Disease Subcategories Research Articles

The validity of death certificates: routine validation of death certification and its effects on mortality statistics

The 3478 death certificates (7.1% of all annual death certificates) of this study comprise those national death certificates in 1995 submitted for validation to the panel representing both medical and nosological expertise. As such, it is highly selected and represents, from the nosological point of view, the most inconsistently filled-in portion of Finnish death certificates. The routine validation procedure is essentially based on exploitation of the extra medical information, i.e. the case history, on the Finnish death certificate form. Altogether, 2813 (80.9%) out of 3478 certificates could be adjusted at the primary panel session; the rest required further clarification. The re-assignment of cause of death by the panel and the impact of panel adjustments on the national mortality statistics is assessed here by comparing the initial death certification and the finally registered underlying cause of death grouped into ICD-9 major categories with special reference to the subcategories of neoplasm, cardiovascular disease (HVD) and unnatural death. A statistically significant decline ( p<0.0001) in deaths, both in the category of symptoms, signs and ill-defined conditions and in the pulmonary circulation disease subcategory of HVD with 37.6 and 35.1%, respectively, was observed. The decrease of 11.1% in the benign or NUD neoplasm subcategory and the increase of 8.6 and 7.0% in the categories of endocrine disease, and musculo-skeletal and connective tissue disease, respectively, are essential observations as to the quality of the cause of death register. The effect on the HVD major category was practically nil. At the HVD-subcategorial level, a decrease of 14.0% for diseases of the veins and lymphatics and other circulatory diseases and an increase of 3.5% for hypertensive diseases (HYP) were the two next most obvious alterations to the diseases of the pulmonary circulation, but were without statistical significance. For ischaemic heart disease and other subcategories, the effects were minor. The unnatural deaths as a whole increased in the final statistics with only 0.9%. In the study data, categorial changes ranged from the decrease of 75.2% for symptoms, signs and ill-defined conditions to the increase of 77.3% for endocrine diseases. In conclusion, the Finnish death certificate form, death certification practices and cause of death validation procedure seem to serve the coding of causes of death for mortality statistics appropriately. The results of the study form a relevant reference background to evaluation of epidemiological studies on mortality.

New markers for cardiovascular disease

Meanwhile, in a search for genetic markers for MI, scientists at INSERM Unit 258 (Paris, France) have found a gene that appears to protect against CHD. Stefann-Martin Herrmann and colleagues focused their attention on P-selectin, an adhesion molecule that is expressed at the surface of endothelial cells. P-selectin plays a role in inflammation but is also known to be involved in the initiation of atherosclerotic plaque formation.In a search for P-selectin polymorphisms in 647 MI patients and 758 healthy controls from France and Northern Ireland (the ECTIM study), they identified 13 variants of the P-selectin gene and found that one variant, Pro715, is more common in healthy people than in MI patients [Herrmann, S-M. et al. (1998) Hum. Mol. Genet. 7, 1277–1284]. How this polymorphism alters the properties of P-selectin remains to be established experimentally.Dr Francois Cambien, senior author of the study, explains why, despite these encouraging results, genetic screening for CHD is some way off: `The major markers of heart attack are not genetic ones. There are two important points to consider: first, we may have explored less than one tenth of the genes related to the risk of heart attack and, second, conventional risk factors are related to broad class of diseases whereas genetic risk factors are more likely to be related to sub-categories of disease. Therefore, clinical sub-entities will have to be defined if we really want to investigate the impact of genetic risk factors.'

The seasonality of schizophrenic births in Barbados

There is growing evidence suggesting that extreme temperatures have an impact on mental disorders. We aimed to explore the effect of extreme temperatures on emergency room (ER) visits for mental health disorders using 2.8 million records from New York State, USA (2009–2016), and to examine potential effect modifications by individuals' age, sex, and race/ethnicity through a stratified analysis to determine if certain populations are more susceptible.To assess the short-term impact of daily average temperature on ER visits related to mental disorders, we applied a quasi-Poisson generalized linear model combined with a distributed lag non-linear model (DLNM). The model was adjusted for day of the week, precipitation, as well as long-term and seasonal time trends. We also conducted a meta-analysis to pool the region-specific risk estimates and construct the overall cumulative exposure-response curves for all regions.We found positive associations between short-term exposure to extreme heat (27.07 ∘C) and increased ER visits for total mental disorders, as well as substance abuse, mood and anxiety disorders, schizophrenia, and dementia. We did not find any statistically significant difference among any subgroups of the population being more susceptible to extreme heat than any other.Our findings suggest that there is a positive association between short-term exposure to extreme heat and increased ER visits for total mental disorders. This extreme effect was also found across all sub-categories of mental disease, although further research is needed to confirm our finding for specific mental disorders, such as dementia, which accounted for less than 1% of the total mental disorders in this sample.

Mast cell distribution and neutral protease expression in acute and chronic allergic conjunctivitis

Allergic eye disease has a variety of clinical manifestations including seasonal atopic conjunctivitis (SAC), perennial atopic conjunctivitis (PAC), atopic keratoconjunctivitis (AKC), and atopic blepharoconjunctivitis (ABC). We have investigated the number, distribution and protease expression of mast cells in normal and diseased conjunctiva with the use of immunohistochemistry in water-miscible resin sections. The median mast cell densities in normal subjects were 17 mm-2 in the bulbar substantia propria and 9 mm-2 in tarsal substantia propria. Mast cells were absent from the normal conjunctival epithelium at both sites. Mast cell densities were increased in the bulbar substantia propria in SAC, AKC and ABC. Tarsal substantia propria showed a significant increase in mast cells in ABC and AKC disease states. Mast cells express a range of proteases which varies according to their anatomic site. Mast cells in connective tissue are described to contain tryptase, chymase, cathepsin-G and carboxypeptidase-A, whereas mucosal mast cells contain only tryptase. In the diseased conjunctiva there was a marked reduction in proteases other than tryptase in the intraepithelial mast cells. There were also significant reductions in protease expression other than tryptase in the bulbar substantia propria in AKC and ABC. There appear to be specific alterations in the distribution of mast cells in the sub-categories of allergic eye disease. The distinction between mucosal and connective tissue mast cell phenotypes is not clear-cut and may depend on the functional state of the mast cells in relation to the microenvironment.

Clinical correlates of distinct immunophenotypic and histologic subcategories of lymphocyte-predominance Hodgkin's disease.

Histologic and paraffin immunohistologic studies were carried out on 32 patients with lymphocyte-predominance Hodgkin's disease (LPHD) seen from 1970 through 1982. While nodular histology was accurately predictive of B-cell phenotype (Leu M1 -/L26+), diffuse histology corresponded to either B-cell or Hodgkin's (Leu M1 +/L26-) phenotype, not invariably predictable even when attention was paid to subtle paragranuloma cytology. Clinical characteristics were compared between histologic (diffuse v nodular) and immunophenotypic (Leu M1 +/L26-, Hodgkin's phenotype, v Leu M1 -/L26+, B-cell phenotype) subgroups. Ten patients have since died, and the median follow-up of the living patients was 14 years (range, 6 to 31). Of the several clinical parameters compared, only axillary nodal presentation was strongly associated with both B-cell phenotype and nodular histology, while male predominance related more to B-cell phenotype than nodular histology. No significant difference in overall survival or relapse rate was apparent among either the histologic or the immunophenotypic subgroups. However, very late but salvageable relapses were associated with nodular histology. The incidences of secondary malignancies and death from Hodgkin's disease (HD) were also comparable between the subgroups. Although difference in clinical presentation may exist, neither the histologic nor the immunophenotypic subcategories of LPHD could be demonstrated to correlate with differences in clinical outcome.

Death certification and coding for ischemic heart disease in Australia.

Trends in ischemic heart disease mortality are of current interest because death rates have declined rapidly in the United States, Australia, and some other countries during the last decade, although they have risen elsewhere. There is a need to assess the quality of the data from which such trends are calculated and to consider what information will be required to monitor accurately future patterns of incidence and mortality for this disease. This paper describes two investigations of routinely collected mortality data for ischemic heart disease in Australia. First, information obtained from a heart attack surveillance study was compared with officially recorded causes of death for a defined population during 1979. Second, mortality trends from 1969 to 1978 were compared between the major Australian states. Both studies showed that mortality data were accurate to within about 10%. However, for acute myocardial infarction and other subcategories of ischemic heart disease, the data were neither valid nor reliable. New diagnostic and coding practices are required before it will be possible to monitor accurately long-term trends in subcategories of ischemic heart disease.