Open Comment Submission 2
Lucy Barnes
2nd Submission
IDSA Open Comments Period
Testing- Question #81
Submitted to IDSA, AAN, ACR Open Comments Period for new Lyme disease guidelines. April 23, 2015- Deadline was extended at the last minute to April 24, 2015 from its original date.
PROJECT PLAN- Guidelines for the Prevention, Diagnosis, and Treatment of Lyme Disease by the Infectious Diseases Society of America, the American Academy of Neurology, and the American College of Rheumatology
Open Comment Period
April 8, 2015
Comments below address
Page 14- Lines 241-242
Question #64. What is the preferred antibiotic treatment regimen for acrodermatitis chronicum atrophicans?
Page 15- Lines 261-262
Question #73. Which tests can aid in the diagnosis of acrodermatitis chronica atrophicans? What is the diagnostic strategy of choice, and when should alternatives be considered?
2006 IDSA Guidelines state: “Available data indicate that acrodermatitis chronica atrophicans may be treated with a 21-day course of the same antibiotics (doxycycline [B-II], amoxicillin [B-II], or cefuroxime axetil [B-III]) used to treat patients with erythema migrans (tables 2 and 3).”
Acrodermatitis Chronicum Atrophicans (ACA)
Testing is not and never has been adequate to prove conclusively that a Lyme infection is present. “Borrelia burgdorferi sensu lato was isolated from the blood of 1/53 (1.9%) patients with borrelial lymphocytoma, 6/176 (3.4%) patients with Lyme neuroborreliosis, 1/13 (7.7%) patients with Lyme arthritis, and 3/200 (1.5%) patients with acrodermatitis chronica atrophicans.”
Source- Isolation of Borrelia burgdorferi sensu lato from blood of adult patients with borrelial lymphocytoma, Lyme neuroborreliosis, Lyme arthritis and acrodermatitis chronicaatrophicans.nnMaraspin V, Ogrinc K, Ružić-Sabljić E, Lotrič-Furlan S, Strle F. Infection. 2011 Feb;39(1):35-40. doi: 10.1007/s15010-010-0062-8. Epub 2010 Dec 10.
http://www.ncbi.nlm.nih.gov/pubmed/21153429
Lyme disease a clinical diagnosis. “There is, however, substantial proof in the literature that antibody titer development after therapy is unpredictable and variable, and moreover it is largely uncorrelated with the clinical course and mode of antibiotic treatment. For example, persistent positive IgG and/ or IgM antibody titers do not indicate treatment failure. Thus, repeated serologic testing is of very limited value for assessing therapy efficacy, and therefore not recommended in the follow-up of dermatoborrelioses patients. Since cultivation of the etiologic agent, Borrelia burgdorferi sensu lato, and polymerase chain reaction are also inadequate for this purpose, the assessment of patients with cutaneous manifestations of Lyme borreliosis in the follow-up rests primarily on the clinical picture.”
Source- Is serological follow-up useful for patients with cutaneous Lyme borreliosis? Mullegger RR, Glatz M. Curr Probl Dermatol. 2009;37:178-82. doi: 10.1159/000213075. Epub 2009 Apr 8
http://www.ncbi.nlm.nih.gov/pubmed/19367102
Inadequate treatment of early Lyme disease leads to more serious complications. “Acrodermatitis chronica atrophicans (ACA) represents the persistent late stage of borreliosis in which Borrelia species may survive for decades. Occasionally, B-cell lymphoma may develop in these patients, and additional neoplastic complications such as basal cell carcinoma or squamous cell carcinoma (SCC) have been reported once each over the past 60 years. Here we describe, to the best of our knowledge, the first case of metastatic SCC in a European patient with long-standing ACA caused by Borrelia burgdorferi sensu stricto. Our case highlights a potential pathophysiological connection of untreated Borrelia infection with the initiation or progression of SCC and should alert dermatologists to this rare complication.”
Leverkus M, Finner AM, Pokrywka A, Franke I, Gollnick H.
Dermatology. 2008;217(3):215-8. doi: 10.1159/000142946. Epub 2008 Jul 8.
http://www.ncbi.nlm.nih.gov/pubmed/18607109
It’s NOT just a European “phenomena” and YES, testing is and remains poor on both sides of the Atlantic. The main clinical features of Lyme borreliosis seem to be the same in Europe and North America; however, the course of erythema migrans is distinct, with multiple erythema migrans and hematogeneous dissemination in early Lyme borreliosis less frequently observed in Europe. Moreover, the skin manifestations borrelial lymphocytoma and acrodermatitis chronica atrophicans are apparently European phenomena. Meningoradiculoneuritis in Lyme neuroborreliosis, with its severe radicular pain, is more prominent in Europe. Similar difficulties exist on both sides of the Atlantic with the serologic diagnosis of Lyme borreliosis.”
Source- Lyme disease: European perspective. Stanek G, Strle F. Infect Dis Clin North Am. 2008 Jun;22(2):327-39, vii. doi: 10.1016/j.idc.2008.01.001. Review.
http://www.ncbi.nlm.nih.gov/pubmed/18452805
Right & Wrong. ACA results from persistent spirochetal infection, however, ACA is not restricted to European patients. “Acrodermatitis chronica atrophicans (ACA) is a slowly progressive lesion located primarily on the extensor (acral) surfaces of the extremities. This chronic lesion, which has inflammatory and atrophic phases, sometimes with fibrotic features, results from persistent spirochetal infection (3, 26). In the United States, Lyme disease is caused only by B. burgdorferi. There, EM lesions are a feature of the illness, but not BL or ACA lesions (38).”
4 weeks of Doxycycline failed to eliminate ACA (persistent Lyme). “Most patients with EM were treated with oral doxycycline for 2 or 3 weeks, and those with BL or ACA were usually given 4 weeks of this medication. A small number of patients received other, comparable regimens. All patients responded to therapy, but in several patients with ACA, skin atrophy persisted or neuropathy resolved slowly.”
Varying Borrelia species can cause ACA. “Although B. afzelii is the most common cause of ACA, each of these Borrelia species has now been recovered from ACA lesions (21, 30).”
Chronic persistent ACA lesion. Thus, depending on the site of the infection, B. afzelii or occasionally other B. burgdorferi sensu lato species may cause an acute, self-limited EM lesion particularly in or near intertriginous sites, a subacute BL lesion on the nipple or ear, or a chronic persistent ACA lesion primarily on extensor surfaces of the extremities.
(The test referenced below should NOT be mentioned or recommended in the new guidelines. This rush to find it- patent it scenario is what prevents people from being diagnosed and treated adequately and properly. Steere should NOT be on the guideline panel, his studies should not be considered or referenced, and Steere`s test should not be a recommended or suggested test in the new guidelines. This is another conflict of interest as has plagued the last set of guidelines.
Publication number
US20130302329 A1
Publication type
Application
Application number
US 13/823,126
PCT number
PCT/US2011/052456
Publication date
Nov 14, 2013
Filing date
Sep 21, 2011
Priority date
Sep 21, 2010
Basic Information- http://www.google.com/patents/US20130302329
Patent
https://docs.google.com/viewer?url=patentimages.storage.googleapis.com/pdfs/US20130302329.pdf
``However, it was chemoattractants for cells of the adaptive immune response that differed most. EM and ACA lesions had high mRNA expression of the T-cell-active chemokines CXCL9 and CXCL10, whereas BL lesions had especially high levels of CXCL13.``
Source- Infect Immun. 2007 Sep; 75(9): 4621–4628.
Published online 2007 Jul 2. doi: 10.1128/IAI.00263-07
Source- Chemokine Signatures in the Skin Disorders of Lyme Borreliosis in Europe: Predominance of CXCL9 and CXCL10 in Erythema Migrans and Acrodermatitis and CXCL13 in Lymphocytoma▿
Robert R. Müllegger,1,* Terry K. Means,2 Junghee J. Shin,2 Marshall Lee,2 Kathryn L. Jones,2 Lisa J. Glickstein,2 Andrew D. Luster,2 and Allen C. Steere2
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951170/
There are additional testing methods- In arthritis and acrodermatitis chronica atrophicans (ACA), IgG serology is 100% positive with very high titers; however IgM serology is only positive in 5 to 10% of the cases. In ACA, culture sensitivity ranges from 20 to 60% and PCR sensitivity from 60 to 90%. Specificity of antibodies, natural exposure to the etiologic agent, and cross-reactivity are critical for the final interpretation of serological assessment. Only the use of "serological profiles" allows the exploitation of detailed results (isotypes, intensity). In this approach, IgG avidity could be constructive. The western-blot is intended to confirm the specificity of antibodies found in screening methods (Elisa).
Source- Med Mal Infect. 2007Jul-Aug;37(7-8):487-95. Epub 2007 Apr 3.
[Laboratory methods for the diagnosis of clinical forms of Lyme borreliosis. (Article in French)1.
http://www.ncbi.nlm.nih.gov/pubmed/17408896
Analysis of the immunoblot-banding pattern revealed positive reactions in all patients against flagellar antigen (41 kDa). Interpretation of the immunoblots revealed positive IgG results in all cases and IgM in five of them. Concluding, ACA develops not only on the extremities, but also on the trunk. The immunoblot technique using Borrelia afzelii antigens is of value in the diagnosis of ACA.
Source- J Med. 1999;30(3-4):267-78.
Clinical features and specific immunological response to Borrelia afzelii in patients with acrodermatitis chronica atrophicans.
Flisiak I1, Schwartz RA, Chodynicka B.
http://www.ncbi.nlm.nih.gov/pubmed/17312680
``Borrelia burgdorferi is difficult to detect in routine biopsy material from patients with skin lesions of borreliosis. In this study, a new immunohistochemical method, focus floating microscopy (FFM), was developed to detect B burgdorferi in tissue sections and was compared with polymerase chain reaction (PCR). By using standard histologic equipment, tissue sections stained with a polyclonal B burgdorferi antibody were simultaneously scanned through 2 planes: horizontally in serpentines and vertically by focusing through the thickness of the section. Borrelia were detected in 47 of 71 ticks, 34 of 66 tick bites, 30 of 32 erythema chronicum migrans cases, 41 of 43 borrelial lymphocytomas, and 50 of 51 acrodermatitis chronica atrophicans cases. FFM proved to be more sensitive than PCR (96.0% vs 45.2%) and nearly equally specific (99.4% vs 100%). All 169 control cases, except 1 false-positive case of secondary syphilis, were negative with FFM. FFM is an easy, quick, and inexpensive method to reliably detect Borrelia in cutaneous tissue sections.``
Source- Am J Clin Pathol. 2007 Feb;127(2):213-22.
Focus floating microscopy: "gold standard" for cutaneous borreliosis?
Eisendle K1, Grabner T, Zelger B.
``Diagnosis of Lyme borreliosis is still based on typical signs of the disease and laboratory techniques can not solve clinical doubts.``
Source- [Clinical picture of Lyme boreliosis].
Flisiak R, Prokopowicz D.
Wiad Parazytol. 1999;45(2):143-9. Review. Polish.
http://www.ncbi.nlm.nih.gov/pubmed/16886455
http://www.ncbi.nlm.nih.gov/pubmed/17210530
Discussion
The 2006 Guidelines recommend providing patients with the same course of antibiotics for the early stages of Lyme disease as for the late, disseminated, multi-system, complex stages presenting years after the original treatment failed. If the original recommended treatment was successful, later stages of Lyme disease would not be of concern, retreatment would not be necessary and people would not be suffering from what the IDSA Guidelines describe in their ‘acrodermatitis chronica atrophicans’(ACA) section as “insidious” multiple subjective and objective symptoms.
Throughout the 2006 Guidelines, author’s mention they have limited or no experience treating people with various stages or presentations of the disease. That one admission should have been the first clue that the authors were not qualified to make recommendations for or against any specific diagnostic or treatment protocol. At the very least, the panel should encourage input from front line treating physicians in order to provide the most successful treatment options for patients.
As a result of the authors failure to be flexible, both in their thinking and their recommendations, people have been misled, misdiagnosed and under treated for active Borrelia infections. It was irresponsible for IDSA authors to take on the responsibility for developing Guidelines for medical conditions they do not understand, refused to review with those having knowledge of the condition and for which they have no experience in treating. This needs to stop. The authors should refrain from making recommendations against treating patients who remain ill after a short course of antibiotics fail. The IDSA’s attempt to set medical standards for the Lyme community, define illness and recommend treatment protocols have been nothing more than a hindrance to clinical judgment and patient autonomy. The 2006 Guidelines mere existence continues to fuel a war where the casualties are human lives. The insult of placing many of the same 2006 guideline panel members on the new panel is beyond shameful.
If the newly appointed panel would substitute the word “cancer” for “Lyme” while reviewing Guidelines, especially in regards to the ACA presentation, this message would become crystal clear. For example, partially treating cancer in the early stages, then withholding treatment until the more advanced stages are reached, then recommending the same unsuccessful treatment as was already prescribed is not only ludicrous, it is an inhumane practice that is not acceptable by any standards for any disease.
Although not listed in the 2006 IDSA Guidelines, the objective and subjective symptoms noted in patients with ACA are endless and well documented. There is no dispute in the medical community that these symptoms arise as a result of inadequately treated Borrelia infection. Live, viable spirochetes have been extracted from ACA lesions from patients never treated originally and also those treated with what was inaccurately purported to be “adequate treatment” by the IDSA. Many patients have suffered for years- between the original treatment prescribed and the eventual presentation of ACA- developing multiple, complex and difficult to treat symptoms as organisms spread throughout their body. Treatment must be continued if it stops Bb progression and provides relief.
Complications associated with the final stages of ACA presentation, such as the difficult-to-treat ulcerations of the skin, which can develop after minor trauma, give rise to the ACA stage being an especially traumatic one for patients. Once at this stage, patient’s lives have often been compromised for years, sometimes for decades and often permanent damage has been done to one or more organ systems that will not subside and cannot be reversed.
Physicians and patients, by way of the IDSA Guidelines, should be presented with a detailed description of the true and full presentation of ACA, including the most recent findings in the Morgellons/Lyme study.
Middelveen MJ, Bandoski C, Burke J, Sapi E, Filush KR, Wang Y, Franco A, Mayne PJ, Stricker RB. BMC Dermatol. 2015 Feb 12;15(1):1. doi: 10.1186/s12895-015-0023-0. http://www.ncbi.nlm.nih.gov/pubmed/25879673
Say NO to Post-Lyme Disease Syndrome. ACA proves it is still an active Borrelia infection. The very existence of acrodermatitis chronica atrophicans lesions in Bb patients shoots down the “post-Lyme syndrome” theory completely. ACA only develops in patients untreated or improperly treated for early Lyme disease, sometimes years after they were infected (even after prescribed what is considered by the previous authors to be “adequate treatment”). If continuing symptoms after treatment were the result of anything other than active infection, ACA would not exist, viable spirochetes would not be detected in ACA lesions years after the initial Lyme infection and antibiotics would not be affective in clearing some of the symptoms associated with ACA.
This begs the following question and is worth repeating- For patients experiencing ongoing subjective symptoms after the IDSA recommended treatment for Lyme disease- how do they develop the ACA presentation if they have ”post-Lyme syndrome”, keeping in mind the authors’ contention is “post-Lyme syndrome” is not caused by active infection? This needs to be addressed and corrected in the upcoming guidelines, as it is false.
Those who develop ACA have the same symptoms listed as the 2006 guideline authors inclusion criteria for “post-Lyme syndrome” (fatigue, widespread musculoskeletal pain, complaints of cognitive difficulties, and subjective symptoms that are of such severity that, when present, they result in substantial reduction in previous levels of occupational, educational, social, or personal activities), yet evidence of viable spirochetes can be found in biopsies of ACA patients and the condition worsens unless the infection is properly and sometimes frequently addressed with antimicrobials.
Additionally, patients with ACA may also experience many of the symptoms included in the “post-Lyme syndrome” exclusion category. The IDSA’s “post-Lyme syndrome” exclusion criteria lists the following signs and symptoms:
An active, untreated, well-documented coinfection, such as Babesiosis; objective abnormalities on physical examination or on neuropsychologic testing; antibiotic refractory Lyme arthritis; late neuroborreliosis associated with encephalopathy, recurrent or refractory objective cognitive dysfunction; a prolonged history of musculoskeletal pains or fatigue; a diagnosis of an underlying disease or condition that might explain the patient’s symptoms (e.g. morbid obesity; medications; autoimmune diseases; uncontrolled cardio-pulmonary or endocrine disorders; malignant conditions within 2 years; known current liver disease; any past or current diagnosis of a major depressive disorder with psychotic or melancholic features; bipolar affective disorders; schizophrenia of any subtype; delusional disorders of any subtype; dementias of any subtype; anorexia nervosa or bulimia nervosa; and active drug abuse or alcoholism at present or within 2 years); laboratory or imaging abnormalities that might suggest an undiagnosed process distinct from post–Lyme disease syndrome, such as a highly elevated erythrocyte sedimentation rate (150 mm/h); abnormal thyroid function; a hematologic abnormality; abnormal levels of serum albumin, total protein, globulin, calcium, phosphorus, glucose, urea nitrogen, electrolytes, or creatinine; significant abnormalities on urine analysis; elevated liver enzyme levels, or a test result suggestive of the presence of a collagen vascular disease; and a positive PCR result.
This also begs the question- If people with ACA were to be placed in a clinical trial, under which category would they be filed? They have signs, symptoms and documentation of active infection, as well as, signs and symptoms of the guideline authors so called “post-Lyme syndrome”, as well as, symptoms mirroring those in the additional exclusion category. The ACA presentation puts quite a big dent in the “post-Lyme syndrome” theory and certainly requires guideline authors to adjust their recommendations to be scientifically and medically accurate.
While making adjustments for the ACA/post-Lyme situation, the Guideline developers may want to reconsider another aspect of the ACA presentation. Progressive allodynia (the exaggerated reaction to pain), is a symptom Guideline authors misunderstood in patients with Lyme disease, yet it is a well-documented, characteristic symptom of active disease progression and, thus, may be a clue to the diagnosis of chronic persisting Lyme disease, especially when accompanied or preceded by the presentation of acrodermatitis chronica atrophicans lesions.
Some have made the assumption allodynia was a condition related to some sort of mental illness in Lyme patients and for that reason the authors indicated patients were not actively infected, but instead, were mentally ill, often prior to contracting Lyme disease. To believe in this unsubstantiated opinion is to say the fruit loops someone ate as a child is the reason they stubbed their big toe as an adult.
As was recently noted in Morgellons- undiagnosed infections can cause multiple symptoms linked or not linked to common diseases. When physical symptoms can not be explained by the guideline authors it does not warrant a slap stick diagnosis of delusional parasitosis or other such unfounded mental disorder. Those who can not or will not relate early symptoms of Bb to late symptoms of Bb- treatment or not- can be said to suffer from delusional guideline preparation syndrome.
Rather than dismissing patient’s complaints or, as in Lyme, declare them cured, or worse, mentally ill because patients remain sick after treatment, perhaps a mention in the new guidelines of the above mentioned condition allodynia, and the fact it is associated with the ACA presentation caused by active infection, would be appropriate.
The truth, the whole truth and nothing but the truth please in the guidelines. The loss of hair, fragility of the skin and the compromised sweat glands associated with ACA leaves patients skin poorly protected and vulnerable. Bacterial super-infections in patients have occurred, adding to the patient’s pain and misery, not to mention the financial burden incurred by treating the additional symptoms. With that in mind, the recommendation against treating Lyme patients due to a possible resistance problem goes right out the window for several reasons. Not treating patients and allowing them to reach the later stages of the disease is actually responsible for super-infections developing, via the complications associated with the ACA presentation. In addition, the Guideline authors and its supporters have previously admitted in other publications that treating Lyme patients for Borrelia infections does not cause resistance problems in the early stages, making that claim mute.
Patients with ACA can experience acral pain, paresthesia, dysesthesia and cognitive dysfunction in conjunction with ACA skin manifestations. Peripheral neuropathy, lymphadenopathy, musculoskeletal pains, and joint damage may also be complicating factors in these patients. Destruction and deformity of the small joints of the hands and the feet is often seen along with, or independent of, additional complications and presentations, such as atrophy of the epidermis, morphea, lichen sclerosus atrophicus, facial edema, and paresis of the brachial plexus.
Fibrotic nodules or bands may be seen on the surfaces of the elbows and the knees. Edema with or without a bluish discoloration to the skin may occur, especially in the earlier stages. Acrodermatitis chronica atrophicans has been described in association with localized amyloidosis, eczema, psoriasis, lupus erythematosus, leprosy, and Hodgkin disease. [i]
Without adequate testing, many Lyme patients have been misdiagnosed with diseases and conditions they do not have, instead of the proper diagnosis of acrodermatitis chronica atrophicans. Scleroderma, livedo, venous insufficiency, Reynaud’s syndrome, edema, cancers and an ongoing aging process have taken the place as a diagnosis for patients who are suffering from ACA.
As scientific knowledge of the active disease progression in ACA becomes more apparent and is further documented, additional concerns can and are raised.
Acrodermatitis chronica atrophicans (ACA) represents the persistent late stage of borreliosis in which Borrelia species may survive for decades. Occasionally, B-cell lymphoma may develop in these patients, and additional neoplastic complications such as basal cell carcinoma or squamous cell carcinoma (SCC) have been reported once each over the past 60 years.[ii]
The only treatment the Guidelines recommend for ACA is a three-week course of the same medication that failed Lyme patients previously and which put them in a chronic infectious state in the first place. Recommendations in the Guidelines do nothing for acutely ill Lyme patients or the late stage ACA patients than suppress clinical judgment and restrict treatment options. Therefore, there should be no recommendations by the IDSA`s new panel when science is lacking and their experience is naught. The stakes are too high and the outcome for patients is bleak with restrictive IDSA Guidelines in place.
The Guidelines state: “Atrophic areas often persist, and little objective improvement can be demonstrated in the neuropathy… However, progression of neurologic involvement is halted, and the neuropathic symptoms of pain and paresthesia are improved [251, 252].”
Throughout the IDSA Guidelines, authors recommend against antibiotic therapy and all other treatment options as a general rule, however, they consider it acceptable to treat a patient presenting with ACA symptomatically, using antibiotics as the drug of choice.
This is only after patients have suffered with late stage disease to a point that there is little hope of reversing the damage, ending their pain or of achieving a complete recovery. The lame and insulting three-week course of antibiotics is simply throwing more of the same medicine at a disease after it has been proven to be an unsuccessful protocol the first time around.
True, it is a “cost-effective” treatment, with an out-of-pocket expense of approximately a $10 copay, however, it is not effective. The money would be better spent on ice cream; at least there would be some temporary pleasure gained before patients realize they are in deep trouble, having no options left while dealing with an infectious disease that has run-a-muck throughout their bodies.
There are no provisions in the IDSA Guidelines for those who fail to recover on the three weeks of “cost-effective” antibiotics offered for any stage of the disease. All doors that may lead to recovery or relief are shut tightly and patients and their health care providers are left with no viable options. Medical guidelines and their authors have a responsibility to not increase suffering by their recommendations. Therefore, the practice of closing the door on all options must be corrected before more are endangered by IDSA Guidelines recommendations.
The Guidelines state: “There are no prospective, randomized studies on treatment.”
A simple search on Pub-Med produced 340 articles dating back to 1948 concerning the manifestations associated with ACA. A search on “chronic Lyme and ACA” produced 107 medical articles, also dating back sixty years. The Guideline authors relied on only three articles to support their original ACA opinions, conclusions and recommendations- they need to include all of the studies, not just their own or what supports their pre-determined positions.
The first referenced article in the previous guidelines was by Persing, et al. [iii] Persing is Vice-President and Director of Cepheid and the Director of Monogram Biosciences. Persing, according to Forbes [iv], pockets a million plus dollars a year income, and along with the IDSA authors and their cohorts, was involved in the failed Lyme vaccine fiasco. Persing is also a Lyme vaccine patent holder (USA #6,045,804) [v], and was an author on the original IDSA 2000 Lyme disease Guidelines. [vi]
Persing’s 1994 report on the ACA rash, which was used to support the IDSA author’s treatment recommendations, revolved around the charts of five (out of 6) European immigrants seen over a period of 49 years at a mid-western clinic between 1912 and 1961. The notes and charts were generated long before Lyme disease was recognized as a complex infectious illness, before tests were developed to detect it, before the infectious organism responsible for the disease was discovered and before anyone knew how the disease was transmitted to humans. The conclusions drawn from Persing’s paper were based on a handful of clinical notes and histopathological findings, with associated documents ranging in age between 45-94 years.
Considering the fact penicillin was not invented until 1928 and Doxycycline (6-Deoxy-5-hydroxytetracycline) was not clinically developed until the early 1960s by Pfizer, Inc., [vii] it seems highly unlikely the historical reminiscing in this article would have much to contribute to the foundation of the 2006 Guidelines treatment protocols for Lyme patients with ACA. This needs to change.
Some of the Guidelines reference authors, along with Persing, have been partners on Lyme related projects with the IDSA panel members. This is a cozy deal, no doubt, but guideline references based on nothing more than papers written by people with no experience treating patients successfully and nothing but massive amounts of additional conflicts of interest to add to the equation, is not a sound basis for restricting treatment to patients and recommending they only receive more of what did not work for them previously. Persing’s inappropriate contribution to the ACA section should, therefore, be discarded.
The second article supporting treatment recommendations refered to untreated ACA patients from Sweden [viii], a huge disappointment considering over 300 studies were available to review, some generated from the United States, the author’s preferred venue.
If the Guidelines authors reviewed this Swedish article for information on ACA, they should have described the ACA presentation in their Guidelines and presented a complete picture in order to promote the use of clinical judgment and patient autonomy. The Swedish article, published over ten years ago, should be discarded as a reference, as it contributed nothing to the treatment recommendations and the Guidelines authors did not report on information concerning the ACA presentation.
The third article chosen by the IDSA panel was, unlike the others, at least written during this century, however, it is by the same Swedish authors mentioned in the second article. The study determined their limited treatment protocol was unsuccessful in resolving many of the presentations accompanying chronic late stage ACA, stating in part:
Despite a good therapeutic effect on ACA lesions, specific antibody values and symptoms of irritative nerve lesions, the objective neurological and neurophysiological findings of nerve deficit remained unchanged. There was no progress of neuropathy findings during the follow-up time. [ix]
In contrast, the IDSA authors claim in the Guidelines that treatment for the ACA presentation:
…resulted in improvement in pain and swelling, diminution in fibrous nodules, and gradual fading of the lesion within 2–6 months [250–252]. Atrophic areas often persist, and little objective improvement can be demonstrated in the neuropathy in uncontrolled studies, regardless of whether antibiotics are administered parenterally…. progression of neurologic involvement is halted, and the neuropathic symptoms of pain and paresthesia are improved.
In 2009, a study mentioned below by Mullegger, et al, determined the diagnostic tests for Lyme were of very little value and that the clinical picture is the key to diagnosis and treatment efficacy concerning the ACA presentation. One medical study discussing treatment of ACA being used as ‘the’ scientific foundation for making decisions does not allow for a well balanced, unbiased, sound recommendation for treatment.
If the IDSA authors must mention treatment recommendations for ACA, their sources should have substance, there should be more than one reliable source (not the authors reports supporting their own opinions), clinical aspects must be considered and the recommendations made must be in conjunction with and include the best-known treatment available. If this cannot be accomplished, no recommendations should be made and all options should remain open.
The IDSA guidelines state: “Although any of the species of Lyme Borrelia may cause the lesion, by far the most common etiologic agent is B. afzelii. Therefore, this manifestation is much more common in Europe than in the United States [243– 246]. “
Rule one: If you don’t look for it, you won’t find it. Without clinical trials and properly educated practitioners experienced in recognizing and treating a specific condition and providing continual feedback, it is impossible to make the above determination.
As more evidence surfaces indicating serologic tests are inadequate for determining exposure to Borrelia, clinicians will be required to educate themselves and depend on their clinical skills to determine if ACA is a problem in the United States. Patients report experiencing the ACA presentation in increasing numbers; however, they are unable to find physicians versed in the diagnosis and treatment of the condition.
As Mullegger’s study determined concerning ACA:
…repeated serologic testing is of very limited value for assessing therapy efficacy, and therefore not recommended in the follow-up of dermatoborrelioses patients. Since cultivation of the etiologic agent, Borrelia burgdorferi sensu lato, and polymerase chain reaction are also inadequate for this purpose, the assessment of patients with cutaneous manifestations of Lyme borreliosis in the follow-up rests primarily on the clinical picture.[x]
The Guidelines failure to include a full and complete assessment of the ACA presentation skews the clinician’s perception of the disease process and removes their ability to utilize clinical judgment in an advantageous manner.
The previous edition of the IDSA Guidelines (2000) allowed for the fact the authors were not educated about a specific Lyme related topic. For example, concerning ophthalmologic manifestations they stated:
Because of the lack of evaluable data on ophthalmologic complications, which are veryrare, the panel was unable to make recommendations concerning keratitis and other possible ocular manifestations of Lyme disease.
Rather than recommend against specific treatments or limit treatment options, in this case they allowed for the fact the science had not provided them with definitive answers. Patients, therefore, were able to seek treatment and be reimbursed by their insurance companies. Clinical judgment and patient autonomy were utilized in this case, as they should always be when discussing or making health care decisions.
Conclusion:
The IDSA Guideline authors and their supporters (as in the case of Persing) have failed to offer scientific validation for their diagnostic and treatment recommendations for the ACA presentation. They indicate in the Guidelines they are unfamiliar with many complications and presentations associated with Lyme disease; they have no experience treating patients with ACA, do not recognize ACA and other conditions in their practice (those who actually treat patients) and have no scientific studies to substantiate their recommendations for ACA. They reject the concept of “chronic” Lyme being caused by active infection, therefore, in their eyes, ACA can not possibly exist. Rather than dismiss ACA, they offer a token treatment of 3 more weeks of antibiotics and leave patients stranded with no other options than perhaps steroids that will perhaps mask the symptoms and infection, but in turn will produce more suffering and early death as a result.
The mere presence of ACA in previously treated patients, years after what was thought to be “adequate treatment”, indicates Lyme disease can be a chronic infectious disease. Multiple Borrelia species in Europe and the United States have the ability to remain sequestered from both antimicrobials and the immune system, hiding in immune-privileged sites, allowing for the development of ACA years after people are exposed, therefore, the recommendations against alternative treatments and the entire misleading and unsubstantiated ACA section should be deleted from the IDSA Guidelines or dealt with accurately and fully. In addition, clinical judgment and patient autonomy should be emphasized.
Please refer to the ACA progression photos in a US Lyme patient with no travel history outside the country. Antibiotic treatment slows or halts progression; it does not eliminate the Bb infection or reverse all of the damage.
https://picasaweb.google.com/AfterTheBite/LymeACAProgression#
Prepared and submitted by:
Lucy Barnes
610 Railroad Avenue
Centreville, MD 21617
Additional References
[i] Bozena Chodynicka, Bozena MD, Schwartz, Robert A. MD, MPH. Acrodermatitis Chronica Atrophicans. Medscape, WebMD, 23 Mar. 2009 http://emedicine.medscape.com/article/1051695-overview
[ii] Leverkus M, Finner AM, Pokrywka A, Franke I, Gollnick H. Metastatic squamous cell carcinoma of the ankle in long-standing untreated acrodermatitis chronica atrophicans. Dermatology. 2008;217(3):215-8. Epub 2008 Jul 8.
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Submitted to Diana Olson and Info@idsociety on April 23, 2015 at 11:12 PM, by emails. Website, once again, would not accept document.