Vaccination is the first line of defense against infections, which is especially important for people with autoimmune diseases. But there are also risks that scientists and doctors are actively discussing when deciding whether to vaccinate for autoimmune diseases.
The topic of autoimmune disorders has been relevant in science for decades, but there is still no exact answer to what causes them. Scientists have put forward several theories. Let’s put them together to understand how an abnormal response to a vaccine occurs and whether vaccinations for autoimmune diseases can be done in theory. As for practice, the reaction is unpredictable, and the patient decides this issue together with the attending physician according to the circumstances.
Possible causes of autoimmune diseases
The production of antibodies against the body's own cells is a normal process for maintaining healthy homeostasis. Provided that he does not go beyond the boundaries of what is permitted. External antigens or improper cell coordination can disrupt the balance of immune forces. Even a simple pathogen attack can lead to a shortage of T-regulators, and they will not have time to eliminate a random autoimmune reaction in time.
The functioning of the immune system is controlled by many genes, and their activity is controlled by a whole galaxy of nuclear factors and auxiliary molecules. A breakdown can occur in any part of this complex mechanism, no matter how old a person is. Hereditary tendencies increase the chances. Both internal and external triggers trigger incorrect gene expression or mutation. Sometimes the sum of a variety of factors is decisive: from absorbed chemicals to severe stress.
Of particular interest is the hypothesis of molecular mimicry : when immune cells confuse an antigen and the tissues of their own body. This is quite possible; their amino acid sequences may be similar.
For example, the hepatitis B virus polypeptide contains a region almost identical to a fragment of the myelin protein. And the body mistakes the products of some pathogens, such as human cytomegalovirus, for its own immunity mediators. A mistake can become fatal and develop into an autoimmune reaction [1].
Can vaccines cause autoimmune disorders?
It is likely that vaccines can cause autoimmune diseases (AIDs) through the same mechanism as infections [2]. There is no direct evidence of such a dependence. It is almost impossible to find out whether vaccination was the trigger for the onset of AIDS. Researchers disagree: the first report isolated cases and try to link them with vaccination, the second experimentally reject such a connection [2–4].
Another important question: how will autoimmune diseases behave after vaccinations, is the risk justified?
There is a possibility that [2.11]:
- the virus from the vaccine will develop into a real infection;
- the effect of the vaccine will not appear at all or will be insufficient;
- autoimmune disease will become more complicated after vaccination.
First things first.
Is there any point in getting vaccinated?
Many people are instinctively afraid of vaccinations, because an injection, in essence, is the injection of a foreign active substance with a sharp needle. This fear was formed by our ancestors to reflexively recoil from the sting of a scorpion or the teeth of a snake, or to swat a mosquito. Often this ancient mechanism prevents people from adequately assessing the benefits of vaccination.
Among patients with AIZ, infectious diseases are twice as common as in the general population and are more severely tolerated [2]. The pathogen not only causes immediate symptoms, but also introduces the risk of complications of AIZ. Some infections can also trigger the occurrence of AIDS in a healthy person. A correlation between the incidence of multiple sclerosis and previously suffered chicken pox, mononucleosis, etc. has been revealed. [5].
Vaccination for autoimmune diseases is the most effective way to avoid infections and associated complications. Whatever the potential risk of a vaccine, the infection itself can cause incalculably more harm [2]. You need to approach the procedure responsibly and make a decision together with your doctor.
Sulfasalazine
Sulfasalazine is an anti-inflammatory and antibacterial agent used in gastroenterology and rheumatology. Inflammatory bowel diseases (Crohn's disease, ulcerative colitis) are a pressing problem in gastroenterological practice. However, despite certain successes in the development of new methods for diagnosing and treating these diseases, there is still a lack of knowledge in the field of the etiology of the development of inflammatory processes in the intestine. Thus, one of the issues facing scientists that needs to be addressed is increasing the effectiveness of already known drugs. The principle “the new is the well-forgotten old,” as it turns out, also works in relation to pharmacology. Sulfasalazine is far from new on the pharmaceutical front: it has been used for more than 50 years. This drug was synthesized by linking two substances with a nitrogen group: aminosalicylic acid and sulfapyridine. The pharmacological effect of the drug is based on the properties of both of its structural components. Salicylic acid with an amino group in position 5 has anti-inflammatory activity, inhibits the synthesis of inflammatory mediators prostaglandins and neutralizes the effect of cyclooxygenase. Sulfapyridine, in turn, has an antibacterial (bacteriostatic) effect aimed at streptococci, gonococci, diplococci and Escherichia coli. After taking sulfasalazine tablets, approximately 25% of the dose is absorbed in the upper gastrointestinal tract, and due to the portal-biliary circulation of bile acids, more than half of this amount is subsequently returned to the intestine.
As a result, about 90% of the drug enters the colon, which should be considered a very high figure. Clinical trials of sulfasalazine showed the effectiveness of the drug in treating mild and moderate forms of ulcerative colitis (improvement was observed in 64-80% of patients, with a 30% improvement when taking placebo). The same studies demonstrated a dose-dependence of the effect of sulfasalazine, with increasing doses often associated with an increased risk of certain adverse reactions.
Another area of application of sulfasalazine is the treatment of rheumatoid arthritis. This is one of the most common chronic joint diseases, which is based on the inflammatory process. In recent years, the capabilities of rheumatologists in the fight against this disabling disease have increased, incl. thanks to the emergence of new drugs. From this point of view, sulfasalazine can be considered as a “new old” drug with antirheumatic activity again proven in the 80s. The positive effect of this drug is associated with its ability to influence the microflora of the large intestine. Clinical studies have shown 63% success in treating patients with the articular form of rheumatoid arthritis after a year of taking the drug.
Sulfasalazine is available only in tablet form. The drug should be taken after meals. The dose and frequency of administration are determined by the attending physician.
Autoimmune diseases and coronavirus vaccination
The risk of contracting COVID-19 is also real for people with autoimmune disorders. The risk of serious complications not only from Covid, but also from AIZ is extremely high. The manufacturers of the first Russian vaccines “Gam-COVID-Vac” and “EpiVacCorona” write in the instructions: “use with caution in AIZ”, since there is not enough data on people in this group [6–7]. The manufacturers of mRNA vaccines, Pfizer and Moderna, also do not contrast autoimmune diseases and coronavirus vaccinations [8–9].
Before getting any vaccination, consult your doctor [2.10]:
- About its safety - whether the vaccine will cause complications of an autoimmune disease.
- About its effectiveness - is there any point in getting vaccinated if immunity works differently, what are the features of vaccination.
- About compatibility with immunotherapy - is it safe, is it effective, is it necessary to change the course of treatment.
Is it possible to get vaccinated?
The vaccine is given only outside periods of exacerbation. The response to the vaccine depends on the type and severity of AIDS, the type of vaccine, the patient’s age, and treatment regimen [2–4].
Types of vaccines [2–4]:
- Live attenuated vaccines are highly effective. However, with reduced immunity, for example, while taking immunosuppressants, a weakened pathogen from a live vaccine can “take root” in the human body. In general, live vaccines are contraindicated in patients undergoing immunotherapy.
- Inactivated vaccines (with a “killed” pathogen) or inert (subunit, split vaccines - with a non-virulent fragment) are weaker than live ones. Adjuvants and revaccination are required. However, they are safer and less demanding on storage conditions than live vaccines.
- Recombinant (vector) vaccines consist of a non-pathogenic viral carrier and a DNA or RNA fragment of the pathogen. Some scientists suggest that the vector may behave like a virus from a live vaccine [11]. This has not been shown in practice. Their effectiveness and safety are comparable to inactivated ones.
- Prior to COVID-19 vaccines, messenger RNA vaccines There is not enough information to talk about the safety of this type of coronavirus vaccine for autoimmune diseases. At the same time, there are no theoretical grounds to assume the opposite.
BE CAREFUL
A patient with reduced immunity can become infected from a household member who has received a live vaccine against rotavirus, polio and some other infections.
Medical Internet conferences
Hemorrhagic vasculitis, described by Schonlein (in 1837) and Henoch (in 1868), is one of the most common and favorable diseases from the group of systemic vasculitis.
The basis of this disease, named Henoch-Schönlein purpura after its discoverers, is an immune complex inflammation with the participation of IgA and complement, occurring mainly in the walls of small vessels of the skin and internal organs [4,7]. According to modern data, the incidence of hemorrhagic vasculitis is 140 cases per 1 million .population. Boys aged 4-17 years are most often affected [3,4,7]. The main diagnostic criterion is a maculopapular hemorrhagic rash (palpable purpura), located on symmetrical areas of the limbs, buttocks, torso and does not disappear with pressure [6,7]. The rash never appears on the face or neck. In 75% of patients, an articular syndrome can be identified, which has the nature of migrating polyarthralgia involving the knee, ankle, and, less often, elbow joints and does not lead to the development of persistent deformities [5].
In 60-80% of children and 40-60% of adult patients, hemorrhagic vasculitis has a pronounced onset with damage to the gastrointestinal tract in the form of intense cramping pain in the mesogastrium, ileal region and dyspepsia, which requires differential diagnosis with acute appendicitis [5,7].
In 35% of cases, abdominal syndrome is manifested by gastrointestinal bleeding (hematemesis, melena, hematochezia), leading to the development of hemorrhagic shock [5,7].
Relatively rare and severe complications at the onset of the disease include intestinal perforation, as well as intestinal obstruction, associated in 70% of cases with intussusception of the small intestine [6].
In the long term, the prognosis for the patient depends on the involvement of the kidneys in the process, which is observed in almost 2/3 of patients [6] and correlates with the severity of the abdominal syndrome [1,5,7]. The clinical manifestation of hemorrhagic vasculitis is considered to be glomerulonephritis with minor nephrotic and urinary syndromes, which has a favorable course in children and a tendency to chronicity in adults [5,6].
In 1/3 of patients, gross hematuria is observed at the onset of nephritis [5]. In isolated cases, nephrotic syndrome with massive proteinuria is observed, which is prone to progression with the development of chronic renal failure [5].
The nature of morphological changes in the glomeruli correlates with the severity of clinical manifestations and varies from minimal mesangial proliferation to severe nephritis with crescents, requiring active immunosuppressive therapy [1,5,6,7]. The proportion of renal glomeruli with crescents of more than 50% of the total number of glomeruli is considered an unfavorable prognostic factor [5].
Occasionally, in the midst of vasculitis, pulmonary hemorrhage, pericarditis, and coronaryitis may develop, leading to heart failure and myocardial infarction. As part of Henoch-Schönlein purpura, cases of cerebrovasculitis have been described, manifested by subarachnoid and intracerebral hemorrhages, persistent headache, seizures and behavioral disorder [2,4,5].
Laboratory signs of hemorrhagic vasculitis are nonspecific [5,6]. An increase in ESR and the amount of acute phase proteins in the blood serum correlates with the clinical activity of the disease. Characterized by moderate hyperthrombocytosis and increased spontaneous platelet aggregation [6]. The concentrations of α2 and γ-globulins in the blood often increase, and circulating immune complexes are detected in more than half of the cases. [7]. In some patients, poly- and monoclonal cryoglobulinemia may be detected [7]. However, normal laboratory data do not exclude the diagnosis of hemorrhagic vasculitis in the presence of clinical symptoms. A typical finding in a skin biopsy for hemorrhagic vasculitis is granulocytic infiltration of the walls of arterioles and venules, as well as fixation of IgA-containing immune complexes in the vascular wall [5,7].
As noted above, Henoch-Schönlein purpura has a favorable prognosis and is highly treatable even in the advanced stage of the disease. However, there are known cases of severe hemorrhagic vasculitis with refractoriness to therapy and the threat of developing chronic renal failure.
To confirm this, we present our own clinical observation.
Patient K.S.A. was admitted to the rheumatology department of the Saratov Regional Clinical Hospital in January 2015 with complaints of isolated small-point hemorrhages on the skin of the lower extremities, on the outer surface of the elbow joints, increasing after physical activity and in an upright position.
From the medical history it is known that in childhood the patient experienced accelerated growth. From 15-16 years of age – pain in the knee and ankle joints of a mechanical nature. I did not receive treatment. In May 2013, small punctate hemorrhagic rashes, non-palpable and non-itching, appeared for the first time on the medial surface of the ankle joints, which resolved on their own after two days. A similar rash appeared periodically and disappeared over the next six months, but with each new exacerbation the patient noted a gradual rise of the rash to the level of the thighs. In October 2013, hemorrhagic vasculitis was diagnosed for the first time. Due to the ineffectiveness of prednisolone (dose 60-120 mg IV), the hospital was treated with dexamethasone 8 mg IV, against the background of which regression of skin rashes was noted with preservation of single elements in the ankle joint area.
In November 2013, intense cramping pain in the epigastrium and a recurrent hemorrhagic rash on the legs appeared. In a clinical blood test, an increase in the level of acute-phase indicators was noted; FEGDS revealed erosive gastroduodenitis. During therapy with prednisolone (8 tablets/day) and plaquenil (200 mg/day), the abdominal manifestations stopped, but skin rashes in the feet area persisted, and a hemorrhagic rash appeared over the elbow joints.
In December 2013, nausea, vomiting “coffee grounds,” and repeated loose stools mixed with scarlet blood clots appeared. No data on surgical pathology were obtained in the hospital. Daily proteinuria was 0.5 g/day, erythrocytes of 40500 were found in Nechiporenko's test. Due to the development of nephritis, prednisolone was prescribed at a dose of 10 tablets/day for a month (followed by a gradual reduction in dose) and sulfasalazine 2 g/day. During therapy, the abdominal syndrome did not recur, but skin rashes and signs of nephritis persisted.
In February, April, June, August, September 2014, pulse therapy with prednisolone 1000 mg was carried out, which led to a decrease in the signs of nephritis (daily proteinuria in August 0.1 g) and incomplete regression of skin manifestations in the form of pinpoint rashes on the legs.
In September 2014, the patient suffered from a sore throat, and therefore took amoxiclav. Against this background, multiple hemorrhagic rashes appeared on the skin of the lower extremities, daily proteinuria was 0.34 g, in the Nechiporenko test - erythrocyturia (9500).
Prednisolone was resumed at a dose of 10 mg/day. in combination with azathioprine 150 mg/day. However, despite treatment, he noted the appearance of abdominal syndrome (diarrhea mixed with blood, vomiting, increase in temperature to 38oC), persistence of skin rashes and signs of nephritis.
In November 2014, the patient had increased erythrocyturia (40.5 - 37.5 thousand in the Nechiporenko test) and a computed tomography scan of the abdominal cavity and retroperitoneal space revealed a microlith of the left kidney; with FEGDS - hemorrhagic gastritis.
Azathioprine was replaced by sulfasalazine at a dose of 2 g/day, the dose of prednisolone remained the same (10 mg/day). During therapy, positive dynamics were noted: regression of skin rashes with the preservation of single small punctate elements on the outer surface of the elbow joints and in the shin area with symptoms of orthostasis. Remission of nephritis could not be achieved.
During a planned hospitalization at the Regional Clinical Hospital of Saratov in December 2014, the patient’s condition was satisfactory, his physique was asthenic. On the skin of the legs and the extensor surface of the elbow joints there are pinpoint, non-palpable hemorrhagic rashes without fusion. On the feet there is residual dark brown pigmentation. Lymph nodes are not palpable. Respiratory rate is 16/min, breathing is harsh, no wheezing. The boundaries of the lungs are not changed. On auscultation, cardiac activity is rhythmic, blood pressure is 110/70 mm Hg. the same on the right and left hands. The abdomen is soft, painless on palpation. Physiological functions are not impaired. In the general blood test, ESR is 5 mm/h, CRP is negative, daily proteinuria is 0.5 g/day.
In the general urine analysis: red blood cells 10-12 per cell, protein 0.11 g. In the Nechiporenko test there are 40.5 thousand red blood cells with FEGDS - focal atrophic gastroduodenitis.
Due to the resistance of nephritis to traditional therapy, it was decided to increase the dose of sulfasalazine to 6 g/day. During treatment, the rash completely disappeared, residual pigmentation was noted on the skin of the legs and above the elbow joints, and the abdominal syndrome did not recur. At discharge, a general urinalysis revealed single red blood cells in the visual field. Daily proteinuria – 0.1 g/l. During dynamic observation in February 2015. No protein was detected in the general urine test; daily proteinuria was negative.
A feature of the described case of hemorrhagic vasculitis is persistent urinary syndrome, refractory to traditional treatment methods
Predictors of severe course and chronicity of nephritis in our patient were: male gender, patient age over 5 years, history of abdominal syndrome. The administration of high doses of sulfasalazine, which is not included in the standard treatment regimen for Henoch-Schönlein purpura, made it possible to achieve complete remission of the disease within a short time.
The effect of vaccines against the background of medications
Drugs that simulate or suppress immunity also affect the effectiveness of vaccines. Decreased response depends on the type, dosage of medication, and duration of use. During treatment with immunomodulators, non-live vaccines are used. The intervals between revaccinations are determined by the results of an antibody titer test [2–4].
It is advisable to check your vaccination status before starting immunotherapy. In 3-4 weeks, if there is no exacerbation and the doctor gives the go-ahead, you can be vaccinated with a live vaccine. As a rule, the immune status is restored 3 months after the end of immunotherapy. In the case of corticosteroids, the period is about a month [2–4].
The reaction to vaccination in each specific case is unpredictable. But the statistics are encouraging. Studies have shown that influenza and pneumococcal vaccines have a complication rate of less than 5% in patients with multiple sclerosis [2–4]. In general, exacerbations of AIDS after the use of non-live vaccines are quite rare. The immune response in people with AIZ who are not undergoing immunotherapy is not much lower than in the population [2–4, 10].
Metypred and Sulfasalazine for reactive arthritis
Natalia
July 19, 2020
Hello. Since May, my feet, forefoot, and instep have been hurting, especially after a night’s sleep, I couldn’t walk on the floor barefoot, I couldn’t stand on my toes, there was a burning sensation in the area where the heel began. In June, my left foot in the area of the 3rd-5th toe became swollen. Before this, in early April, I installed 2 dental implants, in mid-April I lay for 3 days with a temperature of 38-39 and discovered suppuration in the area of one implant. They cleaned and put everything away for me, they said that it was superficial and food got in. Then I took antibiotics Amonsiclav for 7 days. With pain in the feet, I did an ultrasound of the feet (according to the ultrasound, pre-reactive arthritis), took tests for CRP 35.4, RF <20, uric acid 216, ESR 55 (according to Westergon), the rest of the blood flow parameters were normal and consulted a rheumatologist. Diagnosis of reactive arthritis. Treatment was prescribed with Azithromycin for up to 12 days, nalgesin forte 1 t/day for 10 days, Karmalis gel topically, omiprazole for up to 1 month and additional. ASLO tests (negative), smear for chlamydia (negative), HLA B27 (detected) and again CBC, CRP. Now CRP is 14.4 ESR 55 (according to Westergon). My general health has improved significantly, I haven’t taken NPP for a week, I can walk barefoot, stand up on my toes, the pain is moderate, in the morning after sleep it hurts to step on my feet, the swelling persists, at night and at rest the pain does not bother me, I feel like I can do without painkillers. The temperature was always normal. Now the prescription: Metypred 4 mg-1 tab in the morning after meals, Sulfasalazine 1 week-1 tablet 2 times, 2nd week-1 tablet 3 times, then 2 tablets 2 times until 4 months, hepaprotectors, injections for 5 days Texared 20 mg, Calmirex and continue Nalgesin Forte 1 tablet for up to 10 days and for pain. Report in 1-1.5 months with tests of CBC, CRP, biochemistry, AT to double-stranded DNA, ANA, ANF. Only at home I read what medications they prescribed me. And it became scary to take a hormonal drug, due to side effects and addiction, the appearance of pain after withdrawal. Now there is no severe pain. I understand that the ESR is high and an acute inflammatory process means, but the CRP has decreased, and there is an improvement in my health. Is it possible that the ESR will decrease after the injections? I can get them done and get tested. Or are Metipred and Sulfasalazine indicated regardless of ESR? Unfortunately, I can’t ask my doctor these questions, because I make an appointment with him a month in advance. It was only at home that I noticed that there was no indication for how long to take Metipred. Ultrasound conclusion: echographic signs of inflammatory changes in the tarsometatarsal joints of the left and right tibia (wedge-metatarsal and cuboid-metatarsal joints), as well as intertarsal joints, more pronounced on the left, moderate plantar fasciitis on the left.
Age:
38
Chronic diseases:
No
The question is closed
reactive arthritis
Spondylitis
foot pain