Lupus and COVID vaccine: Dr. Thomas recommends not waiting to his patients, read below…
Research regarding the COVID vaccine and lupus patients continues to be done. Should you wait to get yours? Dr. Thomas answer this question below:
“I’ll tell you what I tell my patients, “PLEASE, get your COVID-19 vaccine as soon as it is your turn! However, make sure to ask your doctor first” Why? People are dying left and right. People who did not ever think they would get it – get it. Just this week, I have had 3 patients tell me the horrible, sad story of a loved one or friend who recently died. One was on a ventilator 12 weeks…. 12 weeks! Guess how many similar stories I’ve heard about the COVID-19 vaccine… none.
The COVID-19 vaccines are the most studied vaccines EVER. No vaccine comes close. Over 70,000 people were in the clinical trials for Pfizer and Moderna. And now… millions have been given out with no bad safety signals. Sure, you will have a very sore arm for a week. Sure, you may have achiness, headache, and low-grade fever for a few days. There is always the chance for an allergic reaction (true for any medicine or vaccine … I took my EpiPen with me, just in case.) I’ll take these mild side effects any day over being in the ICU on a ventilator where I could die alone, only able to see my loved ones on FaceTime.
True, patients with autoimmune diseases were excluded from the clinical trials. True, immunosuppressed patients were as well. However, that goes with all vaccine phase I-III clinical trials. If you want to wait for research on lupus patients. You will wait a very long time.
UPDATED September 2021: I cannot wait to get my extra COVID vaccines … specifically my 3rd booster shot!
1/22/21 was a historical day for me! I got my 2nd Moderna vaccine!
PLEASE… everyone… get yours as soon as you can!
The pandemic is at an all-time high. Get your extra COVID vaccines! Lupus patients on immunosuppressants should get their 3rd shot of Moderna or Pfizer now (September 2021).
Be proactive, educate yourself if you are uncertain about the vaccine (but read reputable sites and not the crazy anti-vaccine sites).
I know I’ll make enemies with that comment, but I don’t care. Speaking the truth and hopefully getting someone to save their life is more important than trying to appease those who disagree. As Dr. Anthony Fauci said on the news yesterday, speaking the truth is “Liberating” and “Let the science speak!”
And to Aldene, my vaccinator at United Medical Center, Washington DC, in the video … thank you for saving my life with this God-send!
I updated this post in September 2021. I am recommending the 3rd Moderna and Pfizer vaccines to all my patients who are on immunosuppressant drugs and to all my systemic lupus patients. Supposedly, I should be able to get mine on September 20, 2021, and I cannot wait! I have seen too much death and lingering effects from COVID-19. Dealing with the family members and loved ones who are devastated by the loss of loved ones is difficult. I wish all the vaccine nay-sayers had to care for COVID-19 patients and their families and see the devastation up close. It does not compare to the flu.
Here is my previous post about the vaccine and lupus patients:
Most infected people do not transmit SARS-CoV-2 (the novel coronavirus responsible for COVID-19)
– Some people are “superspreaders,” infecting many people they come into contact with – Who are these superspreaders? How can we identify them so we can super-quarantine them? – We need to figure this out – It is theorized they probably have a “high viral load” (heavily infected, with respiratory droplets that are much more infectious than others)
– Infectiousness occurs before symptoms ever occur
– Infectiousness is at its peak the day before the person develops symptoms
– The infectious period gradually goes away within a week – There are no cases of transmission more than “about a week” after infection symptoms 1st began
– Definite transmission by “fomites” has not been documented – A “fomite” transmission would be touching something the infected person touched – Cannot rule out respiratory spread in presumed fomite transmission cases – However, fomite-transmission is not ruled out and it is still important to wear gloves and disinfect
– The lowest rate of infection is staying at home, never going out, ordering everything like groceries to be delivered, not allowing anyone to come into contact with you (except another person in the home who does the same) – If you must come into contact with others, lowest transmission is when both people wear a good mask and are at least 6 feet apart
– Highest transmission rate = indoor social gatherings and not everyone wearing a mask
How to prepare family for pandemic? Continue social distancing! Continue to avoid large inside gatherings. Practice the “cocoon effect” where you ask all your close contacts to be vaccinated or stay away from you as much as possible. I believe it is a social moral principal for society to protect each other from this devastating infection. This is especially true when that person has a condition that increases their risk of a bad outcome from the infection.
Protect yourself from medical mistakes.
Lupus Question of the day …
It is not uncommon to ask, “can you have lupus with a negative ANA?”
Dr. T responds to the question of “can you have lupus with a negative ANA?”:
1. I hope you kept personal records at home to give to your new doctor. One of my “Lupus Secrets” is to keep copies of your labs, biopsies, and doctor notes, especially those that first made the diagnosis of systemic lupus. The purpose is exactly for situations like this. I had two patients in the past end up having severe flares of their systemic lupus after their drugs were stopped by a new rheumatologist, due to this exact scenario (one had moved, the other changed insurance plans). Having all the records can make a huge difference and prevent this mistake.
2. Around 20% of SLE patients will have their ANA become negative on successful treatment. These are typically patients who go into remission or “low disease activity.” Recent studies also show that they end up having fewer flares than other patients. In the past, we always taught that the ANA never needs repeating once positive the first time in SLE patients because it is not reliable in following disease activity on treatment. However, now, we know that it helps give our patients information about prognosis. If it becomes negative, we can tell our patients, “this is great news! You have a lower likelihood of flaring compared to patients whose ANA stays positive, as long as you keep taking your medications.”
Disclaimer: This is for medical information only and is not for individual medical advice.
Causes of, reasons, and solutions (if needed) when the ANA is negative and one wonders “can you have lupus with a negative ANA?”:
“Can you have lupus with a negative ANA?” Yes… for many reasons as noted below
– When you have systemic lupus erythematosus (SLE) that is under good control on treatment (as in this patient)
PROS = this is great, you are less likely to flare!
CONS = a new doctor could question the diagnosis. Keep all your old records and labs!
– Laboratory error during the workup of SLE, especially when done by the ELISA or multiarray method
SOLUTION = ask for your ANA to be done by 2 different methods, especially by immunofluorescence
or ask for the AVISE Lupus test
– Have SLE plus a different autoantibody, especially anti-SSA antibody and ribosomal-P antibody SOLUTION = check anti-SSA and anti-ribosomal-P if someone has SLE symptoms
or ask for the AVISE Lupus test
– Someone has very early SLE with fluctuating low level ANA levels
SOLUTION = repeat ANA test using two different methods, especially by immunofluorescence
or ask for the AVISE Lupus test
– If have severe hypogammaglobulinemia (immunodeficiency) and have SLE
SOLUTION = ask your doctor to order the AVISE Lupus test
– Childhood SLE
Especially younger children have a much higher chance for ANA negativity
However, they usually become ANA positive as they get older and their lupus worsens
– Cutaneous (skin) lupus
Most patients are ANA negative when it is confined to the skin
To answer this question, you need to understand how the immune system works. One of the key things in the immune system is antigen presentation (figure 30.1A). Antigens are proteins that cause the immune system to make antibodies directed toward those specific antigens for protection. For example, let us say you are infected with parvovirus, which can cause a cold-like illness and sometimes even rash, joint pain, and even a lupus-like illness. The immune system “sees” the proteins (which act as antigens) on this virus, recognizes that they do not belong to the body, and launches an all-out war against the virus. It does this by making antibodies that can attach to the parvovirus antigens, which in turn identifies the virus invaders as the “bad guys.” Subsequently, this alerts other white blood cells of the immune system to attack the virus. The immune system has now learned that parvovirus is a “bad guy.” It is now able to produce these antibodies that recognize parvovirus for the rest of your life. Suppose you are infected by parvovirus ever again. Your immune system’s white blood cells can attack the virus so that you do not get sick from it ever again.
Hydroxychloroquine changes the acidity inside the portions of immune cells that recycle antigen proteins
So now, let us go a little deeper into how the body makes these antibodies in the first place, focusing on a concept called antigen processing (figure 30.1A). This is a very technical discussion that can be skipped by many people reading this book. However, it can be interesting for the person who wants to know more about how anti-malarial medicines work. Macrophages are white blood cells that are responsible for identifying foreign antigens for the immune system. You can think of them as the frontline soldiers that come into contact first with any unusual antigen proteins such as viruses and bacteria invading the body.
Macrophages are often also called “antigen-presenting cells” in immunology. In lupus, where the immune system starts to attack parts of the body itself, the antigens it thinks are foreign are actually antigen proteins naturally occurring in the body. When the macrophages see these antigens (such as proteins from skin cells), they engulf them into little bubbles called vacuoles (follow along in figure 30.1A). The vacuoles break down (or digest) these antigen proteins into numerous smaller components and reassemble them into structures that are then attached to the outside of the macrophage cell surface. The macrophages then show these antigens (antigen presentation) to other white blood cells of the immune system (especially T-cells) so that they can recognize them as being “bad” proteins. This causes other white blood cells (called B-cells) to start making antibodies directed against these antigen proteins. However, in lupus, these antigen proteins that end up being attacked belong to the person’s own body. The antibodies produced to attack the body’s own antigens are called “auto-antibodies.”
A well-known example in systemic lupus erythematosus (SLE) is when ultraviolet (UV) light can damage skin cells. These can then release their inner contents, such as the nucleus and its own DNA, into the surrounding tissues and bloodstream. The lupus immune system can then make anti-DNA autoantibodies that attach to the person’s own DNA from the skin cells (thinking that the DNA is a foreign attacker). This combination of the DNA protein antigen bound to the anti-DNA antibody is called an “immune complex.” These immune complexes can then travel throughout the body, depositing in other tissues where the lupus immune system can cause inflammation and damage. An important example of this is the kidneys. These immune complexes can contribute to kidney inflammation (lupus nephritis). This illustrates how UV light exposure can cause a lupus rash in the area of exposure and in distant parts of the body, like the kidneys.
For this antigen presentation to occur, the macrophages’ vacuoles must have a low pH level (in other words, they must be acidic). Otherwise, the enzymes of the vacuoles that are responsible for processing the antigens will not work. The anti-malarial medicines (such as hydroxychloroquine, Plaquenil) enter the macrophages and subsequently concentrate inside these vacuoles. The anti-malarials have a higher pH level and cause the vacuoles to develop a higher pH level (figure 30.1B). The vacuole enzymes only work under precise pH conditions. This higher pH level in the vacuoles prevents the macrophages’ digesting enzymes from breaking down the antigens to present the T-cells. Therefore, the T-cells cannot “see” these antigens and do not signal the B-cells to make the lupus autoantibodies. Therefore, the anti-malarial medicine calms down the immune system of the person who has lupus. Interestingly, though, it does not actually cause overt immunosuppression. In other words, the immune system can still function normally in different areas and still protects the person from infections and cancer.
Why hydroxychloroquine is not a cure for autoimmune diseases-
After reading the above, one may think it sounds like a cure! It stops autoantibody formation; therefore, it should control lupus completely!
We wish it were that easy. This is just one little tiny part of the immune system. There are many other sections of the immune system that are functioning abnormally in SLE. Also, hydroxychloroquine doesn’t completely stop antigen processing and antibody formation. It is a weak medication. Think of it as “calming down” the process, not eliminating it entirely. And, thank goodness it doesn’t! We need antigen processing to keep working so that our immune system still fights off infections, cancers, etc. The immune system continues to function well with antimalarial drugs. In fact, SLE patients who take hydroxychloroquine are less apt to get infections and cancers compared to patients who do not take it.
Also, this is not the only way that antimalarials work on the immune system. They also work in other ways. For example, we think that inhibiting part of the immune system called toll-like receptors probably plays a more critical role in how antimalarials help in treating lupus. However, delving deeper is beyond the scope of this post.
That would have to be the subject of a different (long) post. The purpose of this article was to just give one part of the story on why a medicine used to treat an infection would work for an autoimmune disease. The immune system is indeed fascinating!
electron microscope of malarial food vacuole (fv) inside the malaria parasite. This is where Plaquenil changes the pH (credit cited below)
How hydroxychloroquine kills malaria-
A similar thing occurs in malaria. Malaria is an infection due to single-celled parasites called Plasmodium that get into humans from mosquito bites. The malaria organisms get into the red blood cells, where they ingest iron-rich hemoglobin. The malaria parasite needs to digest this hemoglobin inside vacuoles within their own bodies (similar to the macrophages of the immune system ingesting antigen proteins inside their vacuoles). The malaria organisms digest the proteins of the hemoglobin to use for food and reproduce. Just as our macrophage vacuoles need an acidic environment to digest antigen proteins, the malaria organisms also require an acidic environment to digest the hemoglobin and dispose of the waste product (the iron-rich heme portion of the hemoglobin). The anti-malarial medicine dissolves into the vacuoles of the malaria organisms and raises their pH levels. The malaria organisms are unable to digest the hemoglobin and to get rid of the heme. The heme molecules combine with the anti-malarial medicine molecules and build up inside the malaria organisms, trapped within their vacuoles. This is toxic to the malaria organisms, and they stop reproducing and hopefully die.
The bottom line is that anti-malarials appear to work by increasing the vacuoles’ pH inside malaria organisms and macrophages. These vacuoles usually ingest hemoglobin (in the case of malaria organisms) or antigen proteins (in the case of macrophages in people with lupus). When the pH is increased, these vacuoles are unable to process these components. In the case of malaria, the malaria organisms die due to the buildup of toxic waste products. In the case of lupus, the macrophages cannot process antigens properly to present them to T-cells. Therefore the immune system is calmed down so that it does not attack the body (such as the skin, joints, or kidneys) as much.
Anti-malarial drugs have other effects on the immune system. However, we will only discuss the above effect as it is simple to illustrate.
Torigoe M, Sakata K, Ishii A, Iwata S, Nakayamada S, Tanaka Y. Hydroxychloroquine efficiently suppresses inflammatory responses of human class-switched memory B cells via Toll-like receptor 9 inhibition. Clin Immunol. 2018 Oct;195:1-7. doi: 10.1016/j.clim.2018.07.003. Epub 2018 Jul 4. PMID: 29981383.
Wang F, Muller S. Manipulating autophagic processes in autoimmune diseases: a special focus on modulating chaperone-mediated autophagy, an emerging therapeutic target. Front Immunol. 2015;6:252. Published 2015 May 19. doi:10.3389/fimmu.2015.00252
Lupus Question of The Day: Is Benlysta for mild lupus nephritis?
Ask Dr. T question and shortened answer about Benlysta in lupus nephritis
Question of the Day:
“I have lupus nephritis and just heard that Benlysta has been approved to treat it. I have stage 3 disease. Is this medication more for people with mild nephritis?“
Dr. T’s Answer:
Types of mild lupus nephritis-
“It all depends upon what your definition is of “mild nephritis.” I would consider ISN/RPS classes 1 (minimal mesangial) and 2 (mesangial proliferative) as mild. They do not need treatment at all (except for Plaquenil/hydroxychloroquine plus often an angiotensin receptor blocker, such as losartan, or an angiotensin converting enzyme inhibitor, such as lisinopril, medicine to lower protein in the urine).
In addition, lupus podocytopathy could also be considered a “mild” type of lupus nephritis. Usually, lupus podocytopathy goes into remission quickly with Plaquenil plus steroids, with a rapid steroid taper. Therefore, for my definitions of “mild” lupus nephritis, Benlysta is not needed.
Benlysta was used in cases of severe lupus nephritis in the BLISS-LN study-
The Benlysta lupus nephritis clinical trial (called BLISS-LN) showed that when Benlysta was added on top of standard of care (Plaquenil, steroids and either mycophenolate or cyclophosphamide) there were significantly more people who improved on Benlysta plus standard of care compared to those who were treated with standard of care alone. More patients had partial or complete responses (including remissions) compared to standard of care (i.e. how we treat lupus nephritis before Benlysta). Plus… there were no significant differences in side effects, which is amazing. Also, more patients who got placebo plus standard of care died or went into complete kidney failure compared to the Benlysta group.
This is all great news. The lupus community is excited about this landmark event: Benlysta being the first FDA-approved drug for lupus nephritis ever. “
UPDATE September 2021: Lupkynis became the second FDA-approved drug for the treatment of lupus nephritis in January 2021.
Donald Thomas, MD, author of “The Lupus Encyclopedia” and “The Lupus Secrets”
Note that this post is for informational purposes only, and is not meant to be specific medical advice. Always seek the advice of your healthcare provider with any questions regarding your own medical situation.