research article Assessment and Comparison of Safety and Efficacy between Topical Capsaicin (0.025%), Capsaicin (0.075%), and Oral Pregabalin in the Treatment of Diabetic Peripheral Neuropathy
Bipin Kumar Sethi1, Nithin Reddy1, Yashwanth Reddy2, Faizuddin Ahmed2*, Lakshmi Tejeshwini2, Sainath Goud2
1Department of Endocrinology, Care Hospitals- Outpatient Centre, Hyderabad, India
2Department of Pharmacy Practice, Guru Nanak University, Hyderabad, India
*Corresponding Author: Faizuddin Ahmed, Department of Pharmacy Practice, Guru Nanak University, Hyderabad, India
Received Date: 11 September, 2022
Accepted Date: 20 September, 2022
Published Date: 23 September 2022
Citation: Sethi BK, Reddy N, Reddy Y, Ahmed F, Tejeshwini L, et al. (2022) Assessment and Comparison of Safety and Efficacy between Topical Capsaicin (0.025%), Capsaicin (0.075%), and Oral Pregabalin in the Treatment of Diabetic Peripheral Neuropathy. J Diabetes Treat 7: 10108. DOI: https://doi.org/10.29011/2574-7568.010108
Abstract
The International Diabetes Federation (IDF) predicts that 1 in 10 adults will suffer from Diabetes by 2030. While the primary focus of clinical professionals remains on the prevention and treatment of this metabolic disease, the chronic complications occurring with diabetes are often underestimated. One such complication is Neuropathy. Patients generally present with neuropathy of the peripheral nervous system but autonomic neuropathy is also well reported. There are limited safe treatment options available for peripheral neuropathy. According to the guidelines published by the American Diabetic Association (ADA) and the American Neurological Association (ANA), pregabalin should be considered the first line of treatment for treating Diabetic Neuropathy. With the growing use of pregabalin, there have been significantly increasing reports of adverse effects with its use; the most common being dizziness, drowsiness, and blurred vision. These adverse effects can negatively affect the patient’s quality of life. Other treatment options including Gabapentin, Nortriptyline, Duloxetine, Venlafaxine, etc have a similar adverse event profile as pregabalin. Therefore, shifting the focus from the systemic route of treatment toward the topical can significantly help in treating the disease while improving the quality of life. One such topical therapy for the treatment of peripheral neuropathy is Topical Capsaicin. It is commonly available in different concentrations, much cheaper, and easy to use. This study aims to compare the safety and efficacy of oral pregabalin and the topical capsaicin ointments in two different concentrations in diabetic neuropathy patient’s.
Keywords: Diabetes, Neuropathy, Pregabalin, Capsaicin, Burning feet
Abbreviations: ADA: American Diabetic Association; AIDS: Acquired Immunodeficiency Syndrome; ANA: American Neurological Association; ANOVA: Analysis of Variance; CGRP: Calcitonin Gene-related Peptide; CIDP: Chronic Inflammatory Demyelinating Polyneuropathy; CKD: Chronic Kidney Disease; DPN: Diabetic Peripheral Neuropathy; DSPN: Distal Symmetric Polyneuropathies; HIV: Human Immunovirus; IDF: International Diabetes Federation; IgA: Immunoglobulin A; IVIG: Intravenous Immunoglobulin; NCV: Nerve Conduction Velocity; NGF: Nerve Growth Factor; NMDA: N-methyl-D-aspartate; NPQ: Neuropathic Pain Questionnaire PSAT: Pain Scores After Treatment; PSBT: Pain Scores Before Treatment; QST: Quantitative Sensory Testing; SD: Standard Deviation; TRPV1: Transient Receptor Potential Vanilloid 1; USFDA: United States Food and Drug Administration.
Introduction
Diabetic Peripheral Neuropathy (DPN) is defined as the presence of signs and symptoms of peripheral nerve dysfunction occurring in people with diabetes, after excluding other causes [1]. It is the most frequent chronic complication associated with Diabetes [2]. It is a heterogeneous condition affecting different parts of the human nervous system and has different clinical presentations [3]. While many patients may present with symptoms of nerve dysfunction, about 50% may be asymptomatic [4]. Early recognition of diabetic neuropathies may help prevent further complications like a poorly healing injury to the insensate foot leading to amputations. Among different types of neuropathies, the most frequently studied are the “Distal Symmetric Polyneuropathies (DSPN),” and “Diabetic Autonomic Neuropathies” [4]. It has now been proven that patients with pre-diabetes can also develop neuropathy [5]. Due to the lack of understanding of the underlying pathophysiology leading to nerve dysfunction, there is a virtual absence of treatment strategies targeting nerve damage [4]. Hence prevention and palliative care of these chronic complications are one of the key components for sustained diabetic care.
The prevalence of symptomatic neuropathy may be as high as 21% [6], while neuropathic deficits are found on examination in up to 50% of all patients with diabetes [7]. Another study estimated that the incidence of DPN in the United States is 28% [8]. In a historical cohort study on 4,400 patients, approximately 50% of the patients developed one or the other types of peripheral neuropathies at the end of the 25th year of follow-up [9]. Depending on the population studied, the prevalence can again range between 6% to 51%. Many studies have also shown that patients with Type-II Diabetes are more prone to develop neuropathy than those with Type-I [10].
The underlying pathophysiological mechanisms involved in causing DPN are not fully elucidated, but there is a consensus that the toxic effects of hyperglycemia are a primary factor for the progression of this chronic complication of diabetes [11,12]. These mechanisms include Polyol pathway hyperactivity, Nitrosative and oxidative stress, Microvascular changes in nerve fibers, Ion channel misregulation, Microglial activation, Central nervous system sensitization and Brain plasticity involving uncontrollable glutamate release and NMDA receptor dysregulation.
Clinical presentation depends on the type of nerve fibers are primarily impaired during the neuropathic conditions, i.e. A