Comparison of both lower leg bone mineral density in single limb knee osteoarthritis patients.

PURPOSE: The relationship between knee osteoarthritis (OA), bone mineral density (BMD), and alignment has not yet been clarified. This study aimed to investigate the relationship between the two limbs in patients with single-limb knee OA. METHODS: Patients who underwent single-limb total knee arthroplasty between March 2019 and February 2021 were retrospectively analyzed. Only patients with Kellgren-Lawrence (KL) grades III and IV on the operated side and KL I and II on the opposite side were included. Patients with traumatic OA, a surgery that could change the alignment of both lower extremities and previous fractures were excluded. The proximal femur BMD on the OA and non-OA sides were compared. In addition, the difference in BMD was compared between a group with a difference in alignment of both lower extremities (> 5°) and a group without a difference (< 5°). RESULTS: In total, 149 patients were included. The BMD T-score of the femoral neck on the OA side was lower than that of the non-OA side (p < 0.001). There was no correlation between BMD and alignment, and there was no difference in BMD according to the difference in alignment. CONCLUSION: The femoral neck BMD of the leg on the side with knee OA was lower than that on the side without OA. However, the alignment difference between the legs did not affect BMD. BMD was lowered because of OA and not because of alignment.

Predictive values of neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and other prognostic factors in pediatric vestibular neuritis patients.

OBJECTIVE: To analyze the relationship between severity and hemodynamic factor in pediatric vestibular neuritis patients and find out their effectiveness as a prognostic factor. STUDY DESIGN: Retrospective review. SETTING: Tertiary medical center. PATIENTS: Pediatric patients diagnosed between January 2010 and December 2019 at a tertiary medical institution who were hospitalized with dizziness. MAIN OUTCOME MEASURE: A study of the duration of spontaneous nystagmus loss and the severity of the disease using questionnaires (PVSQ, DHI) in pediatric patients admitted to Vestibular neuritis (VN) and correlation with NLR, PLR, MPV and RDW conducted at the time of admission. RESULT: This study was conducted on 22 children with VN and 30 children in control group. For the evaluate of the severity of the symptoms of VN patients, two group were classified based on the period from the onset of the symptom to the loss of the spontaneous nystagmus.: mild VN and severe VN, and the PVSQ and DHI questionnaires were used to assess the degree of improvement. PVSQ and DHI score generally improved during spontaneous nystagmus loss, and comparing the severity of the symptoms with the values of NLR, PLR, MPV and RDW showed a positive correlation between the severity of the symptoms and the value of the NLR and PLR value. CONCLUSION: NLR, PLR value is thought to be an efficient indicator of pediatric VN patents and could be a clue to the current unknown cause of childhood VN disease.

Bilateral Orbital Apex Syndrome Related to Sphenoid Fungal Sinusitis.

Orbital apex syndrome (OAS) is a rare condition that usually occurs due to damage to surrounding inner and surrounding bone tissue. Orbital apex syndrome may result from a variety of conditions that cause damage to the superior orbital fissure and to the optic canal leading to optic nerve (II) dysfunction. We recently experienced a rare case of sphenoidal Aspergillosis, which damaged the adjacent cavernous sinus structures and led to the definite symptom of bilateral OAS in a 77-year-old male. We present this rare case with a brief review of these disease's entities.

The Effect of Korean Red Ginseng on Symptoms and Inflammation in Patients With Allergic Rhinitis.

Korean red ginseng (KRG) has been traditionally used in Korea for health improvement. However, the clinical effect of KRG intake on the symptoms in patients with allergic rhinitis remains unknown. Our study was performed to identify the clinical effects of KRG on patients with allergic rhinitis and to examine the effect of KRG on allergic inflammatory reaction. We evaluated 60 patients with allergic rhinitis. All the patients were treated for 4 weeks. The patients were divided into 3 groups, according to the medication. Twenty patients were treated with KRG, 20 patients with the placebo, and 20 patients with the antihistamine. The patients recorded their symptoms in a daily symptom diary card. The patients checked the peak nasal inspiratory flow rate 2 times a day. Total serum immunoglobulin E (IgE) and serum-specific IgE were measured by ImmunoCap method before and after 4-week medication. The Th2 cytokines interleukin-4 (IL-4), IL-5, and IL-10 were checked in the serum before and after the 4-week treatment. The eosinophil counts in the nasal smears were checked. Korean red ginseng group has shown the significant improvement in rhinorrhea, nasal itching, and eye itching. Both the antihistamine and KRG groups showed a significant decrease in total IgE level at the end of treatment. The serum IL-4 level and eosinophil counts in the nasal smears were significantly decreased both in the antihistamine and in the KRG groups. In conclusion, KRG might be a useful treatment modality for patients with allergic rhinitis.

Nrf2-Heme Oxygenase-1 Attenuates High-Glucose-Induced Epithelial-to-Mesenchymal Transition of Renal Tubule Cells by Inhibiting ROS-Mediated PI3K/Akt/GSK-3ß Signaling.

BACKGROUND: Epithelial-to-mesenchymal transition (EMT) is thought to play a significant role in the advancement to chronic kidney disease and contributes to the deposition of extracellular matrix proteins and renal fibrosis relating to diabetic nephropathy. METHOD: We studied the effect of Nrf2-HO-1 signaling on high-glucose- (HG-) induced EMT in normal human tubular epithelial cells, that is, HK2 cells. In short, we treated HK2 cells with HG and sulforaphane (SFN) as an Nrf2 activator. EMT was evaluated by the expression activity of the epithelial marker E-cadherin and mesenchymal markers such as vimentin and fibronectin. RESULTS: Exposure of HK2 cells to HG (60 mM) activated the expression of vimentin and fibronectin but decreased E-cadherin. Treatment of HK2 cells with SFN caused HG-induced attenuation in EMT markers with activated Nrf2-HO-1. We found that SFN decreased HG-induced production of reactive oxygen species (ROS), phosphorylation of PI3K/Akt at serine 473, and inhibitory phosphorylation of serine/threonine kinase glycogen synthase kinase-3ß (GSK-3ß) at serine 9. Subsequently, these signaling led to the downregulation of the Snail-1 transcriptional factor and the recovery of E-cadherin. CONCLUSION: The present study suggests that Nrf2-HO-1 signaling has an inhibitory role in the regulation of EMT through the modulation of ROS-mediated PI3K/Akt/GSK-3ß activity, highlighting Nrf2-HO-1 and GSK-3ß as potential therapeutic targets in diabetic nephropathy.

Nrf2-Heme oxygenase-1 modulates autophagy and inhibits apoptosis triggered by elevated glucose levels in renal tubule cells.

BACKGROUND: Autophagy is a highly balanced process in which lysosomes remove aged and damaged organelles and cellular proteins. Autophagy is essential to maintain homeostasis in the kidneys. METHODS: Using human renal tubule cells HK-2, we assessed the impact of high glucose (HG) on autophagy. We also evaluated the capability of sulforaphane (SFN) to protect the HK-2 cells from HG-induced apoptosis by modulating autophagy. RESULTS: SFN modulated autophagy and decreased apoptosis in the HK-2 cells that were cultured in 250 mM glucose medium for two days. The reactive oxygen species (ROS) levels increased, as expected, in the cells cultured in the 250 mM glucose medium. However, the SFN decreased the ROS levels in the HK-2 cells. The overexpression of heme oxygenase-1 (HO-1) by SFN decreased the expression of LC3 and beclin-1. LC3 and beclin-1 were involved in the downregulation of caspase-3 that was observed in the HG-induced cells. CONCLUSION: The activation of nuclear factor E2-related factor 2 (Nrf2)-HO-1 inhibited ROS expression and subsequently attenuated autophagy and cell apoptosis after HG injury was decreased. HG injury led to the activation of autophagy and HO-1 in order to combat oxidative stress and protect against cell apoptosis. Therefore, HO-1 activation can prevent ROS development and oxidative stress during HG injury, which considerably decreases autophagy and apoptosis.

Fibrillary glomerulonephritis combined with chronic inflammatory demyelinating polyneuropathy.

A 58-yr-old man presented with leg edema and subacute weakness of his bilateral lower extremities. Urinary and serum immunoelectrophoresis revealed the presence of lambda-type Bence Jones proteins. He was ultimately diagnosed with monoclonal gammopathy of undetermined significance (MGUS). A renal biopsy specimen showed fibrillary glomerulonephritis (FGN), which was randomly arranged as 12-20 m nonbranching fibrils in the basement membranes. Immunofluorescence studies were negative for immunoglobulin (Ig)G, IgM, IgA, C3, and kappa light chains in the capillary walls and mesangial areas. A Congo red stain for amyloid was negative. Electromyography and nerve conduction velocity examinations results were compatible with the presence of demyelinating polyneuropathy. This case showed a rare combination of FGN, without Ig deposition, and MGUS combined with chronic inflammatory demyelinating polyneuropathy (CIDP).

Effect of topical vitamin D on chronic kidney disease-associated pruritus: An open-label pilot study.

Chronic kidney disease-associated pruritus (CKD-aP) is a troublesome symptom in patients with end-stage renal disease (ESRD). Recently, vitamin D deficiency has been known to be one of the possible etiologic factors in CKD-aP. However, limited data is available on whether topical vitamin D treatment is effective for relieving CKD-aP. Therefore, the purpose of this study is to evaluate the effectiveness of topically vitamin D for CKD-aP. Twenty-three patients with CKD-aP were enrolled in a single center, open-label study. Patients were instructed to apply a topical vitamin D (calcipotriol) agent (Daivonex solution; LEO Pharma) or vehicle solution twice daily for a month. We assessed the efficacy and safety of topical vitamin D on CKD-aP using clinical and dermoscopic photographs, and questionnaires including the validated modified pruritus assessment score (VMPAS) and visual analog scale (VAS) every 2 weeks. Dry dermoscopic findings showed significant improvement of scale (dryness) on the skin of topical vitamin D-treated patients compared with those of the vehicle group. Both VMPAS and VAS were significantly decreased after 2 and 4 weeks of the topical vitamin D treatment compared with the vehicle, respectively (P < 0.05). No significant side-effects were observed. Topical vitamin D may be one of the safe and effective therapeutic candidates for CKD-aP.

Activation of AMP-activated protein kinase inhibits albumin-induced endoplasmic reticulum stress and apoptosis through inhibition of reactive oxygen species.

BACKGROUND: Endoplasmic reticulum (ER) stress induced by urinary albumin plays an important role in tubulointerstitial injury. We have shown that albumin-induced ER stress is regulated through reactive oxygen species (ROS)-c-Src kinase-mTOR signaling pathways. We postulated that peroxisome proliferator-activated receptor-γ (PPAR-γ) might also act as an upstream signaling molecule between c-Src kinase and mTOR. It has been suggested that AMP-activated protein kinase (AMPK) is involved in attenuation of ER stress. We examined whether and how activation of AMPK suppressed the albumin-induced ER stress and apoptosis in tubular epithelial cells. METHOD: HK-2 cells, a proximal tubular cell line, were used. Protein expressions were measured by Western blot analysis. Intracellular ROS and apoptosis were analyzed by flow cytometry. RESULTS: Albumin-induced PPAR-γ expression and PPAR-γ inhibitor (GW9662) suppressed the albumin-induced ER stress. c-Src kinase inhibitor and GW9662 reduced the albumin-induced PPAR-γ and mTOR, respectively. Metformin (the best known clinical activator of AMPK) and another AMPK activator (AICAR) suppressed the albumin-induced ER stress via inhibition of ROS through induction of endogenous antioxidant thioredoxin. AMPK inhibitor blocked the effect of metformin and AICAR. Our in vivo animal study showed that metformin reduced the renal cortical expression of ER stress protein (GRP78) in protein-overload proteinuria rats. Metformin also reduced the caspase 3-dependent apoptosis induced by albumin. CONCLUSION: PPAR-γ was involved in albumin-induced ER stress as an upstream signaling molecule between c-Src kinase and mTOR. AMPK activation might be beneficial in attenuating the tubulointerstitial injury induced by albumin.

Activation of spleen tyrosine kinase is required for TNF-α-induced endothelin-1 upregulation in human aortic endothelial cells.

Endothelin-1 (ET-1) promotes atherosclerosis. We tested whether spleen tyrosine kinase (Syk) mediates tumor necrosis factor-α (TNF-α)-induced ET-1 upregulation in human aortic endothelial cells (HAECs) and sought to identify the signal pathways involved. TNF-α-induced reactive oxygen species (ROS) activated Syk and phosphatidylinositol 3-kinase (PI3K), which was required for the activation of AP-1 and subsequent ET-1 gene transcription. ROS mediated c-Jun NH(2)-terminal kinase (JNK) is also required for AP-1 activation, but Syk and PI3K regulated AP-1 activation independently of JNK. Through regulation of ET-1 production, Syk could be implicated in atherosclerosis.

Porcelain heart: rapid progression of cardiac calcification in a patient with hemodialysis.

Cardiac calcification usually occurs in patients with end-stage renal disease. However, rapid progression of cardiac calcification is rarely associated with secondary hyperparathyroidism of end-stage renal disease. We report a patient with end-stage renal disease who showed moderate left ventricular hypertrophy at the first echocardiography, and showed severe myocardial calcification and severe mitral valve stenosis 4 years later. We suspected a rapid progression 'porcelain heart' cardiomyopathy secondary to hyperparathyroidism of end-stage renal disease. The patient underwent parathyroidectomy, and considered mitral valve replacement.

Desmopressin improves platelet dysfunction measured by in vitro closure time in uremic patients.

BACKGROUND/AIMS: Desmopressin decreases bleeding time in uremic patients. Although bleeding time is the most frequently used measure of global platelet function, this test has important disadvantages. In vitro closure time (CT) is a relatively new and efficient test of primary hemostasis. We designed a prospective randomized study to evaluate the effect of desmopressin on platelet function, as measured by in vitro CT, in uremic patients. METHODS: Forty-eight uremic patients, about to commence hemodialysis and with prolonged CT, were randomized to infusion with desmopressin (n = 24) or saline alone (n = 24). Complete blood count, prothrombin time, activated partial thrombin time, levels of plasma fibrinogen, von Willebrand factor (VWF), factor VIII (FVIII) and CT were measured before and 1 h after desmopressin or saline infusion. RESULTS: Following desmopressin infusion, collagen/epinephrine and collagen/adenosine diphosphate CT were significantly shortened from 212 +/- 58 to 152 +/- 45 s (p = 0.01) and from 189 +/- 78 to 147 +/- 58 s (p = 0.012), respectively; levels of FVIII and VWF were significantly increased from 188 +/- 66 to 252 +/- 93% (p = 0.017) and from 113 +/- 9 to 121 +/- 9% (p = 0.043), respectively. There were no significant changes in the control group. CONCLUSIONS: Desmopressin improved platelet dysfunction and increased the plasma concentrations of VWF and FVIII, suggesting that desmopressin may play a role in improving the bleeding tendency in uremic patients.