Cerebrospinal fluid glucose and leukocyte responses in experimental meningitis

The fall in cerebrospinal fluid (CSF) glucose and CSF leukocyte response was studied in cats with experimental meningitis. Klebsiella pneumoniae or Streptococcus pneumoniae were injected intracisternally, and the latter organisms were incubated with CSF in vitro. When 10(6)-10(9)K. pneumoniae were incubated with 4 ml of CSF, the time time necessary for the glucose to decrease to less than 10 mg/dl ranged from 6.5 to 2.5 h, at a rate proportional to the size of the inoculum. When the same numbers of bacteria were injected intracisternally, the time ranged from 9 to 3 h, and the CSF leukocyte response did not exceed 1200 WBC/mm3. At this time, only minimal histological changes in brain and choroid plexus were seen. Twenty hours after intrathecal K. pneumoniae, large numbers of leukocytes (up to 4 X 10(4)/mm3) were recovered from the CSF. Regardless of the number of leukocytes, however, hypoglycorrhachia occurred when the CSF contained more than 10(7) bacteria/ml. At this interval, large numbers of leukocytes were seen invading the stroma of the choroid plexus, leptomeninges and perivascular spaces. When 10(8) S. pneumoniae were injected intracisternally, CSF glucose concentration decreased as rapidly as with K. pneumoniae. The spinal fluid leukocyte response to S. pneumoniae was, however, greater than that to K. pneumoniae. These results suggest that under the conditions of these studies, hypoglycorrhachia of bacterial meningitis is the result of metabolism of the bacteria with little contribution from the leukocytes.     

Pancreatic carcinoma associated with marked eosinophilia: a case report

A case of pancreatic carcinoma associated with marked eosinophilia is reported. A 71-yr-old man was admitted to hospital because of melena and abdominal pain. The systematic examinations revealed pancreatic adenocarcinoma with multiple metastases (rectum, lung and brain). The leukocyte count was gradually increased and reached up to 81.7 X 10(9)/l, of which 54% consisted of eosinophils. Colony-stimulating factor (CSF) was detected both in the patient's serum and in the tumor extracts by a normal human bone marrow culture system. The colonies which were stimulated with patient's serum largely consisted of granulocyte, granulocyte/macrophage and eosinophil types. These results suggest that blood leukocytosis and eosinophilia were due to a high concentration of plasma CSF, which was probably produced by the tumor cells.     

A High Level of Colony-Stimulating Activity in a Lung Cancer Patient with Extensive Leucocytosis,and the Establishment of a CSA Producing Cell Line (KONT)

Colony-stimulating activity (CSA) was demonstrated in materials taken from a patient suffering from lung cancer associated with excessive leucocytosis. CSA was detected not only in his urine, serum and pleural effusion but also in the supernatant of cell cultures originating from the effusion. The excessive leukocytosis of the patient might be due to a CSA producing tumor. A cell line (KONT) originating from the CSA producing tumor has been maintained for 4 years and shown to produce mouse- and human-CSA.     

EFFECTS OF ARSENIC TRIOXIDE ADMINISTRATION STYLES ON LEUKOCYTOSIS

ARSENIC trioxide ( As2O3) is effective in thetreatment of acute promyelocytic leukemia(APL) and many other kinds of malignant he-matopathies and solid carcinomas·1-5However, leukocytosisis commonly noticed with As2O3use, which severelythreatens the survi…     

Leukocytosis in acute pulmonary embolism.

PURPOSE: The purpose of this investigation is to assess the level of leukocytosis in acute pulmonary embolism (PE). BACKGROUND: Limited data exist regarding leukocytosis in acute PE. One reason that the prevalence of leukocytosis in acute PE is unknown, despite an extensive number of investigations of PE, may relate to the fact that acute PE is usually associated with other conditions that themselves may cause leukocytosis. METHODS: Hospital records of 386 patients with a diagnosis of acute PE were reviewed retrospectively. Patients with no other possible or definite cause of leukocytosis were analyzed separately. A diagnosis of PE was made by a high-probability interpretation of the ventilation/perfusion lung scan or pulmonary angiogram. RESULTS: Among patients with PE in whom other possible or defined causes for leukocytosis were eliminated, 52 of 266 (20%) had a WBC count > 10,000/mm3. None had a WBC count that was > or = 20,000/mm3. Patients with the pulmonary hemorrhage/infarction syndrome had an increased WBC count in 32 of 183 (17%) vs 20 of 83 (24%) in patients who did not have pulmonary hemorrhage/infarction syndrome (not significant). CONCLUSION: A modest leukocytosis may accompany (and possibly be caused by) PE. Its presence should not dissuade the clinician from objectively pursuing the diagnosis of PE.     

婴幼儿重症百日咳死亡相关因素分析

目的探讨婴幼儿重症百日咳死亡相关因素。方法回顾分析2015年1月1日至2019年10月31日收治的婴幼儿百日咳25例病死病例(死亡组)及80例同期收治的重症存活病例(存活组)的临床资料。结果死亡组男性5例(20.0%),中位发病日龄77天,20例(80.0%)未接种百日咳疫苗;存活组男性47例(58.8%),中位发病日龄83天,63例(78.8%)未接种疫苗。与存活组相比,死亡组男性少、痉挛性咳嗽发生率低、肺实变(或肺不张)发生率高、外周血白细胞(WBC)增多更显著、肺动脉高压发生率高、使用丙种球蛋白比例低,差异均有统计学意义(P0.05)。多元logistic回归分析发现,男性、使用丙种球蛋白(OR=0.03、0.03)为重症百日咳死亡的保护因素,WBC最高值高、肺动脉高压(OR=1.10、13.31)为死亡的危险因素,有痉挛性咳嗽患儿死亡概率更小(OR=0.02)。预测死亡的WBC最高值的最佳临界值为55.37×10~9/L,AUC=0.83(95%CI:0.73～0.93)P0.001。结论未接种疫苗、高WBC血症、肺动脉高压明显增加婴幼儿重症百日咳的病死率,使用丙种球蛋白、早期换血减轻高WBC血症可能改善其预后,慎用激素。     

脑脊液细胞计数与实时荧光定量 PCR 检测结核菌在结核性脑膜炎诊断中的相关性分析

目的：分析结核性脑膜炎（tuberculous meningitis，TBM）脑脊液细胞数变化，探讨其与脑脊液中结核分枝杆菌实时荧光定量聚合酶链反应（real-time fluorescent quantitative PCR，FQ-PCR）检测阳性的相关性。方法选取确诊的结核性脑膜炎患者81例，应用全自动血液－体液细胞分析仪进行脑脊液细胞总数计数、离心甩片作脑脊液细胞涂片，光学显微镜图像分析系统分类计数，应用 FQ-PCR 法检测脑脊液中结核分枝杆菌，两者进行相关性分析。结果 FQ-PCR 法检测 TB-DNA 阳性率为50．6％（41／81），其中 FQ-PCR 阳性组中白细胞总数高于阴性组（P ＜0．05）。且白细胞数与 FQ-PCR 拷贝数呈正相关。FQ-PCR 阳性中脑脊液细胞学表现：以混合型细胞反应为主，其中淋巴细胞比例0．590，中性粒细胞比例0．366。结论结核性脑膜炎脑脊液细胞学大多以淋巴细胞反应为主，脑脊液白细胞数的变化可以反映疾病的严重程度，与 FQ-PCR 联合检测对早期诊断结核性脑膜炎有一定的意义。     

Evaluation of postoperative fever and leukocytosis in patients after total hip and knee arthroplasty

Fever and leukocytosis are common after joint arthroplasty, often resulting in additional studies. This study was conducted to determine the incidence of fever and leukocytosis after joint arthroplasty and the use of tests. We retrospectively reviewed records (n = 426) of patients who underwent knee or hip arthroplasty between February 2006 and April 2008 to determine the incidence of fever and leukocytosis, tests, and results. Sixty-four had fever, and 247 had postoperative leukocytosis. Sixty additional tests were performed; 6 (10%) of 60 tests were clinically relevant. After joint arthroplasty, more than half of patients developed leukocytosis, and nearly 15% developed fever. Diagnostic testing should be based on physical examination or symptomatic findings and not solely on laboratory values or vital signs, decreasing the patient discomfort and potentially lower costs.     

Thrombotic complications of myeloproliferative neoplasms: risk assessment and risk‐guided management

Philadelphia‐negative myeloproliferative neoplasms are considered to be acquired thrombophilic states. Thromboses, both arterial and venous (not rarely in unusual sites), are often the initial events leading to the diagnosis. After diagnosis, the yearly incidence of thrombotic events is highly variable, and ranges from approximately 1% to 10%. The identification of patients at risk who may benefit from antithrombotic therapy remains a challenge, and it is currently based on age and history of thrombotic events. However, the predictive value of these clinical characteristics is rather limited. Few prospective studies and even fewer interventional randomized studies are available, and there are no studies designed to formally validate the use of risk stratification. The implementation of laboratory parameters such as leukocytosis and/or the JAK2 V617F mutation into a scoring system may be of interest. The mechanisms at work leading to thrombosis remain largely speculative, but are likely to be complex and multifactorial, with a prominent role of cell–cell interactions, mostly owing to qualitative changes. The long‐term treatment options to prevent thrombosis are, schematically, aspirin alone as primary prevention for the low‐risk patients, and cytoreduction combined with aspirin for the other patients. In very low‐risk young essential thrombocythemia patients, abstention can even be considered. The optimal duration of anticoagulation after a thrombotic event is not established. All antithrombotic therapies should be balanced with the hemorrhagic risk, which can also be increased in these patients.