Both of the presented patients had positive response to therapy after Rituximab injection as their MMSE increased remarkably. Also Rituximab has decreased FBDS episodes. Moreover, It should be noted that psychotic symptoms in the second patient were also resolved following Rituximab injection. Both patients satisfactorily tolerated Rituximab and had no side effects after injection. In summery this two case reports were successful examples of the treatment of LE with Rituximab.
The exact mechanism of Rituximab in LGI1 patients is still unclear. One possible explanation is that Rituximab targets CD20 on B cells, so it can attenuate B cells and deplete antibodies.[19]
As an increasing number of autoimmune non-paraneoplastic encephalitis cases
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Bases on Finke and colleagues [22] in the long term, LGI1 associated LE will cause structural damage in the hippocampal system and produces various degrees of cognitive impairment.[22] Hence rapid diagnosis and early effective treatment is warranted to decrease long term brain damages. Considering good prognosis after immunotherapy, neurologists should be vigilant about the possibility of LE when a rapidly progressive cognitive disorder is associated with epileptic seizure.[10]
Rituximab is considered to be effective and safe second line treatment for autoimmune encephalitis. Rituximab administration can be initiated in clinically diagnosed Autoimmune encephalitis regardless of autoantibody status when the response to the first line immunotherapies is insufficient. [5]
According to lee et al [5] the effects of Rituximab in the autoimmune and the paraneoplastic LE were comparable. Rituximab targets B cells and T cells are spared, so innate immune system is still working and the rate of infection will be low.[18] Rituximab has advantage of safety in cases of disturbed immune system and simultaneous infections. [23] Given the substantial efficacy and safety, in the future Rituximab might be even considered as a first line therapy for Autoimmune encephalitis.[5] Further studies are necessary to evaluate the efficacy of Rituximab as a first-line
More than one third of the patients do not respond to induction therapy (primary nonresponse) and even among initial responders, the response wanes over time. John Berg has been treating Jeffery Monroe with Adalimumab for his IBD. She had begun to exhibit symptoms / or loss of response that may be attributed to subtherapeutic levels of Adalimumab (ADA) and/or the presence of antibodies to
Encephalitis is a neurological disorder that results in the inflammation of the brain and sometimes the meninges. It is usually due to a viral infection. Most often arboviruses cause encephalitis, by transference via mosquitos to humans and animals. When bitten by an infected mosquito the virus moves from the mosquito into the person’s blood, it then reaches the brain and spinal cord, it multiplies within the central nervous system thus inflaming and damaging nerve cells, this interferes with signals from the brain to the rest of the body. The herpes simplex virus type one can commonly cause encephalitis. HIV has also been noted as an increasing cause of encephalitis. Viral infections like: mumps, chicken pox and measles can also cause encephalitis, but rarely.
The immaturity of the data is underscored by the disposition at the time of analysis. Patients were more likely to have discontinued based on adverse events than to have had disease progress or be continuing therapy. Although tolerability looked better when only patients receiving tremelimumab 1 mg were analyzed, even in that group, 30% of patients had a related grade > 3 adverse event, with 16% of patients discontinuing due to an adverse event and 4% dying from the study therapy. For comparison, in the studies that led to approval of pembrolizumab and nivolumab, grade > 3 related adverse events were seen in 7-10.5%, adverse events led to discontinuation of study therapy in 0.2-3.8% and death was related to study treatment in 0-0.3%.2, 3, 4
Epstein Barr virus (EBV) he explained to me is a type of herpes virus that causes infectious mononucleosis and can also be associated with different cancers. EBV attacks the cells that line the mouth and throat. The virus can affect the lungs, liver, bone marrow and eyes. It is often confused with Chronic Fatigue Syndrome. To me, this sounded like a better prognosis than lymphoma. The doctor explained that there was no treatment for the virus; I should continue my healthy lifestyle. He cautioned me that I would need to watch the swollen lymph nodes and have them checked regularly. I promised that I
Risperdal (Risperidone) has been used for a number of different mental health disorders. It has been used for Schizophrenia, Bipolar I disorder, and to help with irritability in children with Autism. There are a number of different things that will be covered in this paper such as the chemical makeup of the medication, the appearance, side effects, off label use, side effects, administration, and how it works, with other additional information.
Encephalitis literally means an inflammation of the brain, but it usually refers to brain inflammation caused by a virus. It may also be called “acute viral encephalitis or aseptic encephalitis';. Encephalitis is an infectious disease of the Central Nervous System characterized by pathologic changes in both the gray and white matter of the spinal cord and brain. It may be due to specific disease entity such as rabies or an arthropod-borne virus (arbovirus), or it may occur as a sequela of influenza, measles, German measles, chicken pox, herpes virus infection, small pox, vaccinia, or other diseases. The specific viruses involved may vary. Exposure can also occur through insect bites, food or drink, or skin
Evaluate the superiority of brodalumab to ustekinumab by comparing reductions in PASI 100 scores from week 0 to week 12 of treatment.
There are only treatments to suppress symptoms, treat complications related to the disease, and relieve discomfort (Harvery and Zieve). The treatments to suppress symptoms include the use of topical creams to treat skin rash. The topical creams used for the treatment of lupus contain corticosteroids to suppress inflammation and immune activity. The use of corticosteroids is essential to suppresses inflammation and immune response. Corticosteroids work by suppressing T cell secretions of cytokines, and suppressing B cells ability to bind with interleukins (Harvery and Zieve; Simanta, and Mohan). Corticosteroids diminish neutrophils adhesion, chemotaxis, phagocytosis, and secretion of toxic substance (Harvery and Zieve; Simanta, and Mohan). Corticosteroids also reduce the production of prostaglandins and leukotrienes (Harvery and Zieve; Simanta, and Mohan). A more mild treatment method is the use of nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs block prostaglandins, therefore, suppressing blood vessel dilation, inflammation, and pain (Harvery and Zieve). On more aggressive cases of SLE the use of immunosuppressant drugs is required. These drugs impedes the production of immune cells. In 2011, the first biological drug made specificly for the treatment of lupus was approved by the Food and Drug Administration (FDA) (Harvery and Zieve). This drug is called Belimumab. It targets B cells that have lost self-tolerance (Harvery and Zieve; Smcconnell). Because the causes of lupus are not yet well known, there are no prevention
DMTs reduce the relapse rate but some also reduce brain atrophy and slow disease progression. Medications such as one of the injectable INFs or glatiramer acetate are first line recommendations due to their long history of safety and efficacy. However, in the last ten years the options for treatment have grown substantially with the introduction of DMTs with better dosing schedules and administration routes. There are now three oral medications that all have different mechanisms of action: fingolimod, dimethyl fumarate and teriflunomide. They are all now used as first line treatments or to replace INFs or glatiramer acetate in patients who have developed neutralizing antibodies that have reduced the effects of those medications. Several second line treatments have been developed to treat patients who either did not respond to first line treatments or have progressive types of MS. They include an immunosuppressant chemotherapy agent (mitoxantrone) and two monoclonal antibody medications (alemtuzumab and natalizumab). These medications are available by infusion only and have much riskier side effects including the development of other auto-immune disorders and progressive multifocal leukoencephalopathy (which can be fatal). DMTs are approved for patients with relapsing forms of MS, but patients with non-remissive courses have fewer treatment options. For example,
As previously described, leukocytes activated in the periphery are able to adhere to the endothelium of blood vessel walls in order to traffic into the CNS, where re-activation by antigen presentation from perivascular APC leads to inflammation. In 1992, Yednock et al., which would later develop a successful therapy for RRMS patients, made a revolutionary finding. They reported that lymphocytes and monocytes bound selectively to inflamed EAE brain vessels and that this could be reversed with antibodies against VLA-4 (Yednock et al., 1992). When tested in
1. Brodaty, H., Ames, D., Snowdon, J., Woodward, M., Kirwan, J., Clarnette, R., & ... Greenspan, D. (2005). Risperidone for psychosis of Alzheimer's disease and mixed dementia: results of a double-blind, placebo-controlled trial. International Journal of Geriatric Psychiatry, 20(12), 1153-1157.
Infliximab is the first TNF antagonist approved by FDA (1999) and EU (1998). It was formed by chimeric IgG1 antibody and show outstanding treatment effect against Crohn’s disease. It neutralise the biological activity of TNF-α by binding with high affinity to the soluble and transmembrane forms of TNF-α, and inhibits the effective bind of TNF-α with its receptor. It falls in the class of “anti-TNF antibodies” and have the capability of lysing cells involved in the inflammatory process.
Encephalitis is a condition caused by viruses which cause the brain to become inflamed. There are two types of encephalitis one is called primary because the viruses affect the brain itself. Secondary is the viruses travel from some other part of the body that has been affect to the brain. When the virus reaches the brain it begins to multiply causing inflammation. The brain’s white matter can be destroyed. This destruction causes cell death, hemorrhage and edema. The edema begins to compress the blood vessels this causes intracranial pressure (Mayo Clinic, 2011).
A huge caution associated with the use of adalimumab is its ability to reactivate, or make one more susceptible to infection. This is because it inhibits TNFα which plays a role in the fighting of infections. Reactivating the dormant form of tuberculosis (TB) is one of the most important infectious adverse reactions in those taking adalimumab. Consequently, patients are assessed for tuberculosis before being offered adalimumab. Other infections include septicaemia and hepatitis B. As a general rule of thumb, evaluation for infection before, during and 4 months post treatment should occur. Treatment should not be started until the infection is controlled and it is advised that adalimumab be avoided in patients on drugs that alter immune function (e.g. immunosuppressants).
Example of antidepressants that are been approved by the Food and Drug Administration (FDA) commonly used to treat bibliomania are Clomipramine (Anafranil), Fluvoxamine (Luvox CR), Fluoxetine (Prozac), Paroxetine (Paxil, Pexeva) and Sertraline (Zoloft).