Combination therapy of modified electroconvulsive therapy and long-acting injectable aripiprazole for dopamine supersensitivity psychosis: a case report.

In the treatment of schizophrenia, long-term pharmacotherapy with D2-receptor antagonists can induce dopamine supersensitivity psychosis (DSP). We report a male patient with schizophrenia with suspected DSP due to excessive polypharmacy. He was hospitalized for several years. Most psychotropic drugs were reduced and subsequently stopped without the exacerbation of symptoms by administering modified electroconvulsive therapy (mECT). Aripiprazole was then selected as the main drug for treatment, which was subsequently changed to the long-acting injection formulation. He was eventually discharged and returned home. Combination therapy with mECT and aripiprazole, especially the long-acting injectable formulation, may help improve and prevent DSP.

Intravenous Immunoglobulin G Modulates the Expression of Sepsis-Induced Coagulopathy Factors and Increases Serum IgM Levels: A Prospective, Single-Center Intervention Study.

Sepsis and sepsis-related multiple organ failure are major causes of mortality in intensive care unit (ICU) settings. This study aimed to determine the effect of intravenous immunoglobulin G (IVIgG) on different types of immunoglobulin and anti-coagulant factor types in sepsis patients. A single-center observational study of patients with sepsis, severe sepsis, or septic shock was conducted from August 2008 to March 2013. Patients were divided into the IVIgG (immunoglobulin G [IgG] <870 mg/dL; lower normal range) and non-IVIgG (IgG ≥870 mg/dL) groups. The IVIgG group received IVIgG for three days, and other standard medications. Serial measurements were taken of serum IgG, immunoglobulin A (IgA), immunoglobulin M (IgM), total plasminogen activator inhibitor 1 (tPAI-1), and protein C. Patients in the IVIgG treatment group had significantly higher serum IgM level on Days 4 and 7 than on Day 1, but no significant changes in IgM levels were observed in patients in the non-IVIgG group. Patients in the IVIgG treatment had lower tPAI-1 levels on Days 4 and 7 than on Day 1 and increased protein C levels on Day 7 compared to those on Days 1 and 4. There were no significant differences in tPAI-1 levels or protein C levels in the non-IVIgG group, although a similar trend was observed. IVIgG administration increased patients' serum IgM and protein C levels and decreased their serum tPAI-1 levels. IVIgG has potential application for preventing sepsis-induced coagulopathy and disseminated intravascular coagulation.

A case of panspinal epidural abscess that presented with meningeal irritation.

Case: In rare cases, spinal epidural abscess involves the entire spine and can lead to neurological deficits and sepsis if treatment is delayed or suboptimal. A 65-year-old man was admitted with a diagnosis of bacterial meningitis. After admission, magnetic resonance imaging showed a spinal epidural abscess from the cervical to lumbar spine. Blood culture revealed Staphylococcus aureus. The patient was initially treated medically because he had no neurological deficits. Repeat blood culture remained positive and abscesses were found in the mediastinum and bilateral psoas muscles. Outcome: Surgery was carried out and the patient's postoperative course was satisfactory. Conclusion: Spinal epidural abscess can extensively affect the spine and may present with the symptoms of bacterial meningitis. It is essential to examine the entire spine and paraspinal regions and to treat early in cases of spinal epidural abscess.

Ventricular fibrillation by anaphylaxis following consumption of blue_skinned fish.

Case: Approximately 4_h after eating mackerel sushi, a 65_year_old man developed generalized itchiness and redness, after which he became unresponsive. He went into a state of ventricular fibrillation but after he was defibrillated twice, his heartbeat returned. The electrocardiogram obtained immediately after hospitalization showed some ST_segment depression, but a subsequent electrocardiogram showed improvement. Coronary CT showed no obvious stenosis or plaque in the coronary artery. Outcome: Results of an IgE_RAST test confirmed that the level of allergen_specific IgE for mackerel measured <0.10_UA/mL, while the level for anisakis was 1.91_UA/mL. Conclusions: As for the mechanism leading to cardiac arrest, it is thought that the histamines and leukotrienes released from cardiac mast cells caused a coronary artery spasm (Kounis syndrome). This anaphylactic shock is considered to be a result of anisakis allergy, but in general cases of anaphylaxis resulting from consumption of blue_skinned fish.

Suppression of cell invasiveness by periostin via TAB1/TAK1.

We have previously shown that the expression of periostin is significantly downregulated in human bladder cancer tissues and that periostin suppresses cell invasiveness and metastasis of cancer cells. To clarify the molecular mechanism of this suppression by periostin, we searched for periostin-binding proteins and identified TAB1, which interacts with and activates TAK1, by mass analysis of proteins co-precipitated with periostin in 293T cells expressing periostin. The association between periostin and TAB1 was confirmed by a pulldown assay in 293T cells co-tranfected with expression plasmids of periostin, TAB1 and TAK1. TAK1 was also co-precipitated with periostin in this assay. Co-transfection experiments in 293T also showed that periostin could activate TAK1. Introduction of siRNA for TAB1 suppressed TAK1 activation by periostin. Analyses with deletion mutants of periostin revealed that the C-terminal region of periostin was necessary and sufficient for the association with TAB1 and the TAK1 activation. The suppression of invasiveness by periostin was attenuated by siRNA targeting TAK1 or TAB1 in 293T (human embryonic kidney) and T24 (human bladder carcinoma) cell lines. These findings indicate that periostin is involved in the suppression of cell invasiveness via the TAB1/TAK1 signaling pathway.

[Can magnetic resonance imaging of the brain in the acute phase of carbon monoxide intoxication forecast delayed encephalopathy?].

We examined the usefulness of Magnetic Resonance Imaging (MRI) test in the acute phase of carbon monoxide intoxication for forecasting delayed encephalopathy (DE). [Case 1] 26-year-old female. COHb 12%. Takotsubo (Ampulla) cardiomyopathy was supervened. Pallidal disorder was recognized in MRI test in the early stage. Although Prophylactic HBO was performed, DE began. 36 days later, disorder was recognized in large area, such as, in cerebral white matter and callosum, and abnormality was found in WMS-R and MMSE. Since HBO was performed, DE subsided. In MRI test, on the other hand, high signal range in cerebral white matter and callosum were gradually decreased and WMS-R and MMSE were improved. [Case 2] 19-year-old female. COHb 9.4%. The state was considered to be mild but pallidal disorder was found in MRI test at the beginning. DE did not start, then the part of pallidal disorder was narrowed. WMS-R and MMSE showed slightly low level. [Case 3] 19-year-old female. COHb 7.3%. The state was considered to be mild and there was no abnormal findings in MRI test in the early stage. DE did not start. [Case 4] 48-year-old male. COHb 48.9%. Rhabdomylosis was supervened, then ischemic change in a left radiate crown was recognized in the early MRI test. Since the third day, disorientation and restlessness had been developed, so that the patient was transferred to psychiatric department, though it was still difficult to distinguish the case from DE. Although the case is relatively mild, pallidal disorder is recognized in the early MRI test. Pallidal disorder alone can cause memory disorder and cognitive impairment. Even if pallidal disorder alone is recognized in the early MRI test, white matter disorder is developed with time, and then DE begins. If there are no typical carbon monoxide intoxication findings, some cases can be suspected as DE. It is useful to perform serial MRI test in order to prepare for delayed encephalopathy in carbon monoxide intoxication.