A 20\'s primiparous woman, following spontaneous expulsion of intrauterine death of the fetus at 30 weeks of gestation, presented on post-partum day 8 with acute onset flaccid quadriparesis and breathing difficulty, which had rapidly progressed to involve the legs on day 3 up to her upper limbs on post-partum day 5. Following examination, Guillain Barre Syndrome (GBS) with ascending diaphragmatic involvement was diagnosed, and plasma exchange was initiated. She developed raised blood pressure, headache, sudden onset visual loss with 2 episodes of generalized seizures on post-partum day 14. Brain MRI and clinical suspicion helped diagnose Posterior Reversible Encephalopathy Syndrome (PRES). The patient was treated with anticonvulsants and antihypertensive agents. She regained her vision over the next two days, completed the treatment for GBS, and made a good recovery with independence for advanced activities of daily living on follow-up.

Acquired thrombotic thrombocytopenic purpura (TTP) is a rare life-threatening disorder characterized by microangiopathic hemolytic anemia, severe thrombocytopenia, and organ damage. We present the case of a 71-year-old man initially diagnosed with malaria-like symptoms and displaying markers of microangiopathic hemolytic anemia, severe thrombocytopenia, renal injury, and neurological impairment. Despite antimalarial treatment, acquired TTP was suspected. Plasma exchange and immunosuppressive therapy led to clinical improvement, normalizing the platelet count and hemolytic profile. Diagnostic confirmation revealed significantly reduced ADAMTS13 levels. Following the proposed treatment, the patient\'s ADAMTS13 levels normalized. This case illustrates acquired TTP linked to uncomplicated Plasmodium vivax malaria.

Dengue, caused by the dengue virus, presents with various clinical manifestations, including rare neurological complications. Guillain-Barre Syndrome (GBS), an immune-mediated polyradiculoneuropathy, is a rare complication, often triggered by antecedent infections. Herein, we report the case of a 30-year-old male presenting with GBS following dengue fever. His clinical course revealed classic GBS symptoms, including ascending weakness and bulbar involvement, with no noted infection that could plausibly explain a trigger for GBS. Diagnosis entailed cerebrospinal fluid analysis and nerve conduction studies which confirmed acute inflammatory demyelinating polyradiculoneuropathy. Treatment involved plasmapheresis, yielding a positive response. This case underscores the association between dengue and GBS, emphasizing the need for heightened clinical suspicion in endemic regions like Nepal.

UNASSIGNED: A patient with Sjögren\'s syndrome (SS), immune-mediated thrombotic thrombocytopenic purpura (ITTP), and posterior reversible encephalopathy syndrome (PRES) was reported, and all published cases with thrombotic thrombocytopenic purpura (TTP), PRES, and SS were retrieved and analysed. The patient\'s clinical data and treatment procedure have been discussed.
UNASSIGNED: A 45-year-old Chinese female was hospitalized with headache and low platelet count. She had previously presented to a local hospital with a 7-month history of epigastric discomfort and anorexia, and was diagnosed with SS and ITTP. Laboratory investigations after admission showed platelet (PLT) of 13*10^9/L, red blood cell (RBC) fragments of 6 %, ADAMTS13 Activity＜0.2 %, anti-ADAMTS13 IgG of 88.3U/mL. Brain magnetic resonance imaging (MRI) showed gyriform restricted diffusion along with increased T2-FLAIR signal in the left frontal cortex and bilateral parietal temporal cortex. She was diagnosed with SS, ITTP and PRES, and received the treatment of methylprednisolone, cyclosporine, plasma exchange, IVIG, and rituximab. This patient did not experience the recurrence during the 8-month follow-up period.
UNASSIGNED: ITTP and PRES are rare manifestations of SS. After a suspected or confirmed diagnosis of ITTP, plasma exchange and immunosuppressive therapy should be immediately administered. We suggest that rituximab could have additional therapeutic value for SS combined with ITTP and PRES.

Therapeutic plasma exchange (TPE) is used as an effective treatment modality for a variety of autoimmune disorders. Apart from its desired effect of removing pathological blood components, it also can remove coagulation factors and drugs. Currently, there is an insufficient amount of information regarding the use of direct oral anticoagulants in this setting. In this article, we present a case report of a patient with myasthenia gravis and chronic anticoagulation with apixaban who underwent a series of TPE while continuing apixaban treatment. We observed that only 10% of daily dose was removed by the procedure and plasma levels of apixaban corresponded with expected range. TPE was not associated with shortened drug plasma half-life. We did not observe any significant alteration of apixaban pharmacokinetics during the period of TPE therapy, as well as no thrombotic or bleeding events. This case report supports the use of apixaban in patients treated by TPE, nevertheless, to firmly establish apixaban efficacy and safety profile in this clinical setting further research is needed.

BACKGROUND: Acute cerebellitis is a rare complication of pediatric infections. There are many reports that viral infections lead to neurological manifestations, including acute cerebellitis.
METHODS: A retrospective chart review was conducted for pediatric patients diagnosed with enterovirus cerebellitis between 2000 and 2024. The methods involved reviewing clinical and radiological records and assessing the treatment methods.
RESULTS: Case Report We present the case of a 4-year-old immunocompetent child who initially presented with acute encephalopathy followed by truncal ataxia, and eventually received a diagnosis of postinfectious cerebellitis. Enterovirus real-time polymerase chain reaction were positive in the nasopharyngeal swab. Therapeutic plasma exchange (TPE) was started due to neurological deterioration despite IVIG treatment. She improved significantly with TPE, and methylprednisolone treatment and was discharged in good health status. The patient is being followed up as neurologically normal.
CONCLUSIONS: Acute cerebellitis associated with enterovirus is a rare pediatric disorder. Early diagnosis and treatment with TPE in this severe case is thought to be preventive for the potentially fatal complications.

Neuromyelitis optica spectrum disorders (NMOSD) is one of autoimmune inflammatory diseases and is characterized by area postrema syndrome, brainstem syndrome, optic neuritis, and/or myelitis. Typical myelitis is longitudinally extended transverse myelitis (LETM) which extends over three vertebral bodies. Several previous case reports have suggested association between cancer and NMOSD. A 50-year-old woman had breast cancer and underwent mastectomy and, 10 months later, she had developed acutely progressive dysbasia. Spine MRI showed LETM in 13 vertebrae length and blood test revealed positive anti-aquaporin 4 (anti-AQP4) antibody based on enzyme-linked immunosorbent assay with index of over 40. She was treated by intravenous methylprednisolone, plasma exchange, and intravenous immunoglobulin, followed by oral prednisolone. The condition had mostly recovered after the treatment. A small population of NMOSD has the aspect of paraneoplastic neurological syndrome. The age of onset in patients with cancer-associated NMOSD tends to be higher than that in individuals with NMOSD due to any causes of NMOSD.

BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) involves autoimmune and inflammatory responses in the central nervous system, primarily affecting the optic nerves and spinal cord. Atypical presentations such as ataxia and syncope complicate the diagnosis, and lesions in the medulla are easily mistaken for cerebral infarction. This case report emphasizes the need to recognize such manifestations to avoid misdiagnosis and ensure timely treatment.
METHODS: This case report presents an NMOSD female patient who experienced ataxia, syncope, and neuropathic pain during her illness.
METHODS: NMOSD.
METHODS: The patient managed her blood sugar with insulin, controlled neuropathic pain with pregabalin, and underwent 5 plasma exchanges.
RESULTS: Significant improvement was noted 1 week post-plasma exchange, with complete resolution of neuropathic pain and no symptom recurrence reported at 6-month follow-up.
CONCLUSIONS: Atypical manifestations of NMOSD, such as ataxia, syncope, and trigeminal neuralgia, increase diagnostic difficulty. Recognizing these symptoms is crucial to avoid misdiagnosis and ensure timely and appropriate treatment for patients.

BACKGROUND: Thrombotic microangiopathy is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ injury. The pathological features include vascular damage that is manifested by arteriolar and capillary thrombosis with characteristic abnormalities in the endothelium and vessel wall. Thrombocytopenia is one of the common adverse effects of interferon therapy. However, a more serious but rare side effect is thrombotic microangiopathy.
METHODS: We report the case of a 36-year-old Asian male patient with clinical manifestations of hypertension, blurred vision, acute renal failure, thrombocytopenia, and thrombotic microangiopathy. Renal biopsy showed interstitial edema with fibrosis, arteriolar thickening with vitreous changes, and epithelial podocytes segmental fusion. Immunofluorescence microscopy showed C3(+), Ig A(+) deposition in the mesangial region, which was pathologically consistent with thrombotic microangiopathy renal injury and Ig A deposition. The patient had a history of hepatitis B virus infection for more than 5 years. Lamivudine was used in the past, but the injection of long-acting interferon combined with tenofovir alafenamide fumarate was used since 2018. The comprehensive clinical investigation and laboratory examination diagnosed the condition as thrombotic microangiopathy kidney injury caused by interferon. After stopping interferon in his treatment, the patient\'s renal function partially recovered after three consecutive therapeutic plasma exchange treatments and follow-up treatment without immunosuppressant. The renal function of the patient remained stable.
CONCLUSIONS: This report indicates that interferon can induce thrombotic microangiopathy with acute renal injury, which can progress to chronic renal insufficiency.

A 75-year-old man with blurred vision and nasal bleeding was diagnosed with hyperviscosity syndrome and central retinal vein occlusion secondary to Waldenström macroglobulinemia. Serum total protein and IgM levels were undetectable. Because of the severe symptoms, we determined that immediate plasma-exchange treatment was required to decrease the blood viscosity. The initial plasma exchange was performed using the membrane isolation method with a predilution standby. A saline predilution replacement was prepared to decrease the total membrane pressure (TMP); however, the predilution protocol was not used because the planned treatment volume could be achieved without increasing the TMP. After two consecutive days of membrane plasma exchange, all serum biochemical tests were measurable, and IgM was below 4000 mg/dL. After chemotherapy, his visual symptoms improved, and he was discharged. Since it is difficult to assess the risk of elevated TMP prior to initial plasma exchange, membrane plasma exchange with a predilution standby may be a useful strategy for initial plasma exchange for hyperviscosity syndrome in terms of safety and efficiency.