Summary
The title of the article on medical literature is ‘Review of Symptomatic Treatment of Diabetic Neuropathy by Dr. July, M. Wright. Dr. Wright is a specialist in pharmacology and the article attempts to outline how neuropathy symptoms caused by diabetes can be treated.
Background
The literature outlines how diabetes neuropathy has become one of the leading causes of neuropathic symptoms observed in patients with diabetes mellitus. The disparities observed in the various study is due to differences in variables such as duration of diabetes and lack of a definition for neuropathy. In a study conducted in a referral hospital, 8% of the patients with diabetes developed neuropathy, and this percentage increased 50 for patients with more than 25 years with the disease. Another research that did not include patients already having neuropathy, established that 39 percent of patients with Insulin-dependent diabetes mellitus still developed neuropathy. The general realization is that there are no defined symptoms of diabetic neuropathy and as such, it becomes difficult for specialists to diagnose. This is because the pathogenesis of peripheral diabetic neuropathy is already associated with many other diseases and illnesses. These diseases include: “myoinositol deficiency, glycosylation of cellular proteins, Na-K- adenosine-triphosphate (ATPase) deficiency, protein Kinase alterations, endoneurial vascular alterations, endoneurial hypoxemia, and many others. (Wright 690). Since the symptoms of diabetic peripheral neuropathy and these other diseases have been known in the medical field for a long time and there have been various undertakings to try and provide relief for the patients. Some of the undertakings have included attempts at “controlling the blood glucose levels, use of aldose inhibitors, myoinositol, gangliosides, aminoguanidine and vitamins.” (Wright 690).
The literature provides detailed pathophysiology of pain and shows at what point the outlined therapy’s function. In the diabetes peripheral neuropathy involving the large fibers, the associated symptoms include: “loss of sensation of movement, position, vibration, and balance and diminished deep tendon flexes. In the small fibers, the symptoms include loss of pain, temperature, and sensation, paresthesia, and dysesthesia. Most patients experience the symptoms of both large and small fibers.
In outlining the pathophysiology of pain doctors have been able to establish that Diabetes neuropathy is caused by the damage of nerve fibers involved in the pathophysiology of pain. Relief of the symptoms caused by diabetic neuropathy can be attained by using drugs acting on the pain pathway. However, the relationship between pain and pathophysiology of DPN has not been well understood and it is for this reason that therapy has not been conclusively established.
Methods
The research was carried out by MEDLINE between 1966 and 1993 and it sought to establish ways in which patients responded to diabetic neuropathy drugs. 14 studies were then conducted, and they were “limited to prospective, randomized, double-blind and placebo or actively controlled studies.” (Wright 691). Inter-comparisons between the results of the numerous studies were allowed but time was allowed for the variables to be eliminated first. These trials are known as “cross-over trials.” (Wright 692). The trials were based on a conclusive research method that led to the criterion for use in the experiment. The outcome of the results was then compared against the statistics obtained.
Results
Of all the studies conducted by MEDLINE on diabetic neuropathy, 14 were found to meet the criteria initially outlined for the research. The results of this 14 were therefore considered to be authentic. Anti-depressants were the primary drugs in use for the research. The nine patients who were given the placebo never showed any signs of side effects. The nineteen patients who received the two drugs; paroxetine and imipramine showed symptoms with the symptoms of imipramine being highly pronounced. In instances where desipramine and benztropine were used, it was realized that 12 patients who were given desipramine showed relief while only 2 patients who were given benztropine showed relief. In similar research, amitriptyline showed significant pain relief as compared to desipramine. The use of sodium channel antagonists such as lidocaine also established that pain relief was achieved. Although a recently discovered drug called Capsaicin was also used, there was the general realization of discontinuity in terms of the kinds of pain the drug targeted. The strength of the results is that they generally pointed to the fact that drugs affecting the pain pathway could cause relief. The major weakness is explaining the disparities between the drugs. His other weakness was that the mechanism of action of the drugs remained unknown.
Conclusion
The author concluded that generally, antidepressants are the only efficient drugs in the treatment of diabetic neuropathy. However, only selected drugs within this class such as imipramine and amitriptyline can be used since clinical studies have been conducted conclusively. This conclusion carries much credibility since it is backed by comprehensive clinical studies.
Comments
The study was backed by a strong background showing that the problem was there. The study also involved the use of several anti-depressants to establish which ones were effective. The study also sought to develop upon previous studies that had established that there was the possibility of using ant-depressant therapy in attempting to treat DPN. Many studies were conducted within this field but only the ones deemed applicable were chosen. The researcher was also able to accept that the research was still not able to associate the pathophysiology of DPN with the mechanism of action of the drugs.
The major strength of this study is that it allowed for the observation of multiple parameters at the same time. The research looked at the way patients responded to the drugs and compared that to the placebo. The research also looked at how various drugs affected the patients and to what degree. This shows that a lot of information was obtained with this single experiment.
The weakness of the study is that it used many drugs and therefore no drug was studied conclusively in terms of mechanism of action. The other weakness was that the drugs used were not checked for possible side effects not related to providing relief. Some of the side effects can be long-term or even antagonistic. Therefore, unless further research is conducted most of the drugs can still not be used with much confidence.
This research is applicable pharmacologically since it was able to identify the two drugs that can be used effectively against a real and existing problem among diabetics. Since the research has already established that anti-depressant therapy can be used in the treatment of DPN, it provides an opportunity for further clinical studies that may seek to establish the exact mechanism of action of the drugs and perhaps optimize their functions. This can go a long way in relieving patients of the suffering caused by DPN.
Works Cited
Wright, Julie. Review of Symptomatic Treatment of Diabetic Neuropathy, Pharmacotherapy, 1994.