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Simplifying jugular venous pressure (JVP), visibility of the right internal jugular vein above the right clavicle in the sitting position, has been proposed in the management of heart failure (HF) because of its convenience. However, this method may be undervalued for the detection of mildly to moderately increased JVP. Increased JVP on inspiration, known as Kussmaul sign, may be a useful physical finding in this condition. This study consisted of 138 patients who were admitted for the management of HF. Using this simple method, JVP was assessed at rest in the sitting position before discharge; its response to inspiration was also examined if no high JVP was noted at rest. The primary outcome was a composite of cardiac death and hospitalization for worsening HF. Among all the patients, 16 patients (12%) had high JVP at rest and another 16 patients (12%) had high JVP not at rest but on inspiration. During a follow-up period of 249 ± 182 days, a primary outcome event occurred in 63 patients (46%). The incidence of adverse cardiac events was higher in patients with a high JVP at rest (69%; hazard ratio 3.31, 95% confidence interval 1.64 to 6.67, p = 0.0009) and in patients with a high JVP on inspiration (56%; hazard ratio 2.18, 95% confidence interval 1.02 to 4.63, p = 0.043) than in patients without a high JVP in both conditions (41%). In conclusion, a high JVP not only at rest but also on inspiration was associated with a poor prognosis. The response of JVP to inspiration using this simple technique of physical examination may be a new approach in the management of HF.

Abnormal blood pressure response (ABPR) has been reported to be a risk factor for sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). We aimed to elucidate the relationship between ABPR during exercise stress echocardiography (ESE) and impaired left ventricular (LV) contractile reserve based on two-dimensional strain in patients with HCM.Patients with HCM underwent ESE with treadmill exercise. Patients whose blood pressure elevation at maximum workload was lower than 20 mmHg from baseline were classified as having ABPR. Echocardiographic parameters were compared between patients with and without ABPR. Results: Of 26 patients with HCM, nine patients were diagnosed with ABPR. Significant LV outflow tract obstruction (50 mmHg) was provoked only in one patient with ABPR (baseline to the conclusion of the exercise, 15.2 mmHg to 63.0 mmHg). Change in cardiac output (CO) and the ratio of early diastolic velocity to early annular velocity (E/e') from baseline to just after the conclusion of exercise did not differ between patients with and without ABPR (CO, 102±40% vs. 122±45%,In conclusion, impaired LV contractile reserve during exercise might contribute to ABPR in patients with HCM.

Senescent vascular cells are detected in atherosclerotic lesion, and its involvement in the development of atherosclerosis has been revealed; however, whether and the mechanism by which endothelial cell (EC) senescence is causally implicated in atherosclerosis remains unclear. We here investigate a role of EC senescence in atherosclerosis by utilizing EC-specific progeroid mice that overexpress the dominant negative form of telomeric repeat-binding factor 2 under the control of the Tie2 or vascular endothelial cadherin promoter. EC-specific progeria accelerated atherosclerosis in mice with target deletion of ApoE. Mechanistically, senescent ECs were markedly sensitive for inflammation-mediated VCAM-1 induction, leading to enhanced monocyte adhesion. Inhibition of NF-κB signaling abolished the enhanced inflammatory responses in senescent ECs, while NF-κB nuclear translocation in response to TNF-α were similar between young and senescent ECs. We found a higher association of VCAM-1 gene with active histone H3 trimethylated on lysine 4, leading to increased NF-κB accessibility in senescent ECs. Our data revealed that EC cellular senescence causes endothelial hyper-inflammability through epigenetic alteration, which consequently accelerates atherosclerosis. Therefore, EC senescence is a promising therapeutic target for the prevention and/or treatment of atherosclerotic disease in elderly population.

Isolated septal myocardial infarction is an uncommon condition with diagnostic difficulty due to small infarction size and anatomical variations. We report a case of isolated septal myocardial infarction, in which the diagnosis was confirmed not by electrocardiographic, echocardiographic, or angiographic findings, but by nuclear imaging. A 46-year-old man with chest discomfort exhibited ST-segment elevations in leads V1 and V2, and borderline abnormalities of the septal wall motion on echocardiography. Emergency coronary angiography demonstrated delayed flow in the second septal branch of the left anterior descending coronary artery. Intravascular ultrasound showed plaque in the proximal portion of the septal branch without evidence of plaque rupture. No balloon angioplasty or stent implantation was required because the flow delay in the septal branch disappeared after the intravascular ultrasound procedure. Myocardial perfusion-metabolism mismatch, as assessed by resting thallium-201 and iodine-123-beta-methyl-p-iodophenyl-pentadecanoic acid, was seen in the mid-septal region.

Yamanaka R, Hoshino A, Fukai K, Urata R, Minami Y, Honda S, Fushimura Y, Hato D, Iwai-Kanai E, Matoba S. TIGAR reduces smooth muscle cell autophagy to prevent pulmonary hypertension. Am J Physiol Heart Circ Physiol 319: H1087-H1096, 2020. First published September 18, 2020; doi:10.1152/ajpheart.00314.2020.-Pulmonary arterial hypertension (PAH) is a refractory disease. Its prognosis remains poor; hence, establishment of novel therapeutic targets is urgent. TP53-induced glycolysis and apoptosis regulator (TIGAR) is a downstream target of p53 and exhibits functions inhibiting autophagy and reactive oxygen species (ROS). Recently, p53 was shown to suppress PAH progression. Because inhibition of autophagy and ROS is known to improve PAH, we examined the effect of TIGAR on PAH progression. We compared pulmonary hypertension (PH) development between TIGAR-deficient knockout (KO) and wild-type (WT) mice using a hypoxia-induced PH model. Human pulmonary artery smooth muscle cells (PASMCs) were used for in vitro experiments with small interfering RNA (siRNA) to investigate the possible molecular mechanisms. From the analysis of right ventricular pressure, right ventricular weight, and mortality rate, we concluded that the hypoxia-induced PH development was remarkably higher in TIGAR KO than in WT mice. Pathological investigation revealed that medial thickening of the pulmonary arterioles and cell proliferation were increased in TIGAR KO mice. Autophagy and ROS activity were also increased in TIGAR KO mice. TIGAR knockdown by siRNA increased cell proliferation and migration, exacerbated autophagy, and increased ROS generation during hypoxia. Autophagy inhibition by chloroquine and ROS inhibition by N-acetylcysteine attenuated the proliferation and migration of PASMCs caused by TIGAR knockdown and hypoxia exposure. TIGAR suppressed the proliferation and migration of PASMCs via inhibiting autophagy and ROS and, therefore, improved hypoxia-induced PH. Thus, TIGAR might be a promising therapeutic target for PAH.NEW & NOTEWORTHY Pulmonary arterial hypertension is a refractory disease. TP53-induced glycolysis and apoptosis regulator (TIGAR) is a downstream target of p53 and exhibits functions inhibiting autophagy and reactive oxygen species (ROS). By using TIGAR-deficient knockout mice and human pulmonary artery smooth muscle cells, we found that TIGAR suppressed the proliferation and migration of PASMCs via inhibiting autophagy and ROS and, therefore, improved hypoxia-induced PH. TIGAR will be a promising therapeutic target for PAH.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Background Ischemic disease is prevalent in elderly population due to impaired angiogenesis. Endothelial cell (EC) generates energy largely via glycolysis, which is further activated when angiogenesis actively occurs. PFK-1 is one of the most important regulatory enzymes for glycolysis, which is activated by PFKFB3. On the other hand, TIGAR inhibits PFK-1 under the control of p53. Crucial roles of PFKFB3 in EC functions under physiological and pathological conditions have been reported; however, a role of TIGAR in EC angiogenic functions remains to be elucidated. Furthermore, it remains unknown whether and how cellular senescence affect the energy metabolism in EC. Purpose The purpose of this study is to investigate molecular mechanisms underlying EC dysfunction associated with ageing, especially by focusing on endothelial energy metabolism. Method and result Senescent EC showed reduced glucose consumption assessed by [U-13C]-glucose tracer assay in association with increased expression of p53 and TIGAR. Angiogenic capacity assessed by tube-formation assay was reduced in senescent EC. Of note, either silencing of TIGAR by siRNA or lentivirus-mediated overexpression of PFKFB3 improved angiogenic capacity in senescent EC. These results collectively suggest that senescence impairs glycolysis in EC by activating p53-TIGAR axis, which leads to senescence-associated endothelial dysfunction. To analyze an impact of EC senescence in angiogenesis in vivo, we generated EC-specific progeroid mice in which dominant negative form of telomere repeat-binding factor 2 (TRF2) was overexpressed in EC under the control of the TIE2 promoter. After confirming EC-specific senescence in these endothelial progeroid mice, we generated hind-limb ischemia model. Recovery of blood flow assessed by laser doppler velocimeter was significantly impaired in endothelial progeroid mice, indicating that EC senescence is directly and causally implicated in age-related angiogenic dysfunction. Of note, genetic inactivation of TIGAR completely rescued the impaired ischemia-induced neovessel formation in EC-specific progeroid mice. Conclusion Using unique endothelial progeroid mice, we revealed that EC senescence is a bona fide risk for ischemic disease, largely by reducing glycolysis in EC through p53-TIGAR axis. Our data suggest that endothelial energy metabolism is an attracting therapeutic target for the prevention and/or treatment of ischemic diseases, especially in elderly population.

Background Ageing is a significant risk factor for atherosclerotic diseases. Vascular senescence has been considered to play an important role in the progression of atherosclerosis; however, it remains unclear whether endothelial cell (EC) senescence is causally involved in the pathogenesis of atherosclerosis. Purpose The purpose of this study is to elucidate a causative role of senescent EC in the progression of atherosclerosis. Methods Telomeric repeat-binding factor 2 (TRF2) plays a central role in telomere maintenance and protection against end-to-end fusion of chromosome. We previously reported that overexpression of TRF2-dominant negative mutant (TRF2DN) induced premature senescence in EC. We recently generated EC-specific progeroid mice by overexpressing TRF2DN specifically in EC (TRF2DN-Tg), and then generated ApoE-KO/TRF2DN-Tg mice to analyze a role of EC senescence in atherosclerosis. These mice were fed with a high cholesterol-diet, and atherosclerosis was assessed by en face analysis of whole aorta and histological analysis of aortic sinus. In vitro studies to analyze the underlying mechanisms were performed using replicative senescent HUVECs. Results En face analysis of aorta revealed that atherosclerotic lesions were significantly increased in ApoE-KO/TRF2DN-Tg mice comparing with that in ApoE-KO mice at as early as 2 weeks after high-cholesterol diet. Histological analysis of aortic sinus also exhibited accelerated atherosclerosis in ApoE-KO/TRF2DN-Tg mice in association with increased macrophage infiltration. Mechanistically, we found that the induction of adhesion molecules such as VCAM-1, ICAM-1, and E-selectin in response to low-grade inflammatory stimuli was substantially augmented in senescent ECs comparing with that in young ECs. As a result, monocyte adhesion was significantly enhanced in senescent ECs. Of note, eNOS inhibition did not affect the hyper-reactivity of senescent EC to inflammation, while antagonizing NF-kB abolished it. Nuclear translocation of NF-kB in response to inflammation was not different between young and senescent ECs, suggesting that NF-kB transcriptional activity might be enhanced in senescent ECs. Conclusion We revealed a causative role of EC senescence in the progression of atherosclerosis in vivo using unique EC-specific progeroid mice. Our findings revealed that EC senescence is a bona fide risk for atherosclerosis, and thus senescent ECs are attracting pharmacotherapeutic targets for the prevention and/or treatment of atherosclerotic disease in elderly population.

Background: Although metabolic alterations were observed in heart failure (HF), only recently have the mechanisms underlying these changes been identified. Tumor suppressor p53 responds to metabolic changes thorough several mechanisms. One of the p53 targets, TIGAR (TP53-induced glycolysis and apoptosis regulator) reduces glycolysis and suppresses autophagy, which augments ischemic damage, however its role on HF is unclear. Method and Results: In order to investigate TIGAR’s function in HF, we compared myocardial metabolic and functional outcomes between TIGAR deficient (TIGAR–/–) mice and wild-type (TIGAR+/+) mice subjected to chronic thoracic transverse aortic constriction (TAC), a pressure-overload HF model. In wild-type mice hearts, p53 and TIGAR increased markedly during HF development. Eight weeks after TAC surgery, the left ventricular (LV) dysfunction, fibrosis, oxidative damage, and myocyte apoptosis were significantly advanced in wild-type than in TIGAR–/– mouse heart. Further, myocardial high-energy phosphates in wild-type hearts were significantly decreased compared to those of TIGAR–/– mouse heart. Glucose oxidation and glycolysis rates were also reduced in isolated perfused wild-type hearts following TAC than those in TIGAR–/– hearts, which suggest that the upregulation of TIGAR in HF causes impaired myocardial energetics and function. The effects of TIGAR knockout on LV function were also replicated in tamoxifen (TAM)-inducible cardiac-specific TIGAR knockout mice (TIGARflox/flox/ Tg(Myh6-cre/Esr1) mice). Conclusion: The ablation of TIGAR during pressure-overload HF preserves myocardial function and energetics. Thus, cardiac TIGAR targeted therapy to increase glucose metabolism will be a novel strategy for HF.

Vascular senescence is thought to play a crucial role in an ageing-associated decline of organ functions; however, whether vascular senescence is causally implicated in age-related disease remains unclear. Here we show that endothelial cell (EC) senescence induces metabolic disorders through the senescence-associated secretory phenotype. Senescence-messaging secretomes from senescent ECs induced a senescence-like state and reduced insulin receptor substrate-1 in adipocytes, which thereby impaired insulin signaling. We generated EC-specific progeroid mice that overexpressed the dominant negative form of telomeric repeat-binding factor 2 under the control of the Tie2 promoter. EC-specific progeria impaired systemic metabolic health in mice in association with adipose tissue dysfunction even while consuming normal chow. Notably, shared circulation with EC-specific progeroid mice by parabiosis sufficiently transmitted the metabolic disorders into wild-type recipient mice. Our data provides direct evidence that EC senescence impairs systemic metabolic health, and thus establishes EC senescence as a bona fide risk for age-related metabolic disease., Vascular senescence is closely associated with individual ageing, while its causative role remains unclear. Here Barinda et al. generate endothelial cell-specific progeroind mice, and reveal that endothelial cell senescence directly induces metabolic disorders through senescence-messaging secretomes.

Aneurysms of the sinus of Valsalva are characterized by dilatation of at least one of the three aortic sinuses. We experienced a case with unruptured aneurysm of the right sinus of Valsalva, in which serial imaging studies were useful in assessing a rare complication after surgical repair. An asymptomatic 75-year-old man underwent patch closure of the aneurysm orifice because of progressive enlargement of the aneurysm. The postoperative course was uneventful, and computed tomography (CT), performed a week after the patch repair, showed no leakage of contrast medium into the isolated aneurysm. Three months later, echocardiography showed decreased size of the aneurysm with heterogeneous echogenicity and possible blood flow in the aneurysm, findings suggestive of thrombus formation and a recurrent fistula. CT with contrast medium showed partial recanalization between the patched aneurysm and the right sinus of Valsalva. Follow-up echocardiography, performed 1 year after surgery, revealed neither definite aneurysm nor shunt flow of Valsalva. The present case highlights that non-invasive follow-up can be an alternative option when carried out with caution in selected patients with incomplete closure of Valsalva aneurysm.

BACKGROUND Patients with hypertrophic cardiomyopathy (HCM) sometimes develop myocardial fibrosis in association with adverse cardiovascular events. Electrocardiography (ECG) could provide helpful information on myocardial fibrosis in HCM, as in coronary artery disease. METHODS AND RESULTS A total of 60 patients with HCM without bundle branch block underwent cardiac magnetic resonance imaging (CMR). The extent or location of late gadolinium enhancement (LGE) was examined in relation to 12-lead ECG. A notch on QRS was defined as at least 2 consecutive spikes in the same polarity with a reversal of direction ≥90° and the initial negative deflection ≥0.05 mV. LGE was associated with notched QRS, leftward QRS axis, and prolonged QRS duration, but not with any other findings such as abnormal Q waves, R-wave amplitude, or ST-T changes. Notched QRS was most useful in determining the presence or absence of myocardial fibrosis, with a sensitivity of 70% and a specificity of 81% using a cut-off of the number of leads with notched QRS ≥2. The number of notched QRS leads was positively correlated with LGE volume (P

Background Energy starvation and the shift of energy substrate from fatty acids to glucose is the hallmark of metabolic remodeling during heart failure progression. However, ketone body metabolism in the failing heart has not been fully investigated. Methods and Results Microarray data analysis and mitochondrial isobaric tags for relative and absolute quantification proteomics revealed that the expression of D-β-hydroxybutyrate dehydrogenase I (Bdh1), an enzyme that catalyzes the NAD + /NADH coupled interconversion of acetoacetate and β-hydroxybutyrate, was increased 2.5- and 2.8-fold, respectively, in the heart after transverse aortic constriction. In addition, ketone body oxidation was upregulated 2.2-fold in transverse aortic constriction hearts, as determined by the amount of 14 CO 2 released from the metabolism of [1- 14 C] β-hydroxybutyrate in isolated perfused hearts. To investigate the significance of this augmented ketone body oxidation, we generated heart-specific Bdh1-overexpressing transgenic mice to recapitulate the observed increase in basal ketone body oxidation. Bdh1 transgenic mice showed a 1.7-fold increase in ketone body oxidation but did not exhibit any differences in other baseline characteristics. When subjected to transverse aortic constriction, Bdh1 transgenic mice were resistant to fibrosis, contractile dysfunction, and oxidative damage, as determined by the immunochemical detection of carbonylated proteins and histone acetylation. Upregulation of Bdh1 enhanced antioxidant enzyme expression. In our in vitro study, flow cytometry revealed that rotenone-induced reactive oxygen species production was decreased by adenovirus-mediated Bdh1 overexpression. Furthermore, hydrogen peroxide–induced apoptosis was attenuated by Bdh1 overexpression. Conclusions We demonstrated that ketone body oxidation increased in failing hearts, and increased ketone body utilization decreased oxidative stress and protected against heart failure.

Background The 4th heart sound (S4) is commonly heard in patients with hypertrophic cardiomyopathy (HCM). The 3rd heart sound (S3) is also audible in HCM patients regardless of the presence or absence of heart failure. These extra heart sounds may be associated with myocardial fibrosis because myocardial fibrosis has been suggested to affect left ventricular compliance.Methods and Results:The present retrospective study evaluated 53 consecutive HCM patients with sinus rhythm who had no symptoms of heart failure and underwent an initial assessment including phonocardiography, echocardiography, and late gadolinium enhancement (LGE) magnetic resonance imaging (MRI). S3 was detected on phonocardiography in 13% of all patients, and S4 was recorded in 75% of patients. Patients with S3 had a higher incidence of LGE and larger LGE volumes (86% and 11.5±2.4 g/cm, respectively) than patients without S3 (33% and 2.5±0.8 g/cm, respectively; P=0.02 and P=0.002). The presence of S4 was not associated with MRI findings, including the incidence of LGE and LGE volume. The diagnostic value of S3 for the detection of LGE was highly specific (97%), with a low sensitivity (29%). Conclusions Myocardial fibrosis, as assessed by LGE, was associated with S3 but not with S4 in patients with HCM. These results may contribute to the risk stratification of patients with HCM.

Rhabdomyolysis, which is a characteristic occurrence in associated with muscle cell necrosis, develops due to various causes. We herein report a rare case of a patient with rhabdomyolysis after high intensity resistance training, in which markedly elevated levels of serum creatine kinase (CK) and urine myoglobin were observed. A previously healthy 37-year-old man presented with severe myalgia and dark urine after performing high-intensity exercise. The patient's serum CK level was 95,100 U/L and his urine myoglobin level was 160,000 ng/mL. His symptoms and laboratory findings gradually improved with the intravenous administration of saline and no complications (including electrolyte imbalance and acute renal failure) developed.

D-Amino acids are enantiomers of L-amino acids and have recently been recognized as biomarkers and bioactive substances in mammals, including humans. In the present study, we investigated functions of the novel mammalian mitochondrial protein 9030617O03Rik and showed decreased expression under conditions of heart failure. Genomic sequence analyses showed partial homology with a bacterial aspartate/glutamate/hydantoin racemase. Subsequent determinations of all free amino acid concentrations in 9030617O03Rik-deficient mice showed high accumulations of D-glutamate in heart tissues. This is the first time that a significant amount of D-glutamate was detected in mammalian tissue. Further analysis of D-glutamate metabolism indicated that 9030617O03Rik is a D-glutamate cyclase that converts D-glutamate to 5-oxo-D-proline. Hence, this protein is the first identified enzyme responsible for mammalian D-glutamate metabolism, as confirmed in cloning analyses. These findings suggest that D-glutamate and 5-oxo-D-proline have bioactivities in mammals through the metabolism by D-glutamate cyclase.

A 75-year-old man was admitted with abrupt onset of dyspnea during sleep. On examination, his blood pressure was 222/165 mm Hg, pulse was 160 bpm, and oxygen saturation was 75% while breathing ambient air. Heart sounds were difficult to assess because of coarse crackles and his moaning. There was no edema in the extremities. An ECG showed sinus tachycardia with a QRS duration of 111 milliseconds, and a chest radiograph showed pulmonary edema without cardiomegaly. A presumed diagnosis of acute heart failure was made, and isosorbide dinitrate was administered intravenously with supplemental oxygen via a face mask. Cardiac auscultation after stabilization of vital signs showed a holosystolic murmur at the apex and an early systolic click at the left sternal border. Mitral regurgitation resulting from mitral valve prolapse (MVP) was most likely but was not confirmed by transthoracic echocardiography because of a lack of definitive evidence (Figure 1). Of note, another extra sound during early diastole was heard best at the third left sternal border. Figure 1. Apical 2-chamber views of the left ventricle (LV) on transthoracic echocardiography show insufficient coaptation of the mitral leaflets ( A , arrow) and …

Background Right bundle branch block (RBBB) is associated with ventricular septal fibrosis in patients with hypertrophic cardiomyopathy (HCM) after alcohol septal ablation, but little data are available in HCM patients without a history of septal ablation. Methods Magnetic resonance late gadolinium enhancement (LGE) was performed in 59 HCM patients with no history of alcohol septal ablation. The location and extent of LGE were examined in relation to electrocardiographic features including RBBB. Results LGE volume was higher in 7 HCM patients with RBBB (7.3 ± 7.4 g/cm) than in patients without RBBB (2.9 ± 7.4 g/cm, p = 0.016). LGE volume was positively correlated to QRS duration of RBBB (correlation coefficient = 0.93, p = 0.023). The diagnostic value of RBBB was highly specific for the detection of LGE in the ventricular septum, with sensitivity 21% and specificity 94%. Conclusions The presence of RBBB may be a simple marker for detecting ventricular septal fibrosis in HCM patients who had no history of alcohol septal ablation. Further studies are necessary to confirm our findings.

We report here six cases of malignant melanoma in which metastatic lesions were detected first. Of these, two cases showed some peculiar features: one exhibited widespread subcutaneous bleeding, probably due to venous rupture, and the other case had a rare primary lesion on the penis. In the Japanese literature, there have been 46 cases of malignant melanoma in which metastatic lesions were detected prior to the initial ones. The preferential site for metastasis was the lymph node (32 cases). The primary lesion was unknown in 35 patients. The outcomes were available for 36 of the 46 patients; 23 died, including 18 who died within two years.

症例1: 80歳の男性。後頭部の結節及び左下腿後面の皮下結節例。症例2: 80歳の男性。下顎,右側胸部,右大腿,右側腹部,両鼠径部の結節例。症例3: 77歳の男性。頭部,前胸部左側,背部の結節例。症例1,2では皮膚転移巣が原発巣より先に発見された。頭頚部皮膚への膵癌の転移の報告は少ないが,今回の3症例はいずれも後頭部領域に転移巣がみられた。加えて,産業医科大学皮膚科において過去19年間に経験した転移性皮膚癌51例について,統計的に検討した。

熱帯魚飼育歴のある患者の手に生じた皮膚非定型抗酸菌症の2例を報告した。症例1: 31歳の男性。4ヵ月程前に左小指基部に擦過傷受傷, 次第に結節となった。病理組織像はリンパ球を混じた類上皮細胞よりなる肉芽腫であり, 生検組織の培養で抗酸菌集落を認めた。従来よりの同定法とDNA-DNAハイブリダイゼーション法でMycobacterium marinumと同定した。ミノサイクリン内服にて約3ヵ月後に軽快した。症例2: 16歳の女性。半年程前, 右手背示指基部を草の葉で切創受傷。その後同部位および2cm程中枢側にも発赤を生じた。さらに右手関節部にも発赤, 腫脹を生じ拡大して波動を触れるようになった。病理組織像は真皮中層に乾酪壊死を伴う類上皮細胞性肉芽腫を認めた。右手関節部皮下膿瘍の膿汁の培養で抗酸菌集落を認め, Mycobacterium gordonaeと同定した。本菌による症例の報告は比較的稀である。ミノサイクリン内服開始後3ヵ月経過しても軽快せず, リファンピシン, イソニアジド内服に変更し1ヵ月程で軽快した。

Background There are few studies regarding the time-dependent effectiveness of topical calcium gluconate treatment for the experimental hydrofluoric acid (HF) burn. Methods For producing a HF-burn, a drop of 46% or 23% HF solution was put on the back of rats for 3 minutes followed by washing with tap water. Calcium gluconate jelly or ointment was then applied to the burn area at various time intervals. The ointment was applied once a day thereafter. Results The topical calcium gluconate treatment was much more effective if the application was started within 3 hours. On the other hand, if the application was started after 6 hours or more, there was no difference between the groups and the non-treatment groups. Conclusions It is suggested that practitioners should be ready to prepare quickly the calcium gluconate ointment to treat a HF burn, since the calcium gluconate ointment is not commercially available in Japan.