This case was reported in a literature article and described the occurrence of immune-mediated necrotizing myopathy in a 28-year-old female patient who received annual influenza vaccine for prophylaxis. On an unknown date, the patient received annual influenza vaccine unspecified season at an unknown dose. On an unknown date, less than a month after receiving annual influenza vaccine unspecified season, the patient experienced immune-mediated necrotizing myopathy (serious criteria hospitalization and GSK medically significant), muscle weakness (serious criteria hospitalization), tenderness muscle (serious criteria hospitalization), absent reflex (serious criteria hospitalization), dyspnea (serious criteria hospitalization), dysphagia (serious criteria hospitalization), weight loss (serious criteria hospitalization), hypophonia (serious criteria hospitalization), fatigue (serious criteria hospitalization), acute motor axonal neuropathy (serious criteria hospitalization and GSK medically significant), sinus tachycardia (serious criteria hospitalization), muscle atrophy (serious criteria hospitalization), facial weakness (serious criteria hospitalization), muscle edema (serious criteria hospitalization), phagocytosis (serious criteria hospitalization), Schwannoma benign (serious criteria hospitalization), respiratory failure (serious criteria hospitalization and GSK medically significant), inflammation (serious criteria hospitalization), general physical health deterioration (serious criteria hospitalization), unwell (serious criteria hospitalization), mobility decreased (serious criteria hospitalization) and dropped head syndrome (serious criteria hospitalization). The patient was treated with prednisone, Immunoglobulin, SOLU-MEDROL and rituximab. On an unknown date, the outcome of the immune-mediated necrotizing myopathy, muscle weakness, tenderness muscle, absent reflex, dyspnea, dysphagia, weight loss, hypophonia, fatigue, acute motor axonal neuropathy, sinus tachycardia, muscle atrophy, facial weakness, muscle edema, phagocytosis, Schwannoma benign, respiratory failure, inflammation, general physical health deterioration, unwell, mobility decreased and dropped head syndrome were unknown. The reporter considered the immune-mediated necrotizing myopathy, muscle weakness, tenderness muscle, absent reflex, dyspnea, dysphagia, weight loss, hypophonia, fatigue, acute motor axonal neuropathy, sinus tachycardia, muscle atrophy, facial weakness, muscle edema, phagocytosis, Schwannoma benign, respiratory failure, inflammation, general physical health deterioration, unwell, mobility decreased and dropped head syndrome to be possibly related to annual influenza vaccine unspecified season. Additional information was provided. This case was reported in a literature article and described the occurrence of anti-single recognition particle-mediated necrotizing myopathy in a 28-year old female who was vaccinated with unspecified annual influenza vaccine (manufacturer unknown) for prophylaxis. The patient was previously healthy woman. The patient had no family history of neuromuscular disorders. The patient had no exposure to cholesterol-lowering agents, including statins, herbal medication, or recreational drugs. No information on patient's concurrent condition or concomitant medication was provided. On an unspecified date, the patient received unspecified annual influenza vaccine (administration site and route unspecified; dosages unknown; batch number not provided). The age of vaccination was not provided. On an unspecified date, within 2 weeks after vaccination, the patient developed muscle weakness which started in the calves and thighs and spread rostrally to the trunk and arms over the course of 3 weeks. At 5 weeks after vaccination, the patient presented to a local community hospital with profound muscle weakness. The patient could not lift her arms or legs. There was mild muscle tenderness. The patient denied any fever, chills, skin rashes, or other complications after the vaccination. The patient's denied of any visual disturbance, ptosis, dysarthria, dysphagia, or cognitive impairment. On physical examination, the patient's vital signs were stable. The patient's neurological examination showed marked proximal weakness in the upper and lower extremities: strength of 4/5 in the medical research council (MRC) scale in neck flexion, mild bifacial weakness, 3/5 in proximal upper and lower extremities but 5/5 in the hands and feet. Reflexes were absent in the upper extremities and 1+ in the lower extremities. The patient initial creatine kinase (CK) level was 16,095 U/L, which remained elevated despite hydration, initiated for presumed rhabdomyolysis. The patient first muscle biopsy was reportedly inconclusive. The patient was briefly treated with 40-mg daily prednisone without response. The patient's condition continued to worsen. 1 month later, the patient was presented with a significant head drop, dyspnoea, dysphagia, 20-pound weight loss, hypophonia, and fatigue. The patient's motor examination showed (in MRC): deltoid 1/5, biceps 3/5, triceps 2/5, wrist flexion 4/5, wrist extension 4-5 abductor policies brevis 4/5, first dorsal interosseous 4/5, iliopsoas 1/5, quadriceps 3/5, hamstring 3/5, ankle dorsiflexion, and plantar flexion 4/5 bilaterally. The patient's sensory examination was normal but deep tendon reflexes were globally absent. Spinal tap was performed, and patient's cerebral spinal fluid revealed elevated total protein 99 mg/dL with normal cell count and glucose. The cause of the infection was excluded by negative cultures and polymerase chain reaction (PCR). The patient nerve conduction studies (NCSs) were abnormal, with decreased compound muscle action potential amplitudes, normal onset latencies, and normal conduction velocities in the left median and ulnar nerves. Subsequently the patient was hospitalised. At the hospital, the patient was diagnosed with acute motor axonal neuropathy, a variant of Guillain- Barre syndrome (GBS). Subsequently, the patient was treated with a 5-day course of intravenous immunoglobulin (IVIg) with minimal improvement. The patient was discharged to a long-term rehabilitation facility and required feeding tube insertion. The patient was continued to deteriorate and that raised the possibility of alternative disease beyond acute motor axonal neuropathy. The patient was referred to another institution for further evaluation and management. On admission, the patient was afebrile but seemed chronically ill. The patient's ophthalmic, cardiac, pulmonary, and abdominal examinations were unremarkable except for mild sinus tachycardia on electrocardiogram (ECG). The patient's neurologic examination was unchanged with continued muscle weakness especially of all muscle groups (proximal more than distal), diffuse muscle atrophy, severe facial and bulbar weakness, and head drop. Sensation was intact, but reflexes were globally absent. A second nerve conduction study (NCS) showed moderately reduced compound muscle action potential with normal latencies and conduction velocities. The patient's Sensory NCS was completely normal. Motor Nerve Conduction Studies were as follows: The amplitude of right median to abductor policies brevis (APB) of wrist was 0.8 mV and amplitude of right median to APB of elbow was 0.4 mV. The onset latency of right median to APB of wrist was 3.6 milliseconds and onset latency of right median to (APB) of elbow was 6.9 milliseconds. The conduction velocity of right median to APB of elbow was 55 m/s. The amplitude of right ulnar to abductor digiti minimi (ADM) of wrist was 1.7 mV and amplitude of right ulnar to ADM of below and above elbow was 1.6 and 1.5 mV respectively. The onset latency of right ulnar ADM of wrist was 2.3 milliseconds and onset latency of right ulnar to ADM of below and above elbow was 5.5 and 7 milliseconds respectively. The conduction velocity of right ulnar to ADM of below elbow was 56 m/s and above elbow was 67 m/s. The amplitude of right peroneal of extensor digitorum brevis (EDB) of ankle was 1.2 mV and amplitude of right peroneal to EDB of below fibula and lateral popliteal fossa was 1.3 and 1.5 mV respectively. The onset latency of right peroneal to EDB of ankle was 4.2 milliseconds and onset latency of right peroneal to EDB of below fibula and lateral popliteal fossa was 8.9 and 10.2 milliseconds respectively. The conduction velocity of right peroneal to EDB of below fibula was 51 m/s and lateral popliteal fossa was 77 m/s. The amplitude of left tibial to abductor hallucis brevis (AHB) of ankle was 2.8 mV and popliteal fossa was 2.5 mV. The onset latency of left tibial to AHB of ankle was 3.0 milliseconds and popliteal fossa was 9.8 milliseconds. The conduction velocity of left tibial to AHB of popliteal fossa was 37 m/s. Sensory Nerve Conduction Studies are as follows: the amplitude of (antidromic) of right median of wrist was 44.4 mV and palm was 55.4 mV. The onset latency of right median of wrist was 2.3 milliseconds and palm was 1.1 milliseconds. The conduction velocity of right median of wrist and palm was 61 m/s and 58 m/s respectively. The amplitude of right ulnar was 35.8 mV and for right sural was 26.4 mV. The onset latency of right ulnar was 2.2 milliseconds and for right sural was 1.6 milliseconds. The conductance velocity of right ulnar was 58 m/s and for right sural was 67 m/s. The F waves onset latency of right median (APB) was 24.25 milliseconds and F waves onset latency of left tibial (AHB) was 44.88 milliseconds. Electromyography showed abundant fibrillation potentials and positive sharp waves in all tested muscles, and diffuse myopathic units. The patient's creatine kinase level remained elevated at 11,699 U/L and troponin T was elevated at 3.6 ng/mL. Echocardiogram and cardiac magnetic resonance imaging (MRI) were unremarkable without signs of myocarditis or pericardial effusion. The patient's thigh MRI showed diffuse oedema on short T1 inversion recovery and T2 sequences. MRI imaging studies of the thigh muscles. Showed: Axial T1-weighted images (TR/TE: 489/7.32, 3-mm slice thickness) showing normal appearance of left thigh muscle without atrophy. Coronal STIR (TR/TE: 3475/41.52) and axial fat-suppressed T2 weighted images (TR/TE: 2390/82.94) demonstrating marked hyperintense signal in the anterior and posterior compartments of both thighs indicating muscle oedema. The patient's second muscle biopsy was performed from the left rectus femoris muscle and that showed discrete necrotic fibres with phagocytosis and concurrent regenerating fibres. Lymphocytic inflammatory cell infiltration was absent. There was no evidence of perifascicular atrophy or increased endomysial fibrosis. These pathological features were consistent with immune-mediated necrotizing myopathy (IMNM) with minimal inflammation. Histopathological findings of necrotizing myopathy in the left rectus femoris muscle biopsy showed: Hemotoxylin and eosin-stained frozen sections (3200) showing increase in fibre size variability and numerous necrotic fibres undergoing phagocytosis. Also, regenerating fibres including regenerating basophilic cuffs. Alkaline phosphatase (350) highlighting regenerating fibres involving both the perimysium and endomysium. Immunohistochemical stain for CD68 (3100) illustrating several necrotic myofibers infiltrated by CD68(+) macrophages. Extensive rheumatologic workup showed normal complements C3, C4, and all but one of the myositis-specific antibodies (Jo-1, PL-7, PL-12, Mi-2, Ku, EJ, and OJ) returned negative, including SS-A, SS-B, deoxyribonucleic acid (DNA), ribonucleoprotein (RNP), Smith, antinuclear antibodies (ANA), and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR). The anti-single recognition particle (anti-SRP) antibody returned moderately positive. The patient's chest and abdominal computed tomography scans were performed to exclude occult malignancy, a retroperitoneal mass was found. The mass was surgically resected and confirmed to be a benign Schwannoma. After admission, the patient was started on intravenous SOLU-MEDROL (1 g daily for 5 days). Despite this, the patient developed respiratory failure, which required intubation. IVIg at a dose of 2g/kg divided over 5 days was initiated. The patient did not improve and after 1-week rituximab 375 mg/m2 weekly was added to regimen. Using this combination of IVIg and rituximab, the patient slowly demonstrated clinical improvement and down trending of serial CK levels, from 11,700 to 960 U/L after 5 weeks. The patient strength lagged in improvement compared with laboratory studies and patient's eventually required tracheotomy. The monthly IVIg was continued along with Rituximab every 6 months and patient's steroid was gradually tapered off while in a rehabilitation facility. At past outpatient visit, 15 months after initial presentation, the patient's feeding tube and tracheotomy were removed. The patient could ambulate without assistance but still had difficulty climbing up stairs. The patient past CK level was 289 U/L. Motor examination showed significant improvement with mild proximal weakness 4-4+/5 in MRC score in the deltoid, biceps, iliopsoas, and hamstring muscles. This case has been considered as serious due to hospitalisation. The author stated "What triggered the anti-SRP myopathy in this previously healthy young woman is unclear. The onset of her symptoms within 2 weeks after receiving influenza vaccination suggests the possible association to the vaccination". The authors concluded "We here reported a case of a 28-year-old previously healthy woman who presented with features of acute motor axonal neuropathy 2 weeks after receiving an annual influenza vaccination, which worsened despite IVIg therapy. Her diagnosis of IMNM was supported by elevated CK, necrotic myofibers with minimal inflammation on muscle disease, and positive anti-SRP serology. IVIg and rituximab may be a useful treatment modality for anti-SRP myositis, a well-known form of myopathy that is resistant to steroid and other standard of care modalities". Lab Comments: Lab tests were performed on unspecified dates. CSF: Negative cultures and PCR. Nerve conduction study (NCS) 1: decreased muscle action potential amplitudes, normal onset latencies and normal conduction velocities, left median and ulnar nerves. NCS 2: moderately reduced compound muscle action potential with normal latencies and conduction velocities. Sensory NCS were normal. Electromyography (EMG)  abundant fibrillation potentials and positive sharp waves in all tested muscles and diffuse myopathic units. Echocardiogram and cardiac magnetic resonance imaging (MRI): unremarkable without signs of myocarditis or pericardial effusion. Thigh MRI: diffuse oedema on short T1 inversion recovery and T2 sequences. Second muscle biopsy, left rectus femoris muscle: discrete necrotic fibres with phagocytosis and concurrent regenerating fibres. Lymphocytic inflammatory cell infiltration was absent. No evidence of perifascicular atrophy or increased endomysial fibrosis. These pathological features were consistent with immune-mediated necrotizing myopathy (IMNM) with minimal inflammation. Rheumatologic workup: normal complements C3, C4, and all but one of the myositis-specific antibodies (Jo-1, PL-7, PL-12, Mi-2, Ku, EJ, and OJ) were negative, including SS-A, SS-B, deoxyribonucleic acid (DNA), ribonucleoprotein (RNP), Smith, antinuclear antibodies (ANA), and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR). The anti-single recognition particle (anti-SRP) antibody was moderately positive. Chest and abdominal computed tomography scans: retroperitoneal mass.