Understanding the Burden of Tuberculosis Among American Indians/Alaska Natives in the U.S.: A Validation Study

Objective

We validated cases of active tuberculosis (TB) recorded in the Indian Health Service (IHS) National Patient Information Reporting System (NPIRS) and evaluated the completeness of TB case reporting from IHS facilities to state health departments.

Methods

We reviewed the medical records of American Indian/Alaska Native (AI/AN) patients at IHS health facilities who were classified as having active TB using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnostic codes from 2006 to 2009 for clinical and laboratory evidence of TB disease. Individuals were reclassified as having active TB disease; recent latent TB infection (LTBI); past positive tuberculin skin test (TST) only; or as having no evidence of TB, LTBI, or a past positive TST. We compared validated active TB cases with corresponding state records to determine if they were reported.

Results

The study included 596 patients with active TB as per ICD-9-CM codes. Based on chart review, 111 (18.6%) had active TB; 156 (26.2%) had LTBI; 104 (17.4%) had a past positive TST; and 221 (37.1%) had no evidence of TB disease, LTBI, or a past positive TST. Of the 111 confirmed cases of active TB, 89 (80.2%) resided in participating states; 81 of 89 (91.2%) were verified as reported TB cases.

Conclusions

ICD-9-CM codes for active TB disease in the IHS NPIRS do not accurately reflect the burden of TB among AI/ANs. Most confirmed active TB cases in the IHS health system were reported to the state; the national TB surveillance system may accurately represent the burden of TB in the AI/AN population.Tuberculosis (TB) is a bacterial infection caused by Mycobacterium tuberculosis (M. tuberculosis) complex. Treatment for active TB disease requires months of combination drug therapy. Left untreated, TB can result in substantial morbidity and occasionally death. Although the number of TB cases in the United States has steadily declined during the past two decades, TB remains a major health concern within many subgroups, including American Indians/Alaska Natives (AI/ANs). The TB case rate among AI/ANs is estimated at 5.6 per 100,000 population, notably higher than the national average of 3.4 cases per 100,000 population.¹Surveillance of active TB disease is an important component of monitoring and controlling the spread of TB. Currently, annual rates of TB in the U.S. are calculated by the Centers for Disease Control and Prevention (CDC) National Tuberculosis Surveillance System (NTSS).¹ The NTSS is an electronic database that relies on the collaboration of state and local health departments; each person diagnosed with TB disease is verified as an incident case of TB and reported using a standard TB case form. The criteria for TB disease surveillance are based on a laboratory case definition, clinical case definition, or provider diagnosis.^1,2 The laboratory case definition requires isolation of M. tuberculosis complex in culture or detection of M. tuberculosis complex nucleic acids by amplification testing or demonstration of acid-fast bacilli in a clinical specimen when a culture cannot be obtained. The clinical case definition requires (1) a positive tuberculin skin test (TST), (2) signs and symptoms compatible with TB, (3) treatment with at least two anti-TB medications, and (4) a completed diagnostic evaluation. A provider diagnosis is used when the clinical presentation is consistent with TB but the criteria to meet laboratory or clinical case definitions are not met.The Indian Health Service (IHS), an agency of the U.S. Department of Health and Human Services, provides comprehensive health-care services through IHS, Tribal, and Urban Indian facilities (collectively referred to hereafter as IHS) to eligible AI/AN people who are members of 566 federally recognized Tribes. IHS provides care for approximately 2.1 million (62%) of the nation''s estimated 3.4 million AI/ANs.³ The IHS maintains a national database, the National Patient Information Reporting System (NPIRS).⁴ Within NPIRS, diseases and conditions are coded according to the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM).⁵ In addition, IHS is in the process of implementing an electronic health record (EHR) system.⁶ Electronic data collected by IHS have the potential to serve as a resource to better understand the burden and monitor trends of TB disease within the AI/AN population; yet, the accuracy of NPIRS for identifying people with TB disease has not been previously established. Several previous studies in other U.S. populations have cited wide variability (0%–77%) in the positive predictive value (PPV) of ICD-9-CM diagnostic codes for active TB disease.^7–13CDC provides guidance for IHS providers to report all nationally notifiable diseases, including TB, to local and state authorites.^1,2 However, there are no explicit mechanisms for IHS to report cases of TB directly to the NTSS, and the extent to which IHS facilities collaborate with local authorities on case reporting is not well understood.We validated active cases of TB disease within the AI/AN population by reviewing the medical charts of individuals assigned an active TB disease ICD-9-CM code in the inpatient and outpatient NPIRS visit data from 2006 to 2009 to determine the completeness of reporting TB disease by examining whether validated TB cases from IHS facilities were reported to state health departments.     

The relationship between <Emphasis Type="Italic">ACE</Emphasis> genotype and risk of severe hypoglycaemia in a large population-based cohort of children and adolescents with type 1 diabetes

Aims/hypothesis Genetic factors may account for familial clustering related to diabetes complications. Studies have shown a significant relationship between the presence of the deletion (D) allele of the gene encoding ACE and risk of severe hypoglycaemia. This large prospective cohort study assesses this relationship in a large sample of children and adolescents with type 1 diabetes. Subjects and methods We studied 585 children and adolescents (mean age 11.9 ± 4 years, 48.4% males). The frequency of severe hypoglycaemia (an event leading to loss of consciousness or seizure) was prospectively assessed over the 13-year period 1992–2004. Patients were seen with their parents every 3 months and data recorded at each visit. The ACE gene was detected using PCR. Results In our cohort of 585 children, 186 (31.8%) had at least one episode of severe hypoglycaemia, and of these 28.0% had the II genotype, 48.9% had the ID genotype and 23.1% had the DD genotype. This was in agreement with the Hardy–Weinberg proportion. A total of 477 severe hypoglycaemic episodes was recorded with a total of 3,404 person-years of follow-up, giving a total incidence of 14 per 100 patient-years. No significant increase in risk for DD genotype (incidence rate ratio = 0.97, 95% CI 0.61–1.55) relative to II genotype was observed. Conclusions/interpretation This large prospective study concludes that the presence of the D allele of the ACE gene does not predict a significantly higher risk of severe hypoglycaemia in type 1 diabetic children and adolescents.     

THE INFLUENCE OF NITROGEN RETENTION UPON THE REGENERATION OF PLASMA PROTEINS

1. Because of the clinical observation that the capacity to form new plasma proteins is sometimes impaired in cases of nephritis (2), experiments were performed to determine whether the impaired function in the nephritic is related to nitrogen retention. 2. These experiments consisted of producing renal injury by injecting uranium nitrate into standard hypoproteinemic dogs and comparing the rate of blood plasma protein formation under these conditions of nitrogen retention with that in the uninjured dog. 3. Despite elevations in blood N.P.N. to more than ten times normal, no interference with plasma protein formation was observed. These elevations in N.P.N. affected principally the urea and undetermined fractions. 4. Neither elevation in N.P.N. nor proteinuria per se appears to have any effect upon plasma protein production. Possibly the deficient production of plasma proteins in the nephritic is related to a more general disturbance in metabolism in which the elevation in N.P.N. is secondary.     

Modulation of Kupffer cell membrane phospholipid function by n-3 polyunsaturated fatty acids

Dietary n-3 polyunsaturated fatty acids (PUFAs) have been reported to improve clinical outcome in a number of inflammatory diseases including burns and sepsis. One mechanism contributing to the anti-inflammatory effect is the incorporation of n-3 PUFAs into membrane phospholipids which decreases macrophage eicosanoid production. We hypothesize that an additional mechanism for their effects is an alteration of membrane signal transduction that decreases macrophage responsiveness to inflammatory stimuli. Kupffer cells, the fixed macrophages of the liver, were obtained from rats pair fed diets for 6 weeks with 15% of calories supplied as menhaden (high n-3), corn (control), or safflower (high n-6) oils. The effects of the dietary oils on Kupffer cell membrane signal transduction and eicosanoid production were assessed by measuring inositol phospholipid (PI) metabolism, intracellular calcium responses, and prostaglandin E2 (PGE2) production to the inflammatory signals endotoxin (LPS) and platelet activating factor (PAF). The menhaden oil diet resulted in significant incorporation of n-3 PUFAs into total cellular PUFAs compared to corn and safflower oil. (total n-3 PUFAs, 28.1% menhaden vs 2.1% corn vs 1.2% safflower, P less than 0.03). This incorporation altered signal transduction of PAF as both PI turnover (65% +/- 10% of corn oil) and calcium response (0.6-fold vs 5.0-fold for corn oil) were significantly reduced in the menhaden oil group. (P less than 0.05) The menhaden oil diet also reduced significantly PGE2 production in response to PAF and LPS (corn, 348 +/- 23 pg/ml; menhaden, 48 +/- 6 pg/ml, P less than 0.01). We conclude that, in addition to modulating eicosanoid production, n-3 PUFAs can also alter macrophage membrane signal transduction.(ABSTRACT TRUNCATED AT 250 WORDS)     

A Comparison of Mental Health Hospital Admissions in a Cohort of Heroin Users Prior to and After Rapid Opiate Detoxification and Oral Naltrexone Maintenance

Mental health (MH) hospital admissions were investigated in a cohort (N = 1184) of heroin dependent persons using linked health records. All MH in-patient admissions were extracted 36 months before to 36 months after commencing rapid opioid detoxification (ROD) and oral naltrexone. Results show that the incidence rate ratio (IRR) of drug-related and other MH admissions peaked in the 3 months immediately prior to treatment. All categories subsequently declined to baseline levels by 36 months following treatment. The authors conclude that treatment for heroin dependence reduces risk of MH admissions.     

Acute Stress and Cardiovascular Health: Is There an ACE Gene Connection?

Cardiovascular disorders (CVD) are associated with acute and posttraumatic stress responses, yet biological processes underlying this association are poorly understood. This study examined whether renin‐angiotensin‐aldosterone system activity, as indicated by a functional single nucleotide polymorphism (SNP) in the angiotensin converting enzyme (ACE) gene, is associated with both CVD and acute stress related to the September 11, 2001 (9/11) terrorist attacks. European‐American respondents (N = 527) from a nationally representative longitudinal study of coping following 9/11 provided saliva for genotyping. Respondents had completed health surveys before 9/11 and annually for 3 years after, and acute stress assessments 9 to 23 days after 9/11. Respondents with rs4291 AA or TT genotypes reported high acute stress twice as often as those with the AT genotype. Individuals with the TT genotype were 43% more likely to report increased physician‐diagnosed CVD over 3 years following 9/11, when the following variables were included in the model: (a) pre‐9/11 CVD, mental health, and non‐CVD ailments; (b) cardiac risk factors; (c) ongoing endocrine disorders; and (d) significant demographics. The ACE rs4291 TT genotype, which has been associated with HPA axis hyperactivity and higher levels of serum angiotensin converting enzyme (ACE), predicted acute stress response and reports of physician‐diagnosed CVD in a national sample following collective stress. ACE gene function may be associated with both mental and physical health disorders following collective stress.     

Aortic dissection, patent ductus arteriosus, iris hypoplasia and brachytelephalangy in a male adolescent.

We describe a 14-year-old male with dissection of the descending aorta, bilateral iris hypoplasia, striae distensae and brachytelephalangy, the latter being most marked in the thumbs. Inguinal herniae and a patent ductus arteriosus were surgically repaired in infancy. The pattern of abnormalities may constitute a previously undescribed syndrome. The proband died suddenly at the age of 17 years.