The disappearing act: case of a migrating left renal vein stent.

INTRODUCTION: Nutcracker syndrome (NS) is a rare condition in which the abdominal aorta and superior mesenteric artery compress the left renal vein (LRV). One treatment option is the placement of an endovascular stent into the LRV, which carries the risk of stent migration. CASE REPORT: A 30-year-old female with NS status-post LRV stenting 6 months prior presented to the emergency department with suprapubic pain. An incidental finding on abdominal computed tomography scan noted interval removal of LRV stent, which had not been surgically removed. A subsequent chest radiograph showed the stent lodged in the left pulmonary artery. DISCUSSION: To our knowledge, this is the first documented case of LRV stent migration to the pulmonary artery. This case demonstrates the importance of physician awareness of stent migration as a potential complication after stent placement, and careful review of all imaging findings, even if unrelated to the chief complaint.

Racial disparities in access after regulatory surveillance of benzodiazepines.

BACKGROUND: We examined the effects of a prescription-monitoring program on benzodiazepine access among Medicaid enrollees living in neighborhoods of different racial composition. METHODS: We used interrupted time series and logistic regression to analyze data from noninstitutionalized persons aged 18 years or older (N = 124 867) enrolled continuously in New York Medicaid 12 months before and 24 months and 7 years after initiation of the program. We used census data to identify the racial composition of the neighborhoods. Outcome measures were nonproblematic use (short term, within dosing guidelines), potentially problematic use (>120 days' use or more than twice the recommended dose), and pharmacy hopping (filling prescriptions for the same benzodiazepine in different pharmacies within 7 days). RESULTS: There was a sudden, sustained reduction in benzodiazepine use in all the neighborhoods after the program's introduction. Despite the lowest rates of baseline use, enrollees in predominantly (> or = 75%) black neighborhoods experienced the highest rates of discontinuation after introduction of the program. This difference remained 7 years after policy initiation. Compared with white participants, black participants were more likely to discontinue nonproblematic (odds ratio, 1.78; 95% confidence interval, 1.47-2.17) and potentially problematic (odds ratio, 1.77; 95% confidence interval, 1.45-2.17) benzodiazepine use, after adjusting for sex, eligibility status, neighborhood poverty, and baseline use. The program almost completely eliminated pharmacy hopping in all racial groups, although less among white participants (82.6%) vs black participants (88.7%). CONCLUSIONS: A systematic benzodiazepine prescription-monitoring program reduced inappropriate prescribing, with a stronger effect in predominantly black neighborhoods despite lower baseline use. The policy may have resulted in an unintended decrease in nonproblematic use that disproportionately affects black populations.

Characterization of the 1918 influenza virus polymerase genes.

The influenza A viral heterotrimeric polymerase complex (PA, PB1, PB2) is known to be involved in many aspects of viral replication and to interact with host factors, thereby having a role in host specificity. The polymerase protein sequences from the 1918 human influenza virus differ from avian consensus sequences at only a small number of amino acids, consistent with the hypothesis that they were derived from an avian source shortly before the pandemic. However, when compared to avian sequences, the nucleotide sequences of the 1918 polymerase genes have more synonymous differences than expected, suggesting evolutionary distance from known avian strains. Here we present sequence and phylogenetic analyses of the complete genome of the 1918 influenza virus, and propose that the 1918 virus was not a reassortant virus (like those of the 1957 and 1968 pandemics), but more likely an entirely avian-like virus that adapted to humans. These data support prior phylogenetic studies suggesting that the 1918 virus was derived from an avian source. A total of ten amino acid changes in the polymerase proteins consistently differentiate the 1918 and subsequent human influenza virus sequences from avian virus sequences. Notably, a number of the same changes have been found in recently circulating, highly pathogenic H5N1 viruses that have caused illness and death in humans and are feared to be the precursors of a new influenza pandemic. The sequence changes identified here may be important in the adaptation of influenza viruses to humans.

Novel origin of the 1918 pandemic influenza virus nucleoprotein gene.

The nucleoprotein (NP) gene of the 1918 pandemic influenza A virus has been amplified and sequenced from archival material. The NP gene is known to be involved in many aspects of viral function and to interact with host proteins, thereby playing a role in host specificity. The 1918 NP amino acid sequence differs at only six amino acids from avian consensus sequences, consistent with reassortment from an avian source shortly before 1918. However, the nucleotide sequence of the 1918 NP gene has more than 170 differences from avian strain consensus sequences, suggesting substantial evolutionary distance from known avian strain sequences. Both the gene and protein sequences of the 1918 NP fall within the mammalian clade upon phylogenetic analysis. The evolutionary distance of the 1918 NP sequences from avian and mammalian strain sequences is examined, using several different parameters. The results suggest that the 1918 strain did not retain the previously circulating human NP. Nor is it likely to have obtained its NP by reassortment with an avian strain similar to those now characterized. The results are consistent with the existence of a currently unknown host for influenza, with an NP similar to current avian strain NPs at the amino acid level but with many synonymous nucleotide differences, suggesting evolutionary isolation from the currently characterized avian influenza virus gene pool.

Evidence of an absence: the genetic origins of the 1918 pandemic influenza virus.

Annual outbreaks of influenza A infection are an ongoing public health threat and novel influenza strains can periodically emerge to which humans have little immunity, resulting in devastating pandemics. The 1918 pandemic killed at least 40 million people worldwide and pandemics in 1957 and 1968 caused hundreds of thousands of deaths. The influenza A virus is capable of enormous genetic variation, both by continuous, gradual mutation and by reassortment of genome segments between viruses. Both the 1957 and 1968 pandemic strains are thought to have originated as reassortants in which one or both human-adapted viral surface proteins were replaced by proteins from avian influenza strains. Analyses of the genes of the 1918 pandemic virus, however, indicate that this strain might have had a different origin. The haemagglutinin and nucleoprotein genome segments in particular are unlikely to have come directly from an avian source that is similar to those that are currently being sequenced. Determining whether a pandemic influenza virus can emerge by different mechanisms will affect the scope and focus of surveillance and prevention efforts.

A controlled study of the effects of state surveillance on indicators of problematic and non-problematic benzodiazepine use in a Medicaid population.

OBJECTIVE: Benzodiazepines (BZs) are safe, effective drugs for treating anxiety, sleep, bipolar, and convulsive disorders, but concern is often expressed about their overuse and potential for abuse. We evaluated the effects of physician surveillance through a Triplicate Prescription Program (TPP) on problematic and non-problematic BZ use. METHOD: This study uses interrupted time series analyses of BZ use in the New York (intervention) and New Jersey (control) Medicaid programs for 12 months before and 24 months after the New York BZ TPP. The regulation required NY physicians to order BZs on triplicate prescription forms with one copy forwarded by pharmacies to a state surveillance unit. Study participants were community-dwelling persons over age 18 continuously enrolled between January 1988 and December 1990 in New York (n = 125,837) or New Jersey Medicaid (n = 139,405). RESULTS: During the baseline year, 20.2% of New York and 19.3% of New Jersey cohort members received at least one BZ prescription. After the TPP, there was a sudden, sustained reduction in BZ use of 54.8% (95% CI = [51.4%, 58.3%]) in New York with no changes in New Jersey. Significantly greater reductions were experienced by young women, and persons living in zip codes that were urban, predominantly Black, or with a high density of poor households. Increases in potential substitute medications were modest. At baseline, nearly 60% of BZ recipients had no evidence of potentially problematic use. Despite a somewhat greater likelihood of discontinuation of BZ therapy among those with potentially problematic use, the largest impact of the TPP was a substantially greater relative reduction in access to BZs among non-problematic users. CONCLUSIONS: State-mandated physician surveillance dramatically reduces BZ use with limited substitution of alternative drugs, lowers rates of possible abuse, but may severely limit non-problematic BZ use.

A retrospective data analysis of the impact of the New York triplicate prescription program on benzodiazepine use in medicaid patients with chronic psychiatric and neurologic disorders.

BACKGROUND: Benzodiazepines are treatment mainstays for several disorders, but there is often concern about dependency and addiction. In January 1989, New York implemented regulations requiring physicians to order benzodiazepines using state-monitored triplicate prescription forms. OBJECTIVE: The purpose of this study was to assess the effects of the triplicate prescription program (TPP) on changes in use of benzodiazepines and other psychoactive drugs in clinically vulnerable Medicaid populations. METHODS: Using an interrupted time series with comparison series design, psychoactive medication use was examined in the New York (intervention) and New Jersey (control) Medicaid programs before and after implementation of the New York benzodiazepine TPP among community-dwelling Medicaid beneficiaries aged >/=19 years continuously enrolled from January 1988 through December 1990 in New York or New Jersey with diagnoses of schizophrenia, schizophreniform disorder, schizoaffective disorder, schizoid personality disorder, or schizotypal personality disorder; bipolar disorder; epilepsy; and/or panic disorder, agoraphobia without history of panic disorder, social phobia, or specific phobia. RESULTS: A total of 125,837 New York and 139,405 New Jersey Medicaid beneficiaries were continuously enrolled and met the study inclusion criteria. Of these, there were 6054 Medicaid enrollees in New York and 6875 enrollees in New Jersey who were clinically vulnerable patients with >/=1 of the specified diagnoses. New York Medicaid patients with any of these diagnoses experienced a -48.1% relative change (95% CI, -50.0% to -46.2%) in benzodiazepine use at 6 months after TPP implementation, with no decline in use in New Jersey patients. The largest reduction in benzodiazepine use was seen among patients with seizure disorder (-59.9% at 6 months; 95% CI, -63.9% to -55.9%). Although use of substitute drugs increased slightly in New York after the TPP, it did not offset reductions in benzodiazepine use. The effects of TPP were sustained for 7 years of follow-up and had the greatest impact on nonproblematic benzodiazepine use. CONCLUSIONS: During the time period studied in this analysis, the New York TPP reduced benzodiazepine use among chronically ill patients for whom these agents represent effective treatment. Our findings suggest that many patients previously receiving benzodiazepines did not receive any pharmacologic intervention.

Effects of state surveillance on new post-hospitalization benzodiazepine use.

BACKGROUND: Benzodiazepines (BZD) effectively treat anxiety and insomnia accompanying major health events, including hospitalizations. Prescribing regulations to decrease BZD misuse may negatively impact therapeutic uses. OBJECTIVE: To assess the impact of a Triplicate Prescription Program (TPP) on initiation of post-hospitalization BZD prescribing, both overall and among cardiac and cancer patients in the United States. DESIGN: Interrupted time-series of post-hospitalization BZD dispensing events to enrollees in the US Medicaid program in the states of New York (intervention group) and New Jersey (control group), before and after implementation of a TPP. STUDY PARTICIPANTS: Community-dwelling Medicaid enrollees in New York State (n = 67 962) and New Jersey (n = 71 701), hospitalized between 1 January 1988 and 30 November 1990. INTERVENTION: The New York State TPP, implemented on 1 January 1989, requires physicians to prescribe BZD on triplicate prescription forms for state surveillance. OUTCOME MEASURES: Rates and duration of new post-hospitalization use of BZD and substitute medications. RESULTS: Overall, a sudden and sustained 63.5% decrease [95% confidence interval (CI) -58.6% to -68.3%] in new post-hospitalization BZD dispensing-from a baseline rate of 44 discharges with BZD dispensing per 1000 discharges per month-followed the TPP in New York State, without discontinuity in the control state. Patients hospitalized for acute ischemic cardiac events experienced a 72.5% reduction (95% CI -55.5% to -89.4%), and cancer patients a 69.4% reduction (95% CI -36.7% to -100.0%). The TPP did not preferentially reduce BZD use lasting >2 months. Increased substitute use did not offset reductions in BZD use. CONCLUSIONS: By decreasing new short-term post-hospitalization BZD use, the New York State TPP also had unintended effects.

Characterization of the 1918 "Spanish" influenza virus matrix gene segment.

The coding region of influenza A virus RNA segment 7 from the 1918 pandemic virus, consisting of the open reading frames of the two matrix genes M1 and M2, has been sequenced. While this segment is highly conserved among influenza virus strains, the 1918 sequence does not match any previously sequenced influenza virus strains. The 1918 sequence matches the consensus over the M1 RNA-binding domains and nuclear localization signal and the highly conserved transmembrane domain of M2. Amino acid changes that correlate with high yield and pathogenicity in animal models were not found in the 1918 strain. Phylogenetic analyses suggest that both genes were mammalian adapted and that the 1918 sequence is very similar to the common ancestor of all subsequent human and classical swine matrix segments. The 1918 sequence matches other mammalian strains at 4 amino acids in the extracellular domain of M2 that differ consistently between avian and mammalian strains, suggesting that the matrix segment may have been circulating in human strains for at least several years before 1918.

1917 avian influenza virus sequences suggest that the 1918 pandemic virus did not acquire its hemagglutinin directly from birds.

Wild waterfowl captured between 1915 and 1919 were tested for influenza A virus RNA. One bird, captured in 1917, was infected with a virus of the same hemagglutinin (HA) subtype as that of the 1918 pandemic virus. The 1917 HA is more closely related to that of modern avian viruses than it is to that of the pandemic virus, suggesting (i) that there was little drift in avian sequences over the past 85 years and (ii) that the 1918 pandemic virus did not acquire its HA directly from a bird.