PubMed Health⌕ Search

Biomedical subjects

A Qamar

Publications and source records attributed to A Qamar.

14 recordsLinked to original sources

Fractures of the distal third of the clavicle treated by hook plating.

We retrospectively assessed the union and shoulder function following hook plate fixation in 18 patients with Neer type 2 fractures of the lateral end of the clavicle. The average age was 40 (range 22-62) years, and the mean follow-up was 25 (range 6-48) months. Fifteen patients had acute fractures and the rest were non-unions. Complications included two non-unions, one following a deep infection. There were no iatrogenic fractures. Acromial osteolysis was seen in five patients who had their plates in situ. The average pain score at rest was 1 (range 0-4), and the average pain score on abduction was 2.2 (range 0-5). The average Constant score was 88.5 (range 63-100). Patients were asked to rate their shoulder function; three rated it as normal, 11 as nearly normal and one as not normal. Hook plate fixation appears to be a valuable method of stabilising Neer type 2 fractures of the clavicle, resulting in high union rates and good shoulder function. These plates need to be removed after union to prevent acromial osteolysis.

Bone Plates↗

Association between antibody response to toxin A and protection against recurrent Clostridium difficile diarrhoea.

BACKGROUND: We have reported that symptom-free carriers of Clostridium difficile have a systemic anamnestic immune response to toxin A. The aim of this study was to determine whether an acquired immune response to toxin A, during an episode of C. difficile diarrhoea, influences risk of recurrence. METHODS: We prospectively studied 63 patients with nosocomial C. difficile diarrhoea. Serial serum IgA, IgG, and IgM concentrations against C. difficile toxin A, toxin B, or non-toxin antigens were measured by ELISA. Individuals were followed for 60 days. FINDINGS: 19 patients died (30%). Of the 44 who survived, 22 had recurrent C. difficile diarrhoea. Patients with a single episode of C. difficile diarrhoea (n=22) had higher concentrations of serum IgM against toxin A on day 3 of their first episode of diarrhoea than those with recurrent diarrhoea (n=22, p=0.004). On day 12, serum IgG values against toxin A were higher in patients who had a single episode of diarrhoea (n=7) than in those who subsequently had recurrent diarrhoea (n=9, p=0.009). The odds ratio for recurrence associated with a low concentration of serum IgG against toxin A, measured 12 days after onset of C. difficile diarrhoea, was 48.0 (95% CI 3.5-663). INTERPRETATION: A serum antibody response to toxin A, during an initial episode of C. difficile diarrhoea, is associated with protection against recurrence.

Aged↗

Saccharomyces boulardii stimulates intestinal immunoglobulin A immune response to Clostridium difficile toxin A in mice.

Saccharomyces boulardii is a nonpathogenic yeast that protects against antibiotic-associated diarrhea and recurrent Clostridium difficile colitis. The administration of C. difficile toxoid A by gavage to S. boulardii-fed BALB/c mice caused a 1.8-fold increase in total small intestinal immunoglobulin A levels (P = 0.003) and a 4.4-fold increase in specific intestinal anti-toxin A levels (P < 0.001). Enhancing host intestinal immune responses may be an important mechanism for S. boulardii-mediated protection against diarrheal illnesses.

Animals↗

Asymptomatic carriage of Clostridium difficile and serum levels of IgG antibody against toxin A.

BACKGROUND: Clostridium difficile infection can result in asymptomatic carriage, mild diarrhea, or fulminant pseudomembranous colitis. We studied whether antibody responses to C. difficile toxins affect the risks of colonization, diarrhea, and asymptomatic carriage. METHODS: We prospectively studied C. difficile infections in hospitalized patients who were receiving antibiotics. Serial stool samples were tested for C. difficile colonization by cytotoxin assay and culture. Serum antibody (IgA, IgG, and IgM) levels and fecal antibody (IgA and IgG) levels against C. difficile toxin A, toxin B, and nontoxin antigens were measured by an enzyme-linked immunosorbent assay (ELISA). RESULTS: Of 271 patients, 37 (14 percent) were colonized with C. difficile at the time of admission, 18 of whom were asymptomatic carriers. An additional 47 patients (17 percent) became infected in the hospital, 19 of whom remained asymptomatic. The baseline antibody levels were similar in the patients who later became colonized and those who did not. After colonization, those who became asymptomatic carriers had significantly greater increases in serum levels of IgG antibody against toxin A than did the patients in whom C. difficile diarrhea developed (P<0.001). The adjusted odds ratio for diarrhea was 48.0 (95 percent confidence interval, 3.4 to 678) among patients with colonization who had a serum level of IgG antibody against toxin A of 3.00 ELISA units or less, as compared with patients with colonization who had a level of more than 3.00 ELISA units. CONCLUSIONS: We find no evidence of immune protection against colonization by C. difficile. However, after colonization there is an association between a systemic anamnestic response to toxin A, as evidenced by increased serum levels of IgG antibody against toxin A, and asymptomatic carriage of C. difficile.

Aged↗

p38 MAP kinase activation by Clostridium difficile toxin A mediates monocyte necrosis, IL-8 production, and enteritis.

Clostridium difficile toxin A causes acute neutrophil infiltration and intestinal mucosal injury. In cultured cells, toxin A inactivates Rho proteins by monoglucosylation. In monocytes, toxin A induces IL-8 production and necrosis by unknown mechanisms. We investigated the role of mitogen-activated protein (MAP) kinases in these events. In THP-1 monocytic cells, toxin A activated the 3 main MAP kinase cascades within 1 to 2 minutes. Activation of p38 was sustained, whereas stimulation of extracellular signal-regulated kinases and c-Jun NH(2)-terminal kinase was transient. Rho glucosylation became evident after 15 minutes. IL-8 gene expression was reduced by 70% by the MEK inhibitor PD98059 and abrogated by the p38 inhibitor SB203580 or by overexpression of dominant-negative mutants of the p38-activating kinases MKK3 and MKK6. SB203580 also blocked monocyte necrosis and IL-1beta release caused by toxin A but not by other toxins. Finally, in mouse ileum, SB203580 prevented toxin A-induced neutrophil recruitment by 92% and villous destruction by 90%. Thus, in monocytes exposed to toxin A, MAP kinase activation appears to precede Rho glucosylation and is required for IL-8 transcription and cell necrosis. p38 MAP kinase also mediates intestinal inflammation and mucosal damage induced by toxin A.

Animals↗

The Goldman algorithm revisited: prospective evaluation of a computer-derived algorithm versus unaided physician judgment in suspected acute myocardial infarction.

BACKGROUND: It has been nearly a decade since Goldman's computer-driven algorithm to predict myocardial infarction was validated. Despite the potential to avoid admission of patients without acute myocardial infarction (AMI) to the coronary care unit (CCU), the routine use of computer-generated protocols has not been widely adopted. METHODS: Two hundred consecutive patients admitted to a university-affiliated community hospital with the suspected diagnosis of AMI as determined by physicians without the aid of the Goldman protocol underwent a blinded prospective evaluation to assess the performance of the Goldman algorithm in predicting the presence of AMI. Over the same time period, the Goldman algorithm was applied by retrospective chart review in 762 patients with non-AMI admitting diagnoses. Prospective history, physical examination, and electrocardiographic data were obtained within 24 hours of admission to the CCU by a physician blinded to each patient's clinical course. Retrospective chart reviews were conducted for 762 patients with chest pain given with non-AMI diagnoses. RESULTS: The diagnosis of AMI was confirmed in 68.5% (137/200) of patients with suspected AMI admitted to the CCU. In prospective parallel evaluations the Goldman algorithm predicted the presence of AMI in 167 (83.5%) of these 200 patients. All 137 confirmed patients with AMI were correctly identified by the Goldman algorithm. All major in-hospital complications occurred in the 137 patients who were diagnosed as having AMI. Of the 762 patients with chest pain with non-AMI diagnoses, only 27 (3.5%) sustained an AMI. The Goldman algorithm predicted the presence of AMI in 85% (23/27) of these patients. Adherence to the use of Goldman's algorithm in the triage of chest pain could have prevented 16.5% of CCU admissions for AMI. CONCLUSIONS: Routine adherence to the Goldman algorithm for the evaluation of patients with acute chest pain could have decreased the number of CCU admissions for suspected AMI by 16. 5%. Because major in-hospital complications occurred only in patients with AMI, this strategy would result in significant cost savings to our health care system without jeopardizing patient safety.

Algorithms↗

Myocardial infarction in critically ill patients presenting with gastrointestinal hemorrhage: retrospective analysis of risks and outcomes.

OBJECTIVES: To determine the frequency of and risk factors for myocardial infarction (MI) in patients admitted to an ICU with GI hemorrhage, and the effects of MI on mortality and length of stay. METHODS: A retrospective review of the medical records of patients admitted to our ICU with GI hemorrhage was conducted. Charts were reviewed for various demographic, laboratory, and outcome parameters. Patients were categorized as having MI, not having MI, or inadequate data to allow classification. RESULTS: Two hundred thirty admissions to the ICU for GI hemorrhage were reviewed. One hundred thirteen cases had serial creatine phosphokinase (CK) measurements with isoenzymes allowing diagnosis of MI. In these 113 cases, patients' mean age was 67.4+/-1.3 years and the mean APACHE II (acute physiology and chronic health evaluation) score was 10.9+/-0.6. The in-hospital mortality rate was 13/113 (11.5%). Patients who did not survive had a higher admission APACHE II score (15.8+/-2.0 vs 10.2+/-0.5; p = 0.02), lower initial systolic BP (104.5+/-4.4 vs 121.2+/-3.2 mm Hg; p = 0.005), and a longer length of ICU stay (8.3+/-1.8 vs 4.0+/-0.4 days; p = 0.04) than those who survived. Sixteen of 113 patients met enzymatic and ECG criteria for MI. One patient complained of chest pain and nine of 16 had shortness of breath and/or dizziness. Patients with MI had significantly more cardiac risk factors (2.4+/-0.2 vs 1.6+/-0.1; p = 0.006), lower presenting hematocrit (26.0+/-1.3 vs 30.5+/-0.8; p = 0.007), and lower lowest hematocrit in the first 48 h (22.3+/-0.9 vs 25.1+/-0.6; p = 0.01), and tended to have a longer ICU stays (7.9+/-2.2 vs 4.0+/-0.4 days; p = 0.09) than those without MI. Patients who had MI were not more likely to die during hospitalization (risk ratio = 1.8; 95% confidence interval, 0.6 to 5.8). CONCLUSIONS: Myocardial infarction occurs frequently in patients admitted to intensive care with GI hemorrhage. A clinical history of and multiple risk factors for coronary artery disease may help identify patients who are at increased risk of MI, which tends to be associated with a higher acuity of illness and in-hospital mortality. Prospective studies are required to further substantiate these associations.

APACHE↗

An outbreak of enterically transmitted non-A, non-B hepatitis in Pakistan.

An epidemic of enterically transmitted non-A, non-B hepatitis occurred at a college in Sargodha, Pakistan in early 1987. There were 133 clinical cases, an attack rate of approximately 20%. Though the disease was relatively mild, all clinical cases required hospitalization and prolonged convalescence. Nearly all cases were associated with a single water source. The epidemic ended when the water supply was improved. This is the 4th described epidemic of non-A, non-B hepatitis in Pakistan.

Acute Disease↗

Effective resource management using a clinical and laboratory algorithm for chest pain triage.

BACKGROUND: Bridgeport Hospital recently compared the use of a clinical algorithm with unaided physicians for the triage of 200 emergency department (ED) patients with chest pain for coronary care unit (CCU) admission. HYPOTHESIS: Cardiac troponin-T may be an effective adjunct to an established clinical algorithm for accurate selection of patients who are admitted to the CCU for suspected acute myocardial infarction (AMI). It is elevated 6 hours earlier than lactate dehydrogenase fraction 1 (LD1) and may be the most effective test for confirming non Q-wave AMI (usually with ST-T changes and LD1/lactase dehydrogenase > 35%). It is elevated in class 3 angina with a high risk of fatal arrhythmia. STUDY DESIGN: Clinical and electrocardiogram criteria for triage are as defined by Goldman et al. (see references 6 and 11). The exclusion of non-AMI within 4 hours of ED visit using troponin-T (or an alternative test) should allow more rapid treatment of non-AMI patients at a lower intensity of hospital service (e.g., telemetry versus ICU). This should translate into shorter length of stay for non-AMI patients and facilitate thrombolytic therapy with significant resultant medical and cost benefits. LABORATORY DATA: Creatine kinase and its MB isoenzyme (CK-MB) are measured at the time of clinical triage and 4, 8, and 12 hours later. LD1 and total lactase dehydrogenase are measured 12 hours after initial sampling. Cardiac troponin-T is measured at the time of ED arrival and 4 hours later. ANALYSIS OF BENEFIT: The first thing to consider is reducing the cost from stress thalliums for low risk evaluation. The second is the evaluation of active ischemia--unstable angina and diagnosis of missed AMI. The Goldman algorithm eliminates unnecessary admissions to the CCU for chest pain, including unstable angina. There is a difference between AMI and triage for CCU admission (200 patients). CK-MBs allowed for the elimination of 37 non-AMIs. However, we missed eight cases of AMI that would have been LD1 positive (troponin positive) and gained 10 cases of unstable angina that should have been assigned to CCU or a monitored bed. Troponin found six more cases of unstable angina that were CK-MB negative but should have been class 3 unstable angina that could be assigned to at least a telemetry bed. This makes 14 cases of AMI or unstable angina unaccounted for by CK-MB (5.6%). All of the cases were at risk of ventricular arrhythmia within 36 hours. The only question was whether to assign them to CCU or to monitored beds. The third point in the analysis is to examine the savings in operating costs by substitution. The cost model, in selecting a strategy, takes test costs, clinical outcomes, and the cost of clinical algorithms into consideration.

Algorithms↗

Outcomes research is the fifth discipline of the fifth generation of managed care: utility of a single troponin-T.

OBJECTIVE: The fifth generation of managed care is disease management. Diseases have measurable risk in providing laboratory and medical services. The link between managing services and managing risk can be aided by leveraging the laboratory. We wish to remodel laboratory services to fit the needs of the use, thereby using the laboratory for competitive advantage by redesigning a desired output using a formal structured process. Outcomes research is the systems framework for the remodeling process through the link of laboratory output to clinical and financial outcomes. A process redesign model connects the use of laboratory tests to improved medical services by leveraging resources to achieve measurable improvement over current results. This view of outcomes research seeks both competitive advantage and measurable improvements in quality. METHODOLOGY: This approach is illustrated by the patient presenting with chest pain (CP). A majority of the patients rule out for acute myocardial infarction (AMI), including patients with indigestion, shortness of breath, and other clinical findings. This is the basis for an emergency department (ED) CP observation unit to reduce coronary care unit admission rates. When the Goldman algorithm for discharging low-risk patients with CP from the ED using only clinical features and electrocardiographic findings proved difficult to implement, we turned to measuring the diagnostic efficiency of a new cardiac marker to replace the evolutionary changes in creatine kinase (CK) isoenzyme MB. The physicians making the decision were blinded to the results of the study. We fitted the expected characteristics of the test to the expected results for our program. The test was done on the presenting specimen of 293 evaluable patients with a median of 6.5 hours from the time of onset of CP to the time the specimen was drawn. The result was compared with the evolutionary pattern of CK-MB. RESULTS: The sensitivity of the test at presentation to the ED was 85% compared with < 50% for the presenting CK-MB, the false negative results taken earlier than 3 hours or 10 days after the onset of symptoms. Troponin-T effectively identifies non Q-wave AMI much earlier than the CK-MB. This study led to a prospective randomized clinical trial to demonstrate an improved medical and financial benefit from an early rule in or rule out of severe coronary artery ischemia. CONCLUSION: The study supports our hypothesis that the laboratory can systematically redesign its technology strategy and participate in the construction of a clinical pathway for the discharge from ED or admitting decisions with a test 98% sensitive for identifying patients with serious coronary ischemia by 3.5 hours after the onset of symptoms.

Biomarkers↗

Diagnosis of myocardial infarction: integration of serum markers and clinical descriptors using information theory.

OBJECTIVE: We examine the use of information theory applied to a single cardiac troponin T (cTnT) (first generation monoclonal; Boehringer Mannheim Corp., Indianapolis, Indiana) used with the character of chest pain, electrocardiography (ECG) and serial ECG changes in the evaluation of acute myocardial infarction (AMI). We combined a single measure of cTnT (blinded to the investigators) with a creatine kinase MB isoenzyme (CK-MB) measurement to discover the best decision value for this test in a study of 293 consecutive patients presenting to the emergency department with symptoms warranting exclusion of AMI. METHODS: The decision value for determining whether cTnT is positive or negative was determined independently of the final diagnosis by examining the information in the cTnT and CKMB data. Using information theory, an autocorrelation matrix with a one-to-one pairing of the CKMB and troponin T was constructed. The effective information, also known as Kullback entropy, assigned the values for troponin T and for CKMB that have the lowest frequency of misclassification error. The Kullback entropy is determined by subtracting the data entropy from the maximum entropy of the data set in which the information has been destroyed. The assignment of the optimum decision values was made independently of the clinical diagnoses without the construction of a receiver-operator characteristic curve (ROC). The final diagnosis of AMI was independently determined by the clinicians and entered into the medical record. RESULTS: The decision value for cTnT was 0.1 ng/ml as determined by the the information in the data. The method was validated within the same study by mapping the results so obtained into the diagnoses obtained independently by the clinicians using all of the methods at their disposal. The cTnT was different in AMI (n = 60) compared with non-AMI patients (n = 233) (2.08 +/- 0.21 vs. 0.07 +/- 0.10; p < .0001). CONCLUSION: Information theory provides a strong framework and methodology for determining the decision value for cTnT which minimizes misclassification errors at 0.1 ng/ml. The result has a strong correlation with other features in detecting AMI in patients presenting with chest pain.

Creatine Kinase↗

Evaluating a new graphical ordinal logit method (GOLDminer) in the diagnosis of myocardial infarction utilizing clinical features and laboratory data.

OBJECTIVE: We used a new graphical ordinal logit method (GOLDminer) to assess a single cardiac troponin T (cTnT) analysis at the time of admission (first generation monoclonal; Roche BMC Corp., Indianapolis, Indiana), the character of chest pain, and electrocardiographic (ECG)findings in predicting the likelihood of acute myocardial infarction (AMI) in patients presenting with suspected myocardial ischemia. The final diagnosis of AMI was based on serial ECG findings and evolution of CKMB isoenzyme levels in conjunction with clinical findings. SUBJECTS: The study population consisted of 293 consecutive patients who presented at a mean of six hours after onset of chest pain or associated symptoms warranting a "rule-out" for AMI assessment to a university-affiliated community hospital. RESULTS: The odds-ratio for an elevated cTnT (> 0. 1 ng/ml) in AMI was 22.2:1. There was an association between typical chest pain and cTnT (chi square = 78.23, p < .0001) and between abnormal ECG findings and cTnT (chi square = 108, p < .0001). The cTnT yielded diagnostic benefit in addition to chest pain characteristics and ECG findings in AMI. We present the odds-ratios for the combined features in GOLDminer plots. CONCLUSION: We demonstrate how the odds-ratios for AMI are obtained after scaling continuous to ordinal the values for a single cTnT determination alone and with other features in patients presenting with chest pain.

Creatine Kinase↗