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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 19  |  Issue : 2  |  Page : 118-122

Esophageal motility dysfunction and Type 2 Diabetes Mellitus: Indian scenario


1 Senior Advisor, Marine Medicine, INHS Asvini, Mumbai, Maharashtra, India
2 Professor, Department of Physiology, AIIMS, Rishikesh, India
3 Associate Professor, Department of Community Medicine, INHS Asvini, Mumbai, India
4 Associate Professor, Department of Physiology, Armed Forces Medical College, Pune, India

Date of Web Publication13-Feb-2018

Correspondence Address:
Dr. Vivek Verma
Institute of Naval Medicine, INHS Asvini, Colaba Mumbai - 400 005, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jmms.jmms_20_17

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  Abstract 


Introduction: Diabetes mellitus (DM) is a metabolic disorder which affects multiple systems of the body including gastrointestinal (GI) system. A number of researchers have studied the effect of type 2 DM on esophageal motility function in western population, but there are no such studies on Indian population. Objectives: Assessment of esophageal motility functions in patients of type 2 DM and its correlation with duration of diabetes, blood sugar, and glycated hemoglobin (HbA1c). To explore the correlation of GI symptoms with abnormal esophageal motility findings. Materials and Methods: The study was conducted on 42 patients. History of three common GI symptoms was recorded. Esophageal motility functions were assessed using high-resolution GI manometry assembly. Blood sugar (Fasting and Post Prandial) and HbA1c were measured. Results: In the present study, the mean duration of diabetes was 6.21 ± 4.55 year and the mean body mass index of the patients was 25.80 ± 4.93 kg/m2. Twenty-nine patients gave a history of GI symptoms. The mean HbA1Cwas 7.86 ± 1.49 and 62% patients had HbA1Cvalues >7%. Contractile front velocity (CFV) and basal lower esophageal sphincter pressure (BLESP) were the main esophageal motility parameters found to be affected in the study. About 26.19% patients had CFV more than 9 cm/s and 26% patients had abnormal BLESP. Only 5% patient had raised peristaltic amplitude. Conclusion: CFV and BLESP were the main esophageal motility parameters which were affected in the diabetic patients. The association between GI symptoms and CFV was significant. The duration of diabetes negatively correlated with peristaltic amplitude and HbA1Cvalues. Larger studies, especially in India, would be of significance to the clinicians for better symptomatic management of the disease in India.

Keywords: Basal lower esophageal sphincter pressure, diabetes mellitus, esophageal manometry, glycated hemoglobin


How to cite this article:
Verma V, Mohan L, Ray S, Singh S P, Singh Y. Esophageal motility dysfunction and Type 2 Diabetes Mellitus: Indian scenario. J Mar Med Soc 2017;19:118-22

How to cite this URL:
Verma V, Mohan L, Ray S, Singh S P, Singh Y. Esophageal motility dysfunction and Type 2 Diabetes Mellitus: Indian scenario. J Mar Med Soc [serial online] 2017 [cited 2019 Oct 19];19:118-22. Available from: http://www.marinemedicalsociety.in/text.asp?2017/19/2/118/225270




  Introduction Top


Diabetes mellitus (DM) is a metabolic disease which affects multiple systems of the body including gastrointestinal (GI) system. Chronic GI symptoms such as dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, diarrhea, and constipation have been recognized for a long time in association with DM. Rundles in 1945 first studied and drew attention to the effects of diabetes on the gut.[1] Esophageal function has been studied by a number of researchers in both Type 1 and Type 2 DM. DM affects esophageal motility and can lead to esophageal dysmotility in the form of altered Basal Lower Esophageal Sphincter Pressure (BLESP), peristaltic velocity, peristaltic amplitude, multipeak waves, and failure of peristalsis.[2],[3],[4],[5] Stewart et al. in 1976 found altered esophageal motor function in diabetics though esophageal symptoms were infrequent.[6] The esophageal motility is affected by a number of factors including age, body mass index (BMI), gender, and various neurohormonal factors. The duration and control of blood sugar in diabetics, altered autonomic functions and neuropathy are the important variables which affect esophageal motility. A tightly controlled blood sugar can delay or even prevent the effects of diabetes on esophageal motility. Scientific studies in this regard are absent in Indian population group. In the present study, we studied various parameters of esophageal motility function and their correlation with duration of diabetes, blood sugar, and glycosylated hemoglobin (HbA1c). We also explored the association of GI symptoms with esophageal motility.


  Materials and Methods Top


A descriptive observational study was conducted in patients diagnosed as Type 2 DM attending the medical OPD of a tertiary care service hospital. The population of DM Type 2 in the age group of 35–80 in this hospital was estimated to be 1200 per year. Taking the prevalence of esophageal dysmotility for BLESP in diabetic patients to be 58%,[5] and assuming 95% confidence interval and 15% deviation, the sample size was calculated to be 42. A systematic random sampling technique was used to select the patients. Inclusion criteria were patients of DM Type 2 with a minimum of 1 year after diagnosis who were being followed up in the OPD of a tertiary care hospital. Patients diagnosed as Achalasia Cardia by manometry, those suffering from scleroderma, those who had cerebrovascular accident in the past, hemodynamically/metabolically unstable patient who cannot undergo the procedure or patients and who had undergone esophageal surgery for any ailment were excluded. A detailed clinical history of diabetes and GI symptoms was obtained. All patients were given a prior appointment for the test. A written informed consent was obtained from all the patients. Patients taking drugs that may affect GI motility, for example, antacids, calcium channel blockers, and proton pump inhibitors were instructed to suspend use of the drug for at least 24 h before the test.[7] Esophageal functions were assessed using 16 channel high resolutions GI manometry assembly. Blood sugar (fasting and postprandial [PP]) was measured by routine blood test, whereas HbA1c was measured using HbA1C meter: A1c now + (manufactured by Bayer Healthcare LLC California).[8]

Esophageal motility function test and manometry procedure

A high-resolution 16-channel water perfusion GI manometry assembly with electronic pressure transducers manufactured by the Royal Melbourne Hospital, Australia was used for the assessment of esophageal motility function. The patients were asked to sit on the examination table and the catheter was introduced into the esophagus of the patient through the nostril. Once both the upper esophageal sphincter and lower esophageal sphincter (LES) were localized, the patient was asked to lie in the supine position. The reference was set for all the channels in lying down position. The patient was then asked not to swallow for 1 min to record BLESP. A minimum of six consecutive respiratory movements without any swallow were recorded as software analyses pressures at six points. On obtaining the recording for basal pressures, ten consecutive 5 ml water swallows were given to the patients in the right lateral position.[9] The pattern of peristalsis and the relaxation of the upper and LESs with the swallow were recorded. Thereafter, the patient was made to sit and the catheter was gently pulled out of the esophagus and put under water to ensure that all channels were open during the procedure.

Analysis of manometric recordings

BLESP, Peristaltic Amplitude, and CFV were the three outcome measure studied for the esophageal motility function test. BLESP was found to be the most studied parameter and hence was taken for sample size calculation. It was measured at end-expiration at six points and mean value was used for calculations. The maximum pressure in the smooth muscle portion was selected as peristaltic amplitude. Based on the identification of contractile deceleration point and steepest portion of the distal esophageal segment, CFV was calculated. The Smart Mouse™ tool available in ManoView™ was used to calculate the slope.[9] A similar parameter referred to as pressurization front velocity was used in earlier studies.[10] These data were used to define the normative data while calculating whether the parameter was normal or abnormal.

Statistical analysis

All result parameters were recorded on an Excel data sheet. Analysis of the data was done using software SPSS 17 (SPSS Inc., Chicago, IL, USA). Appropriate statistical tests (ANOVA, Pearson coefficient of correlation and Chi-square test) were selected and applied according to the data. The data have been represented as mean + standard deviation, percentages, range. Gender-wise analysis of the data has also been undertaken.


  Results Top


The demographic, anthropometric, blood sugar, and HbA1C profiles of the patients are summarized in [Table 1]. About 62% patients were found to have HbA1C values more than 7%.
Table 1: Demographic, anthropometric, blood sugar, and glycated hemoglobin profile of patients

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Esophageal motility parameters

The results of esophageal motor function are summarized in the [Table 2], [Table 3], [Table 4]. Eleven patients (29%) had peristaltic velocity more than 9 cm/s. About 26% patients had abnormal BLESP. The peristaltic amplitude was found to be higher in females (121.73 ± 42.37 vs. 89.92 ± 21.71). Only two patients (5%) had peristaltic amplitude >180 mm of Hg but both these patients had normal BLESP as well as peristaltic velocity.
Table 2: Manometric parameters

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Table 3: Manometric parameters (gender wise)

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Table 4: Abnormal manometric parameters

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Correlation among esophageal motility function parameters, duration of diabetes, and glycated hemoglobin

The correlation of BLESP with other two parameters of esophageal motility (CFV and peristaltic amplitude) revealed a weak positive association (0.3) with only peristaltic amplitude (P = 0.05) [Table 5]. The peristaltic amplitude was found to have weak negative correlation (0.3) with duration of diabetes [Table 6]. The correlation of HBA1C with various manometric parameter was weakly negative and not significant.
Table 5: Correlation of basal lower esophageal sphincter pressure; contractile front velocity and peristaltic amplitude

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Table 6: Correlation between duration of diabetes and manometric parameters

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The patients were divided into 3 groups based on their BLESP, i.e., <10 mm of Hg, 10–35 and >35 mm of Hg. A total of 6/42 (14.28%) patients were found to have BLESP >35 mm of Hg and 5/42 (11.9%) were found to have BLESP <10 mm of Hg [Table 4]. These three groups were compared using ANOVA (not violating assumptions of homogeneity of variance) for mean value of age, BMI, duration of DM and HbA1C. The groups had equal variance as far as these parameters are concerned. However, when these groups were compared for peristaltic velocity, peristaltic amplitude, and failure of peristalsis, statistically significant difference was found between them with respect to peristaltic velocity and failure of peristalsis. The peristaltic velocity was significantly lower in the group with BLESP <10 mm of Hg and increased with increasing BLESP and was maximum in the group with BLESP >35 mm of Hg. The failure of peristalsis was maximum in the group with BLESP either <10 or >35 mm of Hg and was minimum when BLESP was normal.

Gastrointestinal symptoms

History was taken regarding GI symptoms, namely, retrosternal pain, dysphagia, and vomiting. Any patient giving a positive history of at least one symptom was considered to have GI symptoms. A total of 29 (69%) patients gave a history of having GI symptoms. Retrosternal burning sensation was the commonest symptom reported by patients [Table 7].
Table 7: Gastrointestinal symptoms

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Association of manometric parameters with gastrointestinal symptoms

The association between CFV values and presence or absence of GI symptoms was seen using Chi-square test. 64% of patients with GI symptoms had peristaltic velocity >6.25 cm/s (P = 0.014). Two patients had mean peristaltic amplitude >180 mm of Hg (4.76%). Both these patients had normal BLESP as well as peristaltic velocity. However, both of them had higher BMI as compared to mean BMI [Table 8].
Table 8: Association between contractile front velocity values and gastrointestinal status

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  Discussion Top


In the present study, CFV and BLESP were the most affected motility parameters in patients of DM. Peristaltic amplitude was the least affected parameter. The studies available in the literature have shown varied results, DM has been found to be the causative agent for the esophageal dysmotility and can affect the BLESP, CFV, and amplitude of peristalsis which may or may not cause GI symptoms. Furthermore, the effect of DM on esophageal motility increases with the duration of the disease. A possible explanation for these varied affiliations can be due to the presence/absence of autonomic neuropathy, multitude of confounding factors which alter esophageal motility such as age, gender, blood sugar control, the time of test, diurnal variation, and many more yet unidentified factors.[11],[12],[13],[14] Nonavailability of the normative data for Indian population and wide range of normal motility parameters makes scenario further complex. Nonlinear relationship between altered motility parameter and clinical symptoms needs further attention.

The average duration of diabetes in patients, after detection, in this study was 6.21 ± 4.55 years a statistically significant negative correlation, r = −0.32 was found between duration of DM and peristaltic amplitude. No significant effect of duration was seen on BLESP and peristaltic velocity. The decrease in peristaltic amplitude can be due to degeneration of vagal fibers due to the effect of diabetes. Aging also causes sarcopenia and decreased the strength of contraction of smooth muscle. Also in DM and with increasing age, there is decreased LES tone so a lower strength contraction can clear the bolus through LES.

Aging is significantly associated with changes in esophageal motility. With increasing age, peristaltic amplitude decreases and duration of peristalsis increases but the function remains well coordinated and intact up to 80–90 years of age.[15],[16] In this study, a negative correlation was found among age, BLESP, and peristaltic amplitude, however, there was positive correlation with peristaltic velocity. The reduced BLESP and peristaltic amplitude could be due to degenerative changes and deposition of fibrous tissue which are aggravated by DM. The incidence of reflux also increases with aging.[17]

The mean BMI of the present study population falls in obese category as per the recommendation of Kesavachandran et al.[18] Increased BMI is associated with increased incidence of GERDs, but the association between BMI and BLESP has not been conclusively proven. However, acid reflux can affect the tone of LES by causing structural changes.

Retrosternal burning sensation, dysphagia, and vomiting were the GI symptoms studied in the study population, with retrosternal burning sensation found to be the most common. The retrosternal burning sensation may be attributable to increased incidence of reflux in patients having low BLESP or due to transient LES relaxation (TLESR's) due to hyperglycemia.[19] The findings are similar to those of Corina et al. (65%) and Stewart et al. who found a high incidence of GI symptoms in diabetics.[6],[20] Dyspahgia is a late complication of diabetes and is seen more commonly in patients having other disorders of esophageal motility. Vomiting may be due to decreased LES tone, TLESRs and is aggravated if gastric clearance time is increased due to gastroparesis in DM.[21] It will not be correct to attribute the GI symptoms to DM only as effect of aging will also decrease LES pressure and aggravated by the effect of DM also.[5] The percentage of patients having GI symptoms were higher in patients having abnormal BLESP.

The mean BLESP in females which was less as compared to that in the males, similar findings were described by Dantas et al.[22] About 26% patients were found to have altered BLESP. BLESP is influenced by a number of neurohormonal mechanisms. The decreased BLESP may be due to autonomic neuropathy as a consequence of DM. Increased BLESP in others may be the result of acid induce reflex spasm, increased HbA1C and blood glucose, deposition of advanced glycation products leading to decrease elasticity, day-to-day variation, and denervation hypersensitivity. Structural variation in the muscle of diaphragm surrounding LES can also affect BLESP. Esophageal dysmotility leads to increased circulating levels of Cholecystokinin which can lead to increased contraction of LES.[23] The resultant BLESP is, therefore, a result of balance between neurogenic and myogenic factors, excitatory and inhibitory influences and clasp and sling muscle contributions. In addition, the advanced glycation products which are formed due to increased plasma glucose levels cause morphological and biochemical changes in the muscles forming the LES.[24] The cholinergic activity is affected during hyperglycemia. In healthy volunteers, plasma concentrations of motilin are also less during hyperglycemia when compared with euglycemia.

A normal BLESP is required for proper progression of peristalsis. The BLESP had a weak positive correlation with peristaltic amplitude (P = 0.05). It implies that as the BLESP increases, a higher force of contraction is required to clear the bolus through the LES into the stomach. No statistically significant association was seen between BLESP and GI symptoms although the percentage of patients having GI symptoms was higher in the group with abnormal BLESP.

The peristaltic amplitude was higher in females (P = 0.004). This is in contrast to observation by Dantas RO who found that there was no significant difference in peristaltic amplitude of males and females.[22] This was just an incidental finding and may probably be due to lesser mean age of females as compared to males in our study. Nearly, 64% of patients with GI symptoms had increased peristaltic velocity suggesting that diabetes can lead to increase in peristaltic velocity and disruption of bolus transit causing dysmotility.

Acute hyperglycemia has been shown to have both stimulatory and inhibitory effect on GI motility due to the interaction between neural, hormonal, and local factors; however, we found no correlation among BLESP with blood sugar (F), PP and HbA1C.

Limitations of the study

As it was an invasive study, control group could not be taken among normal individuals and this remains the main limitation of the study. Furthermore, a single measurement of various parameters, which has inherent flaws, was carried out instead of a longitudinal study. A concurrent endoscopic evaluation could have ruled out confounding variables, but due to ethical issues and no definitive indication for such invasive investigation, it was not done.


  Conclusion Top


The study found that DM does cause subtle changes in esophageal motility parameters which may lead to certain GI symptoms. CFV and BLESP were the main esophageal motility parameters which were affected in the diabetics, Peristaltic Amplitude being the least affected. CFV showed a positive correlation with duration of diabetes and BLESP, but negative correlation with HbA1C values. We found a significant positive association between GI symptoms and peristaltic velocity. Peristaltic amplitude correlated negatively with duration of DM. Larger studies, especially in India, would be of significance to the clinicians for better symptomatic management of the disease in India.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Rundles RW. Diabetic neuropathy: General review with report of 125 cases. Medicine 1945;24:111-60.  Back to cited text no. 1
    
2.
Mandelstam P, Siegel CI, Lieber A, Siegel M. The swallowing disorder in patients with diabetic neuropathy-gastroenteropathy. Gastroenterology 1969;56:1-2.  Back to cited text no. 2
    
3.
O'Reilly D, Long RG. Diabetes and the gastro-intestinal tract. Dig Dis 1987;5:57-64.  Back to cited text no. 3
    
4.
Loo FD, Dodds WJ, Soergel KH, Arndorfer RC, Helm JF, Hogan WJ, et al. Multipeaked esophageal peristaltic pressure waves in patients with diabetic neuropathy. Gastroenterology 1985;88:485-91.  Back to cited text no. 4
    
5.
Faraj J, Melander O, Sundkvist G, Olsson R, Thorsson O, Ekberg O, et al. Oesophageal dysmotility, delayed gastric emptying and gastrointestinal symptoms in patients with diabetes mellitus. Diabet Med 2007;24:1235-9.  Back to cited text no. 5
[PUBMED]    
6.
Stewart IM, Hosking DJ, Preston BJ, Atkinson M. Oesophageal motor changes in diabetes mellitus. Thorax 1976;31:278-83.  Back to cited text no. 6
    
7.
Bodger K, Trudgill N. Guidelines for oesophageal manometry and pH Monitoring. Br Soc Gastroenterol 2006. Available from: www.bsg.org.uk. [Last accessed on 2017 Nov 17].  Back to cited text no. 7
    
8.
Professional Procedure Guide for Use of HbA1C. Canada: Bayer healthcare, LLC; 2008. Available from: http://www.a1cnow.com. [Last updated 2006 Nov].  Back to cited text no. 8
    
9.
Bredenoord AJ, Fox M, Kahrilas PJ, Pandolfino JE, Schwizer W, Smout AJ, et al. Chicago classification criteria of esophageal motility disorders defined in high resolution esophageal pressure topography. Neurogastroenterol Motil 2012;24 Suppl 1:57-65.  Back to cited text no. 9
    
10.
Pandolfino JE, Ghosh SK, Rice J, Clarke JO, Kwiatek MA, Kahrilas PJ, et al. Classifying esophageal motility by pressure topography characteristics: A study of 400 patients and 75 controls. Am J Gastroenterol 2008;103:27-37.  Back to cited text no. 10
    
11.
Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:837-53.  Back to cited text no. 11
    
12.
Fouad H, Mervat E, Mousa A. Esophageal motility disorders in patients with diabetes mellitus. Tanta Med Sch J 2008;3:74-87.  Back to cited text no. 12
    
13.
Barnett JL, Owyang C. Serum glucose concentration as a modulator of interdigestive gastric motility. Gastroenterology 1988;94:739-44.  Back to cited text no. 13
    
14.
Annese V, Bassotti G, Caruso N, De Cosmo S, Gabbrielli A, Modoni S, et al. Gastrointestinal motor dysfunction, symptoms, and neuropathy in noninsulin-dependent (type 2) diabetes mellitus. J Clin Gastroenterol 1999;29:171-7.  Back to cited text no. 14
    
15.
Hollis JB, Castell DO. Esophageal function in elderly man. A new look at “presbyesophagus”. Ann Intern Med 1974;80:371-4.  Back to cited text no. 15
    
16.
JoAnne R, Allison DB, Taylor A. Oral, pharyngeal and Esophageal Motor Function in Aging. GI Motility Online; 2006. Available from: http://www.nature.com. [Last accessed on 2016 May 16].  Back to cited text no. 16
    
17.
Ayazi S, Hagen JA, Chan LS, DeMeester SR, Lin MW, Ayazi A, et al. Obesity and gastroesophageal reflux: Quantifying the association between body mass index, esophageal acid exposure, and lower esophageal sphincter status in a large series of patients with reflux symptoms. J Gastrointest Surg 2009;13:1440-7.  Back to cited text no. 17
    
18.
Kesavachandran CN, Bihari V, Mathur N. The normal range of body mass index with high body fat percentage among male residents of Lucknow city in north India. Indian J Med Res 2012;135:72-7.  Back to cited text no. 18
[PUBMED]  [Full text]  
19.
Zhang Q, Horowitz M, Rigda R, Rayner C, Worynski A, Holloway RH, et al. Effect of hyperglycemia on triggering of transient lower esophageal sphincter relaxations. Am J Physiol Gastrointest Liver Physiol 2004;286:G797-803.  Back to cited text no. 19
    
20.
Corina M, Dumitrascu DL. Esophageal Motility Disorders in Diabetes Mellitus: A Manometric Study of Gastrointestinal & Liver Disease; 2000. Available from: http://www.jgld.ro. [Last accessed on 2015 Jun].  Back to cited text no. 20
    
21.
Parkman HP, Camilleri M, Farrugia G, McCallum RW, Bharucha AE, Mayer EA, et al. Gastroparesis and functional dyspepsia: Excerpts from the AGA/ANMS meeting. Neurogastroenterol Motil 2010;22:113-33.  Back to cited text no. 21
    
22.
Dantas RO, Ferriolli E, Souza MA. Gender effects on esophageal motility. Braz J Med Biol Res 1998;31:539-44.  Back to cited text no. 22
    
23.
Borg J, Melander O, Johansson L, Uvnäs-Moberg K, Rehfeld JF, Ohlsson B, et al. Gastroparesis is associated with oxytocin deficiency, oesophageal dysmotility with hyperCCKemia, and autonomic neuropathy with hypergastrinemia. BMC Gastroenterol 2009;9:17.  Back to cited text no. 23
    
24.
Ulrich P, Cerami A. Protein glycation, diabetes, and aging. Recent Prog Horm Res 2001;56:1-21.  Back to cited text no. 24
    



 
 
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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]



 

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