Exp Clin Endocrinol Diabetes 2016; 124(10): 618-621
DOI: 10.1055/s-0042-107242
Article
© Georg Thieme Verlag KG Stuttgart · New York

The Therapeutic Effect of Pancreatic Kininogenase on Treatment of Diabetic Peripheral Neuropathy in Patients with Type 2 Diabetes

Y.-P. Jin*
1   Department of Endocrinology, Nanjing Medical University Affiliated Nanjing Hospital, Nanjing, China
,
X.-F. Su*
1   Department of Endocrinology, Nanjing Medical University Affiliated Nanjing Hospital, Nanjing, China
,
H.-Q. Li
1   Department of Endocrinology, Nanjing Medical University Affiliated Nanjing Hospital, Nanjing, China
,
J.-D. Wu
1   Department of Endocrinology, Nanjing Medical University Affiliated Nanjing Hospital, Nanjing, China
,
B. Ding
1   Department of Endocrinology, Nanjing Medical University Affiliated Nanjing Hospital, Nanjing, China
,
R. Sun
1   Department of Endocrinology, Nanjing Medical University Affiliated Nanjing Hospital, Nanjing, China
,
T. Shan
1   Department of Endocrinology, Nanjing Medical University Affiliated Nanjing Hospital, Nanjing, China
,
L. Ye
2   National Heart Research Institute Singapore, National Heart Centre, Singapore
,
J.-H. Ma
1   Department of Endocrinology, Nanjing Medical University Affiliated Nanjing Hospital, Nanjing, China
› Author Affiliations
Further Information

Publication History

received 05 January 2016
first decision 12 April 2016

accepted 12 April 2016

Publication Date:
04 October 2016 (online)

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Abstract

Background: To determine the therapeutic efficacy and cost-effective of pancreatic kininogenase (PKase) on treatment of diabetic peripheral neuropathy (DPN) compared with Prostaglandin E1 (PGE1) in patients with type 2 diabetes.

Methods: 104 patients with DPN receiving standard glucose control therapy were randomly assigned into 3 groups: Group-A received PKase treatment, Group-B received PGE1 treatment, and Group-C received only standard glucose control therapy. Michigan neuropathy screening instrument (MNSI) score, neurophysiology examination, and nerve conduction velocity were measured.

Results: Standard glucose control therapy significantly reduced hyperglycemia to a similar level in all groups. Questionnaire grading and neurophysiology examination both indicated that no significant difference was found at the end of treatment between Groups -A and -B. Except for the ulnar nerve sensory conduction velocity that was significantly improved in Group-B, the remaining nerve conduction velocity (regardless of sensory or motor nerve conduction velocities) was improved to a similar level in Groups -A and -B. Group-A had significantly reduced questionnaire grading and better improvement in motor nerve conduction velocity of the common peroneal nerve, ulnar nerve, and sensory nerve conduction velocity of the sural nerve as compared with Group-C. However, the medical cost of PKase was only 18.9% of that of PGE1 during one course of treatment.

Conclusions: PKase has the similar therapeutic efficacy as PGE1 on treatment of DPN in patients with type 2 diabetes. However, the medical cost of PKase is one fifth of that of PGE1. Thus, PKase is a cost-effective drug for treatment of DPN.

* equal contribution