Chronic Guillain-Barré syndrome and refractory diarrhea after RYGB: a 9-year longitudinal case report

TL;DR

A man developed chronic neurological issues and severe diarrhea after weight-loss surgery, likely due to long-term nutrient deficiencies.

Contribution

This case suggests a link between long-term micronutrient deficiencies and chronic autoimmune neurological disorders after bariatric surgery.

Findings

The patient experienced progressive neurological deterioration and significant weight loss over 9 years.

Severe deficiencies in vitamin D, calcium, iron, and other nutrients were observed.

Autoimmune dysregulation and gastrointestinal dysfunction led to the need for partial parenteral nutrition.

Abstract

We present a 46-year-old male who developed chronic Guillain-Barré syndrome and refractory diarrhea after undergoing Roux-en-Y gastric bypass, with progressive neurological deterioration and 34.9% total weight loss over 9 years. Serial evaluations demonstrated severe deficiencies include vitamin D, calcium, iron and other nutritions, accompanied by evidence of autoimmune dysregulation. The patient’s condition progressed to require partial parenteral nutrition due to worsening neurological and gastrointestinal dysfunction. This case highlights the critical need for ongoing nutritional monitoring after bariatric surgery and suggests that persistent micronutrient deficiencies may contribute to sustained immune dysfunction, potentially triggering chronic autoimmune neurological disorders in susceptible individuals.

Tables

Table 1. Clinical and biological parameters before and at 6th year after operation

	At baseline	At 6th year after operation	Reference rangec
Clinical parameters
Weight,kg	87.6	56.9
BMI,kg/m2	30.3	19.7
Weight loss, kg(%)		30.6(34.9)
Upper limbs(MRC grade)		4/5
Lower limbs (MRC grade)		3–4/5
Biological parameters
Iron (μmol/L)	14.28	4.77a	7.2–27.7
Folate (nmol/L)	19.6	43.6b	8.8–39.7
Ferritin (ng/mL)	942.8b	273.9	30–400
Vitamin B12 (pmol/L)	1476b	701.7b	148–660
Total 25-OH Vitamin D (nmol/L)	NM	32.7a	>75
Calcium (mmol/L)	2.10	1.78a	2.08–2.6
Albumin (g/L)	48.1	29.4a	40–55
Prealbumin (mg/L)	234	133a	200–400
RBC (×1012/L)	4.89	3.30a	4.3–5.8
Hemoglobin (g/L)	147	95a	130–175
Blood Glucose (mmol/L)	6.8–22.8(72% >13)	5.7–20.3(70% >13)	3.9–6.1
HbA1c (%)	8.7b	5.5	4–6
TSH (μIU/mL)	1.460	0.997	0.27–4.2
Total T4 (nmol/L)	78.45	44.72a	66–181
Stool Fungal Test	Negative	Saccharomyces cerevisiae	Negative

Full text

Introduction

Guillain-Barré syndrome (GBS) is classically an acute, immune-mediated polyneuropathy, with chronic forms account for less than 5% of cases [1–3]. Roux-en-Y gastric bypass (RYGB), while effective for obesity management, carries lifelong risks of micronutrient malabsorption and refractory gastrointestinal complications, including chronic diarrhea [4, 5]. While vitamin deficiencies post-RYGB are well-documented, However, their role in triggering chronic autoimmune neuropathy is poorly understood.

Case report

A 46-year-old male with a 6-year history of poorly controlled type 2 diabetes (HbA1c 9.8%, BMI 30.3 kg/m^2^). The patient presented with severe metabolic dysregulation (random glucose 6–25 mmol/L, predominantly 16–25 mmol/L) due to no adherence with metformin, glipizide, and long-acting insulin, resulting in bilateral diabetic retinopathy (left eye with 6-month blurred vision) and nephropathy (elevated urinary albumin despite preserved glomerular filtration rate), demonstrating progressive microvascular complications from sustained hyperglycemia.

Operation and postoperative course

Laparoscopic RYGB was performed, creating a 30 mL gastric pouch with a 100 cm Roux limb measured from the ligament of Treitz. The patient recovered well, with stable glucose (6.6–9.8 mmol/L) and transient low-grade fever (peak 38.3°C) that resolved spontaneously, By postoperative day 8 (POD 8) he achieved a 4 kg weight loss and was discharged on a semi-liquid diet. At POD 21, progressive neurological deficits emerged: bilateral lower limb weakness (distal 3/5, proximal 3–4/5 Medical Research Council (MRC) grade), distal numbness (feet-predominant), with mild hyperalgesia and dorsal hypoesthesia; urinary retention with suprapubic discomfort; and systemic symptoms (dizziness, anorexia) without febrile or focal neurological deficits. Neurological examination revealed diminished lower limb reflexes, preserved upper limb reflexes, bilateral Lasègue’s sign positivity, and absent meningeal signs, while maintained normal bowel function.

Diagnostic and therapeutic course

The patient showed albuminocytologic dissociation in cerebrospinal fluid, elevated protein 694.3 mg/L and cells 5/μL, and electrophysiological evidence of proximal nerve root involvement (abnormal F-waves and H-reflexes), meeting Brighton criteria for GBS diagnosis. Intravenous immunoglobulin (IVIG) administration after definitive diagnosis, partial neurological recovery was achieved, with distal lower limb strength improving to MRC grade 4/5 by postoperative day 48 and achieved functional independence in ambulation independence. However, the patient subsequently developed gradual-onset diarrhea (1–2 episodes/day, Bristol Type 5–6).

9-year follow-up

The patient received ongoing dietary counseling focusing on nutrition optimization, micronutrient supplementation, and lifestyle adjustments. Despite strict dietary compliance, persistent diarrhea and inadequate intake led to unresolved micronutrient deficiencies. The patient reported chronic diarrhea with 4–8 daily episodes, occasionally exceeding 10. Stools were consistently pasty (Bristol stool scale Type 5–6) without abdominal pain or systemic symptoms. Although combination anti-diarrheal therapy provided partial relief, symptoms often recurred, significantly impacting daily life. Persistent left lower limb weakness resulted in a mild limping gait. While maintaining independent ambulation, they required minimal activities of daily living assistance and reported prolonged squatting difficulty. These residual symptoms did not significantly impair basic self-care.

In 2022 (postoperative year 6), the patient was hospitalized for severe diarrhea evaluation. The patient demonstrated mild distal-predominant weakness (lower limbs 3–4/5 distally and 4/5 proximally, upper limbs uniformly 4/5) with preserved muscle tone but mild atrophy, accompanied by distal lower limb hyperalgesia and dorsal foot hypoesthesia with intact proprioception/vibration. Reflexes showed diminished patellar and Achilles responses with flexor plantar reflexes, while special tests revealed bilateral Lasègue’s sign positivity. Electromyography identified reduced motor conduction velocity in the left tibial nerve (normal latency/amplitude), normal motor and sensory conduction velocities with decreased sensory amplitudes in the right tibial and bilateral median/ulnar/radial nerves, and prolonged F-wave latency (normal occurrence rate) in the right tibial nerve, consistent with sensory fiber impairment affecting all limbs with right tibial F-wave abnormality.

Clinical summary (2016–2025)

The patient developed progressive weight reduction (BMI 19.7 kg/m^2^, 34.9% weight loss) with persistent muscle weakness, refractory diarrhea (4–8 daily Bristol type 6–7), and asymmetric neuropathic weakness, resulting in dependence and work disability. Secondary complications included moderate depression/anxiety (Patient Health Questionnaire-9: 18) exacerbated by medication non-adherence. Further details are provided in (Table 1).

Longitudinal analysis reveals significant metabolic and nutritional alterations over the six-year interval. Marked deficiencies developed in iron metabolism and hematopoietic parameters, accompanied by paradoxical vitamin fluctuations (elevated folate with declining B12). While glycemic control demonstrated substantial improvement, persistent dysregulation was evident through continued hyperglycemic episodes. The metabolic profile shows partial correction of insulin resistance alongside emerging hypocalcemia. Notably, new microbiological findings were identified and hypothyroidism. These findings highlight progressive micronutrient depletion coexisting with partially resolved metabolic dysregulation, suggesting complex pathophysiology requiring multidimensional interpretation.

Discussion

Bariatric surgery has become an important treatment for obesity and T2DM. Significant neurological complications have been reported [6, 7], including postoperative complications range from common manifestations like peripheral neuropathy (60%) and encephalopathy (30%) to rare but severe conditions such as GBS [8–11]. The pathophysiology remains unclear but appears driven by nutrient deficiencies (particularly thiamine [B1] and cobalamin [B12]) that likely trigger immune dysfunction and demyelination [12, 13]. This case demonstrates the occurrence of acute GBS following RYGB. Although IVIG therapy led to initial improvement, the condition progressed into chronic GBS accompanied by refractory diarrhea, suggesting that this persistent diarrhea likely induced malabsorption of multiple nutrients [5, 14]. This highlights the critical need for postoperative surveillance of GBS following bariatric procedures, with particular attention to its potential association with altered immune homeostasis and gut microbiome dysbiosis. These findings hold significant implications for optimizing patient management through prophylactic micronutrient supplementation and structured neurological monitoring protocols in postoperative care [13].