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Onset of Marine-Lenhart syndrome and Graves' ophthalmopathy in a female patient treated with alemtuzumab for multiple sclerosis.
Le Moli, R, Russo, M, Malandrino, P, Vella, V, Belfiore, A, Frasca, F
Hormones (Athens, Greece). 2021;(1):161-165
Abstract
BACKGROUND Immune checkpoint blockade therapy may lead to thyroid dysfunction in 3-7% of treated patients. Alemtuzumab is a CD52 inhibitor leading to thyroid dysfunction in approximately 40% of patients. A female patient was affected by multiple sclerosis (MS) and subclinical hyperthyroidism due to an autonomously functioning thyroid nodule (AFTN). After alemtuzumab treatment, she developed aggressive clinical hyperthyroidism consistent with Marine-Lenhart syndrome. CASE PRESENTATION A 36-year-old woman presented in July 2019 with symptoms of hyperthyroidism and eye complaints. Three years earlier, she was diagnosed with MS. Subclinical hyperthyroidism was diagnosed in April 2017. Thyroid scintigraphy showed an intranodular distribution of 99mTc-pertechnatate consisting of an AFTN in the right lobe of the thyroid. In June 2018, because of the MS, she was treated with alemtuzumab. In November 2018, she was started on methimazole treatment because of the symptoms of hyperthyroidism. In December 2018, thyroid function was normal under methimazole treatment. In June 2019, the patient received a second round of alemtuzumab administration. One month later, she developed symptoms of hyperthyroidism. These symptoms were accompanied by diplopia. Blood tests showed severe hyperthyroidism. Thyroid scintigraphy showed a diffuse distribution of 99mTc-pertechnatate and the presence of a "cool" area in the right lobe of the thyroid, confirmed by ultrasonography. The nodule was diagnosed as a low-risk indeterminate lesion. CONCLUSION We present a case of Graves' disease with active, moderate-to-severe Graves' ophthalmopathy in a patient with pre-existing AFTN presenting with a coexisting, rare case of Marine-Lenhart syndrome associated with immune reconstitution after alemtuzumab treatment.
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A team approach to supporting the nutritional needs of patients living with multiple sclerosis.
Bell, N, Brammer, L
British journal of community nursing. 2017;(3):124-128
Abstract
Multiple sclerosis is the most common cause of non-traumatic disability in young adults, with most diagnoses occurring between the ages of 25-49 years. Nutrition must be managed effectively and holistically to improve health and quality of life. Dysphagia management is collaborative and can enhance nutrition and hydration goals as well as reduce the risk of aspiration pneumonia. A case study demonstrates the specialist clinical skills and frameworks used to achieve nutrition, hydration, safety and patient focused outcomes.
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Retinopathy during interferon-β treatment for multiple sclerosis: case report and review of the literature.
Gaetani, L, Menduno, PS, Cometa, F, Di Gregorio, M, Sarchielli, P, Cagini, C, Calabresi, P, Di Filippo, M
Journal of neurology. 2016;(3):422-7
Abstract
The onset of new visual symptoms in patients with multiple sclerosis is often associated with a neuro-ophthalmologic manifestation of the disease. However, other possible differential diagnoses need to be ruled out, including drug-induced retinal side effects. Although uncommon, retinal side effects of interferon-beta formulations may occur, and need to be promptly recognized and treated by neurologists. In this manuscript, we report the case of a 37-year-old woman affected by multiple sclerosis diagnosed with interferon beta-associated retinopathy and we review the literature with regard to the epidemiology, clinical presentation, management and follow-up of interferon beta-associated retinopathy. Interferon-beta induced retinopathy seems to be an uncommon and a dose-related side effect in multiple sclerosis patients. Retinopathy tends to completely resolve after treatment discontinuation. Neurologists must be aware that immune-modulatory drugs, in particular interferon beta, have been reported to cause retinal side effects. In multiple sclerosis patients complaining of new visual symptoms during interferon-beta treatment, it is thus advisable to perform an ophthalmological assessment to rule out and properly manage retinopathy.
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Autoimmune encephalitis in humans: how closely does it reflect multiple sclerosis ?
Höftberger, R, Leisser, M, Bauer, J, Lassmann, H
Acta neuropathologica communications. 2015;:80
Abstract
INTRODUCTION Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Immunological studies suggest that it is a T-cell mediated autoimmune disease, although an MS-specific target antigen for autoimmunity has so far not been identified. Models of experimental autoimmune encephalomyelitis in part reproduce features of MS, but none of the models so far covers the entire spectrum of pathology and immunology. Autoimmune disease of the nervous system has occasionally been observed in humans after active sensitization with brain tissue or brain cells, giving rise to acute demyelinating polyradiculoneuritis, acute disseminated encephalomyelitis and in rare cases reflecting an inflammatory demyelinating condition similar to acute multiple sclerosis. In this study we analyzed in detail the immunopathology in archival autopsy tissue of a patient who died with an MS like disease after repeated exposure to subcutaneous injections of lyophilized brain cells. RESULTS The pathology of this patient fulfilled all pathological diagnostic criteria of MS. Demyelination and tissue injury was associated with antibody (IgM) deposition at active lesion sites and complement activation. Major differences to classical EAE models were seen in the composition of inflammatory infiltrates, being dominated by B-cells, infiltration of IgM positive plasma cells, profound infiltration of the tissue by CD8(+) T-lymphocytes and a nearly complete absence of CD4(+) T-cells. CONCLUSIONS Our study shows that auto-sensitization of humans with brain tissue can induce a disease, which closely reflects the pathology of MS, but that the mechanisms leading to demyelination and tissue injury differ from those, generally implicated in the pathophysiology of MS through studies in experimental autoimmune encephalomyelitis.
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[Allergic skin rashes by methylprednisolone in a case with multiple sclerosis].
Kuga, A, Futamura, N, Funakawa, I, Jinnai, K
Rinsho shinkeigaku = Clinical neurology. 2004;(10):691-4
Abstract
We reported a 34-year-old woman with multiple sclerosis showing an allergic reaction to methylprednisolone sodium succinate. She was admitted to our hospital with a complaint of hypesthesia in the right side of the face and body. MRI showed several high signal intensity lesions in her brain with Gd-DTPA enhancement effect. She was diagnosed as having an acute relapse of MS from previous episodes and clinical findings. We started a methylprednisolone pulse therapy. After the injection on the first day, skin rashes appeared on her trunk and thigh. On the second day, the skin rashes spread over her whole body. Patch test for methylprednisolone sodium succinate (MP) was positive. The steroid administration was substituted by intravenous injections of betamethasone 100mg/day for three days. Her neurological and radiological findings were successfully disappeared without any side effects. This case indicates the efficacy of substitution therapy of betamethasone for MP.