ORCP-418; No. of Pages 4
ARTICLE IN PRESS
Obesity Research & Clinical Practice (2015) xxx, xxx—xxx
SHORT REPORT
Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review Noman Ishaque a, Bhojo A. Khealani a, Amir H. Shariff b, Muhammad Wasay a,∗ a
Neurology Section, Department of Medicine, Aga Khan University Hospital, Karachi, Pakistan b General Surgery Section, Department of Surgery, Aga Khan University Hospital, Karachi, Pakistan Received 17 November 2014 ; received in revised form 13 January 2015; accepted 1 February 2015
KEYWORDS Bariatric surgery; GBS; Neuropathy; Demyelinating; Obesity
Summary Obesity is a major health problem worldwide. Bariatric surgery has been increasingly used to manage obesity. Many acute as well as chronic neurological complications have been reported after bariatric surgery including Guillain—Barré syndrome (GBS). An autoimmune process has been postulated as the underlying pathophysiology. Most of the reported cases of GBS after bariatric surgery are of the axonal variety. Here, we report a case of a demyelinating variety of GBS in a young woman who presented with acute onset of progressive weakness and paresthesia of all limbs within six weeks after bariatric surgery. She was treated with intravenous immunoglobulin (IVIG) and rehabilitation. She had complete recovery on follow-up. We believe that onset of acute inflammatory demyelinating polyradiculoneuropathy (AIDP), which is demyelinating variety of GBS, is associated with changes in immune system after bariatric surgery. © 2015 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.
Introduction
∗
Corresponding author. Tel.: +92 2134930051. E-mail addresses: [email protected] (N. Ishaque), [email protected] (B.A. Khealani), [email protected] (A.H. Shariff), [email protected] (M. Wasay).
Obesity is a major health problem worldwide and has reached epidemic proportions the world over. Bariatric surgery is currently the only modality that provides a significant, sustained weight loss for the patient who is morbidly obese,
http://dx.doi.org/10.1016/j.orcp.2015.02.001 1871-403X/© 2015 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Ishaque N, et al. Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review. Obes Res Clin Pract (2015), http://dx.doi.org/10.1016/j.orcp.2015.02.001
ORCP-418; No. of Pages 4
ARTICLE IN PRESS
2
N. Ishaque et al.
with resultant improvement in obesity-related comorbidities. The demand for bariatric surgery worldwide is increasing at an exponential rate and in 2008, 344,221 bariatric surgery operations were performed [1]. As the frequency of bariatric surgery is increasing, so is the recognition of different neurologic complications associated with bariatric surgery. No part of the neuraxis is exempt from these potential complications. There are many well-recognized neurologic complications of bariatric surgery including Wernicke’s encephalopathy and peripheral neuropathies [2]. The three clinical patterns of peripheral neuropathies after bariatric surgery are sensory-predominant polyneuropathy, mononeuropathy, and radiculoplexopathies [3]. GBS has been reported as a rare complication of bariatric surgery [2,4] and the reported cases are of the axonal variety. We report a case of demyelinating variety of GBS in a young woman within six weeks after bariatric surgery.
Case report A 30-year-old woman presented with a BMI of 44 in association with polycystic ovarian syndrome and degenerative joint disease. Her obesity proved refractory to dietary measures and exercise and she subsequently underwent a laparoscopic sleeve gastrectomy. The immediate post-operative period was uneventful. She was in regular follow-up with her surgeon and was fully compliant with the recommended diet plan and vitamin supplements. She lost 25% of her excess body weight (EBW) in the first month after surgery. About 6 weeks after surgery she presented with a two-day history of weakness of both lower and upper extremities associated with paraesthesias in her hands and feet. Her neurologic examination was significant for quadriparesis (power of 4/5 in proximal muscles of upper extremities, 3/5 in distal muscles of upper extremities and 4/5 in lower extremities on Medical Research council (MRC) scale), absent brachioradialis, knee and ankle reflexes bilaterally. Babinski’s sign was negative and there was no abnormal sensory sign. Initial laboratory work-up showed: Hemoglobin 14.0, MCV 81.8, Leukocyte count: 7.6, Platelet count: 261, BUN: 10, Creatinine: 0.7, Sodium: 141, potassium: 4.0, ALT: 52, Calcium: 9.2, Phosphorus: 9.8, Serum B12 : 538 and TSH: 0.68 and Albumin: 4.1. Her B12 levels were 538 (lower limit of normal 191) and TSH was 0.68. Copper and zinc levels were not checked.
A detailed electrodiagnostic study was performed (refer to the Table 1, at the end of document) which was significant for absent F responses from right ulnar and bilateral peroneal nerves in addition to morphologically normal but rapidly firing motor unit action potentials on needle EMG examination. Overall these findings were suggestive of an acute neurogenic process affecting mainly the proximal motor nerve segments. Based on clinical and neurophysiologic data, a diagnosis of GBS (demyelinating variety) was made and she was started on intravenous immunoglobulin (IVIG). She was given IVIG in standard recommended dose i.e. 0.4 g/kg/d for 5 days. She was also given gabapentin for sensory symptoms and early rehabilitation was started. The patient improved symptomatically and was discharged on the 6th day of admission with advice for rehabilitation. On follow-up visit in neurology clinic 2 weeks later she was asymptomatic and there was no neurologic deficit. Repeat electrodiagnostic study was repeated 80 days later showed complete recovery from AIDP. The patient is currently 6 months post-surgery with no remaining neurologic deficits. She has lost 64% of her EBW. She remains fully compliant with her diet and exercise regimens.
Discussion The increasing utilization of bariatric surgery has been accompanied by an increased incidence and awareness of related neurologic complications. Neurological complications may result from mechanical or inflammatory mechanisms, but mainly from nutritional deficiencies. Vitamin B12, folate, thiamine, vitamin D, and vitamin E are the most frequent deficiencies. Different patterns of neurologic complications can be observed that may differ based on the time to presentation. At an early stage, immediate peripheral nerve injury, Wernicke’s encephalopathy, and polyradiculoneuropathy are the most frequent. Late complications may appear after years and include optic neuropathy, myelopathy, peripheral neuropathy, and myopathy [5]. The three clinical patterns of peripheral neuropathy after bariatric surgery are sensory-predominant polyneuropathy, mononeuropathy, and radiculoplexopathies [3]. Koffman et al. reviewed 50 case reports of 96 patients with neurologic symptoms after bariatric procedures. The most common presentations were peripheral neuropathy in 60 (62%) and encephalopathy in 30 (31%). Among
Please cite this article in press as: Ishaque N, et al. Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review. Obes Res Clin Pract (2015), http://dx.doi.org/10.1016/j.orcp.2015.02.001
ARTICLE IN PRESS
ORCP-418; No. of Pages 4
Demyelinating neuropathy after bariatric surgery Table 1 Nerve muscle
Nerve conduction studies data at admission. Stim-Site
Latency (ms) R
Motor nerve conduction studies Median (APB) WRIST 3.7 Median (APB) ELBOW 7.4 Ulnar (ADQ) WRIST 2.9 Ulnar (ADQ) D.ELBOW 6.1 Ulnar (ADQ) P.ELBOW 8.7 Posterior Tibial ANKLE 4.8 (AH) Posterior Tibial KNEE 12.6 (AH) Peroneal (EDB) ANKLE 4.9 Peroneal (EDB) D.KNEE 11.6 Peroneal (EDB) P.KNEE 13.1 Peroneal (TA) DFH Peroneal (TA) PFH H.Reflex POP FOSSA 29.4 Nerve
3
Recording-Site
Sensory nerve conduction Median F2 F5 Ulnar SNUFF BOS Radial Sural ANKLE
Stim-Site
studies WRIST WRIST FOREARM CALF
Distance (cm) L
Amplitude (mv)
NCV (m/s)
F-LTN (ms)
R
L
R
L
R
L
R
Duration (ms) L
3.9 7.5 2.9 6.0 9.2 5.0
7.0 22.0 7.0 21.0 10.0 6.5
8.7 8.0 5.2 4.9 1.3 2.6
6.5 6.3 3.3 3.1 1.0 2.3
— 59.0 — 66.0 38.0 —
— 61.0 — 68.0 31.0 —
24.4 — NR — — 45.9
23.0 — 27.4 — — 50.9
8.7 8.9 7.6 8.0 8.2 5.5
7.8 7.9 7.1 7.2 7.2 6.0
13.5
36.0
2.2
1.9
46.0
42.0
—
—
6.4
6.4
4.5 11.3 12.9 3.0 4.2 29.0
9.0 31.0 8.0 11.0 10.0 22.0
2.2 2.1 2.1
1.5 1.5 1.5 4.0 4.0
— 46.0 53.0
— 46.0 50.0 — 83.0
NR — —
NR — — — —
7.5 9.0 9.3
7.6 7.6 7.6 11.9 12.0
Latency (ms) R
L
3.1 3.4 2.4 3.4
3.3 3.4 2.4 3.3
the 60 patients with peripheral neuropathy, 40 (67%) had a polyneuropathy and 18 (30%) had mononeuropathies. Neurologic emergencies including Wernicke’s encephalopathy, rhabdomyolysis, and Guillain—Barré syndrome (GBS) were also reported [6]. GBS is an acute inflammatory neuropathy (immune mediated) which responds to immunomodulating therapy. It has two forms: demyelinating type, the AIDP and axonal variant which is known as acute motor axonal neuropathy (AMAN). The etiology of peripheral neuropathy after bariatric surgery is probably multifactorial, nutritional deficiencies being the most common etiology [7]. The pathophysiology of GBS has been reported to be immunogenic as in GBS otherwise. In a report case of GBS (AMAN variant), after the surgery antibodies like anti-GM1, anti-MAG, anti-GD1a antibodies were found to be positive, supporting immune-mediated pathology [8]. In a second case report, two patients developed GBS about three months after bariatric surgery [2]. In yet another case report, a patient developed GBS almost 5 months after bariatric surgery [4]. Our patient developed symptoms 40 days after bariatric surgery
Distance (cm)
14.00 14.00 10.00 14.00
Amplitude (V)
NCV (m/s)
R
L
R
L
81.00 52.00 44.00 16.00
61.00 60.00 32.00 12.00
45.00 41.00 42.00 41.00
42.00 41.00 42.00 42.00
which is somewhat earlier compared to these reported cases. Obesity alters a normal immune response and increases risk of infections which is improved after the weight reduction [9]. We think that during this recovery period the immune response to infection or stress may be overwhelming, leading to injury to the patient’s own bodily system akin to reperfusion injuries after revascularization.
Conclusion GBS is rarely seen after bariatric surgery but it is important to consider and evaluate this diagnosis in every patient who develops features of acute to subacute neuropathy after bariatric surgery. GBS is a treatable and potentially reversible disease if appropriate therapy such as plasma exchange or IVIG is provided.
Conflict of interest None.
Please cite this article in press as: Ishaque N, et al. Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review. Obes Res Clin Pract (2015), http://dx.doi.org/10.1016/j.orcp.2015.02.001
ORCP-418; No. of Pages 4
ARTICLE IN PRESS
4
N. Ishaque et al.
Author’s contribution Noman Ishaque: data acquisition, data analysis, literature review, manuscript writing, manuscript review. Bhojo Khealani: concept and design, data acquisition, data analysis, manuscript writing, manuscript review. Amir Shariff: data analysis, manuscript review. Mohammad Wasay: concept and design, data analysis, manuscript writing, manuscript review.
References [1] Buchwald H, Oien DM. Metabolic/bariatric surgery worldwide 2011. Obes Surg 2013;23(April (4)):427—36. [2] Chang CG, Helling TS, Black WE, Rymer MM. Weakness after gastric bypass. Obes Surg 2002;12(August (4)): 592—7.
[3] Thaisetthawatkul P, Collazo-Clavell ML, Sarr MG, Norell JE, Dyck PJB. A controlled study of peripheral neuropathy after bariatric surgery. Neurology 2004;63(October (8)):1462—70. [4] Aluka KJ, Turner PL, Fullum TM. Guillain—Barré syndrome and postbariatric surgery polyneuropathies. J Soc Laparoendosc Surg 2009;13:250—3. [5] Landais A. Neurological complications of bariatric surgery. Obes Surg 2014. [6] Koffman BM, Greenfield LJ, Ali II, Pirzada NA. Neurologic complications after surgery for obesity. Muscle Nerve 2006;33(February (2)):166—76. [7] Machado FC, Valério BC, Morgulis RN, Nunes KF, Mazzali-Verst S. Acute axonal polyneuropathy with predominant proximal involvement: an uncommon neurological complication of bariatric surgery. Arq Neuropsiquiatr 2006;64(3-A):609—12. [8] Landais AF. Rare neurologic complication of bariatric surgery: acute motor axonal neuropathy (AMAN), a severe motor axonal form of the Guillain—Barré syndrome. Surg Obes Relat Dis 2014, http://dx.doi.org/10.1016/ j.soard.2014.02.019. [9] Huttunen R, Syrjänen J. Obesity and the risk and outcome of infection. Int J Obes 2013;37:333—40.
Available online at www.sciencedirect.com
ScienceDirect
Please cite this article in press as: Ishaque N, et al. Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review. Obes Res Clin Pract (2015), http://dx.doi.org/10.1016/j.orcp.2015.02.001
ARTICLE IN PRESS
Obesity Research & Clinical Practice (2015) xxx, xxx—xxx
SHORT REPORT
Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review Noman Ishaque a, Bhojo A. Khealani a, Amir H. Shariff b, Muhammad Wasay a,∗ a
Neurology Section, Department of Medicine, Aga Khan University Hospital, Karachi, Pakistan b General Surgery Section, Department of Surgery, Aga Khan University Hospital, Karachi, Pakistan Received 17 November 2014 ; received in revised form 13 January 2015; accepted 1 February 2015
KEYWORDS Bariatric surgery; GBS; Neuropathy; Demyelinating; Obesity
Summary Obesity is a major health problem worldwide. Bariatric surgery has been increasingly used to manage obesity. Many acute as well as chronic neurological complications have been reported after bariatric surgery including Guillain—Barré syndrome (GBS). An autoimmune process has been postulated as the underlying pathophysiology. Most of the reported cases of GBS after bariatric surgery are of the axonal variety. Here, we report a case of a demyelinating variety of GBS in a young woman who presented with acute onset of progressive weakness and paresthesia of all limbs within six weeks after bariatric surgery. She was treated with intravenous immunoglobulin (IVIG) and rehabilitation. She had complete recovery on follow-up. We believe that onset of acute inflammatory demyelinating polyradiculoneuropathy (AIDP), which is demyelinating variety of GBS, is associated with changes in immune system after bariatric surgery. © 2015 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.
Introduction
∗
Corresponding author. Tel.: +92 2134930051. E-mail addresses: [email protected] (N. Ishaque), [email protected] (B.A. Khealani), [email protected] (A.H. Shariff), [email protected] (M. Wasay).
Obesity is a major health problem worldwide and has reached epidemic proportions the world over. Bariatric surgery is currently the only modality that provides a significant, sustained weight loss for the patient who is morbidly obese,
http://dx.doi.org/10.1016/j.orcp.2015.02.001 1871-403X/© 2015 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Ishaque N, et al. Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review. Obes Res Clin Pract (2015), http://dx.doi.org/10.1016/j.orcp.2015.02.001
ORCP-418; No. of Pages 4
ARTICLE IN PRESS
2
N. Ishaque et al.
with resultant improvement in obesity-related comorbidities. The demand for bariatric surgery worldwide is increasing at an exponential rate and in 2008, 344,221 bariatric surgery operations were performed [1]. As the frequency of bariatric surgery is increasing, so is the recognition of different neurologic complications associated with bariatric surgery. No part of the neuraxis is exempt from these potential complications. There are many well-recognized neurologic complications of bariatric surgery including Wernicke’s encephalopathy and peripheral neuropathies [2]. The three clinical patterns of peripheral neuropathies after bariatric surgery are sensory-predominant polyneuropathy, mononeuropathy, and radiculoplexopathies [3]. GBS has been reported as a rare complication of bariatric surgery [2,4] and the reported cases are of the axonal variety. We report a case of demyelinating variety of GBS in a young woman within six weeks after bariatric surgery.
Case report A 30-year-old woman presented with a BMI of 44 in association with polycystic ovarian syndrome and degenerative joint disease. Her obesity proved refractory to dietary measures and exercise and she subsequently underwent a laparoscopic sleeve gastrectomy. The immediate post-operative period was uneventful. She was in regular follow-up with her surgeon and was fully compliant with the recommended diet plan and vitamin supplements. She lost 25% of her excess body weight (EBW) in the first month after surgery. About 6 weeks after surgery she presented with a two-day history of weakness of both lower and upper extremities associated with paraesthesias in her hands and feet. Her neurologic examination was significant for quadriparesis (power of 4/5 in proximal muscles of upper extremities, 3/5 in distal muscles of upper extremities and 4/5 in lower extremities on Medical Research council (MRC) scale), absent brachioradialis, knee and ankle reflexes bilaterally. Babinski’s sign was negative and there was no abnormal sensory sign. Initial laboratory work-up showed: Hemoglobin 14.0, MCV 81.8, Leukocyte count: 7.6, Platelet count: 261, BUN: 10, Creatinine: 0.7, Sodium: 141, potassium: 4.0, ALT: 52, Calcium: 9.2, Phosphorus: 9.8, Serum B12 : 538 and TSH: 0.68 and Albumin: 4.1. Her B12 levels were 538 (lower limit of normal 191) and TSH was 0.68. Copper and zinc levels were not checked.
A detailed electrodiagnostic study was performed (refer to the Table 1, at the end of document) which was significant for absent F responses from right ulnar and bilateral peroneal nerves in addition to morphologically normal but rapidly firing motor unit action potentials on needle EMG examination. Overall these findings were suggestive of an acute neurogenic process affecting mainly the proximal motor nerve segments. Based on clinical and neurophysiologic data, a diagnosis of GBS (demyelinating variety) was made and she was started on intravenous immunoglobulin (IVIG). She was given IVIG in standard recommended dose i.e. 0.4 g/kg/d for 5 days. She was also given gabapentin for sensory symptoms and early rehabilitation was started. The patient improved symptomatically and was discharged on the 6th day of admission with advice for rehabilitation. On follow-up visit in neurology clinic 2 weeks later she was asymptomatic and there was no neurologic deficit. Repeat electrodiagnostic study was repeated 80 days later showed complete recovery from AIDP. The patient is currently 6 months post-surgery with no remaining neurologic deficits. She has lost 64% of her EBW. She remains fully compliant with her diet and exercise regimens.
Discussion The increasing utilization of bariatric surgery has been accompanied by an increased incidence and awareness of related neurologic complications. Neurological complications may result from mechanical or inflammatory mechanisms, but mainly from nutritional deficiencies. Vitamin B12, folate, thiamine, vitamin D, and vitamin E are the most frequent deficiencies. Different patterns of neurologic complications can be observed that may differ based on the time to presentation. At an early stage, immediate peripheral nerve injury, Wernicke’s encephalopathy, and polyradiculoneuropathy are the most frequent. Late complications may appear after years and include optic neuropathy, myelopathy, peripheral neuropathy, and myopathy [5]. The three clinical patterns of peripheral neuropathy after bariatric surgery are sensory-predominant polyneuropathy, mononeuropathy, and radiculoplexopathies [3]. Koffman et al. reviewed 50 case reports of 96 patients with neurologic symptoms after bariatric procedures. The most common presentations were peripheral neuropathy in 60 (62%) and encephalopathy in 30 (31%). Among
Please cite this article in press as: Ishaque N, et al. Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review. Obes Res Clin Pract (2015), http://dx.doi.org/10.1016/j.orcp.2015.02.001
ARTICLE IN PRESS
ORCP-418; No. of Pages 4
Demyelinating neuropathy after bariatric surgery Table 1 Nerve muscle
Nerve conduction studies data at admission. Stim-Site
Latency (ms) R
Motor nerve conduction studies Median (APB) WRIST 3.7 Median (APB) ELBOW 7.4 Ulnar (ADQ) WRIST 2.9 Ulnar (ADQ) D.ELBOW 6.1 Ulnar (ADQ) P.ELBOW 8.7 Posterior Tibial ANKLE 4.8 (AH) Posterior Tibial KNEE 12.6 (AH) Peroneal (EDB) ANKLE 4.9 Peroneal (EDB) D.KNEE 11.6 Peroneal (EDB) P.KNEE 13.1 Peroneal (TA) DFH Peroneal (TA) PFH H.Reflex POP FOSSA 29.4 Nerve
3
Recording-Site
Sensory nerve conduction Median F2 F5 Ulnar SNUFF BOS Radial Sural ANKLE
Stim-Site
studies WRIST WRIST FOREARM CALF
Distance (cm) L
Amplitude (mv)
NCV (m/s)
F-LTN (ms)
R
L
R
L
R
L
R
Duration (ms) L
3.9 7.5 2.9 6.0 9.2 5.0
7.0 22.0 7.0 21.0 10.0 6.5
8.7 8.0 5.2 4.9 1.3 2.6
6.5 6.3 3.3 3.1 1.0 2.3
— 59.0 — 66.0 38.0 —
— 61.0 — 68.0 31.0 —
24.4 — NR — — 45.9
23.0 — 27.4 — — 50.9
8.7 8.9 7.6 8.0 8.2 5.5
7.8 7.9 7.1 7.2 7.2 6.0
13.5
36.0
2.2
1.9
46.0
42.0
—
—
6.4
6.4
4.5 11.3 12.9 3.0 4.2 29.0
9.0 31.0 8.0 11.0 10.0 22.0
2.2 2.1 2.1
1.5 1.5 1.5 4.0 4.0
— 46.0 53.0
— 46.0 50.0 — 83.0
NR — —
NR — — — —
7.5 9.0 9.3
7.6 7.6 7.6 11.9 12.0
Latency (ms) R
L
3.1 3.4 2.4 3.4
3.3 3.4 2.4 3.3
the 60 patients with peripheral neuropathy, 40 (67%) had a polyneuropathy and 18 (30%) had mononeuropathies. Neurologic emergencies including Wernicke’s encephalopathy, rhabdomyolysis, and Guillain—Barré syndrome (GBS) were also reported [6]. GBS is an acute inflammatory neuropathy (immune mediated) which responds to immunomodulating therapy. It has two forms: demyelinating type, the AIDP and axonal variant which is known as acute motor axonal neuropathy (AMAN). The etiology of peripheral neuropathy after bariatric surgery is probably multifactorial, nutritional deficiencies being the most common etiology [7]. The pathophysiology of GBS has been reported to be immunogenic as in GBS otherwise. In a report case of GBS (AMAN variant), after the surgery antibodies like anti-GM1, anti-MAG, anti-GD1a antibodies were found to be positive, supporting immune-mediated pathology [8]. In a second case report, two patients developed GBS about three months after bariatric surgery [2]. In yet another case report, a patient developed GBS almost 5 months after bariatric surgery [4]. Our patient developed symptoms 40 days after bariatric surgery
Distance (cm)
14.00 14.00 10.00 14.00
Amplitude (V)
NCV (m/s)
R
L
R
L
81.00 52.00 44.00 16.00
61.00 60.00 32.00 12.00
45.00 41.00 42.00 41.00
42.00 41.00 42.00 42.00
which is somewhat earlier compared to these reported cases. Obesity alters a normal immune response and increases risk of infections which is improved after the weight reduction [9]. We think that during this recovery period the immune response to infection or stress may be overwhelming, leading to injury to the patient’s own bodily system akin to reperfusion injuries after revascularization.
Conclusion GBS is rarely seen after bariatric surgery but it is important to consider and evaluate this diagnosis in every patient who develops features of acute to subacute neuropathy after bariatric surgery. GBS is a treatable and potentially reversible disease if appropriate therapy such as plasma exchange or IVIG is provided.
Conflict of interest None.
Please cite this article in press as: Ishaque N, et al. Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review. Obes Res Clin Pract (2015), http://dx.doi.org/10.1016/j.orcp.2015.02.001
ORCP-418; No. of Pages 4
ARTICLE IN PRESS
4
N. Ishaque et al.
Author’s contribution Noman Ishaque: data acquisition, data analysis, literature review, manuscript writing, manuscript review. Bhojo Khealani: concept and design, data acquisition, data analysis, manuscript writing, manuscript review. Amir Shariff: data analysis, manuscript review. Mohammad Wasay: concept and design, data analysis, manuscript writing, manuscript review.
References [1] Buchwald H, Oien DM. Metabolic/bariatric surgery worldwide 2011. Obes Surg 2013;23(April (4)):427—36. [2] Chang CG, Helling TS, Black WE, Rymer MM. Weakness after gastric bypass. Obes Surg 2002;12(August (4)): 592—7.
[3] Thaisetthawatkul P, Collazo-Clavell ML, Sarr MG, Norell JE, Dyck PJB. A controlled study of peripheral neuropathy after bariatric surgery. Neurology 2004;63(October (8)):1462—70. [4] Aluka KJ, Turner PL, Fullum TM. Guillain—Barré syndrome and postbariatric surgery polyneuropathies. J Soc Laparoendosc Surg 2009;13:250—3. [5] Landais A. Neurological complications of bariatric surgery. Obes Surg 2014. [6] Koffman BM, Greenfield LJ, Ali II, Pirzada NA. Neurologic complications after surgery for obesity. Muscle Nerve 2006;33(February (2)):166—76. [7] Machado FC, Valério BC, Morgulis RN, Nunes KF, Mazzali-Verst S. Acute axonal polyneuropathy with predominant proximal involvement: an uncommon neurological complication of bariatric surgery. Arq Neuropsiquiatr 2006;64(3-A):609—12. [8] Landais AF. Rare neurologic complication of bariatric surgery: acute motor axonal neuropathy (AMAN), a severe motor axonal form of the Guillain—Barré syndrome. Surg Obes Relat Dis 2014, http://dx.doi.org/10.1016/ j.soard.2014.02.019. [9] Huttunen R, Syrjänen J. Obesity and the risk and outcome of infection. Int J Obes 2013;37:333—40.
Available online at www.sciencedirect.com
ScienceDirect
Please cite this article in press as: Ishaque N, et al. Guillain—Barré syndrome (demyelinating) six weeks after bariatric surgery: A case report and literature review. Obes Res Clin Pract (2015), http://dx.doi.org/10.1016/j.orcp.2015.02.001
