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Clinical Case Reports Jun 2023Autoimmune polyglandular syndrome type 2 (APS II) is a rare autoimmune disease that affects many endocrine glands. We present a case of a 32-year-old man with Addison's...
Autoimmune polyglandular syndrome type 2 (APS II) is a rare autoimmune disease that affects many endocrine glands. We present a case of a 32-year-old man with Addison's disease, autoimmune thyroiditis, and pernicious anemia. Multi-line and timely management are crucial for each association.
PubMed: 37305884
DOI: 10.1002/ccr3.7413 -
Heliyon May 2023A 47-year-old, north african, male patient, has recently been diagnosed with pernicious anemia, treated with weekly intramuscular hydroxocobalamin. 6 weeks after its...
A 47-year-old, north african, male patient, has recently been diagnosed with pernicious anemia, treated with weekly intramuscular hydroxocobalamin. 6 weeks after its initiation, the patient presented a sudden, extensive and monomorphic eruption of inflammatory papulo-pustules and nodules, affecting the face, and the trunk. The eruption was pruritic, and comedones were also present, on the chest. The patient was diagnosed with vitamin B12-induced acneiform eruption. Levels of vitamin B12 were normalized. Hydroxocobalamin was therefore stopped and lymecycline was started, allowing a complete resolution of the lesions within 3 months. Drug intake, sudden and uncommon age of onset, pruritus, a monomorphic pattern and an involvement of extra-seborrheic areas are features that distinguish acneiform eruptions from acne vulgaris.
PubMed: 37305488
DOI: 10.1016/j.heliyon.2023.e16120 -
Chemico-biological Interactions Sep 2023Vitamin B (cyano- or hydroxo-cobalamin) acts, via its coenzymes, methyl- and adenosyl-cobalamin, as a partner for enzymatic reactions in humans catalysed by methionine...
Vitamin B (cyano- or hydroxo-cobalamin) acts, via its coenzymes, methyl- and adenosyl-cobalamin, as a partner for enzymatic reactions in humans catalysed by methionine synthase and methylmalonyl-CoA mutase. As well as its association with pernicious anaemia, human B deficiency may also be a risk factor for neurological illnesses, heart disease and cancer. In the present work the effect of vitamin B (hydroxocobalamin) on the formation of DNA adducts by the epoxide phenyloxirane (styrene oxide), a genotoxic metabolite of phenylethene (styrene), has been studied using an in vitro model system. Styrene was converted to its major metabolite styrene oxide as a mixture of enantiomers using a microsomal fraction from the livers of Sprague-Dawley rats with concomitant inhibition of epoxide hydrolase. However, microsomal oxidation of styrene in the presence of vitamin B gave diastereoisomeric 2-hydroxy-2-phenylcobalamins. The quantitative formation of styrene oxide-DNA adducts was investigated using 2-deoxyguanosine or calf thymus DNA in the presence or absence of vitamin B. Microsomal incubations containing either deoxyguanosine or DNA in the absence of vitamin B gave 2-amino-7-(2-hydroxy-1-phenylethyl)-1,7-dihydro-6H-purin-6-one [N7-(2-hydroxy-1-phenylethyl)-guanine], and 2-amino-7-(2-hydroxy-2-phenylethyl)-1,7-dihydro-6H-purin-6-one [N7-(2-hydroxy-2-phenylethyl)guanine] as the principal adducts. With deoxyguanosine the level of formation of guanine adducts was ca. 150 adducts/10 unmodified nucleoside. With DNA the adduct level was 36 pmol/mg DNA (ca. 1 adduct/0.83 × 10 nucleotides). Styrene oxide adducts from deoxyguanosine or DNA were not detected in microsomal incubations of styrene in the presence of vitamin B. These results suggest that vitamin B could protect DNA against genotoxicity due to styrene oxide and other xenobiotic metabolites. However, this potential defence mechanism requires that the 2-hydroxyalkylcobalamins derived from epoxides are not 'anti-vitamins' and ideally liberate, and therefore, recycle vitamin B. Otherwise, depletion of vitamin B leading to human deficiency could increase the risk of carcinogenesis initiated by genotoxic epoxides.
Topics: Animals; Rats; Humans; DNA Adducts; Vitamin B 12; Xenobiotics; Rats, Sprague-Dawley; Epoxy Compounds; DNA Damage; DNA; Guanine; Deoxyguanosine; Styrenes; Styrene
PubMed: 37302460
DOI: 10.1016/j.cbi.2023.110591 -
Frontiers in Immunology 2023Autoimmune/inflammatory syndrome induced by adjuvants (ASIA) consists of a wide spectrum of symptoms and immunological features that are believed to develop in... (Review)
Review
INTRODUCTION
Autoimmune/inflammatory syndrome induced by adjuvants (ASIA) consists of a wide spectrum of symptoms and immunological features that are believed to develop in predisposed individuals after exposure to an adjuvant, including a silicone breast implant (SBI). Different autoimmune diseases (AIDs) have been associated with ASIA, but ASIA development after SBI in women with Hashimoto thyroiditis (HT) and familial autoimmunity has rarely been described.
CASE REPORT
A 37-year-old woman presented in 2019 with arthralgia, sicca symptoms, fatigue, + antinuclear antibody (ANA), + anti SSA, and + anticardiolipin Immunoglobulin G (IgG) antibodies. She was diagnosed with HT and vitamin D deficiency in 2012. The familial autoimmunity was present: the patient's mother had been diagnosed with systemic lupus erythematosus and secondary Sjogren's syndrome and her grandmother with cutaneous lupus and pernicious anemia. In 2017, the patient had a cosmetic SBI procedure that was complicated by repeated right breast capsulitis. After 2 years of irregular visits due to COVID-19, she presented with + ANA, + anticentromere antibodies both in sera and seroma, sicca syndrome, arthralgias, twinkling in extremities, abnormal capillaroscopic findings, and reduced diffusing capacity of the lungs for carbon monoxide. She was diagnosed with ASIA, and antimalarial and corticosteroid therapy were introduced.
CONCLUSION
In patients with HT and familial autoimmunity, SBI should be carefully considered due to the possibility of ASIA development. Hashimoto thyroiditis, familial autoimmunity, and ASIA seem to be interconnected in the complex mosaic of autoimmunity in predisposed individuals.
Topics: Humans; Female; Autoimmune Diseases; Hashimoto Disease; Adult; Magnetic Resonance Imaging
PubMed: 37287963
DOI: 10.3389/fimmu.2023.1139603 -
Immunologic Research Dec 2023The effects of specific cytokines produced by T cell subsets (such as Th1, Th2, and newly discovered Th17, Treg, Tfh, or Th22) are diverse, depending on interactions...
The effects of specific cytokines produced by T cell subsets (such as Th1, Th2, and newly discovered Th17, Treg, Tfh, or Th22) are diverse, depending on interactions with other cytokines, distinct signaling pathways, phase of the disease, or etiological factor. The immunity equilibrium of the immune cells, such as the Th1/Th2, the Th17/Treg, and the Th17/Th1 balance is necessary for the maintenance of the immune homeostasis. If the balance of the T cells subsets is damaged, the autoimmune response becomes enhanced which leads to autoimmune diseases. Indeed, both the Th1/Th2 and the Th17/Treg dichotomies are involved in the pathomechanism of autoimmune diseases. The aim of the study was to determine the cytokines of Th17 lymphocytes as well as the factors modulating their activity in patients with pernicious anemia. The magnetic bead-based immunoassays used (Bio-Plex) allow simultaneous detection of multiple immune mediators from one serum sample. In our study, we showed that patients suffering from pernicious anemia develop the Th1/Th2 imbalance with a quantitative advantage of cytokines participating in Th1-related immune response, the Th17/Treg imbalance with a quantitative advantage of cytokines participating in Treg-related response, as well as the Th17/Th1 imbalance with a quantitative predominance of cytokines participating in Th1-related immune response. Our study results indicate that T lymphocytes and their specific cytokines play an role in the course of pernicious anemia. The observed changes may indicate the immune response to pernicious anemia or be an element of the pernicious anemia pathomechanism.
Topics: Humans; Cytokines; Anemia, Pernicious; T-Lymphocytes, Regulatory; Th17 Cells; Autoimmune Diseases; Th1 Cells; Th2 Cells
PubMed: 37269464
DOI: 10.1007/s12026-023-09399-9 -
Cureus Apr 2023Anemia is the most common hematological disorder. It is commonly a manifestation of an underlying disease. Its causes are multifactorial, including but not limited to...
Anemia is the most common hematological disorder. It is commonly a manifestation of an underlying disease. Its causes are multifactorial, including but not limited to nutritional deficiencies, chronic conditions, inflammatory processes, medications, malignancy, renal dysfunction, hereditary diseases, and bone marrow disorders. We present a case of a patient exhibiting anemia related to cold agglutin disease and severe B12 deficiency secondary to pernicious anemia.
PubMed: 37252560
DOI: 10.7759/cureus.38208 -
MedRxiv : the Preprint Server For... Mar 2023Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive enzymatic disorder, particularly prevalent in Africa, Asia and the Middle East. In the US,...
BACKGROUND
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive enzymatic disorder, particularly prevalent in Africa, Asia and the Middle East. In the US, about 14% of black men are affected. Individuals with G6PD deficiency are often asymptomatic but may develop hemolysis following an infection or upon consumption of specific medications. Despite some evidence that G6PD deficiency affects the immune system, the long- term health risks associated with G6PD deficiency had not been studied in a large population.
METHODS
In this retrospective cohort study, health records from G6PD deficient individuals were compared to matched controls in a national healthcare provider in Israel (Leumit Health Services). Rates of infectious diseases, allergic conditions and autoimmune disorders were compared between groups.
RESULTS
The cohort included 7,473 G6PD deficient subjects (68.7% men) matched with 29,892 control subjects (4:1 ratio) of the same age, gender, socioeconomic status and ethnic group, followed during 14.3±6.2 years.Significantly increased rates for autoimmune disorders, infectious diseases and allergic conditions were observed throughout this period. Notable increases were observed for rheumatoid arthritis (OR 2.41, p<0.001), systemic lupus erythematosus (OR 4.56, p<0.001), scleroderma (OR 6.87, p<0.001), pernicious anemia (OR=18.70, P<0.001), fibromyalgia (OR 1.98, p<0.001), Graves' disease (OR 1.46, P=0.001), and Hashimoto's thyroiditis (OR 1.26, P=0.001). These findings were corroborated with elevated rates of positive autoimmune serology and higher rates of treatment with medications commonly used to treat autoimmune conditions in the G6PD deficient group.
CONCLUSION
G6PD deficient individuals suffer from higher rates of autoimmune disorders, infectious diseases, and allergic conditions.
PubMed: 37090544
DOI: 10.1101/2023.03.23.23287616