Cerebral oxygenation during exercise in cardiac patients

BACKGROUND: Until recently, compensatory mechanisms have been believed to regulate adequately cerebral blood flow in humans. However, this has been called into question by a series of new investigations suggesting that patients with left ventricular dysfunction suffer from cerebral hypoperfusion. We compared cerebral oxygenation during incremental exercise between patients with valvular heart disease and normal subjects. METHODS: Thirty-three patients with valvular disease and 33 normal subjects performed a symptom-limited incremental exercise test using a cycle ergometer. Oxyhemoglobin at the forehead was continuously monitored during exercise using near-infrared spectroscopy. Respiratory gas measurements were performed on a breath-by-breath basis. RESULTS: The increase in oxyhemoglobin during exercise was significantly lower in the patients with valvular disease than in normal subjects. The change in oxyhemoglobin during exercise (DeltaO(2)Hb) at the forehead was negatively correlated with the slope of the increase in minute ventilation to the increase in carbon dioxide output (DeltaE/DeltaCO(2)), and positively correlated with the peak oxygen uptake (O(2)), gas exchange threshold (GET), and slope of the increase in O(2) to the increase in the work rate (DeltaO(2)/DeltaWR). Among the patients with valvular disease, 15 patients showed a decrease in oxyhemoglobin at the forehead during exercise. When compared with the patients with increased oxyhemoglobin, those with decreased levels exhibited a higher DeltaE/DeltaCO(2) and a lower peak O(2), GET, and DeltaO(2)/DeltaWR. CONCLUSIONS: The present findings strongly suggest that cerebral oxygenation during exercise is dependent on the cardiovascular and pulmonary systems. The study also indicated the presence of cerebral hypoperfusion during exercise in cardiac patients whose cardiac output fails to increase normally.     

Plasma levels of soluble Fas during normal pregnancy

The Fas/Fas ligand system could reportedly help to identify a mechanism for maternal immunotolerance of the fetus in human pregnancy. However, there are few reports on soluble Fas (sFas) which is an inhibitor of apoptosis during normal pregnancy. Therefore, ascertaining plasma sFas levels during pregnancy would be of interest. The subjects studied were 10 nonpregnant healthy women and 20 healthy pregnant women in the first and third trimester with singleton gestations. The plasma sFas was measured by sandwich enzyme-linked immunosorbent assay. The mean concentration of sFas was significantly decreased in normal pregnant women in the first trimester compared to age-matched control subjects, and it did not differ significantly between normal pregnant women in the third trimester and age-matched control subjects. From these results, we presume that the decreased plasma sFas plays an important role in maternal immunotolerance in the first trimester of pregnancy.     

Critical level of cerebral oxygenation during exercise in patients with left ventricular dysfunction.

BACKGROUND: In a recent study the indexes of cerebral oxygenation decreased during maximal exercise in nearly half of all patients with left ventricular dysfunction. Whether these levels decrease severely enough to influence mental status or level of consciousness was evaluated in the present study. METHODS AND RESULTS: Forty-two patients with idiopathic dilated cardiomyopathy (IDC) and 29 healthy subjects underwent a symptom-limited maximal exercise test. The cerebral oxyhemoglobin (O(2)Hb) and tissue oxygenation index (TOI) were continuously monitored using near-infrared spectroscopy. The changes in O(2)Hb and TOI were also measured in 7 subjects: 2 who experienced episodes of reduced consciousness caused by sudden decreases in blood pressure during exercise recovery and 5 who exhibited sustained ventricular tachycardia during an electrophysiological study. The change in cerebral O(2)Hb during exercise in patients with IDC averaged 0.38+/-3.39 micromol/L, significantly lower than in the normal subjects (4.30+/-4.47 micromol/L, p<0.0001). The cerebral O(2)Hb decreased during exercise in 18 of 42 patients with IDC. The change in cerebral TOI in the IDC patients during exercise was significantly less than that in the normal subjects (-2.0+/-4.7 vs 2.1+/-5.8%, p=0.002). The mean decreases in cerebral O(2)Hb and TOI were -5.34 micromol/L and -9.7%, respectively, in the patients with reduced consciousness during exercise recovery, and -2.52 micromol/L and -16.5%, respectively, in those with ventricular tachycardia. CONCLUSION: The indexes of cerebral oxygenation may drop severely enough during maximal exercise in some patients with severe IDC that consciousness is affected.     

Mass‐forming type 1 autoimmune pancreatitis mimicking pancreatic cancer

We reported three cases of mass‐forming type 1 autoimmune pancreatitis (AIP) that were preoperatively suspected to be pancreatic cancer, and reviewed their clinicopathological features. Radiological findings in the patients revealed hypoattenuating masses in the early phase or a stricture of the main pancreatic duct with upstream dilatation, which was consistent with the diagnosis of pancreatic cancer. Histopathologically, the lesions were well demarcated and met all diagnostic criteria for immunoglobulin G4 (IgG4)‐related AIP, including the presence of periductal lymphoplasmacytic infiltration, obliterative phlebitis, storiform fibrosis and abundant IgG4‐positive plasma cells. However, the adjacent uninvolved pancreatic duct and lobular structures were well preserved. And in all patients, none or some of the aforementioned characteristics were observed. We suggest that some cases of focal AIP may progress to more severe grades and exhibit mass formation, although remaining localized. These focal cases of AIP are difficult to distinguish from pancreatic cancer. To our knowledge, this report is the first to present a histopathological comparison of mass‐forming AIP with the adjacent uninvolved pancreatic tissues.     

Adenosquamous carcinoma in the biliary tract: association of the proliferative ability of the squamous component with its proportion and tumor progression

Objectives: The purpose of this study was to evaluate the association of the proliferative ability of squamous cell carcinoma (SCC) component with its proportion and tumor progression in adenosquamous carcinoma (ASC) in the biliary tract.

Methods: Nine patients with ASC in the biliary tract (four each in the gallbladder and the extrahepatic bile duct and one in the ampulla of Vater) who underwent surgical resection were retrospectively reviewed.

Results: The proportion of the SCC component in the primary sites ranged from 30% to 95%. The Ki-67 index of the SCC component was higher than that of the adenocarcinoma component in all cases, regardless of the component ratio in the patients’ primary lesions. Predominance of the SCC component in the advancing region of the tumor, in angiolymphatic invasion and in perineural invasion was observed in most of the cases. The component ratio in metastatic lymph nodes differed from that in the corresponding primary lesions in all six cases with lymph node metastasis. Among these cases, the proportion of the SCC component was increased in the metastatic lymph nodes compared with that in the corresponding primary lesion in two cases, whereas the proportion was decreased in four cases.

Conclusions: The SCC component of ASC in the biliary tract displayed a relatively higher proliferative ability, which might be associated with local invasiveness. However, not only the high proliferative ability of the SCC component but also other biological factors might contribute to tumor progression and metastasis in ASC of the biliary tract.     

Ectopic adrenocorticotropic hormone syndrome in a case of small cell carcinoma of the bladder manifesting as severe muscle weakness

Ectopic adrenocorticotropic hormone syndrome is a paraneoplastic syndrome associated with small cell carcinoma. However, ectopic adrenocorticotropic hormone syndrome is rare in association with small cell carcinoma of the bladder. We report what we believe to be the first case of ectopic adrenocorticotropic hormone syndrome associated with small cell carcinoma of the bladder that manifested as severe muscle weakness due to hypokalemia. An early diagnosis and aggressive potassium replacement is essential for retaining muscle strength. The patient died of pneumonia less than 2 months after the diagnosis. Severe immunosuppression by excess cortisol production was suspected. Control of cortisol levels before chemotherapy might be beneficial in preventing infective complications.     

Ultrastructural and morphometrical evaluation of the parathyroid gland in iron-lactate-overloaded rats

Iron lactate was given to Sprague-Dawley rats intravenously at the dosage of 10 mg/kg/day and the early effects on the parathyroid gland were examined ultrastructurally along with the blood level of parathyroid hormone (PTH) after single, 3-day or 6-day administration. Blood levels of electrolytes and other parameters related to osteoclast dynamics were also measured by blood chemistry and histopathology. The plasma parathyroid hormone (PTH) level was elevated in the single and 3-day dosing group but was reduced in the 6-day dosing group. Histopathologically, an increase of osteoclasts in the primary spongiosa was observed in the 3- and 6-day dosing groups. Image analysis of the parathyroid gland revealed that the average area of the storage granule decreased during a experimental period, with the number of storage granules decreasing in the 3- and 6-day dosing group. The chief cells of the parathyroid gland were moderately atrophied in the 6-day dosing group. These results demonstrate that iron lactate immediately promotes discharge of PTH from the storage granules after the treatment and induces an increase of osteoclasts in the primary spongiosa. The findings collectively suggest a pathophysiological mechanism of iron lactate-induced osteopenia in rats.     

Iron lactate-induced osteopenia in male Sprague-Dawley rats.

Osteopenia was induced in rats fed a diet containing 50,000 ppm (5%) iron lactate for 2 or 4 weeks. Blood chemistry, urinalysis, and bone histomorphometry of the proximal tibial metaphysis were performed. Urinary pyridinoline and deoxypyridinoline and the osteoclast number per bone surface were selected for the measurement of dynamic resorption. The osteoclast surface, eroded surface, and osteoblast surface increased at both ends of the exposure periods, and bone resorption and formation both increased. The bone volume, trabecular thickness, and trabecular number decreased, and the secondary spongiosa of proximal metaphysis showed a marked bone loss. However, no mineralization defect was observed. At the end of the 2-week exposure period, biomarkers of osteoclasts and osteoblasts had increased the most, and the osteoblast surface, osteoclast surface, and osteoclast number per bone surface increased with prolonged exposure. The pathological changes of the bone lesion in iron lactate-overloaded rats were similar to those in rats of the osteoporotic model, because they consisted of changes reflecting the increase of bone resorption and formation without an osteomalacic change. However, the decline of serum parathyroid hormone (PTH) levels was different from that of the osteoporosis model rat. We concluded iron-induced bone lesions probably differ from those of low turnover bone diseases.     

Diagnostic value of antigenemia assay for cytomegalovirus gastrointestinal disease in immunocompromised patients

AIM:To investigate the utility of the cytomegalovirus(CMV)antigenemia assay for the diagnosis of CMV gastrointestinal disease(GID). METHODS:One hundred and thirty immunocompromised patients were enrolled in this study.Patients with a history of anti-CMV treatment and who had not undergone examination using the antigenemia assay were excluded.CMV-GID was defined as the detection of large cells with intranuclear inclusions alone or associated with granular cytoplasmic inclusions by biopsy.Biopsy sections were...