Background The oral chicken immunoglobulin Y (IgY) as a novel model of immunotherapy to control Helicobacter pylori (H. pylori, Hp) infection has gained much interest in recent years. However, none of the current IgY therapies showed a total eradication of H. pylori on patients. Methods In this report, the recombinant antigens of H. pylori, including UreB (1710 bp), BabA2 (1269 bp), and FlaA (399 bp), were, respectively, expressed and purified, and then mixed and subjected to immunize laying hens for the preparation of multivalent anti‐H. pylori immunoglobulin Y (anti‐Hp mIgY). Next, the biological activities of anti‐Hp mIgY, including the recognition to antigens and the inhibition on H. pylori growth, were tested. Moreover, to perform a clinical trial, 94 Hp‐infected patients, according to the values of 13C urea breath test and the characteristics of gastroscopy of volunteers, were enrolled to evaluate the effects of dietary anti‐Hp mIgY against H. pylori infection. After continuous dietary of anti‐Hp mIgY for 2 weeks, the oral administration was terminated. The clinical symptoms of the patients were followed up at 2nd, 4th, and 6th week, respectively, and the 13C urea breath test were re‐examined at 6th week. Results The anti‐Hp mIgY could bind to recombinant antigens very well, and the titers of anti‐Hp mIgY to UreB, Baba2, and FlaA, are 62.5, 125, and 250 μg/ml, respectively. The in vitro antibacterial test showed that the 2 mg/ml of anti‐Hp mIgY could completely inhibit the H. pylori growth for 36 h. After a 2‐week dietary of anti‐Hp mIgY, the value of 13C urea breath test was significantly decreased by 56.0% (25.9 ± 14.1 vs 11.4 ± 9.78, p < 0.001), the total improvement rate of clinical symptoms in volunteers was 87.3%, and the H. pylori eradication rate was 30.6%. Conclusion Two‐week dietary of anti‐Hp mIgY greatly improved the clinical symptoms and the quality of life of Hp‐infected patients, and the H. pylori eradication rate reached up to 30.6%.
Objective. To investigate the clinical characteristics of tracheobronchopathia osteochondroplastica (TO). Methods. The clinical data of six patients with TO from November 2016 to November 2018 were retrospectively analyzed. The etiology, clinical manifestations, diagnosis, and treatment of TO were summarized. Result. All six patients with TO were middle-aged males, confirmed by histopathological examination. The main clinical symptoms were cough, sputum, hemoptysis, chest pain, and repeated pulmonary infection. Some patients could make a preliminary diagnosis by chest CT, and bronchoscopy showed that TO mainly occurred in the trachea and the main bronchus and was more likely to invade the right bronchus. The treatment mainly includes anti-infection, phlegm-resolving, and other symptomatic treatment. Conclusion. TO is a benign disease predisposing to adults, and males are more likely to be affected. Its clinical manifestations are lack of specificity, and the cause may be related to chronic infection. Bronchoscopy combined with histopathological examination is the primary approach for the diagnosis of TO. There is no well-recognized treatment standard for TO, and the judgment of therapeutic effect is inconsistent. It is necessary to improve the understanding of this disease from a clinical perspective.
Increased production of the inflammatory cytokine IL-17A by Th17 cells is a driver of multiple autoimmune disorders, including psoriasis, ankylosing spondylitis (AS) and psoriatic arthritis (PsA). The nuclear receptor RORγt, IL-23 and TGFb are required for the differentiation of Th17 cells. RORγt stabilizes the Th17 phenotype by increasing the expression of IL-23R and inducing the synthesis of IL-17A in Th17 cells. Antibodies targeting IL-23 or IL-17A are highly effective in the treatment of psoriasis, AS and PsA, validating the RORγt /Th17 pathway in human disease. VTP-43742 is an orally active inhibitor of RORgt that is being pursued for the treatment of autoimmune disorders. VTP-43742 binds to RORγt with high affinity (Ki=3.5 nM) and exhibits >1000-fold selectivity versus the RORa and RORβ isotypes. VTP-43742 inhibits Th17 differentiation and IL-17A secretion from mouse splenocytes (IC50=57 nM) without affecting Th1, Th2, or Treg cell differentiation. In the MOG35-55/CFA immunized mouse EAE model, orally dosed VTP-43742 significantly suppressed clinical symptoms, demyelination and mRNA expression of multiple inflammatory markers in the spinal cord. Importantly, VTP-43742 inhibits the secretion of IL-17A from activated hPBMCs (IC50=18 nM) and human whole blood (IC50=192 nM) from healthy and psoriatic donors. Further, VTP-43742 is well absorbed after oral administration in multiple animal species and has pharmacokinetics consistent with once-a-day dosing in humans.
Introduction: Hypophosphatemia is a recently recognized adverse effect of certain intravenous iron formulations. It was previously thought to be asymptomatic and transient, however it can cause severe hypophosphatemia associated with renal phosphate wasting. We present a case of severe hypophosphatemia following intravenous ferric carboxymaltose administration. Clinical Case: A 40-year-old female with history of iron deficiency anemia, Hashimoto’s hypothyroidism and multinodular goiter status post thyroidectomy and obesity status post gastric sleeve presents to the hospital due to dizziness, generalized weakness, bone pain and severe myalgia right after 2nd dose of 750 mg of ferric carboxymaltose administration. She received 1st dose of 750 mg of ferric carboxymaltose a week ago prior to the presentation. She was found to have severe hypophosphatemia with a phosphorus level 1.0 mg/dl (2.4 - 4.8 mg/dl), hypocalcemia with calcium level at 8.7 mg/dl, normal PTH at 40 pg/ml and normal 25-OH Vitamin D level at 59.1 ng/ml. The fractional excretion of filtered phosphate (FEPO4) was 19.5%, supporting renal phosphate wasting. She was hospitalized for 5 days and received intravenous phosphate 45 mmol on hospitalization day 1, 15 mmol on day 2 and 30 mmol on day 3. She was discharged on K-phos Neutral 250 mg TID, Calcium carbonate/Vitamin D3 600 mg/500 IU 2 tablets TID and Calcitriol 0.5 mcg daily. While she was taking K-phos Neutral, Calcitriol and Calcium carbonate/Vitamin D3, her phosphorous level was down to 1.3 mg/dl, which was 4 weeks after 1st dose of ferric carboxymatose administration. She presented to the ED and received intravenous phosphate 15 mmol. She is currently taking K-phos Neutral 250 mg QID, Calcitriol 0.5 mcg daily and Calcium carbonate/Vitamin D3 600 mg/500 IU 2 tablets TID. Her phosphorous levels ranged at 2.5 - 3.0 mg/dl. Her bone pain and myalgia have gradually improved. Conclusion: Clinician should be aware of the side effect of hypophosphatemia following ferric carboxymaltose administration. Recent studies showed that incidence of hypophosphatemia associated with intravenous iron administration was significantly higher in ferric carboxymatose group compared with either iron isomaltoside group or ferumoxytol group. The impact of severe hypophosphatemia should be considered when choosing an intravenous iron medication.
Background Hypocalcemia and hypophosphatemia are known side effects of Denosumab, especially in presence of risk factors including underlying chronic kidney disease, osteoblastic metastasis, high bone turnover states, vitamin D deficiency and preexisting hypocalcemia. We report a unique case of prolonged severe hypocalcemia and hypophosphatemia in a patient with CML on Imatinib, treated with Denosumab for osteoporosis. Clinical case A 73-year-old lady with history of CML, on Imatinib for 4 years and osteoporosis with a chronic L1 compression fracture treated with her second dose of Denosumab 3-months back, presented with complaints of numbness and tingling involving the entire body. Labs revealed severe hypocalcemia (calcium 5.6 mg/dL, ionized calcium 2.93 mg/dL), severe hypophosphatemia, (phosphorus of 0.5mg/dL) and a low normal magnesium level of 1.5mg/dL, with normal ALP, liver and kidney function parameters. Of note she had normal calcium, phosphorus and vitamin D levels before receiving denosumab. Further work-up revealed an elevated PTH level of 241 pg/mL, normal 25 hydroxy vitamin D level of 26.0 ng/ml, slightly low 1,25 (OH) vitamin D of 16pg/ml and an elevated FGF 23 of 299RU/mL (normal <180RU/mL). Her calcium and phosphorus levels remained suboptimal despite treatment with up to 24 grams of calcium carbonate supplementation daily, K-phos 1 packet QID and calcitriol 0.25 mcg TID. 24-hour urine calcium and phosphorus levels were low at 4mg/day and 0.2mg/day respectively. Fractional excretion of phosphate was 13.63%, suggesting renal phosphorus wasting, likely from an elevated FGF23. Bone scan showed no metastatic lesion. After discussion with oncology, Imatinib was held inpatient and she was started on intravenous calcium gluconate infusion, and continued on Calcitriol, vitamin D3 and K-phos supplementation. After receiving almost 18gm of calcium gluconate intravenously over 2 days, her hypocalcemia and hypophosphatemia resolved with improvement in symptoms. Conclusion Hypocalcemia is a recognized adverse effect of Denosumab that is seen in patients with underlying risk factors. Emerging data now suggests the deregulatory effect of long term Imatinib therapy on bone formation by inhibition of osteoclastic activity along with transient increase in osteoblastic activity leading to retention and sequestration of calcium and phosphate in bone, resulting in hypocalcemia and hypophosphatemia. Ours is the first reported case of severe hypocalcemia and hypophosphatemia observed in a CML patient on Imatinib after receiving Denosumab, with resistance to high dose oral calcium and phosphate supplementation, requiring intravenous supplementation and transient discontinuation Imatinib. The elevated FGF 23 likely played a key role in severe hypophosphatemia. This unique case addresses the prospect of occurrence of severe hypocalcemia and hypophosphatemia in patients on Imatinib receiving Denosumab, while questioning the possibility of potentiation of the osteoclast inhibitory effect of this medication when used in patients on long term Imatinib therapy. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
Introduction: Lymphocytic hypophysitis (LYH) is an autoimmune condition in which pituitary gland is infiltrated by lymphocytes, plasma cells and macrophages. It is more common in pregnant and postpartum women, presenting with headache, visual field changes and one or more pituitary hormone impairment. Case Presentation: 32year-old female recently diagnosed with RA complicated by uveitis, presented to our facility with headache, shortness of breath, blurred vision and dysphagia. MRI head revealed a 1.9cm sellar mass with suprasellar extension displacing the optic chiasm. There was clear thickening of the pituitary stalk which raised suspicion for autoimmune hypophysitis. Exam in the ED revealed an anxious female wit hypertension, tachycardia and BMI 30. The rest of the physical exam was unremarkable. Her pituitary gonadal axis workup revealed panhypopituitarism with TSH 0.01uIU/ml, FSH <0.3Miu/ml, LH <0.3mIU/ml, ACTH <5pg/ml, IGF-1 31ng/ml and prolactin 14.4ng/ml. She was started on prednisone 50mg daily and on levothyroxine 150mcg daily. On day 2, she developed polyuria and the work up revealed a serum sodium of 146 meq/L, serum osmolality 315mOsm/kg, urine osmolality 281mOsm/kg and urine output 5.6L in 24hrs. The diagnosis of DI was made and she was started on desmopressin. On day 7, the serum sodium normalized and she did not require any other dose of desmopressin. On the day of discharge, a repeat MRI head was done which showed reduced enhancement of the pituitary which was reassuring. Discussion: LYH is a neuroendocrine disorder characterized by autoimmune inflammation of the pituitary gland with various degrees of pituitary dysfunction. Associated autoimmune diseases are seen in 18%– 50% of cases of AH. The most commonly-associated disease is autoimmune thyroid disease (15%–25%), while concurrent autoimmune conditions including RA are reported as well. Homogenous symmetrical enlargement of the pituitary gland, a thickened non deviated stalk, and a prompt, intense and homogenous enhancement of the mass after gadolinium contrast are the characteristic findings on MRI. Spontaneous resolution is the usual course and surgery is indicated only when the symptoms of sellar compression are serious and progressive. Conclusion: LYH is predominantly a disease of young females. We present this case in order to create awareness about the co-existence of LH with other autoimmune conditions and its usual course of regression with steroids.
Background Subacute thyroiditis, also named giant cell thyroiditis, painful thyroiditis, and de Quervain's thyroiditis, usually presents with neck pain or discomfort, a tender diffuse goiter and mild or moderate elevation of serum free T4 and T3 levels. Here we report a case of subacute thyroiditis patient presenting with severe thyrotoxicosis. Clinical case: A 27-year-old woman with no significant past medical history presents to the emergency room with palpitations and abnormal EKG with heart rate at 160 beats per minute. She developed a sore throat 3 days prior to the presentation, but she did not have neck pain or fever. She reports a 3-month history of hair loss, headaches and weight gain. Labs showed significantly elevated free T4 greater than 7.7 ng/dl (0.8-1.7) and free T3 level at 20.7 pg/ml (2. 0-4.8), and suppressed TSH less than 0. 01 uIU/ml (0.45-4.5) and normal ESR at 15 mm/hour. Her TPO antibody was greater than 1300 u/ml. Thyroid stimulating immunoglobulin (TSI) and TSH receptor antibody (TRab) were obtained but results were pending when she was discharged from the hospital. She has no typical clinical features of subacute thyroiditis with normal ESR and her free T3 and free T4 levels were significantly elevated. She was discharged on Methimazole and Propranolol and to do neck ultrasound as outpatient and follow-up TSI and TRab results and repeat free T4 and T3 in 1 week. Her neck ultrasound revealed mild hypervascularity but no Graves’ features. Her TSI and TRab were negative and free T4 level had no improvement even on significant dose of Methimazole. All the findings argue against Graves’ disease, but support subacute thyroiditis. Then Methimazole was discontinued and Prednisone was started at 20 mg daily and quickly taper to 5 mg daily in 2 weeks then stopped. After on Prednisone for 3 weeks, her free T4 was close to normal at 2. 0 ng/dl, T3 normal at 120 ng/dl, although TSH is suppressed. After stopped Prednisone for 2 weeks, her free T4, T3 and TSH were all back to normal. She is currently euthyroid without any medication at 5 months after her initial presentation. Conclusion Treatment of patients with subacute thyroiditis is pain relief with NSAID or Prednisone when NSAID is not effective. Anti-thyroid medications are rarely effective even in subacute thyroiditis patient with thyroid storm. Our case illustrated the role of corticosteroids in the treatment of subacute thyroiditis patient with severe thyrotoxicosis. Neck ultrasound and thyroid antibodies including TSI and TRab are critical to make a correct diagnosis in subacute thyroiditis patient with severe thyrotoxicosis. Presentation: No date and time listed
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