Thalidomide neuropathy in patients treated for metastatic prostate cancer

Molloy, Fiona; Floeter, Mary Kay; Syed, Nadir Ali; Sandbrink, Friedhelm; Culcea, E.; Steinberg, Seth M.; Dahut, William L.; Pluda, James M.; Krüger, Erwin A.; Reed, Eddie; Figg, William D.

doi:10.1002/mus.1109

Cited by 84 publications

(50 citation statements)

References 28 publications

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“…Local pelvic plexus infiltration could also explain the NCS findings, but would have to be symmetric and widespread and no corroborating clinical features were detected indicating this pathology. A high incidence of peripheral neuropathy in androgen-independent prostate cancer has been reported previously in a study that also recorded onset of symptomatic peripheral neuropathy in six out of 67 patients receiving a daily dose of at least 200 mg (Molloy et al, 2001). In this study, six out of eight men treated for 6 months and all three men treated for 9 months developed a neuropathy.…”

Section: Discussionsupporting

confidence: 77%

An open-label phase II study of low-dose thalidomide in androgen-independent prostate cancer

et al. 2003

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The antiangiogenic effects of thalidomide have been assessed in clinical trials in patients with various solid and haematological malignancies. Thalidomide blocks the activity of angiogenic agents including bFGF, VEGF and IL-6. We undertook an open-label study using thalidomide 100 mg once daily for up to 6 months in 20 men with androgen-independent prostate cancer. The mean time of study was 109 days (median 107, range 4 -184 days). Patients underwent regular measurement of prostate-specific antigen (PSA), urea and electrolytes, serum bFGF and VEGF. Three men (15%) showed a decline in serum PSA of at least 50%, sustained throughout treatment. Of 16 men treated for at least 2 months, six (37.5%) showed a fall in absolute PSA by a median of 48%. Increasing levels of serum bFGF and VEGF were associated with progressive disease; five of six men who demonstrated a fall in PSA also showed a decline in bFGF and VEGF levels, and three of four men with a rising PSA showed an increase in both growth factors. Adverse effects included constipation, morning drowsiness, dizziness and rash, and resulted in withdrawal from the study by three men. Evidence of peripheral sensory neuropathy was found in nine of 13 men before treatment. In the seven men who completed six months on thalidomide, subclinical evidence of peripheral neuropathy was found in four before treatment, but in all seven at repeat testing. The findings indicate that thalidomide may be an option for patients who have failed other forms of therapy, provided close follow-up is maintained for development of peripheral neuropathy.

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Section: Discussionsupporting

confidence: 77%

An open-label phase II study of low-dose thalidomide in androgen-independent prostate cancer

et al. 2003

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“…Several trials have demonstrated that PN was more likely to appear with a high cumulative dose and that it aggravates with the highest administered doses. [47][48][49][50] A few studies have suggested a lower risk of PN with low doses. In two successive trials, Rajkumar et al reported PN in 50-80% of the patients, and this was correlated with the dose and duration of treatment.…”

Section: Incidence Severity and Risk Factors Of Thalidomide-induced mentioning

confidence: 99%

Peripheral neuropathy and new treatments for multiple myeloma: background and practical recommendations

Mohty

El-Cheikh²,

Yakoub-Agha³

et al. 2010

Haematologica

148

137

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haematologica | 2010; 95 (2) 311In multiple myeloma, peripheral neuropathy has for a long time been considered as mainly secondary to the plasma cell dyscrasia itself. With the advent of new targeted drugs such as thalidomide and bortezomib, the iatrogenic neurotoxicity has become the leading cause of peripheral neuropathy. This review discusses the pathogenesis, incidence, risk factors, diagnosis, characteristics, and management of peripheral neuropathy related to new multiple myeloma drugs, mainly bortezomib and thalidomide. The current knowledge of the pathophysiology of the new forms of peripheral neuropathy is still limited. The mechanisms involved depend on the agents used, patient's medical history, and duration of exposure and/or treatment doses or sequence. Diagnosis of such peripheral neuropathy is often easier than treatment. A full anamnesis and regular clinical evaluation are necessary. Electrophysiological assessments may support the diagnosis, although their contribution remains insufficient. Complex clinical features may require a specialized neurological assessment within the context of a multi-disciplinary approach. Finally, early detection of peripheral neuropathy and the use of dose adjustment algorithms as in the case of bortezomib, should help reduce the side effects while maintaining anti-tumor efficacy.

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“…For example, patients receiving cisplatin chemotherapy demonstrate a progressive decline in sensory response amplitudes within the normal range early in the course of cisplatin neuropathy, often before symptoms or objective evidence of sensory neuropathy develop (10,11). In studies involving thalidomide, an average decline of 40% from baseline in the sensory amplitude has been recommended as a physiological level associated with the onset of clinically detectable sensory neuropathy (12). This criterion does not depend on the cause of the neuropathy.…”

Section: Sensory Signs or Absent Or Hypoactive Reflexes) Definite Cmentioning

confidence: 99%

Subclinical Neuropathy Among Diabetes Control and Complications Trial Participants Without Diagnosable Neuropathy at Trial Completion

Albers¹,

Herman²,

Pop‐Busui³

et al. 2007

Diabetes Care

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OBJECTIVE -We sought to evaluate the prevalence of subclinical neuropathy in intensive and conventional treatment groups at completion of the Diabetes Control and Complications Trial (DCCT).RESEARCH DESIGN AND METHODS -We assessed neuropathy using nerve conduction results obtained at DCCT completion after stratifying the DCCT cohort to exclude subjects with progressively less severe degrees of diagnosable neuropathy. We began with those who had confirmed clinical neuropathy (the primary DCCT end point) and eventually excluded all subjects with any clinical or electrodiagnostic evidence of neuropathy.RESULTS -After excluding subjects with confirmed clinical neuropathy at DCCT completion, 8 of 10 nerve conduction measures (including all lower-extremity measures) were significantly improved in the intensive treatment group (O'Brien rank-sum test across all nerve conduction measures, P Ͻ 0.0001). Conduction velocity group differences were substantial, and the peroneal conduction velocity averaged 3.1 m/s faster in the intensive compared with the conventional treatment group (45.1 vs. 42.0 m/s, P Ͻ 0.0001). Numerous significant differences in median and peroneal motor conduction velocities favoring the intensive treatment group persisted, regardless of the exclusion criteria applied.CONCLUSIONS -Intensive and conventional treatment group subjects without diagnosable neuropathy at DCCT completion had significant differences in electrophysiologic measurements favoring the intensive treatment group. Differences in subsequent incident neuropathy between the original treatment groups may reflect, in part, their levels of subclinical neuropathy at DCCT completion, rather than persistent metabolic effects. Diabetes Care 30

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Thalidomide neuropathy in patients treated for metastatic prostate cancer

Cited by 84 publications

References 28 publications

An open-label phase II study of low-dose thalidomide in androgen-independent prostate cancer

An open-label phase II study of low-dose thalidomide in androgen-independent prostate cancer

Peripheral neuropathy and new treatments for multiple myeloma: background and practical recommendations

Subclinical Neuropathy Among Diabetes Control and Complications Trial Participants Without Diagnosable Neuropathy at Trial Completion

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