Queens Hospital Center

Clinical criteria for the classification of patients with hip pain associated with osteoarthritis (OA) were developed through a multicenter study. Data from 201 patients who had experienced hip pain for most days of the prior month were analyzed. The comparison group of patients had other causes of hip pain, such as rheumatoid arthritis or spondylarthropathy. Variables from the medical history, physical examination, laboratory tests, and radiographs were used to develop different sets of criteria to serve different investigative purposes. Multivariate methods included the traditional "number of criteria present" format and "classification tree" techniques. Clinical criteria: A classification tree was developed, without radiographs, for clinical and laboratory criteria or for clinical criteria alone. A patient was classified as having hip OA if pain was present in combination with either 1) hip internal rotation greater than or equal to 15 degrees, pain present on internal rotation of the hip, morning stiffness of the hip for less than or equal to 60 minutes, and age greater than 50 years, or 2) hip internal rotation less than 15 degrees and an erythrocyte sedimentation rate (ESR) less than or equal to 45 mm/hour; if no ESR was obtained, hip flexion less than or equal to 115 degrees was substituted (sensitivity 86%; specificity 75%). Clinical plus radiographic criteria: The traditional format combined pain with at least 2 of the following 3 criteria: osteophytes (femoral or acetabular), joint space narrowing (superior, axial, and/or medial), and ESR less than 20 mm/hour (sensitivity 89%; specificity 91%). The radiographic presence of osteophytes best separated OA patients and controls by the classification tree method (sensitivity 89%; specificity 91%). The "number of criteria present" format yielded criteria and levels of sensitivity and specificity similar to those of the classification tree for the combined clinical and radiographic criteria set. For the clinical criteria set, the classification tree provided much greater specificity. The value of the radiographic presence of an osteophyte in separating patients with OA of the hip from those with hip pain of other causes is emphasized.

In normal plasma, the ratio of the procoagulant activity of factor VIII (VIII(AHF)) to that of the von Willebrand factor activity (ristocetin cofactor, VIII(VWF)) or factor VIII antigen (VIII(AGN)) is approximately 1, but ratios > 1 (e.g., VIII(AHF) > VIII(VWF) or VIII(AGN)) may be observed in some patients with von Willebrand's disease and in the "late" posttransfusion plasmas of patients with this disorder. The lability of VIII(AHF) was studied by incubating plasma, diluted 1:10 in imidazole buffer pH 7.1, for 6 h at 37 degrees C. With normal plasmas, 77+/-12% (SD) of the original VIII(AHF) activity remained after incubation. VIII(AHF) was labile (e.g., 35-55% residual activity) in the "late" posttransfusion plasmas (VIII(AHF) >> VIII(VWF)) of a patient with von Willebrand's disease, but not in the "early" posttransfusion plasmas (VIII(AHF) approximately VIII(VWF)). VIII(AHF) was also labile in the (base-line) plasmas of three patients with von Willebrand's disease in whom the ratios of VIII(AHF) to VIII(VWF) were 4.4 to 8.1, but not in the plasmas of four other patients in whom the ratio was approximately 1. The electrophoretic mobility of factor VIII antigen was increased in two of the three patients with labile VIII(AHF). In both of these patients, and in the late posttransfusion plasmas, labile VIII(AHF) activity could be stabilized by the addition of purified von Willebrand factor (lacking VIII(AHF) activity) or by hemophilic plasma, but not by plasmas of patients with severe von Willebrand's disease. Thus, VIII(VWF) may serve to stabilize VIII(AHF) and this might explain the posttransfusion findings in von Willebrand's disease.

OBJECTIVE: To describe a large cohort of patients who had chest pain following cocaine use, and to determine the incidence of and clinical characteristics predictive for myocardial infarction in this group of patients. METHODS: A prospective observational cohort study of consecutive patients with cocaine-associated chest pain was conducted in six municipal hospital emergency departments (EDs). Demographic variables, drug abuse patterns, medical histories, chest pain characteristics, ECG results, and laboratory data were recorded. Myocardial infarction was the primary endpoint. RESULTS: Fourteen of 246 patients (5.7%; 95% confidence interval [CI], 2.7-8.7%) had myocardial infarction, as diagnosed by elevated CK-MB isoenzyme levels. There were two deaths (0.8%). The patients had a median age of 33 years. The majority were male (71.5%), non-white (83.3%), cigarette smokers (83.3%) who used cocaine regularly. Chest pain began a median of 60 minutes after cocaine use and persisted for a median of 120 minutes. Chest pain was most frequently described as substernal (71.3%) and pressure-like (46.7%). Shortness of breath (59.3%) and diaphoresis (38.6%) were common. There was no clinical difference between patients who had myocardial infarctions and those who did not. Twelve patients had arrhythmias and four had congestive heart failure. All cases requiring intervention were evident upon presentation. An ECG revealing ischemia or infarction had a sensitivity of 35.7% for predicting a myocardial infarction. The specificity, positive predictive value, and negative predictive value of the ECGs were 89.9%, 17.9%, and 95.8%, respectively. CONCLUSIONS: Myocardial infarction in patients who have cocaine-associated chest pain is not uncommon. No clinical parameter available to the physician can adequately identify patients at very low risk for myocardial infarction. Therefore, all patients with cocaine-associated chest pain should be evaluated for myocardial infarction.

Patients with hepatitis C virus (HCV) infection have a greater risk of developing type 2 diabetes mellitus. However, the mechanism of this association is unclear. In this study, we examined the potential defects in upstream insulin signaling pathways in liver specimens obtained from nonobese/nondiabetic subjects with HCV infection. Fasting liver biopsy specimens were obtained from 42 HCV-infected subjects and 10 non-HCV-infected subjects matched for age and body mass index. Liver tissues were exposed to insulin and examined for the contents and phosphorylation/activation status of the upstream insulin signaling molecules by immunoprecipitation and Western blot analysis. HCV infection resulted in a trend toward a 2-fold to 3-fold increase in insulin receptor (IR) and insulin receptor substrate (IRS)-1 contents when compared with non-HCV. In contrast, insulin-stimulated IRS-1 tyrosine phosphorylation was decreased by 2-fold in HCV-infected subjects compared with non-HCV-infected subjects (P <.05). The observed reductions in IRS-1 tyrosine phosphorylation were accompanied by a 3.4-fold decrease in IRS-1/p85 phosphatidylinositol 3-kinase (PI3-kinase) association and a 2.5-fold decrease in IRS-1-associated PI3-kinase enzymatic activity (P <.05 vs. non-HCV). This was accompanied by a marked reduction in insulin-stimulated Akt phosphorylation without any alterations in mitogen-activated protein kinase (MAPK) phosphorylation. Cellular contents of the hepatic p85 subunit of PI3-kinase were comparable between HCV-infected and non-HCV-infected subjects. In conclusion, we found that (1). HCV infection leads to a postreceptor defect in IRS-1 association with the IR and (2). insulin signaling defects in hepatic IRS-1 tyrosine phosphorylation and PI3-kinase association/activation may contribute to insulin resistance, which leads to the development of type 2 diabetes mellitus in patients with HCV infection.

Fifty consecutive outpatients with stable chronic obstructive pulmonary disease were evaluated for lifetime prevalence of psychiatric morbidity. Eight percent had a diagnosis of panic disorder. This finding suggests that this patient population should be monitored for panic disorder.

Currently, accepted protocol which has been developed at the Prenatal Diagnosis Laboratory of New York City (PDL) requires that when a chromosome abnormality is found in one or more cells in one flask, another 20-40 cells must be examined from one or two additional flasks. Chromosome mosaicism is diagnosed only when an identical abnormality is detected in cells from two or more flasks. In a recent PDL series of 12,000 cases studied according to this protocol, we diagnosed 801 cases (6.68 per cent) of single-cell pseudomosaicism (SCPM), 126 cases (1.05 per cent) of multiple-cell pseudomosaicism (MCPM), and 24 cases (0.2 per cent) of true mosaicism. Pseudomosaicism (PM) involving a structural abnormality was a frequent finding (2/3 of SCPM and 3/5 of MCPM), with an unbalanced structural abnormality in 55 per cent of SCPM and 24 per cent of MCPM. We also reviewed all true mosaic cases (a total of 50) diagnosed in the first 22,000 PDL cases. Of these 50 cases, 23 were sex chromosome mosaics and 27 had autosomal mosaicism; 48 cases had numerical abnormalities and two had structural abnormalities. Twenty-five cases of mosaicism were diagnosed in the first 20 cells from two flasks, i.e., without additional work-up, whereas the other 25 cases required extensive work-up to establish a diagnosis (12 needed additional cell counts from the initial two culture flasks; 13 required harvesting a third flask for cell analysis). Our data plus review of other available data led us to conclude that rigorous efforts to diagnose true mosaicism have little impact in many instances, and therefore are not cost-effective. On the basis of all available data, a work-up for potential mosaicism involving a sex chromosome aneuploidy or structural abnormality should have less priority than a work-up for a common viable autosomal trisomy. We recommend revised guidelines for dealing with (1) a numerical versus a structural abnormality and (2) an autosomal versus a sex chromosome numerical aneuploidy. Emphasis should be placed on autosomes known to be associated with phenotypic abnormalities. These new guidelines, which cover both flask and in situ methods, should result in more effective prenatal cytogenetic diagnosis and reduced patient anxiety.

OBJECTIVE: Compare the accuracy and reliability of fetal heart rate identification from maternal abdominal fetal electrocardiogram signals (ECG) and Doppler ultrasound with a fetal scalp electrode. DESIGN: Prospective open method equivalence study. SETTING: Three urban teaching hospitals in the Northeast United States. SAMPLE: 75 women with normal pregnancies in labor at >37 weeks of gestation. METHODS: Three fetal heart rate detection methods were used simultaneously in 75 parturients. The fetal scalp electrode was the standard against which abdominal fetal ECG and ultrasound were judged. MAIN OUTCOME MEASURES: The positive percent agreement with the fetal scalp electrode indicated reliability. Bland-Altman analysis determined accuracy. The confusion rate indicated how frequently the devices tracked the maternal heart rate. RESULTS: Positive percent agreement was 81.7 and 73% for the abdominal fetal ECG and ultrasound, respectively (p = 0.002). The abdominal fetal ECG had a lower root mean square error than ultrasound (5.2 vs. 10.6 bpm, p < 0.001). The confusion rate for ultrasound was 20-fold higher than for abdominal ECG (8.9 vs. 0.4%, respectively, p < 0.001). CONCLUSION: Compared with the fetal scalp electrode, fetal heart rate detection using abdominal fetal ECG was more reliable and accurate than ultrasound, and abdominal fetal ECG was less likely than ultrasound to display the maternal heart rate in place of the fetal heart rate.

Co-occurring or associated psychiatric syndromes (APS) such as depression, obsessive-compulsive disorder (OCD), and panic disorder have largely been hidden from view by exclusion rules that prohibit their being diagnosed in the presence of schizophrenia. This article presents data from a clinical study of APS in chronic schizophrenia and reviews the relevant literature. Thirty-seven chronic schizophrenia patients consecutively admitted to a day program were administered the Structured Clinical Interview for Diagnosis for DSM-IV and the Yale-Brown Obsessive Compulsive Scale symptom checklist. Exclusion rules prohibiting the diagnosis of APS were bypassed. Eighteen patients (48.6%) had one or more APS. Ten patients (27%) had major depression. Eleven (29.7%) met criteria for OCD. Four patients (10.8%) met criteria for panic disorder. These findings suggest that APS may be common in chronic schizophrenia and that there is a need to study these syndromes' clinical validity, including their treatability. A research plan to study the validity of these syndromes further is discussed.

Objective. To examine the incidence of gout over the last 20 years and to evaluate possible changes in associated comorbid conditions. Methods. The medical records were reviewed of all adults with a diagnosis of incident gout in Olmsted County, Minnesota, USA, during 2 time periods (January 1, 1989–December 31, 1992, and January 1, 2009–December 31, 2010). Incident cases had to fulfill at least 1 of 3 criteria: the American Rheumatism Association 1977 preliminary criteria for gout, the Rome criteria, or the New York criteria. Results. A total of 158 patients with new-onset gout were identified during 1989–1992 and 271 patients during 2009–2010, yielding age- and sex-adjusted incidence rates of 66.6/100,000 (95% CI 55.9–77.4) in 1989–1992 and 136.7/100,000 (95% CI 120.4–153.1) in 2009–2010. The incidence rate ratio was 2.62 (95% CI 1.80–3.83). At the time of their first gout flare, patients diagnosed with gout in 2009–2010 had higher prevalence of comorbid conditions compared with 1989–1992, including hypertension (69% vs 54%), diabetes mellitus (25% vs 6%), renal disease (28% vs 11%), hyperlipidemia (61% vs 21%), and morbid obesity (body mass index ≥ 35 kg/m 2 ; 29% vs 10%). Conclusion. The incidence of gout has more than doubled over the recent 20 years. This increase together with the more frequent occurrence of comorbid conditions and cardiovascular risk factors represents a significant public health challenge.

To evaluate the potential teratogenicity and mutagenicity of modern cancer treatment, the authors enumerated from a cooperative clinical trial group 133 pregnancies in 66 women with malignant neoplasms (53% with Hodgkin's disease, 26% with other lymphomas and leukemia, and 21% with solid tumors). The gestations were divided into the following groups: Group 1, 43 pregnancies ending before therapy; Group 2, therapy given at conception or during 32 pregnancies; and Group 3, 58 pregnancies after therapy. Although the total frequencies of abnormalities were similar in Groups 1 and 2 (23% of 35 pregnancies not electively aborted and 28% of 25, respectively), there were slightly more elective abortions and birth defects related to radiation exposure at a susceptible time of gestation in Group 2. Still, there were eight normal infants among the ten fetuses who were liveborn and had first trimester exposure to chemotherapy alone; so, drug therapy early in pregnancy is not inevitably teratogenic. The apparent and surprising excess of abnormal outcomes in Group 3, 40% of 50 pregnancies, was due to low birth weight and premature terminations of pregnancy, rather than an excess of congenital anomalies. The type of unfavorable outcomes in Group 3 and their concentration in the first year posttherapy suggested they could represent defects in factors (e.g., uterine or hormonal) that normally maintain gestations, and not genetic damage to oocytes. Limitations of the data, collected by mail from physicians and their patients, included biases of self-reporting and low statistical power. Prospective study, probably through interinstitutional collaboration, seems necessary, if accurate estimates are to be made of the frequency of certain outcomes, such as spontaneous abortion and minor anomalies.

Risk factors were analyzed and searched for possible predictive parameters for the development of acute myeloid leukemia in 216 reported patients previously treated for Hodgkin's disease. The distribution of histologic subtypes and the stage at diagnosis were similar to that of all patients with Hodgkin's disease. Seventy-five percent of the 216 patients in whom acute myeloid leukemia developed had received both radiotherapy and chemotherapy, 15% chemotherapy only, and 10% radiotherapy only. Of those receiving radiotherapy, 66% were given multiple courses or total nodal irradiation. Of the patients receiving chemotherapy, 77% had received more than eight months of single or combination drug therapy; only 4% had not been exposed to alkylating agents. When acute leukemia developed, 78% of the patients showed no clinical or pathologic evidence of residual Hodgkin's disease. A period of pancytopenia preceded the onset of overt leukemia in at least one-third of the patients. Complete or partial remission of the acute leukemia was achieved in 25% of the patients treated with antileukemic chemotherapy. On the basis of these findings, it is deemed advisable to reexamine the intensity of treatment presently being administered to achieve cure of Hodgkin's disease. Unnecessary or unproved programs of combined radiation therapy and chemotherapy should be avoided. An optimal balance between the risks and benefits of treatment needs to be applied.

Breast cancer in African-American (AA) women occurs at an earlier age than in European-American (EA) women and is more likely to have aggressive features associated with poorer prognosis, such as high-grade and negative estrogen receptor (ER) status. The mechanisms underlying these differences are unknown. To address this, we conducted a case-control study to evaluate risk factors for high-grade ER- disease in both AA and EA women. With the onset of the Health Insurance Portability and Accountability Act of 1996, creative measures were needed to adapt case ascertainment and contact procedures to this new environment of patient privacy. In this paper, we report on our approach to establishing a multicenter study of breast cancer in New York and New Jersey, provide preliminary distributions of demographic and pathologic characteristics among case and control participants by race, and contrast participation rates by approaches to case ascertainment, with discussion of strengths and weaknesses.

Several studies have shown that gingivitis is common in children and adolescents. Introduction of orthodontic devices may exacerbate the gingival inflammation. Orthodontically induced gingival hyperplasia in adolescents, its etiology, and treatment alternatives are discussed. Three instances in which laser therapy was used are described.

Background Sudden unexpected death in epilepsy ( SUDEP ) is the leading cause of epilepsy‐related death. SUDEP shares many features with sudden cardiac death and sudden unexplained death in the young and may have a similar genetic contribution. We aim to systematically review the literature on the genetics of SUDEP . Methods and Results PubMed, MEDLINE Epub Ahead of Print, Ovid Medline In‐Process &amp; Other Non‐Indexed Citations, MEDLINE , EMBASE , Cochrane Database of Systematic Reviews, and Scopus were searched through April 4, 2017. English language human studies analyzing SUDEP for known sudden death, ion channel and arrhythmia‐related pathogenic variants, novel variant discovery, and copy number variant analyses were included. Aggregate descriptive statistics were generated; data were insufficient for meta‐analysis. A total of 8 studies with 161 unique individuals were included; mean was age 29.0 (± SD 14.2) years; 61% males; ECG data were reported in 7.5% of cases; 50.7% were found prone and 58% of deaths were nocturnal. Cause included all types of epilepsy. Antemortem diagnosis of Dravet syndrome and autism (with duplication of chromosome 15) was associated with 11% and 9% of cases. The most frequently detected known pathogenic variants at postmortem were in Na + and K + ion channel subunits, as were novel potentially pathogenic variants (11%). Overall, the majority of variants were of unknown significance. Analysis of copy number variant was insignificant. Conclusions SUDEP case adjudication and evaluation remains limited largely because of crucial missing data such as ECG s. The most frequent pathogenic/likely pathogenic variants identified by molecular autopsy are in ion channel or arrhythmia‐related genes, with an ≈11% discovery rate. Comprehensive postmortem examination should include examination of the heart and brain by specialized pathologists and blood storage.

The absorption of bile acids from the human large bowel was studied in eight patients. All patients had cholecystitis and cholelithiasis and had to undergo cholecystectomy. Cholic acid-(14)C was injected during surgery into the lumen of the cecum, hepatic flexure of the colon, or transverse colon in six patients, under the visual control of the surgeon. Common duct bile was collected by T tube daily for 5 days, and bile acids were extracted. Significant amounts of radioactivity appeared in T tube bile in each patient. T tube bile acids contained a total of 43.6-84.6% of the administered radioactivity; the average for the six patients was 58.9%. The majority of the tracer was excreted during the first 24 hr. In an additional patient cholic acid-(14)C was given in the form of an enema 5 days postoperatively. In this subject 30.8% of the retained radioactivity was excreted through the T-tube in 48 hr. The labeled cholic acid was recovered as both cholic and deoxycholic acid from T tube bile. Thin-layer chromatographic analysis of the bile acid samples indicated that the fraction of radioactivity recovered as deoxycholate increased with time during the postoperative period. Gas-liquid chromatographic analysis showed that the daily total quantity of excreted bile acids increased significantly from the 1st-5th days of the experiment. The amount of cholate excreted in T tube bile increased markedly with time, that of chenodeoxycholate increased moderately, and that of deoxycholate decreased sharply during the 5 days of the experiment. In three patients, injection of radiopaque material mixed with the tracer showed no evidence of regurgitation into the small bowel by serial X-rays. In an additional patient, tube aspirate from the terminal ileum contained no radioactivity. The results indicate that cholic acid is converted to deoxycholic acid in the human colon, and both of these bile acids are absorbed from the human large bowel in significant amounts. These data establish the previously unproved concept that significant absorption of bile acids takes place from the large bowel of man.

Acute myelocytic leukemia occurring many years after intensive radiotherapy and/or chemotherapy has been reported in 82 patients with Hodgkin's disease, 58 patients with multiple myeloma, and 40 patients with chronic lymphocytic leukemia. The precise incidence of this occurrence is uncertain, since the total number of patients at risk is unknown. Most patients with Hodgkin's disease had received intensive radiation therapy. Many also received chemotherapy. One-third of the patients with myeloma were treated only with melphalan. Acute leukemia may occur as part of the natural history of Hodgkin's disease and multiple myeloma; it has been seen with increasing frequency in recent years due to improved survival secondary to better treatment. It is also possible that radiotherapy and/or chemotherapy may be causally related to the development of acute leukemia.

Every eleventh adult has diabetes, and every third has prediabetes. Over 95% of diabetics are of type 2. It is well established that diabetes doubles the risk of heart disease and stroke apart from increasing the risk of microvascular complications. Hence, strict glycemic control is necessary. However, it increases the risk of hypoglycemia, especially in patients with longstanding diabetes. Continuous glucose monitors (CGM) use a sensor to continuously measure the glucose levels in the interstitial fluid every 10 seconds and gives out mean values every five minutes. CGMs are emerging tools in the management of type 2 diabetes. The prime objective of this review is to find out if there is enough supporting evidence, suggesting that continuous glucose monitoring is more effective than self-monitoring of blood glucose (SMBG) in type 2 diabetes. We conducted a systematic literature search in Medline (PubMed) looking for any studies addressing our objective. It is observed that there is a varying level of evidence supporting that employing a CGM can reduce glycated hemoglobin (HbA1c), hypoglycemic events, and increase patient satisfaction. However, some studies reported no significant benefits. This systematic review with meta-analysis concludes that the use of CGM in type 2 diabetes mellitus (T2DM) is beneficial, as it significantly reduces HbA1c compared to the usual method of SMBG. The pooled mean difference in HbA1c was -0.25 (-0.45, -0.06) and statistically significant (at p = 0.01) when comparing CGM to SMBG.

Female genital tract microbiota play a crucial role in maintaining health. Disequilibrium of the microbiota has been associated with increased risk of pelvic infections. In recent years, culture-independent molecular techniques have expanded understanding of the composition of genital microbiota and the dynamic nature of the microbiota. There is evidence that upper genital tract may not be sterile and may harbor microflora in the physiologic state. The isolation of bacterial vaginosis-associated organisms in women with genital infections establishes a link between pelvic infections and abnormal vaginal flora. With the understanding of the composition of the microbiota in healthy and diseased states, the next logical step is to identify the function of the newly identified microbes. This knowledge will further expand our understanding of the causation of pelvic infections, which may lead to more effective prevention and treatment strategies.

Medical errors occur and are sometimes unavoidable. Physicians generally, but not always, have ethical and moral obligations to disclose their errors to the patient. Because common medical errors can be expected, physicians are obligated to work within health systems toward reducing systems flaws that promote errors. However, the obligations of physicians to disclose errors made by others are less clear. This article discusses the professional ethics involved in disclosing and preventing medical errors.

Abstract Twenty‐four cases of breast cancer and acute leukemia and three cases of breast cancer and chronic myelocytic leukemia are reported. An additional 54 cases of acute leukemia and 13 cases of chronic myelocytic leukemia associated with breast cancer from the literature are reviewed. The mean interval between the diagnosis of breast cancer and the occurrence of acute leukemia is 6.9 years. In eight patients, the two diseases occurred simultaneously or within one year of each other. Four patients had acute lymphoblastic leukemia; the remainder had acute myelocytic leukemia or one of its variants. Seven patients received no postmastectomy radiotherapy or chemotherapy and the occurrence of acute leukemia between 1 and 23 years later cannot, therefore, be attributed to the therapy given for the breast cancer. Forty‐one patients received postoperative radiotherapy to the mastectomy site. Combination chemotherapy was administered to eight patients, five of whom were also treated with radiotherapy. Acute leukemia is estimated to occur in patients treated for breast cancer with a sevenfold increased frequency over the expected number. This may be due to an increased risk of a second neoplasm in patients with a primary tumor; alternatively, the acute leukemia may be related to the radiotherapy and/or chemotherapy administered to treat the breast cancer. Late death from leukemia after chemotherapeutic or radiotherapeutic remission of metastatic breast cancer is preferable to morbidity and/or early death from inadequately treated breast cancer.