Imagine diving into the cool waters of the Seine on a hot summer day, with the Eiffel Toweras a backdrop. This scene, which may seem idyllic, has actually been banned for nearly a century. Yet, as the Paris 2024 Olympic Games approach, the issue of swimming in the Seine is resurfacing, raising both hope and concern.

I. Major health risks 

Swimming in the Seine today is not without danger. Water pollution, mainly of microbiological origin due to viruses, bacteria and parasites, poses significant health risks. Here is an overview of the main dangers to which swimmers are exposed.

A. Gastrointestinal infections 

The water of the Seine is often contaminated by bacteria such as Escherichia coli and enterococci, which are indicators of fecal pollution. These bacteria come mainly from untreated wastewater discharges and animal droppings. Accidental ingestion of this water can lead to gastrointestinal infections, manifested by symptoms such as:

 

• Diarrhea
• Stomach ache
• Nausea
• Vomiting

 

These infections can be particularly serious in vulnerable people, such as children, the elderly and those with weakened immune systems.

B. Skin and ENT infections

Skin contact with polluted water from the Seine can cause various skin and ENT (ear, nose, throat) infections. The risks are increased for people with wounds or skin lesions. Possible infections include:

• Dermatitis: inflammation of the skin that can cause redness, itching and rashes.

• Eye infections: conjunctivitis and other eye inflammations.

• Ear infections: external otitis, often painful and bothersome.

• Throat infections: pharyngitis and other inflammations of the upper respiratory tract.

These infections may require medical treatment and, in some cases, lead to more serious complications.

C. Leptospirosis

Leptospirosis, also known as “rat disease,” is a serious bacterial infection transmitted through contaminated rodent urine. This disease can be contracted through skin or mucous membrane contact with contaminated fresh water. Symptoms of leptospirosis may include:

• High fever
• Severe headaches
• Muscle pain
• Chills
• Vomiting

In the most severe cases, leptospirosis can lead to liver, kidney or meningeal complications, and can be potentially fatal if not treated promptly.

II Current status of water quality

The quality of the Seine's water is a major concern for both authorities and citizens. Despite efforts made in recent years, the current state of the river's water remains problematic, particularly with regard to swimming. Let's take a closer look at the results of recent studies and their significance.

A. Results of recent studies

The NGO Surfrider Foundation, known for its commitment to protecting oceans and waterways, has conducted a series of tests on the water quality of the Seine. The results are revealing of the current state of the river:

• Of the 14 tests carried out, only one was deemed satisfactory according to bathing standards.

• The majority of the samples taken showed levels of bacteriological pollution above the authorised thresholds.

• Concentrations of bacteria such as Escherichia coli frequently exceeded acceptable limits for bathing water.

• These results highlight the persistence of water quality problems, despite the sanitation efforts undertaken.

B. Comparison with legislative standards

European and French legislation sets strict standards for the quality of bathing water. These standards are based on the presence of certain bacteriological indicators, including E. coli and intestinal enterococci. Here is how the Seine ranks according to these standards:

	Sample from June 10, 2024	“Excellent” water quality:	“Sufficient” water quality:
E. COLI:	2216 CFU/100 ML	≤ 500 CFU/100 ML	≤ 900 CFU/100 ML
Intestinal enterococci	563 CFU/100 ML	≤ 200 CFU/100 ML	≤ 330 CFU/100 ML

Tests carried out on the Seine show that these thresholds are regularly exceeded, sometimes significantly. For example, concentrations of CFU/100 ml of E. coli were recorded at the Pont Alexandre III in June 2024, well above the thresholds recommended by the and triathlon federations.

C. Factors influencing water quality

• Wastewater discharges: Despite advances in wastewater treatment, overflows can still occur during heavy rains.
• Urban runoff: Rainwater running off impermeable surfaces in the city carries various pollutants into the river.
• Industrial activity: Although regulated, industry continues to contribute to the pollution of the river.
• River traffic: Boats traveling on the Seine can be a source of pollution, particularly through their discharges.

Conclusion

Swimming in the Seine carries significant health risks due to microbiological and chemical pollution of the water. Gastrointestinal, skin, ENT infections and leptospirosis are the main dangers to which swimmers are exposed. Despite considerable efforts to improve water quality, particularly in view of the Paris 2024 Olympic Games, swimming in the Seine remains prohibited and strongly discouraged without specific authorization.

 The identification of a variant of the TLR7 gene as a cause of lupus erythematosus opens the door to the search for more effective treatments for the disease.

Lupus is an autoimmune disease caused by the activation of the immune system against the body's own tissues, leading to inflammation and damage to joints and certain organs. Its causes include both environmental and genetic factors, which have not yet been characterized in detail.

Currently, lupus is an incurable disease. Although there are treatments aimed at alleviating its symptoms, some of them, which focus on reducing the action of the immune system, have the side effect of increasing patients' susceptibility to infections.

This is one of the main reasons why it is necessary to complete the puzzle of genetic factors that influence its development to a greater or lesser extent. Deciphering the genetic causes of the disease will allow us to better understand the biological mechanisms involved in it and identify points where therapeutic action could be taken.

A recent study led by researchers at the Australian National University, with Spanish direction and participation, has just taken a very important step towards better understanding lupus.

The researchers have identified a genetic cause of the disease that offers a new path for the development of treatments: the presence of gain-of-function variants in TLR7, a gene involved in protecting the immune system against viral infections. The results are published in Nature.

Identifying the connection between TLR7 and lupus

The TLR7 gene encodes a receptor, also called TLR7, that recognizes single-stranded RNA molecules derived from viruses and bacteria and activates the immune system in response. In addition, it can also be activated by the nucleoside guanosine and its endogenous derivatives, although this does not normally represent a threat to health because it occurs to a lesser extent.

Previous studies had already suggested that TLR7 function played a role in systemic lupus. Increased activity had been found in some B lymphocytes from patients and some common polymorphisms were associated with the disease. However, until now no genetic change had been identified in the TLR7 gene that had a determining effect on the onset of lupus.

The first direct link between the TLR7 gene and lupus was found when sequencing the genome of Gabriela, a young Spanish girl who had been diagnosed with a severe case of the disease at the age of 7. The severity and early onset of lupus led researchers to believe that it must be a case caused by a single genetic mutation.

By analysing Gabriela's entire genome, the researchers found a variant in the TLR7 gene that was likely to cause lupus: p.Tyr264His. Various elements pointed to the variant as being responsible for the young woman's disease: the variant caused an amino acid change, it was located in a region of the protein conserved between species, and the computer programs used to predict its effects indicated that it was a harmful variant.

As further evidence, the researchers found two more variants in TLR7 when analyzing the whole exome of other patients with systemic lupus, without detecting changes in any other known lupus-related genes in the implicated families.

Mutation causes lupus when introduced into mice

Based on functional studies in cells, the researchers found that the presence of the p.Tyr264His variant produces a TLR7 protein with greater affinity towards certain endogenous ligands with guanosine that, normally, would not activate the protein, which could explain the development of the autoimmune reaction characteristic of lupus.

To confirm the mutation's role in the development of lupus, the researchers introduced the mutation into mice, creating a strain they named kika, in reference to the name Gabriela had given to a stuffed animal she had been given during one of her hospital visits.

The team observed that the mutation (also called kika) was enough to cause lupus in the animals, which developed different autoimmune symptoms and experienced various organ damage.

The results explain why lupus is more common in women

The study also offers an explanation for why 9 out of 10 people with lupus are women. The TLR7 gene is located on the X chromosome, so that people with a male chromosomal sex have one copy, while those with a female sex have two.

As a biological mechanism of dosage compensation, in women one of the two X chromosomes is inactivated in their cells. However, TLR7 escapes inactivation in immune cells, which leads to the fact that in women there may be two active copies compared to the single copy present in male cells.

Thus, if there is an autoimmune response influenced by TLR7, the effect may be greater in women. And if, in addition, they are carriers of a variant that increases the affinity towards endogenous ligands such as the p.Tyr264His variant, its impact would be even greater.

The opposite example has been observed in the case of the response to SARS-CoV-2 infection, where the presence of genetic variants that produce a deficiency in TLR7 has been linked to a higher risk of developing COVID-19 in men.

Relevance for the development of therapies for lupus and other autoimmune diseases

The study shows that the identified TLR7 gain-of-function variant is sufficient to induce lupus, at least in mice. This result, together with previous data, offers an important step forward for the development of therapies for the disease.

“Even though there are only a small number of people with lupus who have variants in the TLR7 gene, we know that many patients have signs of overactivity in the TLR7 pathway,” said Nan Shen, co-director of the China-Australia Centre for Personalised Immunology, who was involved in the study. “By confirming a causal connection between the gene mutation and the disease, we can begin to look for more effective treatments.”

The team is currently working with pharmaceutical companies to develop or adapt treatments targeting the TLR7 gene that could be beneficial for lupus patients.

These treatments could also be relevant for other autoimmune diseases. “There are other systemic autoimmune diseases such as rheumatoid arthritis and dermatomyositis that fit into the same family as lupus,” says Carola Vinuesa, a researcher at the Australian Centre for Personalised Immunology, co-director of the China-Australia Centre for Personalised Immunology and director of the work.

“TLR7 could also play a role in these conditions,” says the researcher, who has formed a new research team at the Francis Crick Institute focused on identifying the mechanisms that contribute to the development of autoimmunity.

Another question that researchers point out as pending resolution is whether certain environmental stimuli such as the presence of viruses that can activate TLR7 (as is the case with SARS-CoV-2, responsible for COVID-19) can exacerbate the effect of the variant.

Reference: Brown, GJ, Cañete, PF, Wang, H. et al. TLR7 gain-of-function genetic variation causes human lupus. Nature. 2022. DOI: https://doi.org/10.1038/s41586-022-04642-z

 Immune thrombocytopenia (ITP) is a disease caused by the destruction of platelets or thrombocytes by the immune system itself. It is therefore an autoimmune disease.

There are different levels of severity and symptoms of ITP depending on the platelet count. The disease is characterised by an increased risk of bleeding. Platelet levels of between 150,000 and 400,000 per microlitre are considered normal.

When these levels decrease temporarily or persistently, without known triggering factors, then we speak of primary ITP. If the platelet count is below these levels, but above 50,000, it is normally asymptomatic and does not cause bleeding. In these cases, the disease will be difficult to diagnose.

If the platelet count is between 30,000 - 50,000, small hemorrhages often occur when there is trauma, blow, etc. If the count is between 10,000 - 30,000, petechiae, metrorrhagia, epistaxis, gingivorrhagia, etc. may occur spontaneously.

In this situation we speak of moderate thrombocytopenia. If the levels fall below 10,000 platelets per microliter, we are dealing with severe thrombocytopenia in which internal bleeding can occur in vital organs with serious consequences.

The origin of primary immune thrombocytopenia is unknown; although there are other forms of secondary thrombocytopenia associated with certain diseases, infections or the taking of certain medications.

Why does immune thrombocytopenia occur?

The decrease in platelet levels is due both to an increased destruction of platelets in the blood and to a defect in their production in the bone marrow. People who suffer from this disease possess certain antibodies, usually of the IgG type (although in some cases IgM and IgA are also involved), which are capable of recognizing certain proteins on the surface of these cells and marking them as if they were foreign elements to the body itself (antigens).

Consequently, platelets and their precursors in the bone marrow are recognized and eliminated by cells of the immune system, such as macrophages.

What precautions should a person with TPI take?

Physical activity should be controlled and free of dangers such as risky or contact sports, which can cause trauma. It is advisable to ask the doctor which activities should be avoided according to the person's lifestyle.

There are medications that can alter platelet activity, which is why it is always a good idea to ask your doctor before taking any medication.

Keeping the immune system in good condition is important to ensure that its response is balanced and that hypo and hyperactivity situations do not occur. In this regard, microimmunotherapy can be a support within a global strategy for treating immune diseases.

Bibliography

1. Karam D. Echevarría S. Diagnosis and treatment of immune thrombocytopenic purpura. Clinical practice guide. Mexican Social Security Institute.
2. Mayo Clinic. Idiopathic thrombocytopenic purpura. Patient Care and Health Information. Diseases & Conditions. Available at: https://www.mayoclinic.org/diseases-conditions/idiopathic-thrombocytopenic-purpura/symptoms-causes/syc-20352325.

  Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation of the joints. It is sometimes confused with osteoarthritis, but they are different inflammatory diseases.

It affects women to a greater extent, possibly due to the influence of estrogens in the generation of inflammation. In addition, women are more susceptible to autoimmune diseases due to methylation of the X chromosome. There is also a certain heredity with regard to connective tissue diseases, so having a mother with a history of the disease is a risk factor.

Rheumatoid arthritis causes pain, stiffness, swelling, and can even cause joint deformity and loss of normal joint movement. It can also be accompanied by fatigue, occasional episodes of fever, or other symptoms such as heart complications, osteoporosis, or lung complications.

The exact causes of this disease are still not fully understood, although it has been shown that the immune system plays a key role in its development and progression. A combination of genetic and environmental factors triggers an abnormal immune response that results in the production of autoantibodies and chronic activation of the immune system. Let's see what happens to the immune system.

The Adaptive Immune Response in Arthritis

The adaptive response  plays a crucial role in this joint disease. Both B cells and T cells, specialized lymphocytes, are altered and are key in the development of the pathology.

Specifically, an increase in CD4+ T cells and a decrease in Regulatory T cells, responsible for maintaining tolerance and preventing immune reactivity to structures and tissues, have been observed in the affected joints. CD4+ T cells produce proinflammatory cytokines such as interleukin 6, tumor necrosis factor alpha (TNF-α), and interferon gamma. All contribute to chronic inflammation and joint destruction.

B cells also play an important role. Immune complexes consisting of autoantibodies and antigens have been found in the joints of people with this disease. Especially B cells producing anti-citrullinated peptide antibodies (ACPA), are closely associated with disease severity and joint destruction in RA.

In addition, B cells can activate T cells and give rise to a vicious circle that perpetuates the inflammatory response.

Proinflammatory environment and cytokines in arthritis

Chronic inflammation is a hallmark symptom of rheumatoid arthritis. The synovial inflammation typical of arthritis has been shown to be mediated by excessive production of proinflammatory cytokines. These cytokines include IL-1β, IL-6, TNF-α, and IL-17, among others.

They promote the migration of inflammatory cells to the joints and stimulate the production of enzymes that degrade cartilage and bone. TNF-α is one of the most studied cytokines in this disease and has been identified as an important therapeutic target to reduce inflammation and disease progression in these patients.

Solving the Immunological Puzzle

Rheumatoid arthritis is a complex autoimmune disease that involves a dysfunctional adaptive immune response and chronic inflammation of the joints. It must be treated by specialists to prevent it from progressing to other locations and to maintain joint functionality.

Many of the available treatments usually help to relieve symptoms, although they do not always treat the root of the problem. In this regard, it is also worth considering approaches that allow the mediators involved to be modulated simultaneously, trying to redirect the immune response both locally and systemically, so that it works optimally, depending on each person's situation.

Immunomodulatory treatments are an option to consider in this case, since they can offer complementary support to symptomatic relief, helping to rebalance inflammatory signaling.

This is precisely the goal of microimmunotherapy. Doctors who use it in patients with rheumatoid arthritis seek to counteract the deregulation that exists in the inflammatory response and its persistence, in order to limit the deterioration of the affected tissue.

It should be noted that microimmunotherapy is based on the use of the same type of molecules and immunological mediators that the immune system uses, in low and very low doses, to work from a physiological point of view, coming as close as possible to the natural functioning of the body.

For example, it can be aimed at down-regulating the action of cytokines such as IL-1 or IL-6, involved in the inflammatory reaction.

In the end, in rheumatoid arthritis as in other autoimmune diseases, it is not just a matter of slowing down immunity, but of returning it to a state of balance.

Bibliography

1. Miguel-Lavariega D, Elizararrás-Rivas J, Villarreal-Ríos E, Baltiérrez-Hoyos R, Velasco-Tobón U, Vargas-Daza ER, Galicia-Rodríguez L. Epidemiological profile of rheumatoid arthritis. Rev Med Inst Mex Seguro Soc. 2023 Sep 4;61(5):574-582. Spanish. doi: 10.5281/zenodo.8316427.
2. van Delft MAM, Huizinga TWJ. An overview of autoantibodies in rheumatoid arthritis. J Autoimmun. 2020 Jun;110:102392. doi: 10.1016/j.jaut.2019.102392. Epub 2020 Jan 3.
3. Radu AF, Bungau SG. Management of Rheumatoid Arthritis: An Overview. Cells. 2021 Oct 23;10(11):2857. doi:10.3390/cells10112857.

 The term lupus means "wolf" in Latin (in German "wolf"). In consulting the medical writings of the ancients, it was noted that this term was used to characterize various skin conditions whose marks are reminiscent of wolf bites. It appears for the first time in medical literature in 916 AD concerning the illness of the Bishop of Liège, Eraclius, lupus, from which he was miraculously cured on the occasion of a pilgrimage to the tomb of St Martin in Tours.

History of Lupus

The observation is reported by Herbert of Tours: "He Eraclius, whom he calls Hildricus, suffered from an ulcerous disease, lupus, which manifested itself by a red line on the forehead." This type of skin condition certainly did not go unnoticed by ancient physicians. The frescoes of ancient Egypt give a fairly accurate reflection of the skin condition of the inhabitants of the Nile Valley. The study of medical papyri, dating from 1000-1700 BC, has made it possible to identify the semiological descriptions of many skin diseases.

Hippocrates, who lived on the island of Kos between 460-375 BC, described ulcerative lesions of the skin that he called Herpes Esthiomenos (Herpes spreading on the skin, Esthiomenos gnawing). Claudius Galen, a Greek physician practicing in Rome between 131-201 AD, used the name Herpes in a less vague sense to designate superficial ulcerations of the skin.

Persian physicians such as Raazes (900 AD) and Avicenna (1000 AD) described the condition under the name "formica corrosiva" which was retained by Paul Aegina, a Greek physician from the island of Aegina, and by Galen. In the writings of the famous School of Medicine of Salerno of the Middle Ages, we find the writings of Rogerius Frugarti who describes lupus characterized by swellings of the extremities. Rolandus devotes the term "noli me tangere" (do not touch me) for diseases affecting the face.

Bernard of Gordon, physician of the School of Montpellier (1305) also mentions the ulcerative form of herpes which he calls lupus. In 1500, Paracelsus introduces the term consolida lupi to describe a disease different from estthiomenos, fistula and cancer. He thus uses the term lupus vorax. Girolamo Mercurialis gives a description of lupus in his treatise "de Morbei-Cutanei" of 1572, the first work of dermatology published in Europe.

In 1750, the name lupus appeared for the first time in an American medical work "A method of Physics" by Philips Barrough. The use of the word lupus will be reserved for red eruptions of the face by Hans van Gersdorf of Strasbourg in 1577 and taken up by Jean Dolaeus in 1684.

In 1790, the British Robert Willan established a first classification of skin diseases in which we find the description of lupus which he clearly separates from "noli me tangere" and herpes. Willan wrote the first atlas of dermatology "Manual on Skin Diseases" which includes many color illustrations entirely drawn by hand, which will greatly delay its publication.

In 1808, a new edition was published in which Willan reserved the name lupus for a nodular eruption of the face that was complicated by ulcers. Two types of lupus were described, tuberculous lupus and lupus vulgaris. After Willan's premature death, his student Thomas Bateman continued his work. A new atlas of skin diseases was published in 1810 that would influence the history of dermatology. In France, the St Louis hospital in Paris developed a dermatology department in 1801, the direction of which was entrusted to Jean-Louis Alibert.

In 1832, he published a work entitled "Descriptions of Skin Diseases observed at St Louis Hospital" with 50 color engravings. In it, he describes "tartars" within which he isolates the reddening scab corresponding to the condition described by his predecessors under the name of lupus. Alibert specifies that esthiomene corresponds to Paracelsus' lupus vorax and Willan's lupus which are associated with tuberculosis.

In 1815, Alibert left the service of the St Louis hospital to Laurent Théodore Biett, a doctor of Swiss origin, who had studied dermatology with Bateman in London and who would therefore apply the classification of dermatoses according to his English masters. His collaborators, Alphée Cazenave and Henri-Edouard Schedel published in 1828 the first edition of the "Practical Abbreviations of Skin Diseases" in which the authors separated different forms of lupus: lupus which destroys on the surface, which destroys in depth and lupus with hypertrophy. They demonstrated that "noli me tangere" is of cancerous origin and therefore clearly separates this condition from lupus.

In the second edition of 1833, the chapter devoted to lupus is supplemented by a particular form which is described under the name of "Erythema centrifugum".

In 1851, Cazenave extended the description of centrifugal erythema by noting skin lesions with atrophy, telangiectasia, fixed erythema and he modified the name to "Lupus Erythematosus". Work on lupus then continued in Vienna, a center of Austro-Hungarian medicine. Ferdinand von Hebra was put in charge of the Dermatology clinic in this city in 1841.

In 1846 he described a condition affecting the face that he called "seborrhea congestiva". He described the very particular appearance of the malar rash as a "butterfly wing".

In 1866, Von Hebra would specify that the condition was identical to that which Cazenave had described under the name of Lupus erythematosus. He therefore rallied to Cazenave's thesis and definitively accepted this term which would be universally retained. The first illustration of lupus erythematosus appeared in 1856 in Von Hebra's Atlas of Skin Diseases which included numerous hand-painted illustrations by his collaborator, the Swiss Anton Elfinger.

In 1866, a young Hungarian doctor, Moriz Kohn, joined Von Hebra's service. A brilliant doctor, polyglot, talented orator, Kohn would perfect the teaching of his master Von Hebra.

In 1869, he published his first article on lupus erythematosus.

In 1871, Moriz Kohn obtained permission to change his surname to KAPOSI and it was under this identity that he continued to publish numerous works.

In 1872, in a detailed treatise, he described the existence of two types of lupus: discoid lupus, exclusively cutaneous, and a disseminated form associating systemic visceral complications including subcutaneous nodules, arthralgia, lymphadenopathy, fever, weight loss, anemia. He called this form "disseminated and aggregated lupus erythematosus". Confusion arose about the adjective disseminated which is related to the cutaneous evolution and not to the multivisceral (systemic) character of the condition.

In 1902, Sequira and Baleau in London published a review of 71 cases of lupus, including 60 discoid and 11 disseminated. They noted the existence in this latter group of a frequency of acroasphyxia (which would later be better known as Raynaud's phenomenon), renal damage as well as pleurisy (pericarditis. Jadasshon, a German dermatologist practicing in Berne, Switzerland, contributed in 1904 to the replacement of the term "disseminated lupus erythematosus" by that of "systemic lupus erythematosus" or better "lupus disease". Sir Williams Osler would confirm the concept of systemic lupus thanks to numerous publications between 1895 and 1904. In 1936, CK Friedberg described the existence of lupus disease without cutaneous manifestations.

Systemic lupus seems to have existed since ancient times. Indeed, a group of researchers under the direction of Marvin Alison and Alejandro Pezza from the Inca Museum in Peru were able to carefully examine a mummy of a 14-year-old girl, dating from 890 BC, whose examination revealed alopecia, pleurisy and pericarditis, glomerulonephritis compatible with systemic lupus. Reproductions of lupus disease are also found in paintings by old masters.

Thus, Rembrandt in 1634 painted the portrait of Maria Bockenolle, the wife of Pastor Elison, in which one can notice the red rash on the face and the joint deformation of the hand.

At the Louvre Museum, one can admire the painting by the French painter Simeon Chardin from 1740, a copy of which from 1746 is in the Hermitage Museum in St. Petersburg, the "Benedicité" on which one can observe the erythema of the little girl's face.

The 20th century opened the era of lupus biology. In 1910, Hank reported the positivity of the Wasserman complement fixation reaction with the serum of lupus patients. In 1846, Hargraves discovered, in the sternal marrow of lupus patients, the presence of particular cells consisting of neutrophil polymorphonuclear cells having phagocytosed the nucleus of another cell which were called LE cells. The following year, Haserick showed that the serum of lupus patients was capable of causing the formation of LE cells with cells from the marrow of normal subjects.

In 1954, Peter Miescher, a Swiss immunologist, succeeded in absorbing serum factor LE with thymus cell nuclei, thus demonstrating that the factor was an anti-nuclear antibody.

In 1957, it was shown that these antibodies reacted with nucleoproteins, that is, the constitutional subunit of chromatin. The same year, Maxime Seligman in Paris showed that the serum of lupus patients causes a precipitate with DNA. This was confirmed by the German Deicher in Henri Kunkel's laboratory and by the Italian Ceppelini. Thus anti-DNA became the specific serological markers of lupus. An important discovery was to revolutionize the practice of immunology.

This is the development by Coons in 1953 of the immunofluorescence technique.

Friou applied it in 1957 to the search for anti-nuclear antibodies but it would not become widespread until 1968 when the first microscopes equipped with UV lighting became widespread in laboratories. From 1975 onwards, the search for anti-nuclear antibodies was carried out on Hep-2 cells, a substrate still used today.

In 1961, Anderson in Glasgow, will show that the antibodies present in the serum of lupus patients precipitated soluble extracts of thymus nuclei. This is the start of work on anti-ENA antibodies for "Extractable Nuclear Antigens", i.e. soluble antigens of the nucleus. In 1966, Tan identified in a lupus patient, Mrs Smith, a first anti-ENA, which was called anti-Sm. Other specificities will be identified in the following years. The sophistication and standardization of anti-nuclear antibody detection techniques will lead to genuine diagnostic progress in lupus disease.

Dermatological lupus has been the subject of treatment attempts since antiquity. At the beginning of the 15th century, the German physician Johan Tollat ​​von Vorchenberg wrote "for lupus caprifolin", that is to say honeysuckle. Medicine at the time used a very rich pharmacopoeia borrowed from the plant and mineral kingdoms. Jonathan Hutchinson, 1880, proposed cod liver oil, arsenic, zinc chloride and mercury nitrate. Anderson added the application of iodine. Gold salts were introduced in 1913 for the treatment of discoid lupus. For that of systemic lupus, quinidine was introduced by JF Payne in 1894, aspirin was used in 1899 by Radcliffe-Crocker and quinine by Mac Lead in 1908.

In 1956, plaquenil was introduced, which is still widely used today.

In 1935, Edward Kendall isolated cortisone, which was used to treat lupus by Hensch. From 1952, immunomodulators such as cyclophosphamide, mycophenolate, azathioprine, and then monoclonals such as rituximab were used. Other therapies are under development.

The first descriptions of lupus focused on dermatological manifestations. Various varieties of cutaneous lupus have been described by dermatologists.

At the end of the 19th century, it was realized that some lupus could be complicated by diffuse visceral manifestations and the dermis of systemic lupus erythematosus replaced that of disseminated lupus erythematosus. Thanks to the development of our knowledge in immunology, it was demonstrated at the end of the 20th century that lupus disease is an autoimmune disease. Immunological tests were developed that allow a precise diagnosis of systemic lupus. On the other hand, the knowledge acquired about the etiology of the disease will allow the implementation of increasingly effective targeted therapies.

Prof. René-Louis HUMBEL

Laboratory of Immunopathology, Luxembourg

BIBLIOGRAPHY:

• 1. Virchow R. Historical Notes on Lupus. Arc Pathol Anat 1865; 32:169-143.
• 2. Russel B. The History of Lupus Vulgaris: Its recognition, Nature, Treatment and Prevention.Pro Royal Soc Med 1954; 48: 127-132.
• 3. Smith CD The History of Lupus Erythematosus: from Hippocrates to Osler.Rheum Dis North Am 1988; 14:1-14.
• 4. Hoshberg MC. The History of Lupus Erythamotosus. Md Med J 1991; 40:871-873.
• 5. Gamarra A. An historical review of Systemic Lupus Erythematosus in Latin America.Med Sci Monit 2004; 10:171-185.
• 6. Mallavaapu RK, Grimsley EW. The History of Lupus Eythematosus. South Lad j 2007; 100:896-898.

 Hey there! If you’re reading this, chances are you or someone you love is navigating the complex world of diabetes. I want to share my journey with you—my highs and lows, my triumphs and challenges. Hopefully, my story can offer some comfort, understanding, and maybe even some helpful tips along the way.

The Diagnosis: A Life-Changing Moment

I still remember the day I was diagnosed with diabetes like it was yesterday. I was feeling unusually thirsty, tired, and had to go to the bathroom all the time. After a routine check-up and some blood tests, my doctor gave me the news: I had diabetes. My world turned upside down.

Q: What are the common symptoms of diabetes?

A: Common symptoms include excessive thirst, frequent urination, extreme fatigue, and blurred vision. If you’re experiencing any of these, it’s important to see a doctor.

The Early Days: Adjusting to a New Normal

The first few weeks after my diagnosis were the toughest. I had to learn how to monitor my blood sugar levels, take my medication, and drastically change my diet. It felt overwhelming, and I often wondered, “Why me?”

Q: How do you manage blood sugar levels?

A: Managing blood sugar involves regular monitoring, taking prescribed medications or insulin, and maintaining a healthy diet and exercise routine. It’s crucial to work with your healthcare team to find the right balance.

Finding My Rhythm: Embracing the Changes

Over time, I found my rhythm. I discovered that a balanced diet and regular exercise made a huge difference in how I felt. I started cooking more at home, focusing on fresh, whole foods. Exercise became my friend—not just for my body, but for my mind too.

Q: What kind of diet is best for managing diabetes?

A: A diet rich in vegetables, whole grains, lean proteins, and healthy fats is generally recommended. Avoiding processed foods and sugary snacks helps keep blood sugar levels stable. Consulting with a nutritionist can provide personalized guidance.

The Support System: Leaning on Others

One of the most important things I learned is that I couldn’t do it alone. My family and friends became my biggest supporters, and I joined a local diabetes support group. Sharing my experiences and hearing from others who understood my struggles made a world of difference.

Q: How can you find support when dealing with diabetes?

A: Support can come from many places—family, friends, healthcare providers, and support groups. Online communities can also be a great resource. Don’t be afraid to reach out and ask for help when you need it.

Living Well with Diabetes: A Continuous Journey

Living with diabetes is a continuous journey. There are good days and bad days, but I’ve learned that it’s okay to have setbacks. What’s important is to keep moving forward, stay informed, and take care of yourself.

Q: What can you do to stay positive while managing diabetes?

A: Staying positive involves maintaining a balanced lifestyle, setting realistic goals, and celebrating small victories. Mindfulness practices, such as meditation and yoga, can also help reduce stress and improve your outlook.

A Message to You: You’re Not Alone

If you’re dealing with diabetes, remember—you’re not alone. It’s a challenging road, but with the right tools, support, and mindset, you can live a full, healthy life. Don’t be afraid to reach out, ask questions, and take it one day at a time.

Q: What’s the most important thing to remember about managing diabetes?

A: The most important thing is to stay proactive and informed. Regular check-ups, monitoring your health, and making lifestyle adjustments are key. Remember, managing diabetes is a marathon, not a sprint.

The Best Foods for People with Diabetes

As someone living with diabetes, I've learned firsthand the impact that diet can have on managing blood sugar levels and overall health. Finding the right foods to eat can sometimes feel like a daunting task, but I've discovered that making smart, informed choices can make a big difference. Here, I'd like to share some of the best foods I've incorporated into my diet to help manage my diabetes effectively.

1. Leafy Greens

Leafy greens like spinach, kale, and Swiss chard are incredibly nutrient-dense and low in carbohydrates, making them an excellent choice for managing blood sugar levels. They're rich in vitamins, minerals, and antioxidants.

Q: Why are leafy greens beneficial for diabetes management?

A: Leafy greens are low in calories and carbohydrates but high in fiber, which helps regulate blood sugar levels. They also provide essential nutrients that support overall health.

2. Berries

Berries such as blueberries, strawberries, and raspberries are packed with antioxidants, vitamins, and fiber. They satisfy my sweet tooth without causing a spike in my blood sugar levels.

Q: Can people with diabetes eat fruits like berries?

A: Yes, berries are a great option because they have a lower glycemic index compared to other fruits, meaning they have a smaller impact on blood sugar levels.

3. Whole Grains

Whole grains like quinoa, brown rice, oats, and barley are much better for blood sugar control compared to refined grains. They provide steady energy and are high in fiber.

Q: What makes whole grains better than refined grains for diabetes?

A: Whole grains are less processed and retain more nutrients and fiber, which slows the digestion and absorption of carbohydrates, helping to prevent blood sugar spikes.

4. Lean Proteins

Including lean proteins such as chicken, turkey, fish, tofu, and legumes in my diet has been essential. They help keep me full and provide the necessary nutrients for muscle maintenance without adding excess fat.

Q: Why is lean protein important for people with diabetes?

A: Lean proteins help stabilize blood sugar levels by slowing the absorption of carbohydrates and promoting satiety, which can prevent overeating.

5. Nuts and Seeds

Nuts and seeds, such as almonds, walnuts, chia seeds, and flaxseeds, are excellent sources of healthy fats, protein, and fiber. They make for great snacks and can be easily added to meals.

Q: How do nuts and seeds benefit blood sugar control?

A: The healthy fats, protein, and fiber in nuts and seeds help slow down the absorption of sugar into the bloodstream, which helps maintain stable blood sugar levels.

6. Non-Starchy Vegetables

Non-starchy vegetables like broccoli, cauliflower, bell peppers, and zucchini are low in calories and carbohydrates but high in essential nutrients. They're versatile and can be included in many dishes.

Q: What is the advantage of eating non-starchy vegetables for diabetes?

A: Non-starchy vegetables have a minimal impact on blood sugar levels and provide vital vitamins, minerals, and fiber that support overall health.

7. Greek Yogurt

Greek yogurt is a great source of protein and probiotics. I enjoy it as a snack or breakfast option, often adding a handful of berries or a sprinkle of nuts for added flavor and nutrition.

Q: Is Greek yogurt a good choice for people with diabetes?

A: Yes, Greek yogurt is higher in protein and lower in carbohydrates compared to regular yogurt, which helps keep blood sugar levels stable. Just be sure to choose plain, unsweetened varieties.

8. Avocados

Avocados are rich in healthy monounsaturated fats, fiber, and a variety of vitamins and minerals. They add a creamy texture to meals and help keep me feeling full longer.

Q: How do avocados help manage diabetes?

A: The healthy fats and fiber in avocados help slow digestion and improve blood sugar control, making them a great addition to a diabetes-friendly diet.

9. Fish High in Omega-3 Fatty Acids

Fish like salmon, mackerel, sardines, and trout are high in omega-3 fatty acids, which are beneficial for heart health—a key consideration for people with diabetes.

Q: Why are omega-3 fatty acids important for people with diabetes?

A: Omega-3 fatty acids reduce inflammation, improve heart health, and may help improve insulin sensitivity, which is crucial for managing diabetes.

10. Beans and Legumes

Beans and legumes such as lentils, chickpeas, and black beans are excellent sources of plant-based protein, fiber, and complex carbohydrates. They provide sustained energy and help keep blood sugar levels stable.

Q: Are beans and legumes good for blood sugar control?

A: Yes, their high fiber content slows the digestion and absorption of carbohydrates, which helps maintain steady blood sugar levels.

Incorporating these foods into your diet can make a significant difference in managing diabetes. Remember, it's all about balance and making informed choices. If you have any questions or need more personalized advice, don't hesitate to reach out to a nutritionist or your healthcare provider. Together, we can navigate the journey of diabetes management and live healthier, happier lives.

Thank you for reading my story. I hope it resonates with you and maybe even helps you on your own journey. If you have any questions or just need someone to talk to, don’t hesitate to reach out. We’re all in this together.