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Epilepsy

Epilepsy Guide

Help When Epilepsy Treatment Doesn't Work

Medically Reviewed by Christopher Melinosky, MD on May 12, 2023

Written by Katherine Kam

7 min read

What Is Refractory Epilepsy?

If your doctor says you have refractory epilepsy, it means that medicine isn't bringing your seizures under control. You might hear the condition called by some other names, such as uncontrolled, intractable, or drug-resistant epilepsy.

Your doctor can try certain things to help keep your seizures under better control. For instance, they might try different combinations of drugs or a special diet.

Your doctor may also put a device under your skin that sends electrical signals to one of your nerves, called the vagus nerve. This may cut the number of seizures you get. A Neuropace device is a reactive neurostimulator that detects seizures and shocks the brain to stop them.

Surgery that removes a part of the brain that causes your seizures may also be an option. With any of these treatments, you may still need to take epilepsy medicine throughout your life.

It's natural to feel anxious when the doctor tells you your epilepsy isn't getting better with the medicine you're taking. You don't have to go through it alone, though. It's important to reach out to family and friends to get the emotional support you need. You might also want to join a support group, so you can talk with other people who are going through the same things you are.

Featured

Tests and a Diagnosis for Epilepsy

Common Types of Seizures

Types of Epilepsy

Causes

Doctors don’t know why some people have refractory epilepsy and others don't. You can have refractory epilepsy as an adult, or your child might have it. About 1 in 3 people with epilepsy will develop it.

Symptoms

The symptoms of refractory epilepsy are seizures despite taking anti-seizure medication. Your seizures could take different forms and last from a few seconds to a few minutes.

You may have convulsions, which means you can't stop your body from shaking.

When you have a seizure, you may also:

Black out

Lose control of your bowels or bladder

Stare into space

Fall down suddenly

Get stiff muscles

Bite your tongue

Getting a Diagnosis

Your doctor has several ways to diagnose refractory epilepsy. They may ask you questions such as:

How often do you have seizures?

Do you ever skip doses of your medicine?

Does epilepsy run in your family?

Do you still have seizures after taking medicine?

Your doctor may also give you a test called an electroencephalogram. To do this, they'll place metal discs called electrodes on your scalp that measure brain activity.

Other tests might include a CT scan of your brain. It's a powerful X-ray that makes detailed pictures of the inside of your body.

You might also need to get an MRI of your brain. It uses magnets and radio waves to make pictures of your brain.

If you need surgery to treat refractory epilepsy, these tests can help doctors find out where your seizures are starting.

Your doctor will most likely want you to report your symptoms regularly. They may try several drugs at different doses.

Questions for Your Doctor

What might be causing my seizures?

Which tests are needed to diagnose refractory epilepsy?

Should I see an epilepsy specialist?

What treatments are available for refractory epilepsy?

What precautions should I take to avoid getting injured during a seizure?

Are there any limits on my activities?

Treatment

Medications. Your doctor may take a second look at the drugs you're taking. They may suggest another medicine, either alone or combined with other drugs, to see if it helps you have fewer seizures.

Many drugs can treat epilepsy, including:

Brivaracetam (Briviact)

Cannabidiol (Epidiolex)

Carbamazepine (Carbatrol, Tegretol)

Cenobamate (Xcopri)

Clobazam (Sympazan)

Divalproex (Depakote)

Dilantin (Phenytek)

Eslicarbazepine (Aptiom)

Felbamate (Felbatol)

Gabapentin (Neurontin)

Lamotrigine (Lamictal)

Levetiracetam (Keppra)

Oxcarbazepine (Trileptal)

Perampanel (Fycompa)

Potiga (Ezogabine)

Primidone (Mysoline)

Rufinamide (Banzel)

Tiagabine (Gabitril)

Topiramate (Topamax)

Vigabatrin (Sabril)

Zonisamide (Zonegram)

Surgery. If you still have seizures after trying two or three anti-epilepsy drugs, your doctor might recommend brain surgery.

It can help a lot if your epilepsy only affects one side of your brain. Doctors call that refractory partial epilepsy.

A surgeon removes the area of your brain that's responsible for your seizures.

It's natural to worry about brain surgery and to wonder if it will affect the way you think or if you'll seem like a different person afterward. Talk with your doctor about what to expect if you choose the surgery or if you don't, so you can weigh the risks and benefits. A lot of people who have the surgery say that getting free of seizures -- or at least making them less common and less intense -- makes them feel much better.

The surgeon usually operates on an area of your head that's behind your hairline, so you won't have noticeable scars.

After it's done, you'll probably need to stay in an intensive care unit of the hospital for a few days. After that, you'll move to a regular hospital room, where you may need to stay for up to 2 weeks.

You should take it easy for a while after you get back home, but you'll probably be able to return to a normal routine in 1 to 3 months. Even with the surgery, you might need to take seizure medication for a few years. You might need to stay on the drugs for the rest of your life.

Talk to your doctor about any side effects you might have from the surgery. You can ask them to put you in touch with other people who've had the surgery, so you can better understand what to expect.

Diet. The ketogenic diet helps some people with epilepsy. It's a high-fat, low-protein, no carb diet. You have to start it in a specific way and follow it strictly, so you need a doctor's supervision.

Your doctor will watch closely to see whether or when you can lower any of your medication levels. Because the diet is so specific, you may need to take vitamin or mineral supplements.

Doctors aren't sure why the ketogenic diet works, but some studies show that children with epilepsy who stay on the diet have a better chance of reducing their seizures or their medications.

For some people, a modified Atkins diet may work, too. It's slightly different from the ketogenic diet. You don't have to restrict calories, protein, or fluids. Also, you don't weigh or measure foods. Instead, you track carbohydrates.

People with seizures that are hard to treat have also tried a low-glycemic-index diet. This diet focuses on the type of carbs, as well as the amount that someone eats.

Electrical stimulation, also known as neuromodulation. This technology works directly on your nerves. It changes or controls nerve activity by sending electrical signals or medicine to a specific area. Methods include:

Cortical stimulation. Temporary electrodes are placed on the surface of your brain. The doctor sends a signal through them at a level low enough that you won’t notice. If it helps, they can be replaced with permanent electrodes for continuous stimulation.

Closed-loop stimulation. The doctor implants a device under your scalp and within your skull. It’s connected to two electrodes placed either on the surface of your brain, in the brain, or both. The electrodes record your brain waves. When the neurostimulator detects seizure-like activity, it sends a small electrical current to your brain that can stop, shorten, or maybe prevent the seizure.

Deep brain stimulation. The doctor implants thin electrodes deep into certain areas of your brain and a pulse generator under your collarbone. Wires under your skin connect the two. The pulse generator sends signals to disrupt abnormal patterns of brain activity.

Vagus nerve stimulation (VNS). The doctor puts a device that looks like a heart pacemaker under your left collarbone. It connects to the vagus nerve in your neck through a wire that runs under your skin. The device sends a current to the nerve, which may cut down on the number of seizures you get or make them less intense.

Clinical trials. You may want to ask your doctor if you could take part in a clinical trial. These trials test new drugs to see if they're safe and if they work. They're often a way for people to try new medicine that isn't yet available to everyone.

Taking Care of Yourself

Stress can sometimes trigger seizures. Talking to a counselor is a great way to find solutions to manage your stress.

Try going to a support group, too. You can talk with people who know what you're going through and who give advice from their own experience.

What to Expect

Even though you have refractory epilepsy, it's still possible to get your seizures under control. It may be a matter of switching to a different treatment.

Your doctor may find a different drug combination that helps. Getting electrical stimulation of the vagus nerve means fewer seizures for about 40% of people who try it. And if a brain surgeon can remove the part of the brain that's causing seizures, the seizures may stop, or at least happen less often and become less intense.

Getting Support

As you are finding out what works best, you'll need a strong network of family and friends who can offer emotional support, especially if your seizures prove hard to control. Having a trusted person to listen to you can be a great comfort when you're going through something tough.

Ask your doctor for information on support groups in your area. You can also find out about support groups by going to the website of the Epilepsy Foundation.

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thxnews · 10 months ago

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FDA Fast Tracks Kyverna's MS Therapy KYV-101

A Leap Forward in MS Treatment

Transforming Multiple Sclerosis Care Kyverna Therapeutics, Inc. (Kyverna), a leading biopharmaceutical company, has achieved a significant milestone with the FDA Fast Track Designation for its innovative CAR T-cell therapy, KYV-101, aimed at treating multiple sclerosis (MS). This designation highlights the therapy's potential to address the unmet medical needs of individuals with refractory progressive MS. Understanding Multiple Sclerosis Multiple sclerosis is a chronic neurodegenerative autoimmune disease, impacting over 2.8 million people worldwide. Additionally, predominantly affecting women and individuals of Northern European descent, MS symptoms range from blurred vision and slurred speech to severe mobility challenges. Furthermore, current treatments focus on relapse reduction and slowing disability progression; however, the disease inevitably worsens over time. The Promise of KYV-101 KYV-101 represents a groundbreaking approach to the treatment of B-cell-driven autoimmune diseases. Furthermore, this autologous, fully human CD19 CAR T-cell product candidate has been designed to target and remove B cells expressing CD19, a protein involved in various autoimmune conditions. Its development is based on extensive research and promising Phase 1 trial results in oncology, published by the NIH in Nature Medicine. Kyverna's Clinical Trials and Research Kyverna is currently conducting pivotal trials for KYV-101 in patients with lupus nephritis, a severe autoimmune disease. Additionally, they are preparing additional trials for systemic sclerosis, myasthenia gravis, and multiple sclerosis. This underscores the therapy's versatility and potential impact across a spectrum of autoimmune disorders. Kyverna's Vision and Pipeline As a patient-centered biopharmaceutical company, Kyverna is committed to revolutionizing the treatment of autoimmune diseases. Its extensive pipeline includes next-generation CAR T-cell therapies, both autologous and allogeneic, tailored for B cell-driven autoimmune diseases. With KYV-101 at the forefront, Kyverna aims to transform the therapeutic landscape for autoimmune conditions. The Significance of FDA's Fast Track Designation The FDA's Fast Track Designation for KYV-101 is a testament to the therapy's potential to fill a critical healthcare gap. Furthermore, this status facilitates the expedited development and review of the therapy, bringing hope to patients suffering from refractory progressive MS. The Future of Autoimmune Disease Treatment Kyverna's breakthrough in CAR T-cell therapy signals a new dawn in autoimmune disease treatment. By harnessing the power of cell therapy, Kyverna is not just advancing a single product but spearheading a movement towards more effective, targeted treatments for autoimmune diseases, including MS.

Summary

The FDA's Fast Track Designation of Kyverna Therapeutics' KYV-101 marks a pivotal moment in the fight against multiple sclerosis. This innovative CAR T-cell therapy holds the promise of significantly improving the lives of those suffering from refractory progressive MS. As Kyverna continues to push the boundaries of medical science, the future for patients with autoimmune diseases looks increasingly hopeful. With KYV-101 leading the way, the potential for transformative treatments in this field is immense, bringing new hope to millions around the globe. Sources: THX News & Kyverna Therapeutics. Read the full article

#Autoimmunediseasescelltherapy #AutologousCD19CART-cell #CART-celltherapy #FDAFastTrackDesignation #InnovativeMStreatmentoptions #KyvernaTherapeutics'KYV-101 #Kyverna'sautoimmunediseaseresearch #Lupusnephritisclinicaltrials #MultipleSclerosistreatment #ProgressiveMStherapyadvancement

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lupusnews · 1 year ago

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#lupus nephritis #living with lupus #chronic inflammation #chronic pain #chronic fatigue #chronic kidney disease #anyone can get lupus

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newswireml · 2 years ago

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Anifrolumab Shows Promise in Refractory Discoid Lupus#Anifrolumab #Shows #Promise #Refractory #Discoid #Lupus

Anifrolumab appears to improve outcomes in patients with refractory discoid lupus erythematosus (DLE), especially in those with severe or recalcitrant disease, a small retrospective study reports. DLE, the most common form of chronic cutaneous lupus erythematosus, can permanently scar and disfigure patients, and traditional treatments such as antimalarials, steroid-sparing immunosuppressive…

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mcatmemoranda · 2 years ago

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I was working up a pt for lupus recently and just had a question about lupus. I wasn't sure what the diagnostic criteria are. It's 2 clinical and 2 serologic criteria, according to this question I just answered. I was reading about lupus recently and Anti-nuclear antibodies are really non-specific. So just because you have ANA doesn't mean you have lupus. Anti-double stranded DNA and Anti-smith antibodies are specific for lupus. I don't like rheumatology.

The diagnosis is made based on a combination of typical clinical manifestations and serologies adding up to 4 points with at least one manifestation in both categories. If lupus nephritis is diagnosed via biopsy, then the presence of either ANA or anti-dsDNA antibodies fulfills the diagnostic criteria.

Hydroxychloroquine reduces arthritis pain in lupus patients and is the preferred initial treatment for lupus arthritis. Essentially every patient should be considered for treatment unless there is a clear contraindication. Hydroxychloroquine is associated with irreversible vision loss secondary to retinal toxicity, with a prevalence that increases over the length of time on the medication (approximately 7.5% of patients after 5 years, increasing to nearly 20% after 20 years of treatment). A baseline retinal examination with continued monitoring every 6–12 months is necessary for patients who are taking this medication long term. Vitamin D supplementation should also be considered because it has immunomodulatory and antifibrotic effects. Azathioprine and cyclosporine are indicated for severe lupus or lupus nephritis. Mycophenolate is indicated for refractory lupus or lupus nephritis. Rituximab is indicated for severe refractory lupus.

#Hydroxychloroquine #lupus

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mferna · 2 years ago

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Corpogen Laboratorio Clínico on Instagram: "🏥Un nuevo estudio muestra que una terapia contra el cáncer puede ayudar a poner en remisión el lupus difícil de tratar.🩺 El lupus es una enfermedad a...

See on Scoop.it - Salud Publica

Corpogen Laboratorio Clínico shared a post on Instagram: "🏥Un nuevo estudio muestra que una terapia contra el cáncer puede ayudar a poner en remisión el lupus difícil de tratar.🩺 El lupus es una enfermedad autoinmune que ocurre cuando el sistema inmunológico comienza a atacar a sus propios tejidos y órganos. No hay cura para el lupus, y los tratamientos no funcionan para muchas de las 1,5 millones de personas que viven con la enfermedad en los Estados Unidos. La nueva terapia toma las propias células T de una persona, las entrena en el laboratorio para que reconozcan células muy específicas, y luego las infunde de nuevo en el cuerpo. En el lupus, la terapia se dirige a CD19, una proteína especifica en la superficie de las células B que son productoras de anticuerpos. El pequeño estudio incluyó a cinco personas con lupus grave que no respondieron a la terapia estándar. Después de unos tres meses de tratamiento, los pacientes mostraron mejoras en los síntomas, incluida la remisión del compromiso orgánico y la desaparición de autoanticuerpos relacionados con la enfermedad. Lo que es más, no necesitaron ningún tratamiento adicional. Los efectos secundarios en el nuevo estudio fueron leves. En los estudios de cáncer, esta terapia causa fiebre y escalofríos, dificultad para respirar y síndrome de liberación de citoquinas, que puede ocurrir cuando las células CAR-T se multiplican y liberan grandes cantidades de citoquinas inflamatorias en circulación. Ahora, los investigadores planean averiguar si el sistema inmunológico realmente ha experimentado un “reset” o reinicio profundo y no existen recaídas con el trascurso del tiempo. Los expertos en lupus están emocionados con los nuevos hallazgos. "Esto es muy, muy importante", dijo Hoang Nguyen, gerente de programa científico senior de Lupus Research Alliance. "No hay una cura real para el lupus, y la eficacia de las terapias actuales es limitada. Esta es la primera vez que un tratamiento eliminó los síntomas del lupus en todos los sujetos tratados en un estudio de 100 días". Con información de Andreas Mackensen et al, Anti-CD19 CAR T cell therapy for refractory systemic lupus erythematosus, Nature Medicine (2022). #CORPOGENLAB #tulaboratorioexperto". Follow their account to see 546 posts.

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didanawisgi · 6 years ago

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Aphthous Stomatitis

Michael C. Plewa; Kingshuk Chatterjee.

Author Information

Last Update: December 2, 2018.

Go to:

Introduction

Aphthous stomatitis is a common ailment, idiopathic in nature, with recurrent painful aphthous ulcers (commonly termed “canker sores”) on the non-keratinized oral mucous membranes.[1][2][3]

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Etiology

The cause of aphthous stomatitis is idiopathic and multifactorial, but likely involves activation of the cell-mediated immune system. Aphthous ulcers are not caused by acute infections and are therefore not contagious. Aphthous stomatitis may be triggered by local trauma, emotional or physiologic stress, allergy or sensitivity (such as to sodium lauryl sulfate present in toothpaste and oral hygiene products, foods such as cinnamon, cheese, citrus, figs or pineapple), toxin exposure (nitrates in drinking water), menstruation, or alterations in the oral microbiome. Malabsorption, enteropathy, or celiac disease may be present. As many as 20% of cases are related to hematinic deficiencies (iron, folate, vitamin B6 and B12), although other deficiencies such as vitamin D, zinc, or thiamine may also be present. Aphthous ulcers are more prevalent in nonsmokers and smokers who quit and less common in individuals with good oral hygiene practices.[4][5][6]

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Epidemiology

Aphthous stomatitis affects approximately 20% of the general population. It is slightly more common in girls and women as well as among affluent socioeconomic classes and countries. Race does not appear to be a factor in the disease. Age of onset may be during childhood, but more commonly in the second and third decade of life, becoming less common with advancing age. Aphthous stomatitis can be a manifestation of Behcet syndrome, systemic lupus erythematosus, reactive arthritis, or inflammatory bowel disease (especially Crohn disease). These disorders may be excluded based on systemic signs and symptoms. [7][8]

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Pathophysiology

Aphthous ulcerations are initially and primarily the result of T cell-mediated immune dysfunction but also may involve neutrophil and mast cell-mediated destruction of the mucosal epithelium. Lesions can have alterations in several intercellular mediators, such as elevations in interferon gamma, tumor necrosis factor-alpha, and interleukins (IL)-2, IL-4 and IL-5, as well as various adhesion molecules involved in cell communication and epithelial integrity. This inflammatory process results in a pseudomembrane containing fibrinous exudate, bacteria, inflammatory cells, and necrotic mucosal cells.

Aphthous ulcers occur on non-keratinized oral mucosae such as along the labial or buccal surfaces, soft palate, the floor of the mouth, the ventral or lateral surface of the tongue, tonsillar fauces, free (marginal or unattached) gingiva adjacent to teeth, and alveolar gingiva in the maxillary and mandibular sulci. In contrast, ulcerations from herpes simplex virus (HSV) involve the keratinized mucosal surfaces such as the attached gingival and dorsum of the tongue, lips, and hard palate.

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History and Physical

Patients may notice a prodrome of burning discomfort a day or two before the onset of ulcerations. Fever, rash, headache, or lymphadenopathy are typically absent and would suggest a different diagnosis such as herpangina or PFAPA syndrome (periodic fever, pharyngitis, adenitis, and oral ulceration). A history of prior ulceration is typical.

On physical exam, patients with aphthous stomatitis are well-appearing and afebrile. Assess for clinical signs of dehydration, especially in infants and children. Involvement of the eye (uveitis) or genitalia suggest other diagnoses, such as Behçet syndrome or MAGIC syndrome (mouth and genital ulcers with inflamed cartilage).

The ulcers of aphthous stomatitis are present as well-circumscribed lesions with central necrotic ulcer with gray, fibrinous exudate surrounded by an erythematous halo on the non-keratinized oral mucosa. Typical locations include the buccal (cheek) and labial (lip) mucosae, the floor of the mouth, the ventral surface of the tongue, and the soft palate. Minor aphthous ulcerations, the most common form of aphthous stomatitis, are less than 1 cm in diameter, round or oval in shape, with yellow or gray pseudomembrane surrounded by an inflammatory red halo, and heal typically within 7-14 days. Major aphthous ulcers are deeper, larger (often 2-3 cm in diameter), may have irregular raised borders, and can take many weeks or months to heal, sometimes with scarring. Much less common are herpetiform recurrent aphthous ulcers, 1 to 2 mm in diameter in clusters of 10 to 100 in groups or throughout the mouth, which usually heal within a few weeks.

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Evaluation

Diagnosis of aphthous stomatitis is clinical, and laboratory testing is usually unnecessary, although diagnostic testing might be considered in persistent, severe, or recurrent cases. [9][8]

A complete blood count demonstrating anemia might suggest hematinic deficiency such as iron, folate, or vitamin B12. Neutropenia might prompt consideration of cyclic neutropenia as a cause of ulcerations.

Gluten-sensitive enteropathy (celiac disease) present in fewer than 5% of recurrent aphthous stomatitis cases and can be identified with serum anti-endomysium antibody and transglutaminase assay.

Consider HIV testing in cases with complex or severe involvement, persistent herpetiform or major aphthous stomatitis, or those involving keratinized mucosa (adherent gingival, dorsum of the tongue, hard palate).

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Treatment / Management

The goals of treatment are to reduce pain (allowing adequate hydration and nutrition), enhance healing, and prevent recurrence. Many treatment options are available for aphthous stomatitis, including topical agents such as local anesthetics (benzocaine), coating or occlusive agents (bismuth subsalicylate, sucralfate, 2-octyl cyanoacrylate, and various bioadherent emollient pastes), antiseptics (chlorhexidine gluconate and hydrogen peroxide), anti-inflammatory agents such as glucocorticosteroids (clobetasol, dexamethasone, fluocinonide, and triamcinolone), amlexanox and metalloprotease inhibitors (antimicrobials tetracycline, doxycycline, or minocycline), honey, and immunomodulatory agents (amlexanox, colchicine, cyclosporine, cyclophosphamide, dapsone, methotrexate, montelukast, thalidomide, or retinoids). [10][11][12]

A step-wise approach to the treatment of aphthous stomatitis involves initial topical anesthetic and occlusive or antiseptic agents for symptom relief of minor cases. First-line treatment of major or minor aphthous stomatitis with significant symptoms is typical with topical steroids in gel or emollient paste (e.g., Orabase) to shorten the duration. Another option would be a one-time local steroid injection, such as triamcinolone. Severe refractory or persistent cases may further be treated with systemic steroids (dexamethasone or prednisone), immunomodulatory agents (listed above), pentoxifylline, or quercetin.

The experimental treatment may include various herbal products or local desiccation (such as with tincture of benzoin), cautery (such as the application of silver nitrate), or even biopsy, all after local anesthesia. Laser therapy may be effective for severe or recurrent cases. Good oral hygiene may prevent recurrences. Dietary supplementation with iron, zinc, or vitamins B1, B2, B6, B12, or C may be useful in individuals with deficiencies of these. A gluten-free diet is important only for those individuals diagnosed with celiac disease.

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Differential Diagnosis

Contact dermatitis

Oral cancer

Herpes simplex

Drug induced lesions

Lupus

Lichen planus

#family medicine #canker sore #aphthous ulcer #aphthous stomatitis #infectious disease #immunology #immune system #Resources

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wheelie-sick · 5 months ago

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hhhh sometimes I just want to scream about all the people who see lupus as an easily treatable nothing disease

and yeah sometimes it is that

but sometimes it's me, moderately immunocompromised from a biologic and despite that having refractory lupus

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furiarossa · 6 years ago

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Supergoldenwolfen

Usually, the aurolupus lycans (also called by some "goldenwolfens") are 1,60-1,78 m tall when in human form. Furiadoro is 1,92 m tall, with a weight ranging between 100 and 160 kg. This particular subspecies, taller and with lighter pigmented skin, is known as "supergoldenwolfen" and it's extremely rare, enough to be considered a legend. Also, even if she has the phenotype of a pure supergoldenwolfen, she is not actually a pureblood and this results in a non-total refractoriness to magic (pure goldenwolfens are totally refractory to magic) and theoretically she could even use very simple basic spells.

Dominant, but not too much

Furiadoro, like the majority of the aurolupus lycans, has a very strong personality and tends to be dominant, but she doesn't want the responsibility that comes from being the alpha female of a pack, so she's just a sort of... bully. Her natural role, if she would have been in a pack, is beta (or lower rank, if someone would be capable of beating her, but that's very difficult).

An ancient spirit

Her spirit is way older than her body, and even if it can't remember everything from its past lives, sometimes knows stuff that she isn't supposed to know. And, oh boys, her body is strong, but her soul is fifty times stronger.

Not her name

Furiadoro (it means "golden fury/ golden rage" in Italian) should have been just a temporary name given to her by September Aster, a young magician. Instead, in the end it stuck and now everyone calls her like this ...

An extra form?

Furiadoro is a lycanthrope with complete cycle: this means that she can reach any possible lycan form, even the intermediate ones that there aren't portrayed here (for example a mix of crinos and human, with claws, some fur and a more solid building, but the basic body shape of a woman). Her appearence is fluid enough that even her facial features could slightly change when she's in human form, so her face could eventually appear a bit different everyday. But the most interesting thing is that she can reach a stadium, called "great crinos" or "monster lycan", that's so rare that only few lycanthropes in history have obtained it. She could stay only a few minutes in this very energy consuming state, but she becomes an enormous wolf-tank, with thick skin, that grows up in size eating the flesh of her enemies and totally abandon herself to instinct and aggressivity.

Relatives

-Blindfury (Father) -September Aster (Best friend) -Alejandro (Brother) -Arban Altan (Mother)

Illustrations:

Furiadoro's forms in detail: Crinos (full moon) | Hispo | Lupus | Human

#reference sheet #artists on tumblr #the way of legends #art #my art #digital art #werewolf #furiadoro #oc #original character #2018 #female

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lupusnews · 1 year ago

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#racial differences in medicine #systemic lupus erythematosus #anyone can get lupus #autoimmune #chronic inflammation

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mcatmemoranda · 5 years ago

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I actually learned about fat embolisms before I even thought of going to medical school when I saw an episode of House where a woman was trapped under a collapsed building and they had to cut her leg off to extricate her. Then she died later from a fat embolus that went to her lungs. Who says you can't learn anything from watching TV?

Anyway, this is the summary on fat embolism syndrome (FES) from UpToDate:

Fat embolism syndrome (FES), a rare clinical syndrome of uncertain pathogenesis, is defined by the presence of fat globules in the pulmonary circulation. FES is most commonly associated with long bone (especially femur) and pelvic fractures. Some cases are associated with trauma in the absence of orthopedic fractures or are nontrauma-related (table 1). (See 'Definition' above and 'Epidemiology and etiology' above and 'Pathogenesis' above.)

●FES typically manifests 24 to 72 hours after the initial insult. The classic triad of findings includes hypoxemia, neurologic abnormalities (eg, confusion, altered consciousness, seizure), and a petechial rash. Less common manifestations include anemia, thrombocytopenia, fever, lipiduria, and coagulation abnormalities; myocardial depression and shock are rare. None of these features are specific for FES. (See 'Clinical presentation' above.)

●When FES is suspected, chest imaging, typically chest radiography and/or computed tomography (CT), should be performed. CT or magnetic resonance imaging (MRI) of the brain should be performed in those with neurologic symptoms. Routine laboratory studies should be drawn including complete blood count and coagulation studies. Measuring free fatty acid or c-reactive protein levels, examining urine or sputum for the presence of fat, and invasive procedures including fat analysis from a wedged sample aspirated from a pulmonary artery catheter, bronchoalveolar lavage fluid, or tissue biopsy are not routinely performed since their diagnostic utility is unclear. (See 'Diagnostic evaluation' above.)

●The differential diagnosis of FES includes other embolization syndromes (thrombus, amniotic fluid, tumor, foreign body, air), acute alveolar filling diseases (eg, heart failure, pneumonia, and acute respiratory distress syndrome) and cutaneus vasculitic disorders (eg, systemic lupus erythematosus). (See 'Differential diagnosis' above.)

●FES is a clinical diagnosis that can be made when the classic triad of hypoxemia, neurologic abnormalities, and the petechial rash occurs in an appropriate clinical setting. However, since the presenting manifestations are nonspecific and the rash occurs in fewer than half of cases, the diagnosis of FES is more commonly made when clinical manifestations occur in the appropriate clinical setting and other relevant diagnoses have been excluded. (See 'Diagnosis' above.)

●Treatment of FES is largely supportive. Systemic corticosteroids are not routinely administered but may be reserved for severe or refractory cases. (See 'Treatment' above.)

●In those at risk of FES, interventions that have been shown to prevent or reduce the incidence and/or severity of FES are early immobilization of fractures, operative correction rather than conservative management (ie, traction alone), and limitation of the intraosseous pressure during orthopedic procedures. We do not advocate for the routine administration of prophylactic postoperative systemic corticosteroid therapy since most cases resolve spontaneously, FES is relatively uncommon, and data to support their use are fundamentally flawed. (See 'Prevention' above.)

●Most patients with FES fully recover spontaneously. In most cases, symptoms are transient and fully reversible, often within a few days, although features may persist beyond one week when FES is severe. Although reported mortality rates range from 5 to 15 percent, the true mortality is probably lower. (See 'Prognosis' above.)

#fat embolism #fat embolism syndrome #FES

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imagecase · 3 years ago

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Deep morphea is a form of localized scleroderma in which inflammation and sclerosis are found in the deep dermis, panniculus, fascia, or superficial muscle, typically in the face, trunk and limbs [1]. Associated clinical findings, including arthralgias, arthritis, contractures, or carpal tunnel syndrome, are frequent and rarely visceral manifestations may occur [1]. Eosinophilia, hypergammaglobulinemia, increased erythrocyte sedimentation; rheumatoid factor, antinuclear antibodies (ANAs) and anti-dsDNA, anti-histones, anti-nucleosome, anticardiolipin antibodies have been reported. Etiology is still uncertain and treatment options are unsatisfactory but include NSAIDs, antimalarial agents, topical and systemic corticosteroids, PUVA, vitamin E, vitamin D3, aminobenzoate potassium, penicillin, retinoids, interferon-gamma, D-penicillamine, methotrexate, cyclosporine, mycophenolate mofetil, cyclophosphamide, azathioprine, bosentan, IV immunoglobulins, abatacept, tocilizumab and rituximab [1,2].

A 42-year old woman went to the rheumatology outpatient clinic, complaining of inflammatory polyarthralgias and lumbar pain, without Raynaud phenomenon history or other systemic symptoms. Physical examination revealed polyarthritis and a hyperpigmented, mildly inflamed and thickened skin in the lower lumbar region (Figure A). She had no sclerodactyly, nor telangiectasias. She presented with raised inflammatory markers; normal blood count, renal and hepatic functions. Its seronegative polyarthritis remitted under methotrexate 20 mg/week, prednisolone 10 mg/day and etoricoxib 90 mg/day. However, the localized skin thickness worsened during several months. Nailfold capillaroscopy remained unremarkable and she evolved with positive direct coombs test, lupus anticoagulant, ANAs (1/320; homogeneous), anti-dsDNA (130,1 U/mL), anti-nucleosome and low titre anti-beta-2-glycoprotein I and anticardiolipin antibodies. The diagnosis of deep morphea was based on the clinical and histopathological findings (Figure D and E) and she began on hydroxychloroquine. Unfortunately, skin biopsy complicated with ulcerations (Figure B) with impaired healing that is slowly improving (Figure C).

Therefore, this is an interesting clinical case of a rare type of localized scleroderma, with an atypical localization and refractoriness to some of the first-line treatments, which became a challenge for the clinicians.

#Morphea

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