Shoulder disorders—Part 2: Examination

Thorough evaluation of patients with shoulder problems should classify patients into discreet diagnostic groups—red flags, impingement syndrome, adhesive capsulitis, shoulder instability. Most rotator cuff tendonitis patients fall into the impingement category. The most important aspect of the initial evaluation is to rule out red flags suggestive of tumor, infection or fracture. If present such patients always require additional testing and often referral.A patient will be classified into the impingement category if there is (a) pain with active shoulder motions (i.e., painful arc), (b) pain with overpressure of passive shoulder elevation (i.e., a positive Neer's test) or horizontal shoulder adduction/internal rotation (Hawkins test), and (c) painfully weak resisted shoulder motions. Impingement syndrome patients should also be evaluated for partial or full-thickness rotator cuff tears, especially if the response to 4–6 weeks of rehabilitation is unsatisfactory.Patients with adhesive capsulitis have severe ROM loss. The most restricted ROMs are with shoulder abduction, external rotation, and flexion. In contrast, patients with shoulder instability are hypermobile. A history of recurrent dislocations is often present. An apprehension sign may be present. SLAP II-IV lesions are common in this patient group and the labrum can be seen to be stretched anterior during many of the functional tests.     

肾移植术后卡氏肺囊虫肺炎5例回顾性分析

目的:观察肾移植术后卡氏肺囊虫肺炎的发生率及治疗效果。方法:选择2003-01/2005-12在中山市人民医院行肾移植的患者112例,患者均知情同意。按是否使用猪抗人淋巴细胞免疫球蛋白分为2组,基础免疫抑制组(n=68)给予环孢素A/他克莫司 吗替麦考酚酯 强的松;抗体诱导组(n=44)给予猪抗人淋巴细胞免疫球蛋白 环孢素A/他克莫司 吗替麦考酚酯 强的松。两组共发生卡氏肺囊虫肺炎5例,其中基础免疫抑制组2例,抗体诱导组3例。5例患者通过普通抗感染治疗,3～7d病情未见好转,遂行支气管镜活检 深部吸痰培养,尽早明确病原体,指导抗菌治疗。比较两组患者卡氏肺囊虫肺炎的发生率,并观察其治疗效果。结果:5例卡氏肺囊虫肺炎患者全部进入结果分析,无脱落。①5例患者经支气管纤维镜肺组织活检确诊为卡氏肺囊虫肺炎,发生率为4.46%,其中抗体诱导组6.82%(3/44)明显高于基础免疫抑制组2.94%(2/68)。②5例卡氏肺囊虫肺炎中2例合并金黄色葡萄球菌感染。以复方磺胺甲恶唑为基础药物进行综合治疗,3例患者临床治愈出院,随访3个月,移植肾及肺功能正常;死亡2例。③5例患者治疗期间均无排斥反应发生。④在发病初期5例患者的CD4/CD8平均值为1.02±0.15,3例治愈患者的CD4/CD8平均值为1.42±0.23,在恢复过程中逐渐升高。2例死亡患者的CD4/CD8平均值为1.10±0.21。结论:早期支气管纤维内镜活检对肾移植术后卡氏肺囊虫肺炎的诊断非常重要,早期诊断、早期治疗是治愈的关键。猪抗人淋巴细胞免疫球蛋白可增加肾移植术后卡氏肺囊虫肺炎的发生率。     

Should we educate about the risks of medication overuse headache?

Background

Medication-overuse headache (MOH) is caused by the regular use of medications to treat headache. There has been a lack of research into awareness of MOH. We distributed an electronic survey to undergraduate students and their contacts via social networking sites. Analgesic use, awareness of MOH, perceived change in behaviour following educational intervention about the risks of MOH and preferred terminology for MOH was evaluated.

Findings

485 respondents completed the questionnaire (41% having received healthcare training). 77% were unaware of the possibility of MOH resulting from regular analgesic use for headache. Following education about MOH, 80% stated they would reduce analgesic consumption or seek medical advice. 83% indicated that over the counter analgesia should carry a warning of MOH. The preferred terminology for MOH was painkiller-induced headache.

Conclusions

This study highlights the lack of awareness of MOH. Improved education about MOH and informative packaging of analgesics, highlighting the risks in preferred lay terminology (i.e. painkiller-induced headache), may reduce this iatrogenic morbidity and warrants further evaluation.     

Facilitating the decrease in fibromyalgic pain during metabolic rehabilitation: an essential role for soft tissue therapies

Recent evidence indicates that fibromyalgia (FMS) is a manifestation of impaired metabolism. In most cases, the cause is primarily inadequate thyroid hormone regulation of cell function. The measurable features of FMS can be improved or relieved in most patients through therapy that is best termed ‘metabolic rehabilitation’. For many patients undergoing metabolic rehabilitation, however, FMS pain scores normalize only after soft tissue treatment controls or eliminates noxious neural input from the musculoskeletal system to the central nervous system. Our studies and clinical experiences convince us that effective soft tissue therapy can expedite the typical patient's improvement or recovery. Neglecting to use such therapy can hinder recovery, even when the patient undergoes expertly conducted metabolic rehabilitation. This paper describes the probable mechanisms by which musculoskeletal lesions can sustain FMS pain, and gives guidelines for treating the FMS patient's soft tissues to facilitate the reduction of pain during metabolic rehabilitation.     

The distribution of infectivity in blood components and plasma derivatives in experimental models of transmissible spongiform encephalopathy

BACKGROUND: The administration of blood components from donors who subsequently develop Creutzfeldt-Jakob disease has raised the issue of blood as a possible vehicle for iatrogenic disease. STUDY DESIGN AND METHODS: We examined infectivity in blood components and Cohn plasma fractions in normal human blood that had been "spiked" with trypsinized cells from a scrapie-infected hamster brain, and in blood of clinically ill mice that had been inoculated with a mouse-adapted strain of human transmissible spongiform encephalopathy. Infectivity was assayed by intracerebral inoculation of the blood specimens into healthy animals. RESULTS: Most of the infectivity in spiked human blood was associated with cellular blood components; the smaller amount present in plasma, when fractionated, was found mainly in cryoprecipitate (the source of factor VIII) and fraction I+II+III (the source of fibrinogen and immunoglobulin); almost none was recovered in fraction IV (the source of vitamin-K-dependent proteins) and fraction V (the source of albumin). Mice infected with the human strain of spongiform encephalopathy had very low levels of endogenous infectivity in buffy coat, plasma, cryoprecipitate, and fraction I+II+III, and no detectable infectivity in fractions IV or V. CONCLUSION: Convergent results from exogenous spiking and endogenous infectivity experiments, in which decreasing levels of infectivity occurred in cellular blood components, plasma, and plasma fractions, suggest a potential but minimal risk of acquiring Creutzfeldt-Jakob disease from the administration of human plasma protein concentrates.     

大肠癌免疫组化表达与临床病理的关系

目的:探讨大肠癌CEA、P53、nm23、Ki-67、MRP免疫组化表达特点和相互关系,及其与临床病理的关系．方法:回顾性分析2003-01／2006-07我院收治的73例大肠癌患者的临床病理及随访资料,并对其石蜡标本采用免疫组化SP染色法检测CEA、P53、nm23、Ki-67、MRP,分析其免疫组化特点及其与临床病理之间的关系．结果:CEA、P53、nm23、Ki-67、MRP在大肠癌中的阳性表达率依次为82．2％、68．5％、75.3％、84．9％和64．4％．CEA、MRP与大肠癌患者的各因素无统计学差异．P53、Ki-67和nm23与肿瘤的Dukes分期和淋巴结转移有关, P53、Ki-67在Dukes C、D期的阳性表达率(依次为82．8％和100％1明显高于Dukes A、B期者(59．1％和75．0％)(P<0．05),而nm23在Dukes C、D期的阳性表达率(58．6％)明显低于Dukes A、B期者(86．4％)(P<0．05)．CEA与nm23的表达呈明显的负相关(r=-0．296,P=0．011),而P53和Ki-67表达之间呈现明显的正相关(r= 0．308,P=0．008),其他各指标间的表达无相关性．nm23、P53和Ki-67与预后因素关系明显,nm23在生存期≥3 a患者的阳性表达率(92．9%)高于生存期<3 a者(71．2％)(P<0．05),而P53和Ki-67在生存期≥3 a患者的阳性表达率(依次为42．9％和64.3％)明显低于生存期<3 a者(74．6％和89．8％)(P<0．05)．结论:P53、Ki-67和nm23的表达与大肠癌的侵袭转移和预后密切相关．CEA可能是大肠癌的侵袭转移的促进因素．MRP所引起的耐药机制是一个相对独立的机制．CEA、P53、nm23、Ki-67可作为判断大肠癌恶性程度、侵袭转移以及预后的指标．     

Development of a marrow transplant regimen for acute leukemia using targeted hematopoietic irradiation delivered by 131I-labeled anti-CD45 antibody, combined with cyclophosphamide and total body irradiation

In an attempt to decrease the relapse rate after bone marrow transplantation (BMT) for advanced acute leukemia, we initiated studies using 131I-labeled anti-CD45 antibody (BC8) to deliver radiation specifically to hematopoietic tissues, followed by a standard transplant preparative regimen. Biodistribution studies were performed in 23 patients using 0.5 mg/kg trace 131I-labeled BC8 antibody. The BC8 antibody was cleared rapidly from plasma with an initial disappearance half-time of 1.5 +/- 0.2 hours, presumably reflecting rapid antigen- specific binding. The mean radiation absorbed doses (cGy/mCi131I administered) were as follows: marrow, 7.1 +/- 0.8; spleen, 10.8 +/- 1.4; liver, 2.7 +/- 0.2; lungs, 2.1 +/- 0.1; kidneys, 0.7 +/- 0.1; and total body, 0.4 +/- 0.03. Patients with acute myelogenous leukemia (AML) in relapse had a higher marrow dose (11.4 cGy/mCi) than those in remission (5.2 cGy/mCi; P = .001) because of higher uptake and longer retention of radionuclide in marrow. Twenty patients were treated with a dose of 131I estimated to deliver 3.5 Gy (level 1) to 7 Gy (level 3) to liver, with marrow doses of 4 to 30 Gy and spleen doses of 7 to 60 Gy, followed by 120 mg/kg cyclophosphamide (CY) and 12 Gy total body irradiation (TBI). Nine of 13 patients with AML or refractory anemia with excess blasts (RAEB) and two of seven with acute lymphocytic leukemia (ALL) are alive disease-free at 8 to 41 months (median, 17 months) after BMT. Toxicity has not been measurably greater than that of CY/TBI alone, and the maximum tolerated dose has not been reached. This study demonstrates that with the use of 131I-BC8 substantially greater doses of radiation can be delivered to hematopoietic tissues as compared with liver, lung, or kidney, which may improve the efficacy of marrow transplantation.     

Degradation of tissue-type plasminogen activator by human monocyte- derived macrophages is mediated by the mannose receptor and by the low- density lipoprotein receptor-related protein

The balance of tissue-type plasminogen activator (t-PA) production and degradation determines its concentration in blood and tissues. Disturbance of this balance may result in either increased or decreased proteolysis. In the present study, we identified the receptor systems involved in the degradation of t-PA by human monocytes/macrophages in culture. Monocytes were cultured and became macrophages within 2 days. At 4 degrees C, 125I-t-PA bound to macrophages with high (apparent dissociation constant [kd], 1 to 5 nmol/L) and low affinity (kd > 350 nmol/L). At 37 degrees C, the cells internalized and degraded t-PA via the high affinity binding sites, which were partially inhibited by mannan. The low affinity binding sites were 6-aminohexanoic acid- inhibitable and not involved in t-PA degradation. Degradation of t-PA was upregulated during differentiation of monocytes to macrophages. Dexamethasone further upregulated the mannan-inhibitable t-PA degradation. Lipopolysaccharide downregulated both mannan-inhibitable and non-mannan-inhibitable t-PA degradation. Non-mannan-inhibitable degradation was completely blocked by recombinant 39-kD receptor- associated protein (RAP, inhibitor of lipoprotein receptor-related protein [LRP]), whereas mannan-inhibitable degradation was blocked by the addition of a monoclonal antibody against the mannose receptor. No differences between the degradation of t-PA and functionally inactivated t-PA were observed. We conclude that human monocyte-derived macrophages are able to bind, internalize, and degrade t-PA. Degradation of t-PA does not require complex formation with plasminogen activator inhibitors. The macrophages use two independently regulated receptors, namely, the mannose receptor and LRP, for the uptake and degradation of t-PA.     

Myocardial siderosis due to hemochromatosis in an individual with hypertrophic cardiomyopathy

A patient with hypertrophic cardiomyopathy (HCM) and transfusion-dependent sideroblastic anemia, who presented with decompensated heart failure, is described. The present case demonstrates the usefulness of cardiac magnetic resonance imaging as a noninvasive imaging modality to assess the etiology of new systolic dysfunction in the setting of HCM. Cardiac magnetic resonance imaging is able to differentiate between the dilated ‘burned-out’ phase of HCM and a concomitant dilated cardiomyopathy secondary to myocarditis or hemosiderosis.     

Acquired immunodeficiency syndrome-associated non-Hodgkin's lymphomas and other malignancies in patients with hemophilia

Non-Hodgkin's lymphoma (NHL) is the most common human immunodeficiency virus (HIV)-associated malignancy in hemophiliacs. We studied the incidence and clinicopathologic features of NHL in 3,041 hemophiliacs followed at 18 US Hemophilia Centers between 1978 and 1989. Of the 1,295 (56.6%) who were HIV(+), 253 (19.5%) developed acquired immunodeficiency syndrome (AIDS), of whom 14 (5.5%) developed NHL. Three NHL occurred in HIV(-) hemophiliacs, for a 36.5-fold greater risk in HIV(+) than HIV(-) hemophiliacs (P < .001). The NHL incidence rate was 29-fold greater than in the US population by Surveillance, Epidemiology, and End Results (SEER) estimates (P < .001). Between 0 and 4 lymphomas have been observed per year between 1978 and 1989. At presentation 13 (92.9%) of the HIV(+) NHL were extranodal. Ten were stage IV, 1 stage II, and 3 stage IE. Ten (71.4%) were high-grade, 3 (21.4%) intermediate-grade, and 1 (7.1%) was a low-grade B-cell lymphoma. Epstein-Barr virus (EBV) DNA was detected in 36% by in situ hybridization, including one central nervous system (CNS) lymphoma. The mean CD4 cell count at NHL diagnosis was 64/mm3, the mean latency from initial HIV infection was estimated to be 59 months, and the median survival was 7 months. The incidence of basal cell carcinoma in HIV(+) hemophiliacs was 18.3-fold greater than in HIV(-) hemophiliacs (P < .001) and 11.4-fold greater than in the US population (P < .001). In conclusion, incidence rates of NHL and basal cell carcinoma in HIV(+) hemophiliacs are significantly increased over rates in HIV(-) hemophiliacs and over rates in the US population. Clinicopathologic presentation of NHL in HIV(+) hemophiliacs is similar to that in HIV(+) homosexual men.