Clinical trials for drugs against diabetic neuropathy: Can we combine scientific needs with clinical practicalities?

Ziegler, Dan; Luft, D

doi:10.1016/s0074-7742(02)50085-4

Cited by 24 publications

(20 citation statements)

References 89 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A meta-analysis of aldose reductase inhibitor trials performed through 1996 revealed only minimal improvement in nerve conduction velocity by 1 m/s after 6 to 13 months of therapy in one trial as the single statistically significant effect to that time. 41 More recently, however, a double-blind, placebocontrolled, phase II study of another aldose reductase inhibitor (fidarestat) demonstrated improvement in all subjective symptoms and in 5 of 8 electrophysiological measures, with no improvement in the placebo group. 42 Phase III trials of this compound are in progress.…”

Section: Aldose Reductase Inhibitorsmentioning

confidence: 99%

“…44 However, no further studies have been performed, and ␥-linolenic acid has not been widely adopted in clinical practice. 41 ␣-Lipoic Acid ␣-Lipoic acid (thioctic acid) has been approved for the treatment of diabetic neuropathy in Germany since the 1960s. 45 It is a free radical scavenger and transition metal chelator with potent antioxidant properties and prevents neuronal and neurovascular injury in animal models of diabetic neuropathy.…”

Section: ␥-Linolenic Acidmentioning

confidence: 99%

See 1 more Smart Citation

The Diabetic Neuropathies

Gooch¹,

Podwall²

2004

The Neurologist

View full text Add to dashboard Cite

show abstract

Section: Aldose Reductase Inhibitorsmentioning

confidence: 99%

Section: ␥-Linolenic Acidmentioning

confidence: 99%

The Diabetic Neuropathies

Gooch¹,

Podwall²

2004

The Neurologist

View full text Add to dashboard Cite

show abstract

“…Ziegler and Luft suggested that, until the mid-1990s, trials were hampered by a generally poor design, short follow-up, and by being limited to patients with advanced DPN [35]. They suggested that trials, involving patients with early DPN, conducted over 3-5 years to establish a delay or arrest in the progression of neuropathy, rather than reversal, were more likely to be successful.…”

Section: Pathogenetic Treatmentsmentioning

confidence: 99%

Treating Diabetic Neuropathy: Present Strategies and Emerging Solutions

Javed¹,

Alam²,

Malik³

2015

Rev Diabet Stud

View full text Add to dashboard Cite

■ AbstractDiabetic peripheral neuropathies (DPN) are a heterogeneous group of disorders caused by neuronal dysfunction in patients with diabetes. They have differing clinical courses, distributions, fiber involvement (large or small), and pathophysiology. These complications are associated with increased morbidity, distress, and healthcare costs. Approximately 50% of patients with diabetes develop peripheral neuropathy, and the projected rise in the global burden of diabetes is spurring an increase in neuropathy. Distal symmetrical polyneuropathy (DSPN) with painful diabetic neuropathy, occurring in around 20% of diabetes patients, and diabetic autonomic neuropathy (DAN) are the most common manifestations of DPN. Optimal glucose control represents the only broadly accepted therapeutic option though evidence of its benefit in type 2 diabetes is unclear. A number of symptomatic treatments are recommended in clinical guidelines for the management of painful DPN, including antidepressants such as amitriptyline and duloxetine, the γ-aminobutyric acid analogues gabapentin and pregabalin, opioids, and topical agents such as capsaicin. However, monotherapy is frequently not effective in achieving complete resolution of pain in DPN. There is a growing need for head-to-head studies of different single-drug and combination pharmacotherapies. Due to the ubiquity of autonomic innervation in the body, DAN causes a plethora of symptoms and signs affecting cardiovascular, urogenital, gastrointestinal, pupillomotor, thermoregulatory, and sudomotor systems. The current treatment of DAN is largely symptomatic, and does not correct the underlying autonomic nerve deficit. A number of novel potential candidates, including erythropoietin analogues, angiotensin II receptor type 2 antagonists, and sodium channel blockers are currently being evaluated in phase II clinical trials.

show abstract

“…However, the selection of patients at the highest clinical need for intensified glycemic intervention could be informed by objective evidence for the presence of early neuropathy. [2] Accurate diagnosis of DSP requires identifying abnormal electrodiagnostic data in combination with neuropathic signs and symptoms. [3,4] This definition correlates well with largefibre dysfunction and is thus effective at detecting the later stages of neuropathy.…”

Section: Introductionmentioning

confidence: 99%