Objective To clarify the influence of the degree of gastric mucosal atrophy on the serum lipid levels before and after the eradication of Helicobacter pylori infection.

Methods The subjects were individuals who underwent an annual detailed medical checkup. Serum anti-H. pylori IgG antibody detection and upper endoscopic examinations were performed in all subjects. Gastric mucosal atrophy was evaluated by the classification of Kimura and Takemoto. The serum levels of total cholesterol, high-density lipoprotein cholesterol (HDLC), low-density lipoprotein cholesterol (LDLC), LDLC/HDLC ratio, and triglycerides were compared among the different degrees of gastric mucosal atrophy in H. pylori-positive subjects. In addition, changes in those serum lipid levels during a two-year period were compared among H. pylori post-eradication cases that showed different degrees of gastric mucosal atrophy prior to eradication.

Results In subjects with higher degrees of gastric mucosal atrophy, the serum levels of total cholesterol, LDLC, and triglycerides were elevated. Furthermore, the LDLC/HDLC ratio in subjects with moderate and severe grades of gastric mucosal atrophy was significantly higher than in subjects with mild atrophy. In subjects with higher degrees of gastric mucosal atrophy, the serum level of LDLC and the LDLC/HDLC ratio were decreased following eradication of H. pylori.

Conclusion Lipid metabolism is influenced by the degree of gastric mucosal atrophy present before the eradication of H. pylori, and the favorable effects of such eradication are significant in patients with higher degrees of atrophy.

Although hyperparathyroidism has been reported to cause acute pancreatitis, little is known about the mechanism involved. This study describes the case of an 86-year-old woman with acute pancreatitis and consciousness disturbance caused by hyperparathyroidism and hypercalcemia, respectively. The consciousness disturbance caused by severe hypercalcemia probably masked the typical symptoms associated with pancreatitis because she did not report abdominal pain during the clinical course.

Cronkhite-Canada syndrome (CCS) is a rare non-inherited disease characterized by gastrointestinal polyposis, chronic diarrhea, ectodermal dysplasia, skin hyperpigmentation, hair loss and nail atrophy. Although the efficacy of corticosteroid and immunomodulatory agents has been demonstrated, no standard therapy regimen has been established, and the prognosis of CCS is still poor due to various complications. We here in report a CCS patient complicated with severe sepsis and disseminated intravascular coagulation who was successfully treated by combined modality therapies, including recombinant human soluble thrombomodulin.

A 75-year-old Japanese woman presented with nausea and appetite loss. Computed tomography showed a radiopaque substance in the stomach. Esophagogastroduodenoscopy revealed bezoars in the stomach, which were endoscopically retrieved. The bezoars were mainly composed of magnesium and oxide. Although bezoar formation associated with magnesium oxide consumption is infrequently encountered, the present case indicates that pharmacobezoar should be considered among the differential diagnoses in patients who demonstrate a radiopaque mass in the digestive tract and have a history of magnesium oxide use.

A 37-year-old obese man who was a social drinker was admitted to our hospital to undergo a detailed examination for liver injury with anti-mitochondrial antibody positivity. Abdominal ultrasonography revealed moderate fatty liver. A histological analysis showed steatosis of approximately 30% of the hepatocytes, focal necrosis, a few ballooning hepatocytes and lobular inflammation suggestive of steatohepatitis, epithelioid granuloma and irregularity of the sequence of the bile duct epithelium accompanied by lymphocyte infiltration suggestive of chronic cholangitis. He was diagnosed with non-alcoholic steatohepatitis complicated with primary biliary cholangitis. His liver injury was improved by weight loss and high-dose ursodeoxycholic acid treatment.

A 79-year-old Japanese woman was diagnosed with acute hepatitis B based on laboratory tests showing positivity for IgM-class antibody against hepatitis B virus (HBV) core and hepatitis B surface antigen (HBsAg) as well as elevated transaminases. A phylogenetic analysis revealed that the HBV strain obtained from the patient belonged to genotype D/subgenotype D1, similar to strains circulating in foreign countries but different from those in Japan. The clinical course was favorable. HBsAg became negative within 10 weeks after the onset. To our knowledge, this is the first report of acute hepatitis B caused by subgenotype D1 HBV in Japan.

A 35-year-old woman was referred to our hospital for the management of acutely decompensated heart failure due to peripartum cardiomyopathy (PPCM). Generally, cardiac examinations are performed after the manifestation of heart failure in patients with PPCM. Thus, reports of serial cardiac examinations before the onset of PPCM are scarce. In this case, we were able to document the serial echocardiographic findings before the onset of life-threatening PPCM. We found that the left ventricular systolic function was preserved at 35 weeks of gestation but declined acutely after delivery at 38 weeks. Although speculative, these findings suggest that left ventricular dilation might precede the onset of PPCM.

A 43-year-old man was diagnosed with acute myocardial infarction (AMI) due to multivessel coronary vasospasm. Accordingly, two coronary vasodilators were administered, and he was discharged without an angina attack. However, from the following day, he reported frequent chest pain and was re-hospitalized. Despite adding multiple coronary vasodilators, it was difficult to completely suppress the angina attack. He also demonstrated hypereosinophilia from the onset of AMI, and his eosinophil count gradually increased up to 6,238/μL. After corticosteroid administration was started, the vasospasm was completely controlled, and his eosinophil count normalized. He remained free from angina attacks for two years with corticosteroid therapy.

Gonadotropin-releasing hormone (GnRH) agonists have been used for the treatment of various diseases. Although autoimmune thyroid disease has been reported as a rare complication of these agents, the symptoms are almost always transient and non-life-threatening. We herein report a rare case of an 83-year-old man receiving GnRH agonist treatment for prostate cancer who developed myxedema coma complicated by acute pancreatitis. This is the first report of myxedema coma potentially associated with a GnRH agonist. The follow-up of the thyroid function is necessary for patients undergoing treatment with GnRH agonists, especially those known to have or to be susceptible to autoimmune thyroid disease.

Neuroendocrine-differentiated prostate cancer (NEPC) is a rare pathophysiology. We herein report a patient diagnosed with conventional prostate adenocarcinoma before hormone therapy, which was later diagnosed as NEPC. The nadir of prostate-specific antigen (PSA) was achieved once. However, adenocarcinoma changed to NEPC in recurrence, and the serum progastrin-releasing peptide (Pro-GRP) and neuron-specific enolase (NSE) values increased. A prostate needle biopsy revealed neuroendocrine differentiation. The chemotherapy regimen was changed, and somatostatin receptor scintigraphy (SRS) helped to determine the distribution and features of lesions as well as the effects of therapy. When prostate cancer worsens despite conventional therapy, NEPC should be considered.

A 76-year-old woman suddenly developed anasarca and a fever, and an examination revealed thrombocytopenia, reticulin fibrosis, and acute kidney injury, yielding the diagnosis of thrombocytopenia, anasarca, fever, reticulin fibrosis, organomegaly (TAFRO) syndrome. Renal replacement therapy and steroid treatment were soon started. Her proteinuria was minor at first; however, once the kidney function improved, nephrotic syndrome occurred. A kidney biopsy showed membranoproliferative glomerulonephritis-like glomerulopathy with massive macrophage infiltration. Although kidney dysfunction is often observed in TAFRO syndrome patients, its detailed mechanism is unclear. This case suggests that TAFRO syndrome involves both acute kidney injury with minor proteinuria and nephrotic syndrome, and these disorders can develop serially in the same patient.

Nivolumab is an anti-programmed cell death-1 (PD-1) antibody that is utilized as an immune checkpoint inhibitor (ICI) for cancer therapy. We herein present the case of a 57-year-old man who developed acute kidney injury during treatment with nivolumab for lung cancer. A renal biopsy revealed acute tubulointerstitial nephritis. Immunohistochemical staining demonstrated marked infiltration of macrophages and T cells together with mild B cell infiltration. Of note, strong CD163⁺ M2 macrophage infiltration was observed. The cessation of nivolumab and high-dose prednisolone therapy improved the renal function of the patient. Further, we review the pertinent literature on renal-infiltrating cells in ICI-induced tubulointerstitial nephritis.

A 64-year-old man was admitted to our hospital for purpuric rash, joint pain, and a fever. He had earlier undergone a follow-up examination for interstitial lung disease. At the current visit, the diagnosis was immunoglobulin A (IgA) vasculitis, based on skin and renal biopsy findings. He developed sudden breathlessness and hemoptysis. Chest computed tomography revealed ground glass opacity in the right lower lung fields, suggesting pulmonary hemorrhaging associated with IgA vasculitis. Despite steroid and cyclophosphamide therapy, and plasma exchange, he died 52 days after admission. Early aggressive therapies may be recommended for old patients with IgA vasculitis who have an additional comorbidities.

We herein report the case of a 52-year-old man with stage IV lung adenocarcinoma. The patient was negative for epidermal growth factor receptor (EGFR) mutations and echinoderm microtubule-associated protein-like 4 (EML4) /anaplastic lymphoma kinase (ALK) rearrangement. He was treated with nivolumab as a third-line chemotherapy. After four cycles of nivolumab treatment, a partial response was observed in the brain and at the primary tumor site. Nivolumab treatment has been continued for 11 months without progression. Immunohistochemistry revealed that the programmed death-ligand 1 (PD-L1) expression was 0% (according to the tumor proportion score).

Our case indicates that the efficacy of programmed cell death 1 inhibitors is not solely predicted by the PD-L1 status, and that immune checkpoint inhibitors might be effective for the treatment of central nervous system metastasis.

The mechanisms underlying anaplastic lymphoma kinase (ALK) resistance have not been well investigated in clinical practice. We herein report the case of a lung cancer patient with carcinomatous meningitis who had an ALK I1171T resistance mutation revealed by direct DNA sequencing of the cerebrospinal fluid after treatment with cytotoxic chemotherapy, crizotinib, and alectinib. I1171T is considered to be sensitive to ceritinib. Although ceritinib was not effective initially, we chose ceritinib again after whole-brain radiotherapy and ventriculoperitoneal shunting. Although the response duration was short, spinal magnetic resonance imaging revealed a marked response. The identification of an acquired ALK resistance mutation will aid in choosing the optimum sequence therapy.

Pembrolizumab, a humanized monoclonal IgG4 antibody directed against programmed death-1, is an immune checkpoint inhibitor that has been introduced for the treatment of non-small-cell lung cancer. However, immune checkpoint inhibitors may cause severe immune-related adverse events. We herein present a case of lung cancer with complete atrioventricular block associated with acute myocarditis, which developed 16 days after the administration of pembrolizumab. The clinical course of this case suggested a strong need for close cardiac monitoring when pembrolizumab is administered on an outpatient basis.

Lymphomatoid granulomatosis (LYG) is a rare lung disorder diagnosed by radiological imaging of multiple pulmonary nodules and occasionally induced by methotrexate (MTX) use. To date, the treatment of LYG has not been standardized. We herein report the case of a patient with grade 3 MTX-related LYG who presented a bulky lung mass. Importantly, the disease condition only improved after the discontinuation of MTX and remained stable for more than 1 year. Chest physicians should be aware that LYG can develop as a single lung mass and spontaneously regress, even without aggressive chemotherapy, following the cessation of MTX.

Nuclear protein in testis (NUT) carcinoma (NUT-C) is an exceedingly rare and aggressive neoplasm. We herein report a case of a 57-year-old man with a rapidly progressing tumor of the thorax and left pleural effusion. The pathological features and immunohistochemical staining of specimens obtained by a transbronchial lung biopsy initially indicated poorly differentiated squamous cell carcinoma. However, given the clinical presentation along with the additional histopathologic features, NUT-C was considered. Immunohistochemical staining for NUT was positive in the pleural fluid cell block, confirming the diagnosis of NUT-C. This report indicates the utility of immunohistochemical staining for diagnosing NUT in the pleural fluid cell block.

We herein report a case of long-lasting pure red cell aplasia (PRCA) after major ABO-incompatible allogeneic stem cell transplantation (SCT) for acute lymphoblastic leukemia. The patient needed red blood cell (RBC) transfusion every week after SCT. On day 236, he was diagnosed with odontogenic infection, and the serum levels of Interleukin (IL)-6 were elevated to 12.1 pg/mL. After that, the numbers of reticulocyte rapidly began to increase, and RBC support was not needed from day 251. No standard care for PRCA following SCT has been established. The IL-6 elevation caused by the odontogenic infection therefore appears to have been affected by the improvement in PRCA.

Mild hemophilia A is caused by a missense mutation in the FVIII gene that is responsible for a decrease in the FVIII:C to between 5% and 40%. The development of FVIII inhibitors has been reported in 3-13% of patients with mild hemophilia. Genetic risk factors for the development of inhibitors in mild hemophilia have been investigated. In the present study, we encountered a case of mild hemophilia with an FVIII inhibitor and identified the mutation responsible: a novel Phe595Cys mutation in the FVIII gene. In addition, this study showed that the inhibitor recognized exogenous wild-type FVIII and autologous mutant FVIII.

We describe the cases of two sisters with spastic paraplegia 11 (SPG11). The younger sister developed relapsing lesions in the brain white matter with enhancement during the acute phase that mimicked multiple sclerosis (MS). The elevation of myelin basic protein in the cerebrospinal fluid (CSF) suggested demyelination, but a normal IgG index, the absence of oligoclonal bands, and the ineffectiveness of steroid treatment indicate that an autoimmune mechanism may not have been involved. In these affected sisters, we identified novel compound heterozygous mutations in the SPG11 gene. Our cases indicate the possible existence of a broader phenotypic spectrum of SPG11 mutations.

Nocturnal hypertension (NH) is a symptom of cardiovascular dysautonomia in multiple system atrophy (MSA); however, care and medication are often insufficient. We herein report a patient with MSA who showed posterior reversible encephalopathy syndrome (PRES) caused by hypertension during sleep. He presented clinically with total blindness; T2-weighted magnetic resonance imaging showed high signal intensities in the bilateral subcortical occipital-temporal lobes. His PRES was completely reversed by blood pressure control. NH may contribute to the development of PRES. The appropriate assessment and management of hemodynamic changes in MSA, including NH, is necessary to prevent severe complications such as PRES.

A 42-year-old Japanese man with hereditary angioedema suffered accidental trauma to his jaw in Shizuoka Prefecture, Japan, which gradually caused facial edema. Since plasma-derived human C1 inhibitor (pdh C1-INH) was unavailable, he had to be transferred to Juntendo University Hospital in Tokyo. Due to his severe edema, he suffered asphyxiation leading to cardiopulmonary arrest upon arrival. The patient was resuscitated and promptly treated with pdh C1-INH. In Japan, the self-administration of pdh C1-INH is not allowed, and every prefecture does not always possess stocks of pdh C1-INH. This case emphasizes the need for urgent improvements in treatment availability in Japan.

A 78-year-old man had a fever and exhibited disordered consciousness, which led to his transportation to our hospital. On arrival, he exhibited discharge from the ear. Because extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli was detected in the ear discharge and cerebrospinal fluid specimens, it was inferred to be the causal bacteria. Pulsed-field gel electrophoresis indicated the same ESBL-producing E. coli pattern in the patient's ear discharge, external auditory canal granulation, cerebrospinal fluid, and stool, indicating their common molecular epidemiological origin. Although ESBL-producing E. coli is an extremely rare cause of bacterial meningitis, it should be considered as a potential causal bacteria for community-acquired meningitis.

Vertebral aspergillosis is a rare infectious disease with a high mortality rate. We herein report a 70-year-old woman with acute myelogenous leukemia with myelodysplasia-related changes, nontuberculous mycobacteriosis, and bronchiectasis who presented with a fever and cough. Her clinical symptoms and laboratory test results suggested febrile neutropenia and pneumonia. However, her clinical course was further complicated by lower extremity weakness. Magnetic resonance imaging of the spine showed consolidation contiguously spreading toward the epidural space between the T4 and T5. Cytological testing of the pleural effusion revealed Aspergillus fumigatus. We also review and summarize previously reported cases of vertebral aspergillosis in Japan.

Valacyclovir, a prodrug of acyclovir, is the first-line treatment for herpes zoster, but the renal function must be monitored, because acyclovir is metabolized by the kidneys. We herein report a case of valacyclovir-induced neurotoxicity with no preceding renal impairment. An 88-year-old man was admitted because of an impaired consciousness after the administration of valacyclovir at 3,000 mg daily for herpes zoster on the chest. His consciousness level gradually improved with hydration and valacyclovir withdrawal. It was later confirmed that the level of acyclovir on admission had been 35.45 μg/mL in the blood and 36.45 μg/mL in the cerebrospinal fluid.