Comparison of biochemical markers and cervical length for predicting preterm delivery

AIM: To examine the clinical utility of several prognostic factors for predicting preterm delivery. METHODS: One hundred and nineteen patients with a singleton pregnancy admitted to our hospital because of symptoms of preterm labor were included in this study. Maternal serum C-reactive protein (CRP), transvaginal sonographic measurement of cervical length (CL), granulocyte elastase (EL) in cervical secretions, fetal fibronectin (fFN), alpha-fetoprotein (AFP), and insulin-like growth factor binding protein-1 (IGFBP-1) in vaginal secretions were examined on admission. EL, fFN, AFP, and IGFBP-1 were measured by bed-side test kits. Correlation between each factor and the duration of pregnancy (from admission to delivery) was investigated. RESULTS: A significant correlation was found between the duration of pregnancy and CRP (r= -0.37, P<0.001), but not CL. The duration was significantly shorter in the fFN-positive group than in the negative group (P=0.0015). However, no significant difference was observed between the positive group and the negative group for each of CL, EL, AFP and IGFBP-1. CONCLUSION: Association between the duration of the pregnancy and two biochemical markers (CRP and fFN) was confirmed. As they can be examined quickly and easily, they are quite useful for estimating prognosis of preterm labor.     

No child should suffer from vitamin K deficiency‐induced bleeding disorders

We encountered an 11‐day‐old male neonate with vitamin K deficiency‐induced intracranial hemorrhage, despite receiving oral vitamin K₂ (menaquinone‐4) prophylaxis according to Japanese guidelines. This case suggests that the current vitamin K deficiency‐bleeding prophylaxis programs cannot prevent bleeding completely. Better prophylaxis programs using both intramuscular and oral administration should be considered.     

Spinal cord stimulation for the treatment of pain and toe ulceration associated with systemic sclerosis: a case report

Systemic sclerosis is a complex disease characterized by extensive fibrosis, microvascular alterations, and additional sequelae. Microvascular alterations can cause painful ulcers and necrosis; however, conservative or surgical treatment is often challenging in terms of healing. The study aimed to describe a toe ulcer with systemic sclerosis and its’ successful treatment with spinal cord stimulation. An 83-year-old woman, who was diagnosed with systemic sclerosis over the past decade, was distressed by a non-healing toe ulcer for an extended period of time. The patient underwent spinal cord stimulation treatment with the expectation of pain relief and an improvement in microcirculatory insufficiency. Her pain scales and microcirculation improved, and the toe ulcer healed. Furthermore, the frequency of Raynaud’s symptoms was reduced, and the patient’s pain decreased. There was no recurrence of the ulcer and she no longer needed a cane for walking.     

Rhabdomyolysis Caused by Gefitinib Overdose

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are common therapeutic agents for EGFR mutation-positive advanced non-small-cell lung cancer. There has been no report of rhabdomyolysis caused by an overdose of EGFR-TKIs. We herein review the existing literature on the subject and report a rare case of rhabdomyolysis due to an overdose of gefitinib, an EGFR-TKI.     

Quantitative Evaluations of Posterior Staphylomas in Highly Myopic Eyes by Ultra-Widefield Optical Coherence Tomography

PurposeTo determine the shape of posterior staphylomas using ultra-widefield optical coherence tomographic (UWF-OCT) images and to identify the factors contributing to the shape and grade of the staphylomas in eyes with pathologic myopia.MethodsThis was an observational case series study. Highly myopic patients who were ≥40 years old with wide or narrow type of macular staphylomas were studied. High myopia was defined as a myopic refractive error (spherical equivalent) greater than −8.0 diopters (D) or an axial length (AL) > 26.5 mm. The maximum diameter and depth of the staphylomas were measured in the 12 radial scans of UWF-OCT images by ImageJ software and were compared between the two types of staphylomas.ResultsWe studied 197 eyes of 138 patients with a mean age of 64.7 ± 10.4 years and mean AL of 30.0 ± 1.9 mm. The AL was significantly longer in the eyes with the narrow type than the wide type of staphyloma (P = 0.036). Multiple regression analyses showed that age was significantly correlated with the maximum depth/maximum diameter ratio (wide type, P < 0.001; narrow type, P = 0.003) of both types of staphylomas. The AL was significantly correlated with the depth/diameter ratio of only the narrow type of staphylomas (P = 0.005).ConclusionsThe significant correlations of age and AL with the wide and narrow types of posterior staphylomas indicate that the factors for their formations may be distinctly different. Quantitative analyses of UWF-OCT images are helpful in determining the shape of the staphylomas.     

Disease-associated CIAS1 mutations induce monocyte death, revealing low-level mosaicism in mutation-negative cryopyrin-associated periodic syndrome patients

Cryopyrin-associated periodic syndrome (CAPS) is a spectrum of systemic autoinflammatory disorders in which the majority of patients have mutations in the cold-induced autoinflammatory syndrome (CIAS)1 gene. Despite having indistinguishable clinical features, some patients lack CIAS1 mutations by conventional nucleotide sequencing. We recently reported a CAPS patient with mosaicism of mutant CIAS1, and raised the possibility that CIAS1 mutations were overlooked in "mutation-negative" patients, due to a low frequency of mosaicism. To determine whether there were latent mutant cells in "mutation-negative" patients, we sought to identify mutation-associated biologic phenotypes of patients' monocytes. We found that lipopolysaccharide selectively induced necrosis-like cell death in monocytes bearing CIAS1 mutations. Monocyte death correlated with CIAS1 up-regulation, was dependent on cathepsin B, and was independent of caspase-1. Cell death was intrinsic to CIAS1-mutated monocytes, was not mediated by the inflammatory milieu, and was independent of disease severity or anti-IL-1 therapy. By collecting dying monocytes after lipopolysaccharide treatment, we succeeded in enriching CIAS1-mutant monocytes and identifying low-level CIAS1-mosaicism in 3 of 4 "mutation-negative" CAPS patients. Our findings reveal a novel effect of CIAS1 mutations in promoting necrosis-like cell death, and demonstrate that CIAS1 mosaicism plays an important role in mutation-negative CAPS patients.     

Case of venous angioma with chronic encapsulated hematoma

We would like to report a rare case of a venous angioma with a chronic encapsulated hematoma, in a 31-year-old woman who was admitted to our hospital in November, 2005. Her neurological examination was noted to be normal. A CT was performed which showed an isodense mass in the left cerebellar hemisphere. This finding was confirmed on MR imaging, which showed a hyperintense mass on T1-weighted imaging, and a hypo to isointense area on T2-weighted images. T1-weighted images with Gd-DTPA enhancement revealed a dilated vein and, as a result, an angiogram was obtained. The venous phase demonstrated medullary veins converging on a central vein, which is usually known as a caput medusae. Follow up T1-weighted images with Gd-DTPA enhancement showed peripheral ring enhancement and expansion of the capsulated hematoma. Total removal of the hematoma and its capsule was performed in July, 2006. The hematoma was seen both inside and outside the tough capsule. A histological examination revealed that the capsule consisted of an outer collagenous layer and an inner granulated layer with deposits of hemosiderin. The hemorrhage rate of a venous angioma has been reported as between 0.22-0.61% per year. We thought that the initial small hemorrhage from the venous angioma resulted in the development of an encapsulated hematoma, and the total hematoma had expanded not only inside due to the hemorrhage of the capsule, but also outside because of the venous angioma.     

Locally applied cilostazol suppresses neointimal hyperplasia and medial thickening in a vein graft model.

BACKGROUND: Pathological changes in vein grafts begin immediately after arterial circulation is applied to the grafts. Chemical mediator stimulation and mechanical strain induce neointimal hyperplasia and medial thickening of the vein grafts, resulting in their failure. We investigated the inhibitory effect of locally applied cilostazol, an inhibitor of cyclic adenosine monophosphate phosphodiesterase III, on neointimal hyperplasia and medial thickening of the grafts. METHODS AND RESULTS: We established a distal anastomotic stricture model of femoral vein-abdominal aorta interposition grafting in rats. In this model, neointimal hyperplasia was observed not only at the distal anastomotic sites, but also in the graft body at postoperative day 14 and was markedly progressed at day 28. A strong expression of tenascin-C was found in the media and neointima of the graft body. In the grafts around which cilostazol was administered locally using Pluronic gel, neointimal hyperplasia was significantly suppressed compared with control grafts treated with the gel alone, with the mean neointimal cross-sectional area reduced by 87.1% for the graft body and by 78.9% for the distal anastomotic sites and mean medial cross-sectional area of the graft body reduced by 54.2% at day 28 versus the control. Cilostazol treatment decreased cell proliferation and the number of tenascin-C-producing cells seen by in situ hybridization, but the expression of tenascin-C protein was not suppressed. CONCLUSION: We concluded that a single perivascular application of cilostazol inhibits neointimal hyperplasia and medial thickening of vein grafts in a rat model.