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Daniel J. Clauw - One of the best experts on this subject based on the ideXlab platform.
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Prodrome and non Prodrome phenotypes of bladder pain syndrome interstitial cystitis
Urology, 2018Co-Authors: John W. Warren, Ningbo Jian, Lisa Gallicchio, Daniel J. ClauwAbstract:Objective To test the hypothesis that risk factors for bladder pain syndrome/interstitial cystitis (BPS/IC) in women differ between those with and without the BPS/IC Prodrome. Materials and Methods Incident cases of BPS/IC and healthy controls were recruited nationally. More than half the BPS/IC cases reported subsyndromal urinary symptoms for decades before onset of BPS/IC and were identified as having the Prodrome. Risk factors for BPS/IC were examined separately for cases with and without the Prodrome using a set of matched controls. Results Two risk factors distinguished 178 Prodrome from 134 non-Prodrome cases. One was “UTIs” in the year before BPS/IC onset, possibly a manifestation of the Prodrome itself. The other was the presence of the maximal number of nonbladder syndromes (NBSs): Prodrome cases were 12 times more likely than non-Prodrome cases to have ≥4 NBSs. Additional risk factors for Prodrome and/or non-Prodrome cases were the direct association of exogenous female hormones, as well as 3 inverse associations: type 2 diabetes mellitus, multiple pregnancies, and current daily smoking. Conclusion Prodrome cases developed urinary symptoms in their early 20s (ie, the Prodrome) and were at very high risk of numerous NBSs. Non-Prodrome cases developed urinary symptoms in their early 40s (ie, full-blown BPS/IC) and were no more likely than controls to have the maximal number of NBSs. These findings are consistent with recent suggestions of two BPS/IC phenotypes: one with systemic and psychosocial manifestations and the other more specific to the bladder. Additionally, several risk factors identified here might be hints of related or causal nervous system pathophysiologies.
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Prodrome and Non-Prodrome Phenotypes of Bladder Pain Syndrome/Interstitial Cystitis.
Urology, 2018Co-Authors: John W. Warren, Ningbo Jian, Lisa Gallicchio, Daniel J. ClauwAbstract:Objective To test the hypothesis that risk factors for bladder pain syndrome/interstitial cystitis (BPS/IC) in women differ between those with and without the BPS/IC Prodrome. Materials and Methods Incident cases of BPS/IC and healthy controls were recruited nationally. More than half the BPS/IC cases reported subsyndromal urinary symptoms for decades before onset of BPS/IC and were identified as having the Prodrome. Risk factors for BPS/IC were examined separately for cases with and without the Prodrome using a set of matched controls. Results Two risk factors distinguished 178 Prodrome from 134 non-Prodrome cases. One was “UTIs” in the year before BPS/IC onset, possibly a manifestation of the Prodrome itself. The other was the presence of the maximal number of nonbladder syndromes (NBSs): Prodrome cases were 12 times more likely than non-Prodrome cases to have ≥4 NBSs. Additional risk factors for Prodrome and/or non-Prodrome cases were the direct association of exogenous female hormones, as well as 3 inverse associations: type 2 diabetes mellitus, multiple pregnancies, and current daily smoking. Conclusion Prodrome cases developed urinary symptoms in their early 20s (ie, the Prodrome) and were at very high risk of numerous NBSs. Non-Prodrome cases developed urinary symptoms in their early 40s (ie, full-blown BPS/IC) and were no more likely than controls to have the maximal number of NBSs. These findings are consistent with recent suggestions of two BPS/IC phenotypes: one with systemic and psychosocial manifestations and the other more specific to the bladder. Additionally, several risk factors identified here might be hints of related or causal nervous system pathophysiologies.
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urinary symptoms as a Prodrome of bladder pain syndrome interstitial cystitis
Urology, 2014Co-Authors: John W. Warren, Ursula Wesselmann, Patty Greenberg, Daniel J. ClauwAbstract:Objective To test the hypothesis that more bladder pain syndrome/interstitial cystitis (BPS/IC) cases than controls report pre-onset urinary symptoms. Methods In a risk factor study, the date of BPS/IC onset (index date) was systematically determined in 312 female incident cases; the mean age at onset was 42.3 years. Frequency-matched controls were compared on pre–index date medical history. Results Three pre–index date symptoms were more common in BPS/IC cases: pelvic pain with urinary features, frequency, and bladder pain; 178 cases (57%) vs 56 controls (18%) had at least 1 symptom ( P Conclusion Before the onset of BPS/IC, pelvic pain with urinary features, frequency, and/or bladder pain were reported by more than half the cases. Prodromal women recalled abnormal urinary symptoms decades before the onset of BPS/IC. The Prodrome was associated with prior NBSs and predicted not only BPS/IC but also its poor prognosis. These data generated 2 hypotheses: that (1) prodromal symptoms are different from BPS/IC symptoms and (2) pain amplification links NBSs, the Prodrome, the appearance of BPS/IC, and its poor prognosis. Recognition of the Prodrome might provide opportunities for prevention of fully developed BPS/IC.
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Urinary symptoms as a Prodrome of bladder pain syndrome/interstitial cystitis.
Urology, 2014Co-Authors: John W. Warren, Ursula Wesselmann, Patty Greenberg, Daniel J. ClauwAbstract:Objective To test the hypothesis that more bladder pain syndrome/interstitial cystitis (BPS/IC) cases than controls report pre-onset urinary symptoms. Methods In a risk factor study, the date of BPS/IC onset (index date) was systematically determined in 312 female incident cases; the mean age at onset was 42.3 years. Frequency-matched controls were compared on pre–index date medical history. Results Three pre–index date symptoms were more common in BPS/IC cases: pelvic pain with urinary features, frequency, and bladder pain; 178 cases (57%) vs 56 controls (18%) had at least 1 symptom ( P Conclusion Before the onset of BPS/IC, pelvic pain with urinary features, frequency, and/or bladder pain were reported by more than half the cases. Prodromal women recalled abnormal urinary symptoms decades before the onset of BPS/IC. The Prodrome was associated with prior NBSs and predicted not only BPS/IC but also its poor prognosis. These data generated 2 hypotheses: that (1) prodromal symptoms are different from BPS/IC symptoms and (2) pain amplification links NBSs, the Prodrome, the appearance of BPS/IC, and its poor prognosis. Recognition of the Prodrome might provide opportunities for prevention of fully developed BPS/IC.
John W. Warren - One of the best experts on this subject based on the ideXlab platform.
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Prodrome and non Prodrome phenotypes of bladder pain syndrome interstitial cystitis
Urology, 2018Co-Authors: John W. Warren, Ningbo Jian, Lisa Gallicchio, Daniel J. ClauwAbstract:Objective To test the hypothesis that risk factors for bladder pain syndrome/interstitial cystitis (BPS/IC) in women differ between those with and without the BPS/IC Prodrome. Materials and Methods Incident cases of BPS/IC and healthy controls were recruited nationally. More than half the BPS/IC cases reported subsyndromal urinary symptoms for decades before onset of BPS/IC and were identified as having the Prodrome. Risk factors for BPS/IC were examined separately for cases with and without the Prodrome using a set of matched controls. Results Two risk factors distinguished 178 Prodrome from 134 non-Prodrome cases. One was “UTIs” in the year before BPS/IC onset, possibly a manifestation of the Prodrome itself. The other was the presence of the maximal number of nonbladder syndromes (NBSs): Prodrome cases were 12 times more likely than non-Prodrome cases to have ≥4 NBSs. Additional risk factors for Prodrome and/or non-Prodrome cases were the direct association of exogenous female hormones, as well as 3 inverse associations: type 2 diabetes mellitus, multiple pregnancies, and current daily smoking. Conclusion Prodrome cases developed urinary symptoms in their early 20s (ie, the Prodrome) and were at very high risk of numerous NBSs. Non-Prodrome cases developed urinary symptoms in their early 40s (ie, full-blown BPS/IC) and were no more likely than controls to have the maximal number of NBSs. These findings are consistent with recent suggestions of two BPS/IC phenotypes: one with systemic and psychosocial manifestations and the other more specific to the bladder. Additionally, several risk factors identified here might be hints of related or causal nervous system pathophysiologies.
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Prodrome and Non-Prodrome Phenotypes of Bladder Pain Syndrome/Interstitial Cystitis.
Urology, 2018Co-Authors: John W. Warren, Ningbo Jian, Lisa Gallicchio, Daniel J. ClauwAbstract:Objective To test the hypothesis that risk factors for bladder pain syndrome/interstitial cystitis (BPS/IC) in women differ between those with and without the BPS/IC Prodrome. Materials and Methods Incident cases of BPS/IC and healthy controls were recruited nationally. More than half the BPS/IC cases reported subsyndromal urinary symptoms for decades before onset of BPS/IC and were identified as having the Prodrome. Risk factors for BPS/IC were examined separately for cases with and without the Prodrome using a set of matched controls. Results Two risk factors distinguished 178 Prodrome from 134 non-Prodrome cases. One was “UTIs” in the year before BPS/IC onset, possibly a manifestation of the Prodrome itself. The other was the presence of the maximal number of nonbladder syndromes (NBSs): Prodrome cases were 12 times more likely than non-Prodrome cases to have ≥4 NBSs. Additional risk factors for Prodrome and/or non-Prodrome cases were the direct association of exogenous female hormones, as well as 3 inverse associations: type 2 diabetes mellitus, multiple pregnancies, and current daily smoking. Conclusion Prodrome cases developed urinary symptoms in their early 20s (ie, the Prodrome) and were at very high risk of numerous NBSs. Non-Prodrome cases developed urinary symptoms in their early 40s (ie, full-blown BPS/IC) and were no more likely than controls to have the maximal number of NBSs. These findings are consistent with recent suggestions of two BPS/IC phenotypes: one with systemic and psychosocial manifestations and the other more specific to the bladder. Additionally, several risk factors identified here might be hints of related or causal nervous system pathophysiologies.
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urinary symptoms as a Prodrome of bladder pain syndrome interstitial cystitis
Urology, 2014Co-Authors: John W. Warren, Ursula Wesselmann, Patty Greenberg, Daniel J. ClauwAbstract:Objective To test the hypothesis that more bladder pain syndrome/interstitial cystitis (BPS/IC) cases than controls report pre-onset urinary symptoms. Methods In a risk factor study, the date of BPS/IC onset (index date) was systematically determined in 312 female incident cases; the mean age at onset was 42.3 years. Frequency-matched controls were compared on pre–index date medical history. Results Three pre–index date symptoms were more common in BPS/IC cases: pelvic pain with urinary features, frequency, and bladder pain; 178 cases (57%) vs 56 controls (18%) had at least 1 symptom ( P Conclusion Before the onset of BPS/IC, pelvic pain with urinary features, frequency, and/or bladder pain were reported by more than half the cases. Prodromal women recalled abnormal urinary symptoms decades before the onset of BPS/IC. The Prodrome was associated with prior NBSs and predicted not only BPS/IC but also its poor prognosis. These data generated 2 hypotheses: that (1) prodromal symptoms are different from BPS/IC symptoms and (2) pain amplification links NBSs, the Prodrome, the appearance of BPS/IC, and its poor prognosis. Recognition of the Prodrome might provide opportunities for prevention of fully developed BPS/IC.
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Urinary symptoms as a Prodrome of bladder pain syndrome/interstitial cystitis.
Urology, 2014Co-Authors: John W. Warren, Ursula Wesselmann, Patty Greenberg, Daniel J. ClauwAbstract:Objective To test the hypothesis that more bladder pain syndrome/interstitial cystitis (BPS/IC) cases than controls report pre-onset urinary symptoms. Methods In a risk factor study, the date of BPS/IC onset (index date) was systematically determined in 312 female incident cases; the mean age at onset was 42.3 years. Frequency-matched controls were compared on pre–index date medical history. Results Three pre–index date symptoms were more common in BPS/IC cases: pelvic pain with urinary features, frequency, and bladder pain; 178 cases (57%) vs 56 controls (18%) had at least 1 symptom ( P Conclusion Before the onset of BPS/IC, pelvic pain with urinary features, frequency, and/or bladder pain were reported by more than half the cases. Prodromal women recalled abnormal urinary symptoms decades before the onset of BPS/IC. The Prodrome was associated with prior NBSs and predicted not only BPS/IC but also its poor prognosis. These data generated 2 hypotheses: that (1) prodromal symptoms are different from BPS/IC symptoms and (2) pain amplification links NBSs, the Prodrome, the appearance of BPS/IC, and its poor prognosis. Recognition of the Prodrome might provide opportunities for prevention of fully developed BPS/IC.
Jeffrey M Gelfand - One of the best experts on this subject based on the ideXlab platform.
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episodic bradycardia as neurocardiac Prodrome to voltage gated potassium channel complex leucine rich glioma inactivated 1 antibody encephalitis
JAMA Neurology, 2014Co-Authors: Georges Naasan, Bm Bettcher, Sarosh R Irani, Michael D Geschwind, Jeffrey M GelfandAbstract:Importance Voltage-gated potassium channel complex antibody (VGKCc-Ab) encephalitis is an immunotherapy-responsive syndrome usually associated with causative antibodies that target the leucine-rich, glioma inactivated 1 (LGI1) protein. Although it is expressed throughout the brain, LGI1 is not known to be expressed in cardiac tissue. We describe a novel neurocardiac Prodrome of VGKCc-Ab/LGI1-encephalitis. Observations Among 14 patients with VGKCc/LGI1-Ab encephalitis evaluated in the University of California, San Francisco Autoimmune Encephalitis Clinic and Rapid Dementia Research Program, 3 patients (2 men and 1 woman; aged 53, 55, and 64 years) exhibited episodic bradycardia that preceded the onset of encephalopathy by approximately 2 months and was severe enough to lead to pacemaker implantation. Serum LGI1-Ab results were positive when tested at the time of the subsequent encephalopathy. All 3 patients developed hyponatremia; none had faciobrachial dystonic seizures or malignancy. Brain magnetic resonance imaging was abnormal in 2 cases. None of the patients experienced further symptomatic bradyarrythmias after 1.7 to 7 years of follow-up. Conclusions and Relevance Episodic bradycardia is a distinctive neurocardiac Prodrome of VGKCc/LGI1-Ab encephalitis. The neuroanatomical localization most likely relates to insular and temporal lobe involvement, cortical regions that modulate cardiac autonomic function. Further study is needed to determine if recognition of this neurocardiac Prodrome and earlier institution of immunosuppression can prevent the development of encephalopathy.
Jm Gelfand - One of the best experts on this subject based on the ideXlab platform.
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Episodic bradycardia as neurocardiac Prodrome to voltage-gated potassium channel complex/leucine-rich, glioma inactivated 1 antibody encephalitis.
'American Medical Association (AMA)', 2014Co-Authors: Naasan G, Bm Bettcher, Jm GelfandAbstract:IMPORTANCE: Voltage-gated potassium channel complex antibody (VGKCc-Ab) encephalitis is an immunotherapy-responsive syndrome usually associated with causative antibodies that target the leucine-rich, glioma inactivated 1 (LGI1) protein. Although it is expressed throughout the brain, LGI1 is not known to be expressed in cardiac tissue. We describe a novel neurocardiac Prodrome of VGKCc-Ab/LGI1-encephalitis. OBSERVATIONS: Among 14 patients with VGKCc/LGI1-Ab encephalitis evaluated in the University of California, San Francisco Autoimmune Encephalitis Clinic and Rapid Dementia Research Program, 3 patients (2 men and 1 woman; aged 53, 55, and 64 years) exhibited episodic bradycardia that preceded the onset of encephalopathy by approximately 2 months and was severe enough to lead to pacemaker implantation. Serum LGI1-Ab results were positive when tested at the time of the subsequent encephalopathy. All 3 patients developed hyponatremia; none had faciobrachial dystonic seizures or malignancy. Brain magnetic resonance imaging was abnormal in 2 cases. None of the patients experienced further symptomatic bradyarrythmias after 1.7 to 7 years of follow-up. CONCLUSIONS AND RELEVANCE: Episodic bradycardia is a distinctive neurocardiac Prodrome of VGKCc/LGI1-Ab encephalitis. The neuroanatomical localization most likely relates to insular and temporal lobe involvement, cortical regions that modulate cardiac autonomic function. Further study is needed to determine if recognition of this neurocardiac Prodrome and earlier institution of immunosuppression can prevent the development of encephalopathy
Bm Bettcher - One of the best experts on this subject based on the ideXlab platform.
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Episodic bradycardia as neurocardiac Prodrome to voltage-gated potassium channel complex/leucine-rich, glioma inactivated 1 antibody encephalitis.
'American Medical Association (AMA)', 2014Co-Authors: Naasan G, Bm Bettcher, Jm GelfandAbstract:IMPORTANCE: Voltage-gated potassium channel complex antibody (VGKCc-Ab) encephalitis is an immunotherapy-responsive syndrome usually associated with causative antibodies that target the leucine-rich, glioma inactivated 1 (LGI1) protein. Although it is expressed throughout the brain, LGI1 is not known to be expressed in cardiac tissue. We describe a novel neurocardiac Prodrome of VGKCc-Ab/LGI1-encephalitis. OBSERVATIONS: Among 14 patients with VGKCc/LGI1-Ab encephalitis evaluated in the University of California, San Francisco Autoimmune Encephalitis Clinic and Rapid Dementia Research Program, 3 patients (2 men and 1 woman; aged 53, 55, and 64 years) exhibited episodic bradycardia that preceded the onset of encephalopathy by approximately 2 months and was severe enough to lead to pacemaker implantation. Serum LGI1-Ab results were positive when tested at the time of the subsequent encephalopathy. All 3 patients developed hyponatremia; none had faciobrachial dystonic seizures or malignancy. Brain magnetic resonance imaging was abnormal in 2 cases. None of the patients experienced further symptomatic bradyarrythmias after 1.7 to 7 years of follow-up. CONCLUSIONS AND RELEVANCE: Episodic bradycardia is a distinctive neurocardiac Prodrome of VGKCc/LGI1-Ab encephalitis. The neuroanatomical localization most likely relates to insular and temporal lobe involvement, cortical regions that modulate cardiac autonomic function. Further study is needed to determine if recognition of this neurocardiac Prodrome and earlier institution of immunosuppression can prevent the development of encephalopathy
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episodic bradycardia as neurocardiac Prodrome to voltage gated potassium channel complex leucine rich glioma inactivated 1 antibody encephalitis
JAMA Neurology, 2014Co-Authors: Georges Naasan, Bm Bettcher, Sarosh R Irani, Michael D Geschwind, Jeffrey M GelfandAbstract:Importance Voltage-gated potassium channel complex antibody (VGKCc-Ab) encephalitis is an immunotherapy-responsive syndrome usually associated with causative antibodies that target the leucine-rich, glioma inactivated 1 (LGI1) protein. Although it is expressed throughout the brain, LGI1 is not known to be expressed in cardiac tissue. We describe a novel neurocardiac Prodrome of VGKCc-Ab/LGI1-encephalitis. Observations Among 14 patients with VGKCc/LGI1-Ab encephalitis evaluated in the University of California, San Francisco Autoimmune Encephalitis Clinic and Rapid Dementia Research Program, 3 patients (2 men and 1 woman; aged 53, 55, and 64 years) exhibited episodic bradycardia that preceded the onset of encephalopathy by approximately 2 months and was severe enough to lead to pacemaker implantation. Serum LGI1-Ab results were positive when tested at the time of the subsequent encephalopathy. All 3 patients developed hyponatremia; none had faciobrachial dystonic seizures or malignancy. Brain magnetic resonance imaging was abnormal in 2 cases. None of the patients experienced further symptomatic bradyarrythmias after 1.7 to 7 years of follow-up. Conclusions and Relevance Episodic bradycardia is a distinctive neurocardiac Prodrome of VGKCc/LGI1-Ab encephalitis. The neuroanatomical localization most likely relates to insular and temporal lobe involvement, cortical regions that modulate cardiac autonomic function. Further study is needed to determine if recognition of this neurocardiac Prodrome and earlier institution of immunosuppression can prevent the development of encephalopathy.
