, including whether the tick-borne illness can be passed from mother to baby in the womb.

Hinckley and four Public Health Agency of Canada scientists authored a recent report that reviewed 59 cases of pregnant mothers carrying Lyme disease and their pregnancy outcomes. The results were published in the November 2018 peer-reviewed science journal PLOS One, showing that 36 of the 59 fetuses had been harmed. Complications ranged from miscarriage and stillbirth to congenital abnormalities, respiratory distress and heart abnormalities.

“It is clear, however, that pregnant women who suspect that they might have contracted Lyme disease should see their health-care provider as quickly as possible to receive appropriate treatment and reduce the chance of poor fetal outcomes,” said Hinckley.

PHAC denied requests from the Herald to speak with any of the agency’s four scientists that coauthored the study. The Herald contacted the study’s lead author Lisa A. Waddell by email and phone but did not get a response.

The question remains, why do pregnant mothers with untreated Lyme disease risk harming their unborn baby?

Determining cause

The authors of the systematic review failed to provide a specific cause for any of the 36 pregnancies resulting in harm to the fetus, nor could they definitively say whether Lyme disease factored in any of the congenital malformations. The study couldn’t rule out transplacental transmission, that the bacteria causing Lyme disease, B. burgdorferi, could be passed from mother to baby in utero.

“It is biologically plausible that transplacental transmission of B. burgdorferi occurs given our understanding of transplacental spirochete transmission for other species of spirochetes (T. pallidum) in humans,” said the study. “However, the evidence in this systematic review on congenital malformations does not provide sufficient evidence to exclude or confirm a role for B. burgdorferi in congenital malformations.”

The study calls for more research to settle the debate.

But the topic of in utero transmission of Lyme disease is not new and cases of it have been documented over the decades. As far back as 30 years ago the federal Department of Health acknowledged it as a legitimate form of transmission, stating in a June 1988 Canada Diseases Weekly Report that,

“Transplacental transmission of B. burgdoferi has been documented and may be associated with an increased risk of adverse pregnancy outcome.”

That it occurs is not up for debate, argues biologist Vett Lloyd of the Mount Allison University Lyme Research Network.

“There is evidence from epidemiological studies that the Lyme disease bacteria can be transmitted from mother to child,” said Lloyd, who’s also a leading Canadian tick expert. “There is also evidence from case studies of this.

“But what we don’t know are the answers to questions important to pregnant mothers: How often does this occur? Is it with every pregnancy when the mother is infected or one in 10? One in 100? One in a million?”

We know what we don’t know

Ultimately, the study illustrates how much researchers don’t know about the impact of Lyme disease in pregnancy, she says. If in utero transmission occurs and the B. burgdorferi bacterium passes the placenta to the baby what happens then? In children and adults Lyme disease has the potential to target every vital organ.

“If it is transmitted in utero to a child, that increases the number of people who can potentially be infected,” said Lloyd. “There is no reason to think that a newborn would be any less affected by Lyme disease than an adult — the opposite would be a reasonable assumption.

This problem is compounded if a mother doesn’t know that she is infected with the Lyme disease bacteria, becomes pregnant while being treated or becomes infected while pregnant.”

The Herald made several attempts to speak to Dr. Robert Strang, the province’s chief medical officer of health, about the findings of the study but he declined to be interviewed. In an email statement Strang reaffirmed one of the main conclusions of the study: “There is not enough evidence to confirm that Lyme disease during pregnancy has any adverse effect on the fetus, Lyme disease can be effectively treated in pregnancy and that further research is needed,” stated Strang.

Strang’s statement also defends the way the province treats Lyme disease, including in pregnant mothers. “Nova Scotia’s approach to the diagnosis and treatment of Lyme disease, including Lyme disease in pregnancy, is based on current scientific evidence and is consistent with national and international evidence-based guidelines.”

Sue Faber, co-founder of LymeHope and a registered nurse, says PHAC is ignoring decades of documented proof of transplacental transmission and insists it’s only a matter of time before the medical community is forced to acknowledge it as a legitimate form of transmission that results in congenital Lyme disease — babies being born with the disease.

Over the year, her Lyme advocacy group has gotten thousands of letters from people across the country convinced family members have fallen victim to congenital Lyme disease. She also says a follow up study is needed to look at some of these families.

When the time comes that the medical community accepts that babies can contract the disease in utero it will be “a game changer,” she says.

“For Lyme disease to be passed from mother to child in pregnancy challenges and deconstructs the status quo from Lyme being only a tick-borne disease to one that can be transmitted from human-to-human, mother-to-baby,” said Faber. “Once we acknowledge that this disease changes and we have a big problem on our hands.”

Anna Maddison, spokeswoman for PHAC, admits more research is required to better understand if there may be adverse effects of Lyme disease during pregnancy. She did not say what current or future research is planned to target questions around transplacental Lyme disease.

But Maddison did point to a new Pan-Canadian Lyme Disease Research Network and that part of its research mandate will include working with patients and families to help address gaps in knowledge. The Society of Obstetricians and Gynecologists of Canada is also reviewing current evidence on the effects of Lyme disease and other tick-borne diseases on pregnancy, she says.

“The aim is to equip health-care providers and women with evidence-based information and tools on Lyme disease and other tick-borne diseases during pregnancy,” said Maddison.

But Faber says she sees little evidence that PHAC is responding to the findings of the study with the urgency it deserves.

“Medical and scientific research needs to follow the precautionary principal,” said Faber. “If there’s a risk, it needs to be addressed. We have identified that human-to-human transmission is possible, and even if it’s plausible there’s a social responsibility to protect the public from exposure to harm.”

_________________

**Comment**

The truly despicable thing is the potential for congenital transmission has been known about for decades yet nothing has been done.  Authorities continue to deny, deny, deny despite the lack of research.  You’d think that research in this area would be a high priority knowing Lyme is the #1 vector-borne disease in the U.S.  But no.  They want more climate data….

How many have been infected congenitally?  God only knows.

I find it highly interesting that the minute the Zika scare came out, they KNEW it was sexually transmitted and announced it with abandon.

With Lyme/MSIDS……crickets.

We desperately NEED transmission studies.  We need to know ALL the bugs that can transmit it, if it’s spread congenitally, via breast milk, tears and other bodily fluids, via blood transfusion, organ transplants, etc.

We also desperately need to know the cumulative effects of Lyme with the various coinfections (polymicrobial nature).

For more:  https://madisonarealymesupportgroup.com/2018/06/19/33-years-of-documentation-of-maternal-child-transmission-of-lyme-disease-and-congenital-lyme-borreliosis-a-review/

https://madisonarealymesupportgroup.com/2019/01/27/mothers-on-a-mission-to-prove-lyme-disease-can-be-passed-to-unborn-child/

https://madisonarealymesupportgroup.com/2018/11/17/young-boy-infected-congenitally-with-lyme-speaks-in-ottawa-house-of-commons/

https://madisonarealymesupportgroup.com/2018/07/24/congenital-transmission-of-lyme-myth-or-reality/

https://madisonarealymesupportgroup.com/2019/01/10/transmitted-in-the-womb-children-battle-lyme-disease-from-birth/

https://madisonarealymesupportgroup.com/2018/12/22/doctors-public-left-in-the-dark-on-danger-to-babies-from-lyme/

https://madisonarealymesupportgroup.com/2018/02/26/transplacental-transmission-fetal-damage-with-lyme-disease/

https://madisonarealymesupportgroup.com/2018/05/24/new-berlin-mom-given-life-altering-lyme-disease-diagnoses-after-pregnancy/

https://madisonarealymesupportgroup.com/2017/10/15/pregnancy-in-lyme-dr-ann-corson/

https://madisonarealymesupportgroup.com/2019/01/28/who-removes-congenital-lyme-from-diagnostic-reference/

https://madisonarealymesupportgroup.com/2018/11/11/gestational-lyme-other-tick-borne-diseases-dr-jones/

https://madisonarealymesupportgroup.com/2018/08/16/why-do-officials-continue-to-deny-gestational-lyme/

https://madisonarealymesupportgroup.com/2018/10/05/canada-acknowledges-maternal-fetal-transmission-of-lyme-disease/

Category:

Lyme, Pregnancy, research, Transmission

Sjogren’s Syndrome: Clinical Benefits of Low-dose Naltrexone Therapy

https://ldnresearchtrust.org/sites/default/files/sjogrens%20publication.pdf

Sjogren’s Syndrome: Clinical Benefits of Low-dose Naltrexone Therapy

Scott Zashin 1

1. Rheumatology, University of Texas Southwest Medical Center, Dallas, USA Corresponding author: Scott Zashin, szashin823@aol.com

 

Abstract

Sjogren’s Syndrome is a chronic autoimmune disorder that causes the inflammation of the lacrimal and salivary glands, resulting in dryness of the eyes and mouth. In addition, fatigue and musculoskeletal pain, often described as aching, is very common. Treatment directed toward alleviating the fatigue and pain associated with Sjogren’s is currently very limited. This report describes a case of a 47-year-old female with suspected Sjogren’s based on long-standing dry eyes, dry mouth, joint pain, fatigue, elevated measures of inflammation, and a positive rheumatoid factor. She failed standard therapy but improved clinically with low-dose naltrexone therapy.

Introduction

Low-dose naltrexone (LDN) is a unique compound that has pain-relieving and anti- inflammatory properties. Limited studies have shown benefit in helping relieve the pain in patients with fibromyalgia and improving disease activity in autoimmune conditions such as inflammatory bowel disease and multiple sclerosis. As a result, it seems reasonable that the medication might be useful in Sjogren’s Syndrome, an autoimmune condition that is associated with pain and inflammation.

Case Presentation

A 47-year-old female was diagnosed with Sjogren’s Syndrome six years ago by another rheumatologist, based on her history of eye and mouth dryness. She was found to have a negative rheumatoid factor at that time, but her sedimentation rate by modified Westergren (erythrocyte sedimentation rate, ESR) was recorded as low as 48 and as high as 61 (normal: less than 20 mm/h). Her C-reactive protein (CRP) was 1.74 (normal less than 0.80 mg/dl). Two years ago, she saw a second rheumatologist who agreed with the diagnosis of Sjogren’s Syndrome. At that time, her rheumatoid factor was now elevated at 69 IU/ml (normal: less than 14 IU/m/). Her antinuclear antibody (ANA) and Sjogren antibodies (SS-A and SS-B) were absent. Her anti-CCP antibody and 14.3.3 ETA protein were normal. Her ESR was 48 and her CRP was 1.42. Past medical history included a diagnosis of fibromyalgia. She also had a history of breast cancer that had been in remission for 20 years, a generalized seizure disorder, and elevated liver tests with normal biopsy. Additional medical issues included symptoms of neuropathy, anxiety, and depression. A prior sleep study did not reveal evidence of sleep apnea. She first came to see this author 18 months ago, seeking another opinion, with complaints of fatigue, severe musculoskeletal pain, as well as dryness of her eyes and mouth.

Her daily medications to help with her symptoms of Sjogren’s Syndrome and fibromyalgia included Lexapro, Restasis, meloxicam 15 mg, vitamin D3, magnesium, tramadol 100 mg daily prn, salagen 5 mg tid prn, and hydroxychloroquine 400 mg daily. Her exam demonstrated widespread trigger points affecting both sides of her body, above and below her waist. Her blood work was remarkable for an ESR of 37 and a CRP of 0.77. Her alanine aminotransferase (ALT) was 40 U/L (normal 6-29 U/L).

She elected to try low-dose naltrexone (LDN), which was compounded using a short-acting filler and started at 1.5 mg daily with instructions to increase the medication weekly by 1.5 mg. She came back to see me two weeks after starting the medication and was taking 3 mg daily. She stated that she felt terrific. Her lab was remarkable for a normal ESR of 25 and a CRP of 2.33. Her ALT was normal.

She was seen in follow-up 16 months ago and remained on 3 mg of naltrexone. She felt well but complained of neuropathic pain. Her ESR was now 20. CRP was not ordered. Her ALT was 31 U/L. She was seen in follow-up 14 months ago and remained on 3 mg of naltrexone and continued to feel well without stiffness or pain. She noted that, previously, it would take her all day to feel better. Her ESR remained at 20 and CRP was only minimally increased at 0.87.

She was then seen in follow-up 11 months ago with complaints of increased achiness. She had widespread tender points. She was given a short course of corticosteroids with symptomatic improvement in place of meloxicam. Naltrexone was increased on that visit to 4.5 mg. On the day of that visit, her ESR was 40 and CRP was 25.7 ( current normal value less than 8 mg/L). She was again seen in follow-up nine months ago, doing well on 4.5 mg of naltrexone. Hydroxychloroquine was discontinued a few weeks earlier due to a prolonged QTc interval. Her ESR was back down to 20 and CRP was down to 10.9.

Overall, the patient noted significant clinical benefit with her fatigue and pain within two weeks of starting low-dose naltrexone but no significant change in her dry eyes or mouth. She continues to do well on low-dose naltrexone four months after stopping hydroxychloroquine due to the electrocardiogram (EKG) abnormalities. While her symptoms improved, what is most interesting about this case is that her clinical improvement was associated with an improvement in her inflammatory markers.

Discussion

In the initial pilot study that used low-dose naltrexone in the treatment of fibromyalgia, the baseline sedimentation rate was a significant predictor of clinical response to LDN [1]. It was of interest to note that this patient’s dramatic clinical response to LDN correlated with an improvement in her ESR. It is postulated that low-dose naltrexone has a beneficial effect on the immune system due to the following mechanisms.

Low-dose naltrexone blocks mu-, delta-, and other opioid receptors. These receptors are present in the cells of the immune system. This inhibition may result in an upregulation of endorphins, which in addition to decreasing pain, may have a beneficial effect on the immune abnormalities by suppressing cell growth [2].

Low-dose naltrexone inhibits microglia activity. Microglia are immune cells in the central nervous system that, when stimulated, produce inflammatory products that may be associated with pain, fatigue, cognitive dysfunction (brain fog) sleep, and mood disorders. Low-dose naltrexone inhibits toll-like receptors that are found in microglia cells. As a result, the production of inflammatory substances declines with resulting symptomatic improvement [3- 4]. The inhibition of these toll-like receptors has been postulated to be responsible for the effectiveness of hydroxychloroquine, a standard therapy in diseases such as Sjogren’s Syndrome and systemic lupus.

Overall, LDN is well-tolerated. The 50 mg standard dose of naltrexone is Food and Drug Administration (FDA) approved in the treatment of alcohol dependence and for inhibiting the effects of opioids. Low-dose naltrexone is sometimes used to help alleviate the symptoms of patients with chronic conditions, including fibromyalgia [1], Crohn’s disease [5-6], and multiple sclerosis [7]. The use of LDN at this low dose and for these indications is considered “off-label” use. In other words, it has not undergone the rigorous testing needed to get the approval of the FDA. Side effects include but are not limited to vivid dreams (most patients take the medication in the evening, but morning dosing of the medication may help with this issue). Patients may experience a reduction in pain relief from narcotics for at least six to 24 hours after taking low-dose naltrexone. In addition, low-dose naltrexone should not be used in patients who are currently receiving opioid analgesics due to the possibility of acute opioid withdrawal. The medication should be avoided until it is felt that the narcotics are out of the patient’s system. Those patients taking thyroid replacement may require a lower amount of thyroid medication so periodic monitoring is indicated. The elevation of liver enzymes is a potential risk with naltrexone treatment but is not felt to be common with low-dose therapy. Other potential side effects may include but are not limited to gastrointestinal disturbances, such as stomach cramps and diarrhea, agitation, anxiety, flu-like symptoms, and headaches. The drug should be compounded with short-acting fillers, so calcium carbonate should be avoided. The most common starting dose is 0.5 mg daily in the evening and increased weekly up to a target dose of 4.5 mg. The drug can be started at higher doses. The drug should be stopped at a minimum of 24 hours prior to the time narcotics may be needed for pain relief for a scheduled surgical procedure. In my practice, I will ask patients to temporarily discontinue low-dose naltrexone 72 hours in advance of taking narcotics if the patient is new to therapy, to ensure pain relief [8-11].

Conclusions

Based on a Medline review, this is the first peer-reviewed case report of a patient with Sjogren’s Syndrome who was treated with low-dose naltrexone and obtained clinical benefits. As a result of this case, further study is needed to determine if low-dose naltrexone will subsequently prove to be a useful medication for treating Sjogren’s Syndrome.

Additional Information

Disclosures

Human subjects: Consent was obtained by all participants in this study. Conf licts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: I prescribe low dose naltrexone to patients in my medical practice.

References
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  5. Smith JP, Stock H, Bigaman S, Mauger D, Rogosnitzky M, Zagon I: Low-dose naltrexone therapy improves active Crohn’s disease. Am J Gastroenterol. 2007, 102:820-828.
  6. Raknes G, Simonsen P, Smabrekke L: The effect of low-dose naltrexone on medication in inflammatory bowel disease: a quasi experimental before-and-after prescription database study. J Crohns Colitis. 2018, 12:677-686.
  7. Gironi M, Martinelli-Boneschi F, Sacerdote P, et al.: A pilot trial of low-dose naltrexone in primary progressive multiple sclerosis. Mult Scler. 2008, 14:1076-1083.10.1177/1352458508095828
  8. Low dose naltrexone. (2018). Accessed: 2018: http://www.lowdosenaltrexone.org/.
  9. LDN Research Trust. (2018). Accessed: 2018: https://www.ldnresearchtrust.org/.
  10. Dickson, Windham, Smith, et al.: The LDN Book . Linda Elsegood (ed): Chelsea Green Publishing, White River Junction, VT; 2016.
  11. Moore E, Wilkinson S: The Promise of Low Dose Naltrexone Therapy. McFarland & Company Inc, Jefferson NC; 2009

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For an overview of Sjogren’s:  https://www.hopkinsrheumatology.org/rheumtv/sjogrens-syndrome-disease-overview/  (3 Min Video)  Please notice symptoms are quite similar to Lyme/MSIDS.  

Sjögren’s Syndrome is an autoimmune disease that is found primarily in women, where inflammation at the salivary and lacrimal glands causes dryness of the eyes and mouth. However, it’s also a systemic disease that affects the entire body, producing joint pain and fatigue, and damaging internal organs. As many as four million Americans suffer from Sjögren’s Syndrome, which often overlaps with other rheumatic diseases making it very common to misdiagnose or overlook. Unfortunately, many patients are not diagnosed on time, which makes it much more difficult to treat. In this video, the Director of the Jerome L. Greene Sjögren’s Syndrome Center, Dr. Alan Baer, discusses the symptoms and problems that many patients with Sjögren’s Syndrome face.

If you search the internet with the words Lyme & Sjogren’s, tons of blogs will pop up with people with both. There isn’t much if any science on the two, however. This is another problem with research in Lyme-land – nobody is studying the effects of Lyme triggering or in conjunction with other syndromes within the body.  A big problem.

Excerpt from The Lyme Book:  http://www.lymebook.com/beg_signs_symptoms.pdf

Lyme disease can trigger autoimmunity, so some people will present with rheumatoid arthritis, lupus, Sjogren’s, Hashimoto’s thyroiditis or any number of autoimmune diseases. It may not be that these diagnoses are incorrect; it may just be that the Lyme infection has unbalanced the immune system sufficiently to trigger the autoimmune mechanism. Where there is autoimmune disease with sufficient evidence of Lyme disease (either through lab work or clinically), treating the Lyme will often improve, if not eliminate, the autoimmunity.

The key concept to grasp here is that of underlying cause. Western medicine has somehow distanced itself from the quest for discovery of the underlying cause of illness. As is the case with bromyalgia or chronicfatigue syndrome, the diagnosis describes a set of symptoms but does not explain why they occur.

For more:  https://madisonarealymesupportgroup.com/2016/12/18/ldn/

https://madisonarealymesupportgroup.com/2018/10/30/ldn-an-overview-of-clinical-applications/

https://madisonarealymesupportgroup.com/2017/06/12/ldn-reduced-pro-inflammatory-cytokines-in-fm-after-eight-weeks/

https://madisonarealymesupportgroup.com/2018/05/18/bullseye-low-dose-naltrexone-lyme-disease-documentary/  Very informative documentary put out by the LDN Research Trust on Lyme/MSIDS.  Dr. Horowitz, Dr. Toups, Dr. Schweig, Dr. Windham, Dr. Holtorf, & Dr. Schwarzback, speak on everything from testing, to diet, to inflammation, and how LDN can help Lyme/MSIDS patients.

https://madisonarealymesupportgroup.com/2018/07/16/low-dose-naltrexone-for-lyme-living-with-lyme-podcast/

https://madisonarealymesupportgroup.com/2019/01/16/ldn-cbd/

 

 

 

 

 

 

 

 

 

 

 

Category:

Activism, Inflammation, Pain Management, research, Treatment

First Case of B. corocidurae in Native European Presenting as Meningitis With Cranial Polyneuritis & Cavernous Sinus Thrombosis

https://www.ncbi.nlm.nih.gov/m/pubmed/30818047/

Meningitis with cranial polyneuritis and cavernous sinus thrombosis by Borrelia crocidurae. First autochthonous case in Europe.

Malincarne L, et al. Int J Infect Dis. 2019.

Abstract

Borrelia crocidurae is endemic in West Africa, where it represents the leading cause of tick-borne relapsing fever (TBRF). TBRF typically presents with high fever and systemic symptoms, followed by recurrent episodes. Neurological complications may occur during febrile relapses. B. crocidurae is considered the most neurotropic agent of TBRF and is associated to severe neurological manifestations i.e. meningitis and encephalitis.

To date, European cases of B. crocidurae infection have been reported in travelers returning from endemic areas. We report the first autochthonous case in Europe of B. crocidurae infection, presenting as meningitis with cranial polyneuritis and cavernous sinus thrombosis that were not preceded by classical febrile recurrences.

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**Comment**

This is important as it shows again that Borrelia burgdorferi is not the only borrelia we need to be concerned about.  While endemic in Africa, this case is in a non-traveling European demonstrating the prolific spread of ticks and subsequently the pathogens they carry:  https://madisonarealymesupportgroup.com/2019/03/09/danish-study-shows-migrating-birds-are-spreading-ticks-their-pathogens-including-places-without-sustainable-tick-populations/

https://madisonarealymesupportgroup.com/2018/11/07/ticks-on-the-move-due-to-migrating-birds-and-photoperiod-not-climate-change/

It also demonstrates once again that current CDC 2-tiered testing will NEVER pick this up.  

Cranial polyneuritis = inflammation of many nerves simultaneously.

Cavernous sinus thrombosis =  when the immune system creates a blood clot to prevent bacteria or other pathogens from spreading within a cavity at the base of the brain which drains deoxygenated blood from the brain back to the heart. Typically it is caused by an infection. The clot increases pressure inside the brain which can cause damage.  Mortality is 30%.  

Symptoms of cavernous sinus thrombosis may include:

Tests for Cavernous Sinus Thrombosis

Doctors may order brain scans, including CT and MRI scans, to look for cavernous sinus thrombosis. They may also test blood or spinal fluid to check for signs of infection.

Treatment of Cavernous Sinus Thrombosis

Doctors treat cavernous sinus thrombosis with high-dose antibiotics. These are usually given though an IV drip.

Corticosteroid medications may also be used to reduce swelling. Blood thinners are sometimes given.

Surgery may be needed to drain the site of the initial infection.

Source:   https://www.webmd.com/brain/cavernous-sinus-thrombosis

 

 

 

 

 

Category:

Lyme, research