Post by Admin/ Traveler on Sept 2, 2019 16:59:16 GMT
The Clinical, Symptom, and Quality-of-Life Characterization of a Well-Defined Group of Patients with Posttreatment Lyme Disease Syndrome
Alison W. Rebman, Kathleen T. Bechtold, Ting Yang, Erica A. Mihm, Mark J. Soloski, Cheryl B. Novak and John N. Aucott
"Background: The increased incidence and geographic expansion of Lyme disease has made it the most common vector-borne infection in North America. Posttreatment Lyme disease syndrome (PTLDS) represents a subset of patients who remain ill following standard antibiotic therapy for Lyme disease. The spectrum of symptoms and their impact on quality of life remain largely unexplored among patients with well-documented PTLDS.
Objective: To characterize a case series of patients with well-documented PTLDS compared to a sample of healthy controls.
Methods: Sixty-one participants met the proposed case definition for PTLDS. Twenty-six healthy controls had neither a clinical history of Lyme disease nor current antibodies to Borrelia burgdorferi. Participants with PTLDS and controls were evaluated by physical exam, clinical laboratory testing, standardized questionnaires, and a 36-item current symptom list.
Results: Compared to controls, participants with PTLDS reported significantly greater fatigue, pain, sleep disturbance, and depression (Fatigue Severity Scale: 50.0 ± 10.6 vs. 19.8 ± 8.6; Short-Form McGill Pain Questionnaire: 13.7 ± 8.3 vs. 0.8 ± 1.9; Pittsburgh Sleep Quality Index: 10.1 ± 4.7 vs. 4.1 ± 2.1; Beck Depression Inventory-II: 15.1 ± 7.7 vs. 2.2 ± 3.2; p < 0.001 for each), and significantly lower quality of life (SF-36 Physical Component Score: 33.9 ± 9.7 vs. 55.1 ± 6.2; Mental Component Score: 42.9 ± 10.1 vs. 54.2 ± 5.4; p < 0.001 for each). Nineteen non-PTLDS-defining symptoms were found to be significantly more severe among participants with PTLDS than controls, including sleep difficultly and visual complaints. Initial delayed or misdiagnosis was characterized in 59.0% of participants with PTLDS, and 32.2% had abnormal vibratory sense.
Conclusion: Although physical exam and clinical laboratory tests showed few objective abnormalities, standardized symptom questionnaires revealed that patients with PTLDS are highly and clinically significantly symptomatic, with poor health-related quality of life. PTLDS patients exhibited levels of fatigue, musculoskeletal pain, sleep disturbance, and depression which were both clinically relevant and statistically significantly higher than controls. Our study shows that PTLDS can be successfully identified using a systematic approach to diagnosis and symptom measurement. As the prevalence of PTLDS continues to rise, there will be an increased need for physician education to more effectively identify and manage PTLDS as part of integrated patient care."
(Trav here: Now, this is what cracks me up/pisses me off - I'm posting what they (IDSA) has determined to be the definition of Post Treatment Lyme Disease Syndrome("PTLDS") below. So my question, because I'm in a totally different group that is simply not recognized, is what about all those that never got the treatment they needed in time??? They are STILL being ignored, as if we simply don't exist.)
"In 2006, the Infectious Diseases Society of America (IDSA) published a proposed case definition for PTLDS (21). Briefly, this definition relies on prior physician-documented Lyme disease, treatment with standard of care antibiotics, and the development of significant fatigue, widespread musculoskeletal pain, and/or cognitive difficulties that last for a period of at least 6 months, and began within 6 months of a Lyme diagnosis and recommended treatment (21). Patients can be excluded for a range of symptoms, conditions, or laboratory abnormalities that could be associated with or explain the symptomatology of PTLDS (21). As antibodies to B. burgdorferi are known to fall over time in treated patients regardless of clinical outcome (7, 22–24), and convalescent antibodies after treatment of early Lyme disease are positive in 65% of patients (25), presence of reactive antibodies is not part of this definition. In the clinical setting, PTLDS is largely an historical diagnosis that hinges on the ability to document symptom onset after an episode of physician-documented Lyme disease that was adequately treated with standard of care antibiotics."
(Trav here again, I'm skipping over a lot of the article to only post certain aspects. If you would like to see the article in it's entirety, please follow the link at the top of this page.)
"Discussion
This study represents the first to compare patients with rigorously defined PTLDS to non-Lyme infected controls on a range of clinical, laboratory, symptom, and quality-of-life parameters. We found that physical exam and clinical laboratory tests showed few abnormalities. However, standardized questionnaires revealed that these patients are highly symptomatic, with clinically significantly poorer quality of life compared both to healthy controls and the US population. These findings were consistent regardless of whether participants met criteria for the initial LD-probable or LD-confirmed group. There was some evidence for greater initial misdiagnosis and more severe current symptoms among the LD-probable group.
Results from the physical exam and laboratory testing in our sample of patients with PTLDS did not show a pattern of significant objective abnormalities. The most notable exception was the higher rate of diminished vibratory sensation on physical exam among participants with PTLDS (32.2%), compared to the 5% expected to fall below the age-adjusted cutoffs used in this analysis (29). This abnormality were not only present among those with a prior diagnosis of neurologic Lyme disease or a later diagnosis of neuropathy but also among those without a specific prior neurologic diagnosis. This finding was also observed in a previous population-based study, in which decreased vibratory sense was noted in 29% of a sample of individuals with prior Lyme disease, and was one of the sole physical exam findings to differ significantly from controls (17). Additionally, although only found in a small subset of our sample (3.4%), two participants met criteria for postural orthostatic tachycardia syndrome, an autonomic condition that has been previously reported following Lyme disease (37). Laboratory tests, including complete blood count, complete metabolic count, and C-reactive protein, showed no significant difference between participants with PTLDS and controls. The rates of current two-tier IgG-WB positivity among those with confirmed early (7/36, 19.4%) and late (4/6, 66.7%) Lyme disease were similar to those found in a 10- to 20-year follow-up study of treated patients assessed to have good overall health (22), further emphasizing that current serology cannot be used as a diagnostic marker for PTLDS.
By contrast, participants with PTLDS reported prominent symptoms that are often diverse and can be moderate to severe in nature. We expected that current symptom severity of fatigue, pain, and cognitive complaints would be higher among PTLDS participants than controls, given that presence of at least one of these symptoms was included in both the IDSA proposed case definition and our enrollment criteria. Indeed, severe levels of each of these were reported by 50.0 (30/6), 28.3 (17/60), and 23.3% (14/60) of participants with PTLDS, respectively, compared to none of the controls for each. Standardized questionnaire scores on fatigue and pain for these participants were also considerably worse than clinically relevant cutoffs (FSS: 55.9 ± 5.9; SF-MPQ: 15.9 ± 6.9; p < 0.001 for both). Previous studies have suggested that fatigue and cognitive symptoms are common, and may be particularly important contributors to decreased functioning in this syndrome (38, 39). As Lyme disease incidence continues to increase in endemic regions and spread to new geographic areas (2), PTLDS is likely to be increasingly relevant in the differential diagnosis of patient-reported symptoms commonly encountered by the general internist.
Participants with PTLDS also reported significantly higher severity of an additional 19 diverse symptoms that were not part of the IDSA criteria but which could be diagnostically and clinically relevant. Among these, sleep difficulty was the most frequently reported current symptom, and the symptom with the highest difference in proportion reporting “moderate” or above between cases and controls, suggesting that it may be a clinically important component of this syndrome. Sleep difficulty has been previously identified in the context of Lyme disease (40), and was found to correlate highly with fatigue in one study (17). In our sample, severe sleep difficulty was reported by 31.7% (19/60) of participants with PTLDS and none of the controls, and their PSQI scores were significantly worse than the clinically relevant cutoff for poor sleep quality (PSQI: 14.0 ± 3.5, p < 0.001). Additionally, severe visual clarity issues and photophobia were reported by 5.0 (3/60) and 8.3% (3/60) of our sample of participants with PTLDS respectively, compared to none of the controls. Although ophthalmologic signs can occur in untreated disease, persistent subjective symptoms have not been described extensively in PTLDS (41, 42). Finally, those symptoms not statistically significantly different between participants with PTLDS and controls notably included objective signs of rheumatologic, neurologic, or ocular involvement (such as joint swelling, drooping facial muscle, and double vision) that traditionally distinguish untreated Lyme disease from the posttreatment phase (21, 43).
We found further evidence that the physical and mental health-related quality of life of patients with PTLDS is often lower than both controls and US population means. Poor health-related quality-of-life baseline values were previously reported in both US and European treatment trials among patients with persistent symptoms following Lyme disease (1.5–2 SD below the PCS population mean and 0.5–1.5 SD below the MCS population mean) (23, 44). As Klempner and colleagues note, these low scores are comparable to patients suffering from congestive heart failure or osteoarthritis (23). They are also consistent with results from our sample, with more than half of the participants with PTLDS found to have SF-36 PCS that were 1.5 SD below the population mean, and 41.0% had MCS that were 1 SD below the population mean. Scores below these cutoffs were not found among any of the controls.
Delayed or misdiagnosis of early Lyme disease has been hypothesized by some to be less common in recent decades as knowledge of appropriate treatment regimens and serologic testing methods has increased (45). However, as identified in this study and in our previous chart review (8), these risk factors for PTLDS may still be part of the community landscape of Lyme disease diagnosis and treatment. In the current study, we found evidence of exposure to non-recommended antibiotics (such as sulfamethoxazole or cephalexin), steroids, or an extended duration of greater than 30 days from illness onset to initiation of recommended treatment in 59% of the sample of participants with PTLDS. Notably, the rate of delayed or misdiagnosis was also significantly higher among those with initial LD-probable compared to LD-confirmed presentations (79 vs. 50%, p = 0.033). We hypothesize that this is due to the non-specific nature of the symptoms in the LD-probable group, which may be more frequently overlooked or attributed to viral illnesses.
Although our study sample was largely recruited from a subset of those referred to an academic referral research center and clinic for PTLDS, our participants’ initial Lyme disease was diagnosed and treated in a range of clinical settings. We chose a retrospective design in the current study in order to capture this heterogeneity, and to capitalize on a more representative and generalizable view of PTLDS in the community setting. Participants included in prospective studies are often ideally and uniformly treated, and limited to specific clinical presentations by design (46, 47). We hypothesize that such factors may contribute to discrepant findings in symptom severity between prospective studies, which tend to report milder residual symptoms following treatment (46, 47), and community-based retrospective studies such as ours and others (16, 17) that describe a higher symptom burden with more significant impacts on quality of life (48).
Our study is limited by the fact that no definitive biomarker exists either for B. burgdorferi infection or PTLDS. As such, we cannot be completely certain that our participants with PTLDS had initial signs and symptoms that were correctly attributed to Lyme disease at illness onset. To minimize this risk, we required medical record documentation to establish the initial signs and symptoms, diagnosis, and treatment for Lyme disease that adhered to the IDSA proposed case definition, which few prior studies have done. We also cannot be completely certain that these symptoms are attributable to PTLDS and not other co-morbidities, as was suggested by a recent publication (49). To address this potential confounding effect, our study compared participants with PTLDS to a healthy control group recruited following the same exclusionary criteria, which included a range of conditions independently associated with fatigue, pain, and cognitive dysfunction. Furthermore, while the inclusion of LD-probable patients could also presumably lower specificity of our findings, our analysis did not find a prominent pattern of difference between LD-probable and LD-confirmed groups. Lastly, our study is limited by an inability to address the possibility of recall bias for those variables which were based on self-report and not medical record review.
Our comprehensive case series suggests that the patient-reported symptoms of PTLDS and their effect on life functioning can be clinically significant and long-lasting, regardless of initial Lyme disease presentation. In the absence of a diagnostic biomarker, this study shows that PTLDS can be successfully characterized using a systematic and standardized approach to patient evaluation. This includes special attention to identifying a medical history of initial missed or delayed diagnosis of Lyme disease, which are potentially important risk factors for the development of PTLDS. We speculate that the pattern of symptoms identified in this study could be a tool for the diagnosis of PTLDS, and that well-validated symptom surveys could be used in the future to both identify and monitor treatment progress in patients with PTLDS. Physicians practicing in Lyme disease-endemic areas need to remain alert for the diagnosis of PTLDS when evaluating patients with otherwise unexplained symptoms and prior Lyme disease.
Further research is needed to delineate specific risk factors for PTLDS and the mechanisms of illness in this group of patients in order to guide improvements in diagnostic specificity and treatment options. Biosamples from this cohort of participants will be an important resource for future investigations into both the identification of molecular biomarkers of disease and addressing potential underlying biological mechanisms in PTLDS. Until then, the symptoms of PTLDS, which can be severe and significantly impact quality of life, need to be more effectively identified, validated, and managed as part of integrated patient care. As the prevalence of PTLDS will continue to rise, there will be an increasing need for physician education toward this end."
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Trav here again - this leaves a ton of questions in my mind, starting with: If the tests are so inaccurate as to be delivering both false negatives and false positives (according to their belief), then how in the world can anyone say that the "non-infected" were really not infected??? And, just how does that skew the results of these findings?
While this is a wonderfully positive statement: "Our comprehensive case series suggests that the patient-reported symptoms of PTLDS and their effect on life functioning can be clinically significant and long-lasting, regardless of initial Lyme disease presentation." - how can they then say, in the very next sentence this sort of thing??? "In the absence of a diagnostic biomarker, this study shows that PTLDS can be successfully characterized using a systematic and standardized approach to patient evaluation. This includes special attention to identifying a medical history of initial missed or delayed diagnosis of Lyme disease, which are potentially important risk factors for the development of PTLDS."
For people like me, that were infected as a very young child, but not diagnosed until much later in life (37 yrs later for me) - how the heck can I remember the details that they want to know? I have a memory that has been badly affected by these diseases, so we will just be ignored???
This is NOT just a fight to avoid the term PTLDS, but a fight for inclusion for everyone that has been affected by these diseases.
Alison W. Rebman, Kathleen T. Bechtold, Ting Yang, Erica A. Mihm, Mark J. Soloski, Cheryl B. Novak and John N. Aucott
"Background: The increased incidence and geographic expansion of Lyme disease has made it the most common vector-borne infection in North America. Posttreatment Lyme disease syndrome (PTLDS) represents a subset of patients who remain ill following standard antibiotic therapy for Lyme disease. The spectrum of symptoms and their impact on quality of life remain largely unexplored among patients with well-documented PTLDS.
Objective: To characterize a case series of patients with well-documented PTLDS compared to a sample of healthy controls.
Methods: Sixty-one participants met the proposed case definition for PTLDS. Twenty-six healthy controls had neither a clinical history of Lyme disease nor current antibodies to Borrelia burgdorferi. Participants with PTLDS and controls were evaluated by physical exam, clinical laboratory testing, standardized questionnaires, and a 36-item current symptom list.
Results: Compared to controls, participants with PTLDS reported significantly greater fatigue, pain, sleep disturbance, and depression (Fatigue Severity Scale: 50.0 ± 10.6 vs. 19.8 ± 8.6; Short-Form McGill Pain Questionnaire: 13.7 ± 8.3 vs. 0.8 ± 1.9; Pittsburgh Sleep Quality Index: 10.1 ± 4.7 vs. 4.1 ± 2.1; Beck Depression Inventory-II: 15.1 ± 7.7 vs. 2.2 ± 3.2; p < 0.001 for each), and significantly lower quality of life (SF-36 Physical Component Score: 33.9 ± 9.7 vs. 55.1 ± 6.2; Mental Component Score: 42.9 ± 10.1 vs. 54.2 ± 5.4; p < 0.001 for each). Nineteen non-PTLDS-defining symptoms were found to be significantly more severe among participants with PTLDS than controls, including sleep difficultly and visual complaints. Initial delayed or misdiagnosis was characterized in 59.0% of participants with PTLDS, and 32.2% had abnormal vibratory sense.
Conclusion: Although physical exam and clinical laboratory tests showed few objective abnormalities, standardized symptom questionnaires revealed that patients with PTLDS are highly and clinically significantly symptomatic, with poor health-related quality of life. PTLDS patients exhibited levels of fatigue, musculoskeletal pain, sleep disturbance, and depression which were both clinically relevant and statistically significantly higher than controls. Our study shows that PTLDS can be successfully identified using a systematic approach to diagnosis and symptom measurement. As the prevalence of PTLDS continues to rise, there will be an increased need for physician education to more effectively identify and manage PTLDS as part of integrated patient care."
(Trav here: Now, this is what cracks me up/pisses me off - I'm posting what they (IDSA) has determined to be the definition of Post Treatment Lyme Disease Syndrome("PTLDS") below. So my question, because I'm in a totally different group that is simply not recognized, is what about all those that never got the treatment they needed in time??? They are STILL being ignored, as if we simply don't exist.)
"In 2006, the Infectious Diseases Society of America (IDSA) published a proposed case definition for PTLDS (21). Briefly, this definition relies on prior physician-documented Lyme disease, treatment with standard of care antibiotics, and the development of significant fatigue, widespread musculoskeletal pain, and/or cognitive difficulties that last for a period of at least 6 months, and began within 6 months of a Lyme diagnosis and recommended treatment (21). Patients can be excluded for a range of symptoms, conditions, or laboratory abnormalities that could be associated with or explain the symptomatology of PTLDS (21). As antibodies to B. burgdorferi are known to fall over time in treated patients regardless of clinical outcome (7, 22–24), and convalescent antibodies after treatment of early Lyme disease are positive in 65% of patients (25), presence of reactive antibodies is not part of this definition. In the clinical setting, PTLDS is largely an historical diagnosis that hinges on the ability to document symptom onset after an episode of physician-documented Lyme disease that was adequately treated with standard of care antibiotics."
(Trav here again, I'm skipping over a lot of the article to only post certain aspects. If you would like to see the article in it's entirety, please follow the link at the top of this page.)
"Discussion
This study represents the first to compare patients with rigorously defined PTLDS to non-Lyme infected controls on a range of clinical, laboratory, symptom, and quality-of-life parameters. We found that physical exam and clinical laboratory tests showed few abnormalities. However, standardized questionnaires revealed that these patients are highly symptomatic, with clinically significantly poorer quality of life compared both to healthy controls and the US population. These findings were consistent regardless of whether participants met criteria for the initial LD-probable or LD-confirmed group. There was some evidence for greater initial misdiagnosis and more severe current symptoms among the LD-probable group.
Results from the physical exam and laboratory testing in our sample of patients with PTLDS did not show a pattern of significant objective abnormalities. The most notable exception was the higher rate of diminished vibratory sensation on physical exam among participants with PTLDS (32.2%), compared to the 5% expected to fall below the age-adjusted cutoffs used in this analysis (29). This abnormality were not only present among those with a prior diagnosis of neurologic Lyme disease or a later diagnosis of neuropathy but also among those without a specific prior neurologic diagnosis. This finding was also observed in a previous population-based study, in which decreased vibratory sense was noted in 29% of a sample of individuals with prior Lyme disease, and was one of the sole physical exam findings to differ significantly from controls (17). Additionally, although only found in a small subset of our sample (3.4%), two participants met criteria for postural orthostatic tachycardia syndrome, an autonomic condition that has been previously reported following Lyme disease (37). Laboratory tests, including complete blood count, complete metabolic count, and C-reactive protein, showed no significant difference between participants with PTLDS and controls. The rates of current two-tier IgG-WB positivity among those with confirmed early (7/36, 19.4%) and late (4/6, 66.7%) Lyme disease were similar to those found in a 10- to 20-year follow-up study of treated patients assessed to have good overall health (22), further emphasizing that current serology cannot be used as a diagnostic marker for PTLDS.
By contrast, participants with PTLDS reported prominent symptoms that are often diverse and can be moderate to severe in nature. We expected that current symptom severity of fatigue, pain, and cognitive complaints would be higher among PTLDS participants than controls, given that presence of at least one of these symptoms was included in both the IDSA proposed case definition and our enrollment criteria. Indeed, severe levels of each of these were reported by 50.0 (30/6), 28.3 (17/60), and 23.3% (14/60) of participants with PTLDS, respectively, compared to none of the controls for each. Standardized questionnaire scores on fatigue and pain for these participants were also considerably worse than clinically relevant cutoffs (FSS: 55.9 ± 5.9; SF-MPQ: 15.9 ± 6.9; p < 0.001 for both). Previous studies have suggested that fatigue and cognitive symptoms are common, and may be particularly important contributors to decreased functioning in this syndrome (38, 39). As Lyme disease incidence continues to increase in endemic regions and spread to new geographic areas (2), PTLDS is likely to be increasingly relevant in the differential diagnosis of patient-reported symptoms commonly encountered by the general internist.
Participants with PTLDS also reported significantly higher severity of an additional 19 diverse symptoms that were not part of the IDSA criteria but which could be diagnostically and clinically relevant. Among these, sleep difficulty was the most frequently reported current symptom, and the symptom with the highest difference in proportion reporting “moderate” or above between cases and controls, suggesting that it may be a clinically important component of this syndrome. Sleep difficulty has been previously identified in the context of Lyme disease (40), and was found to correlate highly with fatigue in one study (17). In our sample, severe sleep difficulty was reported by 31.7% (19/60) of participants with PTLDS and none of the controls, and their PSQI scores were significantly worse than the clinically relevant cutoff for poor sleep quality (PSQI: 14.0 ± 3.5, p < 0.001). Additionally, severe visual clarity issues and photophobia were reported by 5.0 (3/60) and 8.3% (3/60) of our sample of participants with PTLDS respectively, compared to none of the controls. Although ophthalmologic signs can occur in untreated disease, persistent subjective symptoms have not been described extensively in PTLDS (41, 42). Finally, those symptoms not statistically significantly different between participants with PTLDS and controls notably included objective signs of rheumatologic, neurologic, or ocular involvement (such as joint swelling, drooping facial muscle, and double vision) that traditionally distinguish untreated Lyme disease from the posttreatment phase (21, 43).
We found further evidence that the physical and mental health-related quality of life of patients with PTLDS is often lower than both controls and US population means. Poor health-related quality-of-life baseline values were previously reported in both US and European treatment trials among patients with persistent symptoms following Lyme disease (1.5–2 SD below the PCS population mean and 0.5–1.5 SD below the MCS population mean) (23, 44). As Klempner and colleagues note, these low scores are comparable to patients suffering from congestive heart failure or osteoarthritis (23). They are also consistent with results from our sample, with more than half of the participants with PTLDS found to have SF-36 PCS that were 1.5 SD below the population mean, and 41.0% had MCS that were 1 SD below the population mean. Scores below these cutoffs were not found among any of the controls.
Delayed or misdiagnosis of early Lyme disease has been hypothesized by some to be less common in recent decades as knowledge of appropriate treatment regimens and serologic testing methods has increased (45). However, as identified in this study and in our previous chart review (8), these risk factors for PTLDS may still be part of the community landscape of Lyme disease diagnosis and treatment. In the current study, we found evidence of exposure to non-recommended antibiotics (such as sulfamethoxazole or cephalexin), steroids, or an extended duration of greater than 30 days from illness onset to initiation of recommended treatment in 59% of the sample of participants with PTLDS. Notably, the rate of delayed or misdiagnosis was also significantly higher among those with initial LD-probable compared to LD-confirmed presentations (79 vs. 50%, p = 0.033). We hypothesize that this is due to the non-specific nature of the symptoms in the LD-probable group, which may be more frequently overlooked or attributed to viral illnesses.
Although our study sample was largely recruited from a subset of those referred to an academic referral research center and clinic for PTLDS, our participants’ initial Lyme disease was diagnosed and treated in a range of clinical settings. We chose a retrospective design in the current study in order to capture this heterogeneity, and to capitalize on a more representative and generalizable view of PTLDS in the community setting. Participants included in prospective studies are often ideally and uniformly treated, and limited to specific clinical presentations by design (46, 47). We hypothesize that such factors may contribute to discrepant findings in symptom severity between prospective studies, which tend to report milder residual symptoms following treatment (46, 47), and community-based retrospective studies such as ours and others (16, 17) that describe a higher symptom burden with more significant impacts on quality of life (48).
Our study is limited by the fact that no definitive biomarker exists either for B. burgdorferi infection or PTLDS. As such, we cannot be completely certain that our participants with PTLDS had initial signs and symptoms that were correctly attributed to Lyme disease at illness onset. To minimize this risk, we required medical record documentation to establish the initial signs and symptoms, diagnosis, and treatment for Lyme disease that adhered to the IDSA proposed case definition, which few prior studies have done. We also cannot be completely certain that these symptoms are attributable to PTLDS and not other co-morbidities, as was suggested by a recent publication (49). To address this potential confounding effect, our study compared participants with PTLDS to a healthy control group recruited following the same exclusionary criteria, which included a range of conditions independently associated with fatigue, pain, and cognitive dysfunction. Furthermore, while the inclusion of LD-probable patients could also presumably lower specificity of our findings, our analysis did not find a prominent pattern of difference between LD-probable and LD-confirmed groups. Lastly, our study is limited by an inability to address the possibility of recall bias for those variables which were based on self-report and not medical record review.
Our comprehensive case series suggests that the patient-reported symptoms of PTLDS and their effect on life functioning can be clinically significant and long-lasting, regardless of initial Lyme disease presentation. In the absence of a diagnostic biomarker, this study shows that PTLDS can be successfully characterized using a systematic and standardized approach to patient evaluation. This includes special attention to identifying a medical history of initial missed or delayed diagnosis of Lyme disease, which are potentially important risk factors for the development of PTLDS. We speculate that the pattern of symptoms identified in this study could be a tool for the diagnosis of PTLDS, and that well-validated symptom surveys could be used in the future to both identify and monitor treatment progress in patients with PTLDS. Physicians practicing in Lyme disease-endemic areas need to remain alert for the diagnosis of PTLDS when evaluating patients with otherwise unexplained symptoms and prior Lyme disease.
Further research is needed to delineate specific risk factors for PTLDS and the mechanisms of illness in this group of patients in order to guide improvements in diagnostic specificity and treatment options. Biosamples from this cohort of participants will be an important resource for future investigations into both the identification of molecular biomarkers of disease and addressing potential underlying biological mechanisms in PTLDS. Until then, the symptoms of PTLDS, which can be severe and significantly impact quality of life, need to be more effectively identified, validated, and managed as part of integrated patient care. As the prevalence of PTLDS will continue to rise, there will be an increasing need for physician education toward this end."
-------------------------------------------------------------------------------------------------------------------------------------
Trav here again - this leaves a ton of questions in my mind, starting with: If the tests are so inaccurate as to be delivering both false negatives and false positives (according to their belief), then how in the world can anyone say that the "non-infected" were really not infected??? And, just how does that skew the results of these findings?
While this is a wonderfully positive statement: "Our comprehensive case series suggests that the patient-reported symptoms of PTLDS and their effect on life functioning can be clinically significant and long-lasting, regardless of initial Lyme disease presentation." - how can they then say, in the very next sentence this sort of thing??? "In the absence of a diagnostic biomarker, this study shows that PTLDS can be successfully characterized using a systematic and standardized approach to patient evaluation. This includes special attention to identifying a medical history of initial missed or delayed diagnosis of Lyme disease, which are potentially important risk factors for the development of PTLDS."
For people like me, that were infected as a very young child, but not diagnosed until much later in life (37 yrs later for me) - how the heck can I remember the details that they want to know? I have a memory that has been badly affected by these diseases, so we will just be ignored???
This is NOT just a fight to avoid the term PTLDS, but a fight for inclusion for everyone that has been affected by these diseases.