Case Presentation: Patient is a 57-year-old female with past medical history significant for alcohol use disorder who presented to an outside facility with one month history of bilateral lower extremity (BLE) weakness associated with nausea, vomiting, diarrhea, and weight loss. CT abdomen pelvis showed evidence of diverticulitis. She was treated with antibiotics and discharged. Patient was readmitted for continued vomiting and diarrhea. Gastrointestinal (GI) work up, including infectious and inflammatory panels, was unremarkable. Neurology was consulted as her weakness progressed. Her presentation of diarrhea, ascending weakness, and sensory deficits raised concern for Guillain-Barré syndrome (GBS). She was given intravenous immunoglobulin (IVIG) over two days. Cerebrospinal fluid showed albuminocytological dissociation. Electromyography (EMG) and nerve conduction study (NCS) showed severe axonal sensorimotor polyneuropathy with moderate to severe neuropathic recruitment without active denervation potentials. Both findings were consistent with possible GBS. Her symptoms improved, and she was discharged to a rehabilitation facility with close follow up with neurology. Patient returned to the hospital two weeks later with worsening weakness. Labs from her prior admission were positive for SSA and ANA that raised concern for a rare presentation of Sjogren’s Syndrome. Although she did not have other autoimmune symptoms and did not meet diagnostic criteria per rheumatology, patient was transferred to our facility for salivary gland biopsy and Schirmer’s test. Schirmer’s test showed moderate left eye dryness. Salivary gland biopsy did not show evidence of Sjogren’s syndrome. Patient underwent extensive work up per neurology recommendations, such as micronutrient levels, heavy metals screening, and paraneoplastic panel, and was found to have multiple nutrient deficiencies such as vitamins B1, D, folate, copper and zinc. Thiamine, vitamin D, folate, copper, and zinc were repleted. Repeat EMG/NCS had shown severe sensory predominant length dependent axonal peripheral polyneuropathy with superimposed myosin myopathy. Considering her presentation, history of alcohol use disorder, micronutrient deficiencies, and EMG/NCS results, patient was diagnosed to have acute nutritional axonal neuropathy (ANAN).
Discussion: ANAN is a condition caused by micronutrient deficiencies, such as vitamins B1 and B61. Risk factors include “alcohol use disorder, bariatric surgery, and anorexia”1. In this case, the patient’s initial presentation raised suspicion of GBS that delayed the actual diagnosis until patient developed further progression of her neurological symptoms causing significant disability. Literature shows similar reports where patients with ANAN were initially thought to have GBS and treated with IVIG1. In our case, IVIG seemed to help temporarily, but confounded the real clinical picture causing delayed diagnosis. Our patient was noted to have significant copper deficiency along with other micronutrient deficiencies. Copper deficiency, although rare in the general population3, has been reported to cause axonal length dependent sensory predominant peripheral neuropathy2 .
Conclusions: ANAN is a condition whose prognosis is guarded and depends on early recognition and treatment. This case emphasizes the importance of exploring all differential diagnoses, including micronutrient deficiencies in the setting of polyneuropathy.