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.

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%.

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 &gt;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.