Predictors of hyperglycaemic individuals who do not follow up with physicians after screening in Japan: A cohort study

Aims

Although people screened as being hyperglycaemic often fail to follow up with physicians for clinical assessment, epidemiologic findings on the frequency and predictors of not following up (hereafter, “no follow-up”) are lacking. The purpose of this study was to examine the no follow-up rate with physicians after screening for diabetes and predictors of no follow-up.

Methods

We assessed cases of no follow-up with physicians within six months after screening based on medical claims data from employee-based social health insurance programs in Japan, for people aged 20 to 68 years from 2005 to 2010.

Results

Among 3878 screened participants with hyperglycaemia, 2527 (65%) did not follow up with their physicians within six months after screening. Multiple logistic regression analysis revealed that younger age and lower blood glucose level predicted no follow-up among both men and women, while lower body mass index and negative proteinuria also predicted no follow-up among men. Treatment for dyslipidaemia facilitated follow-up among both genders, and treatment for hypertension or depression facilitated follow-up among men.

Conclusions

Approximately two thirds of individuals screened as having hyperglycaemia did not follow up with their physicians within six months after screening. Predictors of no follow-up were younger age and milder hyperglycaemia. Being on treatment for co-morbidities tended to facilitate follow-up.     

Elevated serum anti-phosphatidylcholine IgG antibodies in patients with influenza vaccination-associated optic neuritis

Introduction

Because the optic nerve is mainly comprised from phospholipids such as phosphatidylcholine, the association between optic neuritis, anti-phospholipids antibodies and vaccination was examined.

Subjects

Two female pediatric patients suddenly presented bilateral optic neuritis after administration of trivalent inactivated influenza vaccine.

Methods

These two patients and another 11 patients with central nervous system demyelinating diseases were examined these anti-phospholipids antibodies. And immune histopathology was examined using serum derived from a patient with optic neuritis.

Results

High serum titer of anti-phosphatidylcholine antibody levels were detected during acute phase in patients with optic neuritis. The patient's serum IgG antibodies were found to have stained the capillary endotheliums in the preserved autopsied optic nerve. Patients with optic neuritis had significantly elevated serum levels of anti-phosphatidylcholine antibody in comparison to the other patients without optic neuritis.

Conclusion

Anti-phosphatidylcholine antibodies may be one of the causes of optic neuritis.     

The muscle findings in a pediatric patient with live attenuated oral polio vaccine-related flaccid monoplegia

A pediatric patient, who was given live-attenuated oral polio vaccine twice without distinct gait disturbance during infancy, begun to present limp at 3 years. His gait disturbance became remarkable with aging. At 7 years, he was unable to dorsiflex the left ankle, and presented flaccid monoplegia of the left lower extremity, and the left Achilles tendon reflex was diminished. Magnetic resonance imaging revealed multiple crack-lines in the left anterior tibial muscle, but was unable to detect any distinct lesion at responsible level of L4, L5 and S1 anterior horn cells’ degeneration. Electromyography showed continuous fibrillation potentials, but muscle biopsy presented nearly normal in this muscle. The serum levels of polio antibody type 1 and type 2 titers were elevated 64× respectively, while the type 3 antibody titer was not elevated 4×. This patient was diagnosed as live attenuated oral polio vaccine-related flaccid monoplegia, with mild clinical course.     

Pharmacological inhibition of mitochondrial membrane permeabilization for neuroprotection

Recent data have provided important clues about the molecular mechanisms underlying certain neurodegenerative diseases. Most cell death in vertebrates proceeds via the mitochondrial pathway of apoptosis. Mitochondria contain proapoptotic factors such as cytochrome c and AIF in their intermembrane space. Furthermore, mitochondrial membrane permeabilization (MMP) is a critical event during apoptosis, representing the “point of no return” of the lethal process. Modern medicine is developing an increasing number of drugs for neurodegenerative disease, but no neuroprotective treatment has yet been established. While current treatments temporarily alleviate symptoms, they do not halt disease progression. This paper briefly reviews the pharmacological inhibition of mitochondrial membrane permeabilization for neuroprotection.