Hemodialysis as a Risk Factor for Ceftriaxone‐Associated Pseudolithiasis in Adults

Ceftriaxone‐associated biliary pseudolithiasis is common among children; however, there are only a few reports of pseudolithiasis in adult patients on HD. This retrospective cohort study included 278 adult patients on ceftriaxone therapy from 1 February 2016 to 1 September 2018. Pseudolithiasis was defined as a new development of sludge or stones in the gallbladder within 60 days of ceftriaxone therapy. After excluding patients with preexisting gallstones and a history of cholecystectomy, 113 patients on maintenance HD, and another 98 patients were enrolled as the HD and control group, respectively. Thirteen patients developed pseudolithiasis. Its incidence was significantly higher in the HD group than that in the control group. Multivariate logistic regression analyses showed that development of pseudolithiasis was significantly associated with HD and ceftriaxone dose. Therefore, HD in patients receiving ceftriaxone therapy appears to be associated with a risk of pseudolithiasis. These findings highlight the need for careful follow‐up.     

Multicystic biliary hamartoma mimicking intrahepatic cholangiocarcinoma: report of a case

Multicystic biliary hamartoma (MCBH) is a rare cystic disease of the liver. A 69-year-old man was referred to our hospital with radiographic abnormality. Physical examination of the patient was unremarkable, and he denied any previous medical, travel, or surgical history. An abdominal computed tomography (CT) scan demonstrated a 3-cm low-density lesion in segment 3 of the liver, with dilation of the intrahepatic bile duct. The peripheral site of this lesion was slightly enhanced in the arterial phase. In the portal phase, the peripheral site was enhanced more clearly and showed a honeycomb-like dilated bile duct. Ultrasonography also revealed that the lesion was an irregularly shaped mass. On magnetic resonance imaging (MRI), T1-weighted images revealed a low-density mass and T2-weighted images revealed a dappled-density mass with honeycomb-like dilated bile duct and dilation of major intrahepatic bile duct. The patient was diagnosed with intrahepatic cholangiocarcinoma (ICC) and underwent left hepatectomy. However, pathological findings revealed that the lesion was MCBH. Our case highlights the potential difficulties in differentiating between MCBH and ICC under such circumstances.     

Mitochondrial ubiquitin ligase MITOL blocks S-nitrosylated MAP1B-light chain 1-mediated mitochondrial dysfunction and neuronal cell death

Nitric oxide (NO) is implicated in neuronal cell survival. However, excessive NO production mediates neuronal cell death, in part via mitochondrial dysfunction. Here, we report that the mitochondrial ubiquitin ligase, MITOL, protects neuronal cells from mitochondrial damage caused by accumulation of S-nitrosylated microtubule-associated protein 1B-light chain 1 (LC1). S-nitrosylation of LC1 induces a conformational change that serves both to activate LC1 and to promote its ubiquination by MITOL, indicating that microtubule stabilization by LC1 is regulated through its interaction with MITOL. Excessive NO production can inhibit MITOL, and MITOL inhibition resulted in accumulation of S-nitrosylated LC1 following stimulation of NO production by calcimycin and N-methyl-D-aspartate. LC1 accumulation under these conditions resulted in mitochondrial dysfunction and neuronal cell death. Thus, the balance between LC1 activation by S-nitrosylation and down-regulation by MITOL is critical for neuronal cell survival. Our findings may contribute significantly to an understanding of the mechanisms of neurological diseases caused by nitrosative stress-mediated mitochondrial dysfunction.     

Pivot technique combined with mandibular backward distraction osteogenesis for the patient with high risk for relapse

Severe skeletal relapse is one of the most difficult problems after mandibular advancement, and the management to overcome such problems tends to require more compromised methods and longer treatment period. We described that mandibular backward distraction osteogenesis with maxillomandibular fixation at an appropriate occlusion. Furthermore, to avoid inappropriate distraction vector, the distal plates of the distraction device were fixed with 1 screw to work as a pivot after the manipulation of the condyle to the glenoid fossa at the end of distraction activation. This technique was applied to 3 female patients with mandibular deficiency. The intraoral distractors were set on the lateral surface of the mandibular body; the fixation of the distal plate was fixed with 1 monocortical screw to make the proximal segment including the condyle manipulating at the end of the distraction phase by releasing the maxillomandibular fixation. The distraction rate was 1 mm/d, and the latency period was 7 days. The follow-up period after mandibular backward distraction osteogenesis ranged from 26 to 56 months. No specific complication, such as broken device, severe infection, or bony nonunion, occurred. Postoperative relapse was not observed during the follow-up period. This technique might become 1 choice to apply for mandibular deficiency in a patient with high risk for relapse.     

Diabetic ketoacidosis accompanied by hypothermia: a case report

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus and is caused by insulin insufficiency. Hypothermia is defined as a core temperature of less than 35°C and is sometimes accompanied by DKA. We report two patients with diabetes who were admitted for DKA accompanied by hypothermia.     

Sequential monitoring of serum IL-6, TNF-α, and IFN-γ levels in a CAEBV patient treated by plasma exchange and immunochemotherapy

We report the case of a female patient with chronic active Epstein?CBarr virus infection (CAEBV) accompanied by hemophagocytic syndrome (HPS). On admission, she presented with severe liver dysfunction and disseminated intravascular coagulation with elevation of serum IL-6, TNF-??, and IFN-?? levels. Plasma exchange (PE) followed by immunochemotherapy with prednisolone, cyclosporine A, and VP16 was performed. PE decreased serum cytokine levels dramatically and improved liver function. Following immunochemotherapy, CAEBV became inactive. Four months after discharge, however, CAEBV relapsed with HPS, and serum cytokine levels were extremely elevated again. There was no response to immunochemotherapy, and the patient died 1?day after admission. We examined the cytokines in five additional untreated-CAEBV patients and determined that they were elevated above the normal level in all patients. These results suggest that inflammatory cytokines may have roles in the development of CAEBV, and that their depletion can be an effective treatment for this disease.