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Autoimmune comorbidity in achalasia patients.
Romero-Hernández, F, Furuzawa-Carballeda, J, Hernández-Molina, G, Alejandro-Medrano, E, Núñez-Álvarez, CA, Hernández-Ramírez, DF, Azamar-Llamas, D, Olivares-Martínez, E, Breña, B, Palacios, A, et al
Journal of gastroenterology and hepatology. 2018;(1):203-208
Abstract
BACKGROUND AND AIM Idiopathic achalasia is a rare esophageal motor disorder. The disease state manifests local and systemic inflammation, and it appears that an autoimmune component and specific autoantibodies participate in the pathogenesis. The study aims to determine the prevalence of autoimmune and chronic inflammatory diseases in patients with achalasia and compare the results with those from patients with gastroesophageal reflux disease (GERD). METHODS It was a cross-sectional and included 114 patients with idiopathic achalasia and 114 age-matched and sex-matched control patients with GERD. Data on the presence of autoimmune and inflammatory diseases, the time of presentation, and any family history of autoimmune disease were obtained from the hospital's medical records. RESULTS Seventy three (64%) were female patients (mean age: 42.3 ± 15.5; median disease duration: 12 months). We identified the presence of autoimmune disease in 19 patients with achalasia (16.7%), hypothyroidism was the main diagnosis, and it was present in 52.6% of patients compared with 4.2% in controls. Thirteen of the 19 achalasia patients (68.4%) with autoimmune disease had history of familial autoimmunity. We identified 11 achalasia (9.6%) and 5 GERD patients (4.16%) with an inflammatory condition. Compared with the GERD, the achalasia group was 3.8 times more likely to have an autoimmune disease (95% CI: 1.47-9.83), 3.0 times more likely to have thyroidopathies (95% CI: 1.00-9.03), and 3.02 times more likely to suffer from any chronic inflammatory disease (95% CI: 1.65-6.20). CONCLUSIONS The non-negligible number of patients with autoimmune diseases identified among the patients with idiopathic achalasia supports the hypothesis that achalasia has an autoimmune component.
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Efficacy of Vitamin K2 for Glucocorticoid-induced Osteoporosis in Patients with Systemic Autoimmune Diseases.
Shikano, K, Kaneko, K, Kawazoe, M, Kaburaki, M, Hasunuma, T, Kawai, S
Internal medicine (Tokyo, Japan). 2016;(15):1997-2003
Abstract
Objective Vitamin K2 (menatetrenone) is an effective treatment for patients with postmenopausal osteoporosis. We herein performed a subanalysis of patients with systemic autoimmune diseases undergoing glucocorticoid therapy in our previous prospective study. Methods Sixty patients were categorized into a group with vitamin K2 treatment (n=20, Group A) and a group without vitamin K2 treatment (n=40, Group B). All patients were treated with bisphosphonates. Results Serum levels of osteocalcin and undercarboxylated osteocalcin decreased significantly after the start of glucocorticoid therapy in both groups, while the serum osteocalcin level was significantly higher in Group A than Group B during the third (p=0.0250) and fourth weeks (p=0.0155). The serum level of the N-terminal peptide of type I procollagen, a bone formation marker, decreased during glucocorticoid therapy, but was significantly higher in Group A than Group B during the fourth week (p=0.0400). The bone mineral density and fracture rate showed no significant differences between the two groups. Conclusion Although vitamin K2 improves bone turnover markers in patients with osteoporosis on glucocorticoid therapy, it has no significant effect on the bone mineral density and fracture rate after 1.5 years of treatment.
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3.
Routine supplement of prebiotics and probiotics to newborn infants is not recommended.
Shafai, T
Pediatrics. 2009;(3):e543-4; author reply e544
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4.
Effect of alendronate on glucocorticoid-induced osteoporosis in Japanese women with systemic autoimmune diseases: versus alfacalcidol.
Takeda, S, Kaneoka, H, Saito, T
Modern rheumatology. 2008;(3):271-6
Abstract
Glucocorticoids-induced osteoporosis is a serious problem for patients with systemic autoimmune disease requiring relatively long-term glucocorticoid treatment. Effectiveness of alendronate for the prevention of glucocorticoids-induced osteoporosis was evaluated in comparison with that of alfacalcidol in Japanese women with autoimmune disease excluding rheumatoid arthritis. Loss of bone mass was evaluated with bone mineral density (BMD) of lumber vertebrae, bone resorption was with urinary N-telopeptide for type I collagen (NTX), and bone formation was with serum bone-specific alkaline phosphatase (B-ALP). A total of 33 patients who were treated with oral glucocorticoids (>or=5 mg/day of prednisolone equivalence) for more than 6 months were randomized into two groups; alendronate group (n = 17) received 5 mg/day of alendronate, and alfacalcidol group (n = 16) received 1.0 mug/day of alfacalcidol for 24 months with glucocorticoids. The dose of alendronate was the maximal dose approved in Japan. BMD had tendency to decrease with alfacalcidol, while increase with alendronate. The difference in BMD change between the two groups was significant by 4.3% at 18 months and by 4.2% at 24 months (both P < 0.05). Bone resorption was significantly reduced only with alendronate; NTX was decreased by 28 to 35% at 6 to 24 months (P < 0.05), but not changed with alfacalcidol at 24 months. The bone formation was found to be unchanged according to the B-ALP measured between the two groups. In conclusion, the treatment of 5 mg alendronate daily is more effective than alfacalcidol for preventing the glucocorticoid-induced osteoporosis by the mechanism of reducing bone resorption in Japanese women with systemic autoimmune disease.
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Pharmacokinetics of enteric-coated mycophenolate sodium: comparative study in patients with autoimmune disease and renal allograft.
Neumann, I, Fuhrmann, H, Kanzler, M, Fang, IF, Jaeger, A, Graf, H, Bayer, P, Kovarik, J
Expert opinion on pharmacotherapy. 2008;(6):879-86
Abstract
BACKGROUND Recently, mycophenolic acid drugs have gained interest in the treatment of autoimmune diseases. However, only limited pharmacokinetic data are available on enteric-coated mycophenolate sodium in non-transplant indications. OBJECTIVE This study compared the pharmacokinetics of mycophenolic acid from enteric-coated mycophenolate sodium in patients with autoimmune disease and renal transplant recipients. METHODS Twelve autoimmune disease patients (mainly with antineutrophil cytoplasmic antibody-associated vasculitis) and 11 stable renal transplant patients, all of whom had been on enteric-coated mycophenolate sodium for > or = 10 weeks, received an oral dose of enteric-coated mycophenolate sodium of 720 mg under fasting conditions. Blood samples for the determination of mycophenolic acid in the plasma were collected over 24 h. RESULTS Overall, no significant difference was found between both groups for their 0 - 12 h and 0 - 24 h areas under the concentration-time curve, C(max), T(max), C(0 h), C(12 h) and C(24 h), although the mean C(max) was numerically higher by 39% in the autoimmune disease patients (autoimmune disease 27.3 +/- 17.4 mg/l and renal transplant 19.6 +/- 15.7 mg/l). Patients on concomitant ciclosporin tended to have a lower mycophenolic acid exposure than patients on a non-ciclosporin regimen. The intersubject variabilities in the mycophenolic acid pharmacokinetics were high in both patient populations (around 40% for the area under the curve values). Both groups exhibited a weak and non-significant correlation between their mycophenolic acid trough (C(12 h)) levels and mycophenolic acid 0 - 12 h area under the curve (autoimmune disease r = 0.482 and renal transplant r = 0.138), whereas in the autoimmune disease group the mean C(1.5 h) and C(2 h) concentrations provided a satisfactory association with the 0 - 12 h area under the curve (for both r > 0.7 and p < 0.001). CONCLUSION These data suggest that mycophenolic acid exposure (in terms of the area under the curve) from enteric-coated mycophenolate sodium is comparable in autoimmune disease and renal transplant patients. The mycophenolic acid trough levels did not reflect the systemic exposure to mycophenolic acid adequately; a limited sampling strategy for estimating mycophenolic acid exposure in autoimmune disease patients should include times around C(1.5 h) and/or C(2 h) reflecting T(max) if further studies confirm its usefulness.
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Treatment of refractory blistering autoimmune diseases with mycophenolic acid.
Marzano, AV, Dassoni, F, Caputo, R
The Journal of dermatological treatment. 2006;(6):370-6
Abstract
BACKGROUND Immunosuppressive drugs are used as steroid-sparing agents in the management of blistering autoimmune diseases. Mycophenolic acid (MPA) is a relatively new adjuvant drug that selectively inhibits T and B lymphocyte proliferation by suppressing de novo purine synthesis. OBJECTIVE To evaluate the efficacy of MPA in refractory blistering autoimmune diseases and the safety profile of a recent formulation, enteric-coated mycophenolate sodium (EC-MPS), in comparison with mycophenolate mofetil (MMF). PATIENTS AND METHODS Twelve patients with various bullous dermatoses (three pemphigus vulgaris, one pemphigus herpetiformis, three bullous pemphigoid (BP), two cicatricial pemphigoid (CP) and three epidermolysis bullosa acquisita (EBA)) were enrolled in the study. In 10 cases, MPA was administered in combination with systemic corticosteroids, while in two patients with severe diabetes mellitus MPA was employed as monotherapy. The total time on MPA varied from 2 to 8 months. Four patients were given MMF (2,000 mg daily), seven received EC-MPS (1,440 mg daily) and one received both sequentially. RESULTS Complete remission, lasting for a mean time of 6.1 months, was achieved in 10 patients. Partial remission was obtained in two patients with disseminated CP and EBA. Both MMF and EC-MPS were well tolerated, but the latter was better in terms of gastrointestinal adverse effects. CONCLUSIONS MPA may be proposed as a first-line adjuvant agent for pemphigus as well as for refractory BP and CP. MPA monotherapy has to be considered in selected cases of BP and pemphigus. The highly promising results obtained in EBA suggest a future key role for MPA in the management of this disease.
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Transplantation osteoporosis and corticosteroid-induced osteoporosis in autoimmune diseases: experience with alfacalcidol.
Dequeker, J, Borghs, H, Van Cleemput, J, Nevens, F, Verleden, G, Nijs, J
Zeitschrift fur Rheumatologie. 2000;:53-7
Abstract
The effect of alfacalcidol therapy on bone mineral density at the spine and proximal femur was evaluated in 112 transplant recipients (59 heart, 26 liver and 27 lung); 45 transplant cases served as controls (included in a randomised way in a placebo group) and in 42 rheumatoid arthritis cases. Liver and lung transplantation cases had before transplantation a lower bone density at the spine and femur compared to heart transplant cases. Heart transplant cases lost considerably more bone immediately after transplantation than liver and lung transplant recipients. A positive effect of 2 years alfacalcidol treatment (0.5-1 microgram/day) on bone loss was observed in all treated groups. Alfacalcidol was particularly effective against trabecular bone loss at the spine in rheumatoid arthritis patients and transplant recipients. There is a manifest difference in evolution between organ transplant groups and bone sites measured. Liver and lung transplant recipients respond better to therapy than cardiac recipients.
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The peculiar autoimmunity of primary biliary cirrhosis.
Mackay, IR, Whittingham, S, Fida, S, Myers, M, Ikuno, N, Gershwin, ME, Rowley, MJ
Immunological reviews. 2000;:226-37
Abstract
Autoantibodies to mitochondria (AMA, anti-M2) are a serologic hallmark of primary biliary cirrhosis (PBC). These react with three structurally and functionally related multienzymic complexes, the 2-oxoacid dehydrogenase complexes, but chiefly with the E2 subunit of pyruvate dehydrogenase complex (PDC-E2). Their very dose (95%) and specific association with PBC underpins the autoimmune concept of pathogenesis of that disease, notwithstanding several non-congruent features. Detailed studies, including structural analysis of epitopes, do not disclose how these autoantibodies originate. Their ubiquity in PBC has overshadowed the existence of a second set of relatively PBC-specific autoantibodies to nuclear antigens for which reactants have been cloned and characterized. These include centromeric proteins; proteins of the nuclear pore complex; nuclear dot proteins, which include Sp-100 and the promyelocytic leukemia antigen; and a recently identified autoantigen, SOX13. Certain of these reactants are DNA-binding proteins with transcriptional regulatory activity. Thus serum from individuals with the same clinical syndrome can have autoimmune reactivity to disparate mitochondrial and nuclear constituents in different cellular compartments. Antibody probing of phage displayed random peptide libraries, together with epitope scanning using overlapping sequential octameric peptides from the PDC-E2 sequence, showed that the discontinuous motifs MH, FV(E) and SYP contributed to a predicted conformational antibody epitope in the inner lipoyl domain of PDC-E2.