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Table of Contents
ORIGINAL ARTICLE
Year : 2020  |  Volume : 22  |  Issue : 3  |  Page : 175-179

Subclinical peripheral neuropathy in patients with chronic obstructive pulmonary disease without hypoxemia


1 Department of Chest Diseases, Karapınar State Hospital, Konya, Turkey
2 Department of Chest Diseases, Selcuk University Medical Faculty, Konya, Turkey
3 Department of Neurological Diseases, Selcuk University Medical Faculty, Konya, Turkey

Date of Submission06-Mar-2020
Date of Decision05-Apr-2020
Date of Acceptance02-May-2020
Date of Web Publication31-Dec-2020

Correspondence Address:
Dr. Hatice Yurtgun
Department of Chest Diseases, Karapinar State Hospital, Karapinar, Konya
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejop.ejop_21_20

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  Abstract 


AIM: The aim of the study was to determine the prevalence of subclinical peripheral neuropathy (PNP) in stable chronic obstructive pulmonary disease (COPD) patients without severe hypoxemia.
MATERIALS AND METHODS: Fifty-six (52 men and 4 women) patients with COPD without severe hypoxemia, 25 healthy smokers, and 24 healthy nonsmokers were included in the study. The latency, amplitude, and velocity measurements of right and left median motor nerve, tibial motor nerve, peroneal motor nerve, median sensory nerve, sural sensory nerve, right ulnar motor nerve, and right ulnar sensory nerve were performed.
RESULTS: A high proportion of PNP was detected in the COPD group compared to the smoker and nonsmoker control groups (41.1%, 36.0%, and 33.3%, respectively). However, the difference between the groups was not statistically significant (P = 0.784). However, some of the electrophysiological measurements were statistically significantly worse in the COPD group (P < 0.05). In the COPD group, a correlation was not detected between PNP and duration of COPD, age, body mass index, smoking status (pack/year), forced vital capacity %, forced expiratory volume in 1 s %, SO2, and C-reactive protein values (P > 0.05).
CONCLUSION: The present study demonstrates that the PNP may be an extrapulmonary manifestation of COPD. The physician should be aware of the possibility of PNP in COPD patients without severe hypoxemia.

Keywords: Chronic obstructive pulmonary disease, electromyelography, peripheral neuropathy


How to cite this article:
Yurtgun H, Tülek B, Ekmekçi H, Kanat F, Süerdem M. Subclinical peripheral neuropathy in patients with chronic obstructive pulmonary disease without hypoxemia. Eurasian J Pulmonol 2020;22:175-9

How to cite this URL:
Yurtgun H, Tülek B, Ekmekçi H, Kanat F, Süerdem M. Subclinical peripheral neuropathy in patients with chronic obstructive pulmonary disease without hypoxemia. Eurasian J Pulmonol [serial online] 2020 [cited 2021 Jan 22];22:175-9. Available from: https://www.eurasianjpulmonol.com/text.asp?2020/22/3/175/305717




  Introduction Top


Chronic obstructive pulmonary disease (COPD) is primarily characterized by the presence of irreversible airflow limitation resulting from airway inflammation and remodeling often associated with the development of parenchymal destruction and emphysema.[1] Increasing evidence indicates that COPD is a complex disease involving more than airflow obstruction. Patients with COPD can have multiple coexisting systemic effects and comorbidities that extend beyond the lung.[2] Comorbidities including coronary artery disease, diabetes mellitus, osteoporosis, muscle weakness, anemia, depression, and anxiety are frequent in COPD.[3]

Peripheral neuropathy (PNP) could occur in patients with COPD, but the actual prevalence and clinical importance of PNP is still unclear in COPD.[4],[5],[6] Therefore, PNP is not included in the list of COPD comorbidities. Although the adverse effects of chronic respiratory failure on the central nervous system are well known, its effects on the peripheral nervous system have not been emphasized adequately. Smoking, chronic hypoxia, and older age could be contributing factors for the development of PNP in COPD. We aimed to determine the prevalence of subclinical PNP in stable COPD patients without the diagnosis of PNP and severe hypoxemia.


  Materials and Methods Top


Study design

The study was approved by the ethics committee, and informed consent was obtained from the participants (July 15th, 2011; 2012/203). Eighty stable patients with COPD patients and eighty healthy volunteers were enrolled. Healthy volunteers constituted forty nonsmokers and forty smokers. The diagnosis of COPD was based on the Global Initiative for Chronic Obstructive Lung Disease.[1] All patients had at least a 10 pack-year history of cigarette smoking or exposure to biomass and postbronchodilator (400 μg salbutamol) forced expiratory volume in 1 s and forced vital capacity (FEV1/FVC) ratio of <70% predicted. The Vitamin B12, folic acid, and thyroid hormone concentrations were measured in addition to routine hemogram and biochemical tests in COPD patients and healthy control group in order to exclude risk factors for PNP.

There was no clinical evidence of neuropathy in any patient. None of the patients was using systemic steroids and neurotoxic drugs.

Exclusion criteria

  1. Patients with the disease that can cause polyneuropathy (diabetes mellitus, alcoholism, malignancies, lung surgery, and renal and thyroid diseases)
  2. Low Vitamin B12 and folic acid levels
  3. Oxygen saturation <90%
  4. Patients who had an exacerbation of the disease in the past 6-month period and present smokers.


A total of 24 patients with abnormal thyroid function test results (n = 14) or Vitamin B12 and folate values (n = 10) were excluded from the study. In healthy nonsmoker group, patients with abnormal thyroid function test results (n = 10) and Vitamin B12 and folate values (n = 6), and in the healthy smoker group, patients with abnormal thyroid function test results (n = 5) and Vitamin B12 and folate values (n = 10) were excluded from the study. Fifty-six (52 men and 4 women) patients with COPD, 25 (23 men and 2 women) healthy smokers, and 24 (22 men and 2 women) healthy nonsmokers were included in the study.

Respiratory function tests

Respiratory function tests were performed in patients with COPD and smokers in the control group. Vmax (Viasys-Healthcare®-2007 GmbH, Hoechberg, Germany) was used for the measurement of respiratory function tests. Each participant performed a maximal expiratory flow maneuver in the sitting position until three acceptable measurements were obtained, and the best result was recorded. Respiratory function tests such as FEV1, FVC, and FEV1/FVC were evaluated. After three measurements, the best values were taken into consideration.

Electrophysiologic study

Electrophysiologic study was performed using Nihonkohden MEB-9002K VMA EP/EMG Measuring System 2005 USA brand electromyograph in the electromyography laboratory. The measurements of conventional motor and sensory nerve conduction latencies, amplitudes, and velocities were performed bilaterally from the upper and lower extremities. The latency, amplitude, and velocity measurements of the right and left median motor nerve, tibial motor nerve, peroneal motor nerve, median sensory nerve, sural sensory nerve, right ulnar motor nerve, and right ulnar sensory nerve were performed.

Statistical analysis

Data were analyzed using the IBM Statistical Package for the Social Sciences version 11.5 (SPSS Inc., Chicago, IL, USA). A normal distribution of the quantitative data was checked using the Shapiro–Wilk test. Parametric tests were applied to data of normal distribution (independent t-test and one-way analysis of variance). The distribution of categorical variables in both groups was compared using the Pearson's Chi-square test. Continuous data were presented as mean ± standard deviation. All differences associated with a chance probability of 0.05 or less were considered statistically significant.


  Results Top


Age, body weight, height, and body mass indices (BMIs) of the three study groups did not differ statistically significantly [Table 1]. The mean duration of illness in COPD patients was 7.55 ± 5.28 years, and the mean number of exacerbations was 0.88 ± 0.99. The mean SaO2% in the COPD group was 94.92 ± 1.31. A statistically significant difference was not detected between COPD group and the smokers in the control group as for smoking (43.82 ± 22.89 vs. 46.20 ± 17.87 pack-years, respectively) (P = 0.431). Spirometric values were statistically significantly lower in the COPD group (FVC, FEV1, and FEV1/FVC) when compared with smokers in the control group [Table 2].
Table 1: Intergroup comparisons of age, body weight, height, and body mass indices of the patients

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Table 2: Spirometric values of the group with chronic obstructive pulmonary disease and smokers in the control group

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The latency, amplitude, and velocity of the right and left median motor nerve, tibial motor nerve, peroneal motor nerve, and right ulnar motor nerve are shown in [Table 3]. A statistically significant difference was seen between groups as for left tibial motor nerve latencies and velocities, right tibial motor nerve velocities, and left and right peroneal nerve velocities. Significantly prolonged left tibial nerve latencies and left peroneal nerve latencies were observed in the COPD group. The latency, amplitude, and velocity of the right and left median sensory nerve, sural sensory nerve, and right ulnar sensory nerve are shown in [Table 4]. A statistically significant difference was seen as for right sural sensory nerve latencies, amplitudes, and velocities and right ulnar nerve velocities. A significant prolongation of right sural sensory nerve latencies was observed in the COPD group. The percentage of PNP was 41.1% (23/56) in the COPD group, 36% (9/25) in healthy smokers, and 33.3% (8/24) in healthy nonsmokers. A statistically significant difference was not found between distributions of the cases with established PNP (P = 0.784). In the COPD group, a correlation was not detected between PNP and duration of COPD, age, BMI, smoking status (pack/year), FVC%, FEV1%, and SaO2.
Table 3: Latency, amplitude, and velocity of the right and left median motor nerve, tibial motor nerve, peroneal motor nerve, and right ulnar motor nerve in chronic obstructive pulmonary disease and control groups

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Table 4: Latency, amplitude, and velocity of the right and left median sensory nerve, sural sensory nerve, and right ulnar sensory nerve in chronic obstructive pulmonary disease and control groups

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  Discussion Top


We have found higher rates of PNP in patients with COPD compared to healthy smokers and healthy nonsmokers (41.1%, 36.0%, and 33.3%, respectively). Although the higher rate of PNP observed in COPD patients was not statistically significant, a significant retardation of lower extremity nerve conduction velocities was detected in the COPD group, and some latency values were significantly higher than that in the control group. In the COPD group, no correlation was found between PNP and age, duration of illness, number of exacerbations, BMI, smoking, and levels of FEV1, FVC, and SaO2.

Fifty-two of 56 COPD patients composing the study group are male because COPD is seen more frequently in the male population in our country. In our country, COPD is much more common in men because the smoking rates are much higher in males compared to females, and occupational exposure poses a significant risk to men. In an epidemiological study conducted in our country in 2008, only 80 of 1160 COPD patients were women.[7]

Visser et al. found no significant difference in electrophysiological measurements between smokers and nonsmokers in their study.[8] Similarly, in our study, there was no significant difference between the electrophysiologic measurements of the smoker and nonsmoker control groups.

The association of COPD and PNP was first reported by Appenzeller et al. in 1968.[9] Investigations about the frequency of PNP in COPD continued in the subsequent years. Studies usually have shown that peripheral nerve functions may deteriorate in patients with COPD. Faden et al. performed the first serious clinical study in this area in 1981.[4] They compared the neurophysiological and clinical findings of 23 COPD patients who are active smokers with an age-matched control group with normal pulmonary function tests. They demonstrated subclinical motor and sensory conduction slowdown in 87% of the patients in the COPD group. Agrawal et al. found PNP in 17% of the thirty COPD patients who are active smokers.[6] Nowak et al. reported clinically significant PNP in 20% and subclinical PNP in 4% of the patients.[10] Poza and Martí-Massó detected electrophysiologic abnormalities in 87% of COPD patients.[11] Jann et al. reported PNP in 63%, whereas Ozge et al. reported PNP in 55% of the patients.[12],[13] In our study, PNP was present in 41.1% of the COPD group. Significant differences between the ratios of clinically significant or subclinical PNP have been reported in studies in COPD patients. In general, the frequency of PNP appears to be higher in cases of hypoxemia and/or hypercapnia. On the other hand, in all of the studies in the literature, case numbers are not high enough to generate a general idea of the incidence of PNP in COPD because they generally involve small groups.


  Conclusion Top


COPD is a chronic disease that affects a large number of extrapulmonary organs and systems and therefore has significant systemic effects. Previous studies and our findings show that PNP, with its sensory and motor components, can be regarded as one of the systemic effects of COPD. As the shortcomings of our work, the number of patients was low, and we did not investigate the markers of systemic inflammation and did not question the quality of life. In order to obtain stronger results, it is possible to work with larger categorized groups in terms of sociodemographic and clinical characteristics. Both the effects of PNP on the clinic and prognosis of COPD and the effect of PNP treatment on the clinic and natural course of the disease should be the subject of further studies.

Acknowledgment

This work was derived from the thesis of the first author and supported by the Scientific Research Foundation of the Selcuk University, Konya, Turkey (Project No: 11102038).

Financial support and sponsorship

The study was financially supported by the Scientific Research Foundation of the Selcuk University, Konya, Turkey (Project No: 11102038).

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: Report; 2018.  Back to cited text no. 1
    
2.
Barnes PJ, Celli BR. Systemic manifestations and comorbidities of COPD. Eur Respir J 2009;33:1165-85.  Back to cited text no. 2
    
3.
Negewo NA, Gibson PG, McDonald VM. COPD and its comorbidities: Impact, measurement and mechanisms. Respirology 2015;20:1160-71.  Back to cited text no. 3
    
4.
Faden A, Mendoza E, Flynn F. Subclinical neuropathy associated with chronic obstructive pulmonary disease: Possible pathophysiologic role of smoking. Arch Neurol 1981;38:639-42.  Back to cited text no. 4
    
5.
Kayacan O, Beder S, Deda G, Karnak D. Neurophysiological changes in COPD patients with chronic respiratory insufficiency. Acta Neurol Belg 2001;101:160-5.  Back to cited text no. 5
    
6.
Agrawal D, Vohra R, Gupta PP, Sood S. Subclinical peripheral neuropathy in stable middle-aged patients with chronic obstructive pulmonary disease. Singapore Med J 2007;48:887-94.  Back to cited text no. 6
    
7.
Gunen H, Hacievliyagil SS, Yetkin O, Gulbas G, Mutlu LC, Pehlivan E. Prevalence of COPD: First epidemiological study of a large region in Turkey. Eur J Intern Med 2008;19:499-504.  Back to cited text no. 7
    
8.
Visser NA, Notermans NC, van Berkhout FT, van den Berg L, Vrancken AF. Chronic obstructive pulmonary disease is not a risk factor for polyneuropathy: A prospective controlled study. Chron Respir Dis 2017;14:327-33.  Back to cited text no. 8
    
9.
Appenzeller O, Parks RD, MacGee J. Peripheral neuropathy in chronic disease of the respiratory tract. Am J Med 1968;44:873-80.  Back to cited text no. 9
    
10.
Nowak D, Brüch M, Arnaud F, Fabel H, Kiessling D, Nolte D, et al. Peripheral neuropathies in patients with chronic obstructive pulmonary disease: A multicenter prevalence study. Lung 1990;168:43-51.  Back to cited text no. 10
    
11.
Poza JJ, Martí-Massó JF. Peripheral neuropathy associated with chronic obstructive pulmonary disease. Neurologia 1997;12:389-94.  Back to cited text no. 11
    
12.
Jann S, Gatti A, Crespi S, Rolo J, Beretta S. Peripheral neuropathy in chronic respiratory insufficiency. J Peripher Nerv Syst 1998;3:69-74.  Back to cited text no. 12
    
13.
Ozge A, Atiş S, Sevim S. Subclinical peripheral neuropathy associated with chronic obstructive pulmonary disease. Electromyogr Clin Neurophysiol 2001;41:185-91.  Back to cited text no. 13
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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