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• W4313236997 abstract "A 28-year-old African American man with a history of Budd-Chiari syndrome status post–orthotopic liver transplantation presented with recurrent fevers and aseptic meningitis. Eight months prior to presentation at our hospital, the patient developed symptoms of headache and focal weakness of the right arm and right leg. Magnetic resonance imaging (MRI) of the brain revealed abnormal T2-weighted and fluid-attenuated inversion recovery (FLAIR) signals within the left paramedian midbrain. Lumbar puncture showed lymphocytic pleocytosis and elevated protein levels. Extensive infectious evaluation detailed below was negative. Home medications at that time included prednisone 5 mg daily and tacrolimus (for transplant immunosuppression). He was diagnosed as having central pontine myelinolysis likely secondary to tacrolimus. Tacrolimus was discontinued and changed to cyclosporine. Three months thereafter, he presented with headache, ptosis, anisocoria, and high fevers. MRI showed an abnormal T2 and FLAIR signal within the left paramedian midbrain with associated abnormal enhancement extending along the left cranial nerve III. Lumbar puncture revealed neutrophilic predominance with elevated protein levels. During hospitalization, he developed a papular rash over his chest. A shave biopsy was obtained, which was consistent with pustular folliculitis. The most likely etiology was believed to be bacterial, though cultures were negative. He also had negative syphilis, tuberculosis (TB), herpes simplex virus (HSV), and HIV tests. The patient was empirically treated with antibiotics with a delayed resolution of the rash. Two months later, he presented with headache, fevers, nausea, vomiting, and leukocytosis. Lumbar puncture showed neutrophilic predominance and elevated protein levels. Infectious evaluation was again negative, though the patient received treatment with multiple antibiotics and antiviral therapy. Stress-dose hydrocortisone was administered following clinical deterioration, and cyclosporine was withheld due to concerns of toxicity. The patient was started on mycophenolate mofetil (MMF) and sirolimus with subsequent gradual clinical and MRI improvements. Two months thereafter, the patient was admitted to the hospital after 3 days of worsening headache, nausea, vomiting, photophobia, tachycardia, and high fevers. Admission laboratory testing was notable for leukocytosis. Lumbar puncture revealed neutrophil predominance, with elevated protein levels and normal glucose levels. MRI of the brain was notable for abnormal/increased signaling throughout the pons. The patient again received treatment with broad-spectrum antibiotics and antiviral therapies along with stress-dose hydrocortisone due to his history of adrenal insufficiency. The Infectious Disease department was consulted, who noted the presence of oral ulcerations. The patient noted that he had recurrent aphthous ulcerations over the preceding past 5 years. A slit-lamp examination was performed at this time and did not show any evidence of an inflammatory eye disorder. The patient continued to have cranial nerve III palsy. Rheumatology was consulted for evaluation of his recurrent aseptic meningitis, oral ulcers, and inflammatory-appearing central nervous system (CNS) lesions. The patient had a history of Budd-Chiari syndrome diagnosed 3 years prior to presentation following subacute presentation of weight loss, fatigue, and abdominal bloating. Evaluation revealed extensive thrombosis of the inferior vena cava (IVC) and right atrium for which he was started on anticoagulation. Extensive testing for hypercoagulable disorders, including antiphospholipid syndrome (APS) was negative. He had a rapid progression to acute liver failure, and he underwent liver transplantation with a complicated postoperative course including recurrent pneumothorax, thoracic wall metastatic methicillin sensitive Staphylococcus aureus abscess, adrenal insufficiency, and recurrent bleeding issues requiring exploratory laparotomy. The patient had no history of tobacco, alcohol, or illicit drug use, as well as no recent travel or contact with other people who were sick. He was not sexually active. He had no known family history of autoimmune, autoinflammatory, or neuromuscular disease. Additional symptoms included chronic headaches (including intermittently between neurologic flares), lethargy, and occasional nonspecific abdominal pain. He endorsed some blurry vision. The review of systems was negative for frank eye pain or redness. Notably he reported no history of genital ulcerations, malar rash, photosensitive rashes, sinus pressure, dry eyes, dry mouth, alopecia, dyspnea at rest or with exertion, hemoptysis, cough, chest pain, melena, hematochezia, diarrhea, dysuria, hematuria, joint pain, joint swelling, Raynaud's phenomenon, paresthesias, or focal weakness. Vital signs included a temperature of 101.8°F, heart rate of 103 beats per minute, blood pressure of 108/68 mm Hg, respiratory rate of 22 breaths per minute, and room air oxygen saturation of 99%. His oral examination revealed a buccal aphthous ulcer; palpation of the ulcer did not cause pain. General dental hygiene was fair with a few cavities. There was no parotid gland hypertrophy, and salivary pooling was normal. His examination was also notable for acneiform lesions on his face and healed hyperpigmented lesions over his bilateral lower extremities. He had no conjunctival injection. His lungs had diminished breath sounds. The patient had a normal and regular heart rate and rhythm. No abnormal heart sounds, murmurs, or rubs were noted. Distal pulses were normal. The abdomen was soft and nontender, and no organomegaly was noted. He had multiple well-healed scars on his abdomen. He had no palpable nodes in the cervical, supraclavicular, axillary, or inguinal areas. No scrotal ulcerations were noted. There was one small 1-cm circumferential, shallow ulceration noted at the glans of the penis. Musculoskeletal examination revealed normal spinal curvatures, and no deformities of the joints were noted. The patient had a complete range of motion of his joints with no evidence of synovitis. The neurologic examination revealed subtle left eyelid ptosis, left superior rectus palsy, subtle left lower facial weakness, left- greater than right-beating nystagmus on sustained gaze, mild bilateral ataxia on finger-to-nose test, significant ataxia on heel-to-shin test, and mild bilateral dysdiadokinesia. The patient had weakness of the left upper extremity (4/5 strength). The rest of his motor examination was normal. Generalized hyperreflexia was noted. Sensory examination was intact to light touch bilaterally without extinction. Admission laboratory work was notable for neutrophilic leukocytosis (Table 1). Lumbar puncture revealed 354 nucleated cells with 93% polymorphonuclear cell (PMNs), elevated protein levels, and normal glucose levels (Table 2). Infectious evaluation including bacterial, fungal, and viral etiologies were negative, including syphilis, TB, HSV, and HIV. Testing for antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), and HLA–B51 was negative. Chest radiography was normal without evidence of hilar adenopathy or parenchymal infiltration. Axial T2/FLAIR MRI sequencing of the brain (Figure 1) was notable for abnormal/increased signal throughout the pons, especially the right pons. Sagittal T1-weighted MRI sequencing of the brain (Figure 2) was notable for areas of hypointensitiy, suggestive of lesions in the pons. MRI of the abdomen (axial T1-weighted postcontrast portal venous phase) (Figure 3) was notable for abnormal liver parenchymal enhancement with early enhancement of the caudate lobe and central liver. There was delayed enhancement of the periphery, with a near complete occlusive thrombus of the intrahepatic IVC. These findings are consistent with Budd-Chiari syndrome. In summary, our patient is a young African American man with a history of Budd-Chari status post–orthotopic liver transplantation receiving immunosuppression treatment with a regimen including tacrolimus (and later cyclosporine) who had recurrent episodes of fever, oral/genital ulcerations, biopsy-proven pustular folliculitis, and aseptic meningitis with brainstem parenchymal disease. Because this patient presented with neuroinflammatory lesions and a history of Budd-Chiari, we will focus on the intersection of these diagnoses. Budd-Chiari syndrome is hepatic venous outflow tract obstruction that can originate anywhere between the small hepatic veins, IVC, and right atrium, excluding obstruction due to cardiac disease, pericardial disease, or sinusoidal obstruction syndrome (venoocclusive disease) (1-3). The disorder can be termed “primary” due to reduced venous flow secondary to intrinsic venous disease (i.e., thrombosis or phlebitis) or “secondary” due to extrinsic compression or invasion of the hepatic veins or IVC (i.e., malignancy) (3). Because this patient had no evidence of extrinsic obstruction or malignancy, we will focus primarily on causes of primary Budd-Chiari syndrome. An underlying disorder can generally be identified in 75–80% of patients with primary Budd-Chiari syndrome (2-5). In general, the underlying disorder can be grouped into 1 of 4 different etiopathogenic classes of disease: 1) inherited thrombophilia, 2) acquired thrombophilia, 3) systemic inflammatory disease, or 4) hormonal factors (2-5). These are shown in the table below (Table 3). Because this patient underwent an extensive hypercoagulable evaluation at the time of Budd-Chiari presentation and had no evidence of underlying malignancy, acquired and inherited thrombophilias can be excluded. Next, we will focus on neuroinflammatory lesions in systemic inflammatory and autoimmune diseases. This patient previously underwent multiple, extensive searches for infectious etiologies due to recurrent febrile presentations and immunosuppressed status; however, no pathogenic organism could be identified. While there are a number of CNS-limited inflammatory diseases, we will focus on those associated with systemic disease, since this patient had fevers, mucocutaneous lesions, and a history of thrombosis/Budd-Chiari syndrome, all suggestive of a systemic inflammatory process. Several inflammatory rheumatic diseases have well-described CNS manifestations (6-9). These are shown in Table 4. Notably, this list intersects with the list of systemic and inflammatory diseases that are associated with Budd-Chiari syndrome. Our remaining discussion of the differential diagnosis focusses on those overlapping diagnoses while considering this patient's other manifestations. SLE is an autoimmune inflammatory disease known for its multiorgan and variable presentations. It can present with recurrent fevers, mucocutaneous lesions, neuropsychiatric symptoms, and even thrombosis (10-14). Presentation of neuropsychiatric lupus may occur in up to 40–50% of patients and can be variable ranging from personality and behavioral changes to psychosis, seizure, encephalopathy, or stroke (15, 16). Structural lesions can be identified on imaging and can manifest as demyelinating disease (with cerebral and cord lesions or pachymeningitis) or as a thrombotic presentation (with clinical or subclinical stroke). The thrombotic presentation of SLE is generally due to concurrent APS. Pathogenic antiphospholipid antibodies can be found in at least 20–30% of SLE. Fever was recently added to the clinical criteria for the diagnosis of lupus after 54% of patients reported this as a manifestation during the first year of disease, and fever was shown to occur more frequently in patients in an early-SLE cohort compared to non-SLE patients (10). Oral ulcers have long been a clinical criterion used for the classification of lupus, as they are common in SLE, with a prevalence of 51% in one large cohort study (11). SLE has 3 classic rashes (acute cutaneous lupus, subacute cutaneous lupus, and discoid lupus) and a number of other nonspecific cutaneous findings that could suggest the diagnosis of SLE. Despite the numerous cutaneous presentations, pustular folliculitis is not a rash associated with SLE (12). Importantly, this patient was ANA negative and thus should not be classified as having lupus according to the most recent American College of Rheumatology criteria (11). Primary SS is a systemic autoimmune disease characterized by hypofunction of salivary glands and possible systemic multi-organ disease (17). In primary SS, chronic inflammation of exocrine glands leads to a clinical picture dominated by mucosal dryness symptoms. While there are a number of peripheral and autonomic nervous system disorders associated with primary SS, we will focus on the CNS manifestations given this patient's presentation. Primary SS can have a variety of CNS manifestations, which can broadly be classified into focal or multifocal involvement and diffuse abnormalities. Focal or multifocal involvement includes multiple sclerosis–like syndromes, neuromyelitis optica spectrum disorders, amyotrophic lateral sclerosis–like syndromes, and stroke. Diffuse abnormalities can include cognitive dysfunction, dementia, psychiatric abnormalities, and aseptic meningoencephalitis (18). Patients with SS with neurologic manifestation usually have polymorphous (mixed) inflammatory exudates in cerebrospinal fluid (CSF), composed predominantly of lymphocytes, but including variable numbers of plasma cells, neutrophils, and erythrocytes. In addition, in a study by de la Monte et al, all 14 SS patients with neurologic manifestations in their CSF had large, atypical, morphologically distinct mononuclear cells, which were not found in our patient (19). Additionally this patient's SSA and SSB antibodies were negative, and he had no clear exocrine symptoms clinically, thus SS is less likely. Sarcoidosis can have a wide variety of multi-organ disease. Dermatologic manifestations in particular are clinically heterogenous but usually will suggest non-necrotizing granulomatous inflammation. A number of patients with sarcoidosis may present with neurologic manifestation at disease onset. Neurologic syndromes from sarcoidosis may include cranial mononeuropathy, encephalopathy, and aseptic meningitis. Serum angiotensin-converting enzyme testing only has modest sensitivity/specificity. Generally, 90% of patients with sarcoidosis have pulmonary involvement at time of diagnosis. Definitive diagnosis is based on findings of granulomas on biopsy (either at the site of the CNS or elsewhere) at time of syndrome presentation, which our patient did not have. The patient did not have any pulmonary involvement that would have been consistent with sarcoidosis. Lastly, the patient had pustular folliculitis and oral ulcerations that were otherwise unexplained by sarcoidosis (20). Granulomatosis with polyangiitis can have neurologic manifestations including mononeuritis multiplex, sensory neuropathy, cranial nerve abnormalities, and CNS mass lesions. Pachymeningitis (diffuse thickening of the dura mater) has also been described as a manifestation of AAV. The lack of sinusitis, pulmonary symptoms including pulmonary opacities, peripheral neuropathy, and renal involvement makes this diagnosis less likely (21). Moreover, he was ANCA negative, which also makes this diagnosis less likely. The patient also had no history of asthma or any documented eosinophilia to consider eosinophilic granulomatosis with polyangiitis, for which ANCA is less sensitive. Sweet syndrome is characterized by tender, edematous, and inflamed papules, plaques, and nodules that histologically consist of a dermal infiltrate of neutrophils with nuclear fragmentation. Sweet syndrome presents in 3 clinical settings: classic (or idiopathic), malignancy-associated, and drug-induced. Oral involvement is uncommon in classic Sweet syndrome. However, individuals with Sweet syndrome related to hematologic malignancies often develop oral ulcers, particularly on the buccal mucosa or tongue (22). CNS involvement in Sweet syndrome, neuro-Sweet syndrome, is rare but has been reported (23). Sweet syndrome can also cause fever and recurrent aseptic meningitis that can be PMN or lymphocyte predominant. Peripheral leukocytosis with neutrophilia is the most common laboratory abnormality in patients with Sweet syndrome. Nonspecific inflammation markers, such as erythrocyte sedimentation rate and C-reactive protein level, are also frequently elevated in patients with Sweet syndrome (24). While Sweet syndrome is certainly a consideration in this patient, it is a diagnosis of exclusion. Moreover, venous thromboses (such as Budd-Chiari syndrome) and oral ulcerations are less common in classic Sweet syndrome. This patient also lacked any definitive features suggestive of a hematologic malignancy. Familial autoinflammatory syndromes present with recurrent episodes of inflammation without evidence of infection or autoantibodies. These may be characterized by episodes of fever, rash, arthritis, peritonitis, and eye inflammation with elevations in acute-phase reactants that normalize between flares. Patients can also present with oral aphthous ulcers. Although it is definitely a consideration in this patient, autoinflammatory syndromes usually present very early in life, often in the first decade. Usually there is also a strong family history, whereas our patient did not have a known family history of autoinflammatory disease. It is also a diagnosis of exclusion. Moreover, venous thrombosis (such as Budd-Chiari syndrome) and genital ulcers are not common in classic autoinflammatory syndromes. CNS involvement in autoinflammatory syndromes is rare but has been reported (25). IBD is also an important consideration in cases of recurrent oral ulcerations. Uveitis, peripheral arthritis, and erythema nodosum are examples of extra-gastrointestinal manifestations that may be seen in IBD. These generally respond well to immunosuppressive therapy. This patient had nonspecific gastrointestinal symptoms such as nausea and abdominal pain. However, he did not have bloody stool or chronic diarrhea, which are more specifically associated with IBD. Moreover, venous thrombosis and Budd-Chiari syndrome are not specifically associated with IBD compared to other systemic autoimmune disorders. CNS involvement is also rare in IBD but has been reported (26). The patient had recurrent aphthous ulcers verified by history and examination; a shallow genital ulceration verified by examination; biopsy-proven, recurrent pustular folliculitis; and recurrent aseptic meningitis with brainstem parenchymal disease leading to a diagnosis of Behçet syndrome. His Budd-Chiari syndrome (hepatic vein thrombosis) was believed to also be attributable to Behçet syndrome. After the working diagnosis of Behçet syndrome in association with Budd-Chiari syndrome was made, treatment was initiated with glucocorticoids and infliximab (IFX). Dexamethasone (DEX) was selected as the steroid of choice given the neurologic involvement in this patient, and the dose was tapered from 4 mg of DEX down to a stable dose of 1 mg daily with the addition of IFX. It was difficult to obtain repetitive peripheral IV access for IFX infusions, and the patient did not desire a long-term central catheter; thus, it was elected to prescribe adalimumab (ADA) instead. His response to ADA was excellent, as it had been to IFX. In the background he received maintenance therapy with transplant immunosuppressive medications. Concerns were initially raised regarding the possibility of a flare in Behçet syndrome due to calcineurin inhibitors (especially cyclosporine). It was elected to prescribe tacrolimus instead of cyclosporine (with the goal of a lower trough than usual). MMF was up-titrated from the usual transplant dose of 500 mg twice daily to 1,000 mg twice daily. With this approach, the patient did very well. While he had a persistent cranial nerve III palsy, he had no further recurrent flares of fevers or aseptic meningitis. His oral ulcerations also dramatically decreased in terms of frequency. After more than a year of recurrent admissions for aseptic meningitis, the patient remained stable and admission-free from the hospital after the implementation of the therapies above. Behçet syndrome was initially described by Dr. Hulusi Behçet in 1937 who described the triad of oral aphthous ulcerations, genital ulcers, and relapsing uveitis (27). The diagnosis of Behçet syndrome is clinical, and no specific laboratory findings are included in the diagnostic criteria, making the diagnosis difficult (28). It can often take many years for the disease to be diagnosed, like in our case. The International Criteria for Behçet's Disease (ICBD) is the international criteria for diagnosis/classification of Behçet syndrome created in 2006. In this scoring system, ocular lesions or recurrent oral or genital aphthosis are 2 points. Skin, vascular, or CNS involvement is 1 point. Positive pathergy test is also 1 point. Three or more points are required to consider the patient as a case of Behçet syndrome (29). Our patient had recurrent oral and genital aphthosis with skin, vascular, and neurologic manifestations. He did not develop uveitis. Behçet syndrome can affect vessels of all sizes in the arterial and venous system (30). Vasculitis with thrombosis in large vessels is common, with lower extremity deep vein thrombosis being the most common form of Behçet syndrome vascular involvement. Venous disease in Behçet syndrome is believed to result from endothelial inflammation leading to thrombosis. Treatment involves control of systemic inflammation rather than anticoagulation. Immunosuppressants, with or without steroids, are used in the management of vascular involvement in Behçet syndrome. Several retrospective studies have shown prolonged survival and reduction in relapse rate with immunosuppressants and steroids. In resistant cases, anti–tumor necrosis factor agents can be used (31). Anticoagulation in the treatment of venous disease in Behçet syndrome has been debated. Studies have shown that anticoagulation could increase the risk of aneurysmal rupture. Budd-Chiari syndrome is a rare but severe venous form of Behçet syndrome that is caused by the obstruction of the venous outflow tract that transports blood from hepatic veins into the IVC (12). Most cases of Budd-Chiari syndrome are related to thrombosis resulting from one or several prothrombotic conditions; however, Behçet syndrome has been linked to Budd-Chiari syndrome. This condition is associated with a high risk of complications and death due to portal hypertension and liver failure (33). Nervous system involvement is seen in about 5–10% of all cases. Since the neurologic involvement in this syndrome is so heterogeneous, it is difficult to diagnose, predict its course, and treat, as in our patient's case. CNS involvement can primarily be categorized into cerebral venous sinus thrombosis compared to parenchymal disease. Isolated behavioral syndrome and peripheral neurologic involvement is rare in Behçet syndrome. CNS involvement is more commonly observed in men than women. Parenchymal disease can be acute or chronic progressive. Fever and high CSF counts are commonly found in acute disease. Both lymphocytic- and neutrophilic-dominant pleocytosis have been noted in the CSF. Parenchymal disease may involve periventricular white matter, the basal ganglia, or the brainstem. Brainstem involvement is uncommon with most other rheumatic disorders and multiple sclerosis and should thus raise suspicion for Behçet syndrome. Biopsy (if performed) often reveals neuronal necrosis, lymphocytic infiltration, and gliosis (34). Currently, treatment options for neuro-Behçet disease are based mostly on case reports and case series. Azathioprine, cyclophosphamide, interferon-α, and anti–tumor necrosis factor agents are often used for long-term preventive treatment. Cyclosporine and tacrolimus both share a common pathway for their immunosuppressive effects by inhibiting calcineurin. They are widely used in allograft rejection. There are some case reports of the effectiveness of tacrolimus for the treatment of uveitis in patients with Behçet syndrome. However, a large retrospective review demonstrated that cyclosporine carries a risk of neurologic manifestation flares in Behçet syndrome (35). In concordance, the 2018 update to the EULAR guidelines for the management of Behçet syndrome recommend avoiding cyclosporine for the treatment of Behçet syndrome (36). It is probable that the use of calcineurin inhibitors in our patient may have led to some of the neurologic manifestations of Behçet syndrome. Behçet syndrome. All authors were involved in drafting the article or revising it critically for important intellectual content, and all authors approved the final version to be published. Dr. KC had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. KC, Nandan, Ford, Desai. KC, Nandan, Ford, Desai. KC, Nandan, Ford, Desai. Disclosure Form Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article." @default.
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• W4313236997 title "Unfolding a Case of <scp>Budd‐Chiari</scp> Syndrome and Recurrent Aseptic Meningitis" @default.
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