scholarly journals Treatment of Postherpetic Neuralgia With Gastroretentive Gabapentin: Interaction of Patient Demographics, Disease Characteristics, and Efficacy Outcomes

2015 ◽  
Vol 16 (12) ◽  
pp. 1300-1311 ◽  
Author(s):  
Daniel Kantor ◽  
Sunil Panchal ◽  
Vikram Patel ◽  
Iwona Bucior ◽  
Richard Rauck
2021 ◽  
Vol 25 (12) ◽  
pp. 990-994
Author(s):  
J. Phillipson ◽  
N. Kuruppu ◽  
T. Chikura ◽  
C. McLachlan ◽  
L. McNeill ◽  
...  

BACKGROUND Treatment of TB is often extended beyond the recommended duration. The aim of this study was to assess prevalence of extended treatment and to identify associated risk factors. We also aimed to determine the frequency and type of adverse drug reactions (ADR) experienced by this study population.METHODS We performed a retrospective cohort study of all patients treated for active TB at Christchurch Hospital, Christchurch, New Zealand, between 1 March 2012 and 31 December 2018. Data for 192 patients were collected on patient demographics, disease characteristics and treatment characteristics, including planned and actual duration of treatment and ADRs.RESULTS Of 192 patients, 35 (18.2%) had treatment extended, and 85 (46.5%) of 183 with fully drug-susceptible TB received ≥9 months treatment. The most common reasons for extension were persistent or extensive disease and ADR. Extended treatment duration was not associated with any patient or disease characteristics. We found 35 (18.2%) patients experienced at least one ADR. The most common ADRs were hepatitis, rash and peripheral neuropathy.CONCLUSION TB treatment extension beyond WHO guidelines is common. Further research is needed to guide management of those with slow response to treatment. Methods for early detection of ADR, systems to improve adherence and therapeutic drug monitoring are potentially useful strategies.


2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 467-467
Author(s):  
M. Teo ◽  
S. O'Reilly ◽  
E. Moylan ◽  
D. G. Power

467 Background: Clinical trials have shown that tumor KRAS status predicts response to anti-EGFR monoclonal antibodies in metastatic colorectal cancer (mCRC). We sought to compare distribution of wild-type and mutated KRAS in an Irish population and identify clinicopathologic correlates. Methods: From our prospectively maintained database we retrospectively identified patients with mCRC and documented KRAS status between Jan 2007 to June 2010. Medical notes were examined for patient demographics and disease characteristics. Variables were extracted and compared using unpaired t test and chi2 test. Results: 52 patients were identified, 29 (55.8%) with mutated (mt) and 23 (44.2%) with wild type (wt) KRAS from tumor tissue. Males accounted for 61.5% (n=31). Median age at diagnosis of metastatic disease for the KRASmt group was 66.4 years (range 56.7-82.1) and for the KRAS wt group was 64.2 years (40.1-76.8), p= 0.08. 21 (72.4%) of the KRASmt group and 16 (69.6%) of the KRASwt group had metastatic disease at presentation (p=0.81). For patients who presented initially with localised disease, time to development of metastases was 22.5mo (range 14-37.6) for the KRASmt group and 16.7mo (3.2-123.7) for the KRASwt (p=0.30). 21 (72.4%) of KRASmt and 17 (74.1%) of KRASwt tumors had left-sided primary (p = 0.84) with equal numbers of primary tumor resection in both groups. There was no statistical difference in TN-stage or the presence of liver metastases. Numbers of patients with KRASmt tumors with one, two and three or more different sites of metastases was 22 (75.9%), 5 (17.2%), and 2 (6.9%), and in KRASwt tumors there was no significant difference: 18 (78.3%), 4 (17.4%), and 1 (4.3%), respectively (p = 0.93). Median CEA at diagnosis for both groups were 19.7 μg/l (range 1.2-5958) and 6.1 (1.3-696.9; p = 0.11). Conclusions: We found that the ratio of KRASmt to KRASwt tumours in an Irish population is comparable to that in large international trials. Our analysis revealed no association between KRAS status and clinicopathologic variables. The inclusion of BRAF status, not readily available in our institution, may help define poor prognosis tumors. At present there is no validated molecular biomarker that is superior to standard clinicopathologic variables. No significant financial relationships to disclose.


2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e15180-e15180
Author(s):  
Julia Warr ◽  
David Yam ◽  
Leah VanDraanen ◽  
Shannon Goodall ◽  
Angie Giotis ◽  
...  

e15180 Background: ZOL therapy is associated with severe (i.e., grade ≥ 3) hypocalcemia and hypophosphatemia in a subset of patients with metastatic CRPC. However, as opposed to the distinct clinical picture of hypocalcemia, the symptoms of hypophosphatemia are less pathognomonic. Furthermore, serum phosphate abnormalities are not regularly reported. Methods: To characterize the rate and clinical impact of severe hypophosphatemia in CRPC patients undergoing ZOL therapy, we identified CRPC patients receiving at least 3 doses of ZOL at our Centre between 01/2004 and 03/2011. Patient demographics, disease characteristics and laboratory parameters were extracted using the Oncology Symptom Control and Information Resource database, and by means of manual chart review. Results: 12 of 90 evaluable patients developed grade ≥ 3 hypophosphatemia (nadir) after 364±299 days (mean±SD) following the first dose of ZOL. While only one patient presented with concomitant severe hypocalcemia, the hypophosphatemia nadir coincided with rising PSA readings in 9 out of 11 informative patients. Severe ZOL-associated hypophosphatemia identified patients with worse outcome (median overall survival from time of CRPC diagnosis to death 685 days) compared to patients without documented hypophosphatemia (907 days, HR 0.52, p=0.049; n=42), or patients with grade 1-2 hypophosphatemia (1035 days, HR 0.44, p=0.016; n=36). Otherwise, the prognostic nomogram developed by Armstrong et al appears not to capture the poor prognosis of patients with severe ZOL-associated hypophosphatemia. Conclusions: Grade 3-4 hypophosphatemia occurs in about 15% of CRPC patients undergoing ZOL therapy and is associated with worse prognosis when compared to patients with absent or mild hypophosphatemia. The latter is usually transient and likely related to increased parathyroid hormone levels due to calcium decreases as a consequence of bisphosphonate therapy. On the other hand, the distinct clinical behavior of CRPC presenting with ZOL-associated severe hypophosphatemia suggests that secreted tumor-associated factors such as fibroblast growth factor 23 may contribute to this phenomenon.


Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Niveditta Ramkumar ◽  
Jesse A Columbo ◽  
Pablo M Camblor ◽  
A. James O’Malley ◽  
Philip P Goodney

Introduction: Outcomes for atherectomy remain poorly characterized. Our objective was to use instrumental variable (IV) analysis to compare long-term amputation rates in patients receiving atherectomy versus other traditional peripheral vascular interventions (PVI) approaches. Methods: We queried the Medicare-linked Vascular Quality Initiative registry for patients undergoing PVI from 2010-2015. The exposure was treatment: atherectomy (+/- balloon angioplasty) versus other PVI types. The primary outcome was amputation. We used the proportion of atherectomy procedures of all PVIs performed at each hospital as an IV and compared the estimates from IV analysis to multivariable Cox regression and propensity-matched estimates. Results: In this cohort of 19693 patients, 2103 (10%) received atherectomy. Compared to patients receiving other PVI, patients receiving atherectomy were more likely to have a femoropopliteal artery (65% vs 48%, p<0.001) treated with worse disease severity (TASC B and greater: 77% vs 69%, p<0.001). The 5-year overall amputation rate was 31% (158 amputations per 1000 patients/year) in patients receiving atherectomy versus 24% (105 amputations per 1000 patients/year) for other PVIs (log-rank p<0.001). Without adjustment, patients undergoing atherectomy were 40% more likely to have an amputation (Figure 1). After adjusting for patient demographics, comorbidities, and disease characteristics, this effect was mitigated to 15% and 16% for multivariable Cox and propensity-matched approaches, respectively. However, after the IV adjusted analysis accounted for unmeasured confounders, patients receiving atherectomy versus non-atherectomy PVI were 78% more likely to have an amputation. Conclusions: Patients receiving atherectomy were more likely to have an amputation. Unmeasured confounders such as selection bias may play an important role in the long-term risk of amputation for patients undergoing atherectomy.


2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 5587-5587
Author(s):  
Albiruni Ryan Abdul Razak ◽  
Hui Kong Gan ◽  
Gregory Russell Pond ◽  
Kattleya M Tirona ◽  
Eric Xueyu Chen ◽  
...  

5587 Background: There is increasing evidence that NCF abnormalities may occur in cancer pts. Data on pre-treatment NCF in HNC pts are lacking. This study reports NCF in pts with newly diagnosed, curable HNC compared to controls. Methods: HNC pts underwent a 2-hour battery of NCF tests prior to radio +/-chemo(bio)therapy. Domains tested were intelligence (IQ), memory, language, attention, processing speed, executive function and manual dexterity. Test performances were transformed into Z-scores using normative data (score < -1 signified deficit). Pts also had self-reported assessments for NCF, quality of life (QOL), fatigue and affect. Data obtained were compared to non-cancer controls who underwent the same tests. Results: Eighty HNC and 30 control subjects were assessed. Objective NCF testing demonstrated that HNC and control cohorts were similar across all domains, except for IQ, with pts having higher scores (mean 0.55 vs 0.12, p=0.03). However, individual analysis showed that 39% of HNC and 43% of control subjects had abnormal Z-scores in ≥ 2 domains. Multivariable analysis of factors associated with ≥ 2 abnormal NCF domains included: low education level, significant smoking history (≥ 10 pack year), previous mild brain injury, gender, and group (pt vs control). Amongst pts, HPV -ve status and non-oropharyngeal tumors were also associated with decreased NCF. Pts reported statistically worse subjective baseline symptoms compared to controls: NCF (mean FACT-COG 33.7 vs 18.2, p=0.002), QOL (FACT H&N 33.8 vs 14.9), fatigue (FACT-F 35.1 vs 15.1), anxiety (HADS 7.0 vs 3.1) and depression (HADS 3.9 vs 1.2), p<0.01 for all five parameters. Conclusions: Objectively assessed NCF was similar between HNC pts and controls, but a proportion of participants in both cohorts have multi-domain abnormal Z-scores. Several patient demographics and disease characteristics were associated with abnormal NCFs. Subjectively, pts reported worse NCF, QOL, fatigue and affect. These data suggest that participant and disease characteristics may play a larger role in determining NCF than previously shown. Whether such characteristics impact subsequent NCF is under investigation in a longitudinal study.


2020 ◽  
Vol 26 (11) ◽  
pp. 1669-1681
Author(s):  
Kentaro Murate ◽  
Keiko Maeda ◽  
Masanao Nakamura ◽  
Daisuke Sugiyama ◽  
Hirotaka Wada ◽  
...  

Abstract Background and Aims The therapeutic efficacy and safety of ustekinumab for Crohn’s disease (CD) have been reported from randomized controlled trials and real-world data. However, there are few studies describing the identification of patients most suitable for ustekinumab therapy. The aim of this study was to prospectively evaluate the patients receiving ustekinumab and identify predictors of the treatment efficacy. Methods Patients with moderate to severe active CD scheduled to receive ustekinumab were enrolled. The responders and nonresponders were compared at weeks 0, 8, 24, and 48 by evaluating patient demographics, simple endoscopic scores (SES-CD), ustekinumab and cytokine concentrations, and cellular fractions. Results The clinical response and clinical remission rates in the 22 enrolled patients were 59.1% and 31. 8% at week 8, 68.2% and 45.5% at week 24, and 54.4% and 40.9% at week 48, respectively. There were no significant differences in patients’ demographic and disease characteristics at baseline between responders and nonresponders. A combination of low SES-CD and high serum TNF-α concentration at baseline showed a good correlation with the clinical response. Serum TNF-α concentration was decreased because of the therapy. The ratio of CD4+TNF-α cells at baseline was significantly higher in responders than in nonresponders; however, the ratios of CD45+CD11b+TNF-α and CD45+CD11c+TNF-α cells were not different. The ratio of CD4+ TNF-α cells decreased with the treatment in the responders but not in the nonresponders. Conclusions The combination of 2 factors, namely higher serum TNF-α concentration and lower SES-CD at baseline, may assist clinicians in selecting the appropriate therapy for patients with moderate to severe CD.


2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S430-S431
Author(s):  
I Chu ◽  
R Little ◽  
M Sparrow ◽  
M Ward

Abstract Background Data on outcomes following de-intensification of anti-TNF therapy in inflammatory bowel disease (IBD) are limited and concerns about relapse limit the willingness to de-escalate. This study aimed to evaluate rates of successful de-escalation at 12 months and to determine factors that may predict success. Methods Single-centre retrospective study of IBD patients on dose-intensified infliximab (IFX) or adalimumab (ADA) for secondary loss of response. De-escalation was considered in patients achieving sustained biomarker normalisation. Patients were followed for 12 months post-de-escalation and classified as ‘successes’ if remaining on reduced dose anti-TNF or ‘failures’ if requiring re-escalation, steroids, surgery or enrolment into a clinical trial. Patient demographics, disease characteristics, biomarkers (faecal calprotectin (FCP), C-reactive protein (CRP), albumin), anti-TNF drug levels and thiopurine metabolites were collected. Results Of 24 patients (20 CD, 4 UC), 18 received IFX and 6 received ADA. Patients on IFX were de-escalated to 5 mg/kg 8-weekly (89%) or 10 mg/kg 6-weekly (11%), while patients on ADA were de-escalated to 40 mg fortnightly (83%) or 40 mg weekly (17%). Fifteen out of 24 (63%) patients were successes 12 months post-de-escalation. Of the 9 failures, median time to failure was 6 months (IQR 4.6–9.9) – 6/9 failures required re-escalation of anti-TNF therapy and 3/9 entered a clinical trial. Re-escalation successfully recaptured response in 6/6 (100%) patients after a median of 1.4 years follow-up (IQR 1.1–2.3). Albumin at de-escalation was higher in the success group compared with failures (38 g/l vs. 36 g/l, p = 0.025). There was no significant difference in CRP, FCP, anti-TNF drug level or 6-TGN level between the two groups. There was no difference in IFX levels between successes and failures at the time of de-escalation (5.5 vs. 7.5, p = 0.524) as well as 6 months (3.1 vs. 5.1, p = 0.628) and 12 months (3.2 vs. 6.1, p = 0.457) post de-escalation. There were insufficient data for ADA drug level comparison post-de-escalation. Conclusion Nearly two-thirds of patients remained on reduced anti-TNF dosing at 12 months post-de-escalation. All patients who failed de-escalation were recaptured after dose re-escalation. Other than albumin, no baseline predictors for the success or failure of de-escalation could be identified, although cohort size is small, follow-up was short and the majority of patients achieved sustained biomarker normalisation prior to de-escalation. De-escalation may be considered in patients on intensified anti-TNF therapy in sustained deep remission.


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