OBJECTIVE -To estimate the global number of excess deaths due to diabetes in the year 2000.RESEARCH DESIGN AND METHODS -We used a computerized generic formal disease model (DisMod II), used by the World Health Organization to assess disease burden through modeling the relationships between incidence, prevalence, and disease-specific mortality. Baseline input data included population structure, age-and sex-specific estimates of diabetes prevalence, and available published estimates of relative risk of death for people with diabetes compared with people without diabetes. The results were validated with population-based observations and independent estimates of relative risk of death.RESULTS -The excess global mortality attributable to diabetes in the year 2000 was estimated to be 2.9 million deaths, equivalent to 5.2% of all deaths. Excess mortality attributable to diabetes accounted for 2-3% of deaths in poorest countries and over 8% in the U.S., Canada, and the Middle East. In people 35-64 years old, 6 -27% of deaths were attributable to diabetes.CONCLUSIONS -These are the first global estimates of mortality attributable to diabetes. Globally, diabetes is likely to be the fifth leading cause of death. Diabetes Care 28:2130 -2135, 2005D iabetes is a serious illness with multiple complications and premature mortality, accounting for at least 10% of total health care expenditure in many countries (1). However, routinely reported statistics based on death certification seriously underestimate mortality from diabetes (2), because individuals with diabetes most often die of cardiovascular and renal disease and not from a cause uniquely related to diabetes, such as ketoacidosis or hypoglycemia (3).Most international mortality statistics, including those published by the World Health Organization (WHO), are based solely on the "underlying cause of death" as recorded on the death certificate, even in the presence of other information. Complex methods have been developed for estimating cause-specific mortality for some conditions (AIDS, tuberculosis) but not for diabetes (4).Based on routine statistics, recent World Health Reports estimated mortality from diabetes in the world as 987,000 deaths for the year 2002 (5), which was 1.7% of total world mortality. There were estimated to be at least 170 million people with diabetes in the world in the year 2000 (6); therefore, mortality attributable to diabetes could be expected to be much higher, since diabetes is a serious and chronic condition. The aim of this study was to provide a more realistic estimate of the number of deaths attributable to diabetes. RESEARCH DESIGN AND METHODS Model and dataTo estimate the number of deaths attributable to diabetes in the year 2000, we used a software program, DisMod II, developed for the Global Burden of Disease 2000 study (7,8) and routinely used by WHO for disease estimates. The DisMod II disease model is that of a multistate life table that describes a single disease. There are two causes of death, from the disease and from "all othe...

Objective-To establish the relation between socioeconomic status and the agesex specific prevalence of type 1 and type 2 diabetes mellitus.

This large series suggests that the patients with classical pituitary apoplexy, who are without neuro-ophthalmic signs or exhibit mild and non-progressive signs, can be managed conservatively in the acute stage.

Alström syndrome (OMIM 203800) is an autosomal recessive disease, characterized by cone-rod retinal dystrophy, cardiomyopathy and type 2 diabetes mellitus, that has been mapped to chromosome 2p13 (refs 1-5). We have studied an individual with Alström syndrome carrying a familial balanced reciprocal chromosome translocation (46, XY,t(2;11)(p13;q21)mat) involving the previously implicated critical region. We postulated that this individual was a compound heterozygote, carrying one copy of a gene disrupted by the translocation and the other copy disrupted by an intragenic mutation. We mapped the 2p13 breakpoint on the maternal allele to a genomic fragment of 1.7 kb which contains exon 4 and the start of exon 5 of a newly discovered gene (ALMS1); we detected a frameshift mutation in the paternal copy of the gene. The 12.9-kb transcript of ALMS1 encodes a protein of 4,169 amino acids whose function is unknown. The protein contains a large tandem-repeat domain comprising 34 imperfect repetitions of 47 amino acids. We have detected six different mutations (two nonsense and four frameshift mutations causing premature stop codons) in seven families, confirming that ALMS1 is the gene underlying Alström syndrome. We believe that ALMS1 is the first human disease gene characterized by autosomal recessive inheritance to be identified as a result of a balanced reciprocal translocation.Alström syndrome was initially mapped to an interval of 6.1 cM between loci D2S286 and D2S327 (refs 3-5). Although several candidate genes have been investigated, no mutations have previously been identified [6][7][8] . We have shown that the 2p13 breakpoint in the individual with the 46,XY,t(2;11)(p13;q21)mat translocation is between these loci by metaphase fluorescence in situ hybridization (FISH) analysis using the BACs RP11-355F16 (containing D2S286) and RP11-480F1 (located 150 kb proximal to D2S327) as probes. The BAC RP11-582H21 crosses the translocation breakpoint (Fig. 1a,b) and is overlapped by RP11-79N18, which contains CCT7, a member of a chaperonin gene

OBJECTIVE -There is a lack of continuous longitudinal population-based data on lower extremity amputation (LEA) in the U.K. We present here accurate data on trends in diabetesrelated (DR) LEAs and non-DRLEAs in the South Tees area over a continuous 5-year period.RESEARCH DESIGN AND METHODS -All cases of LEA from 1 July 1995 to 30 June 2000 within the area were identified. Estimated ascertainment using capture-recapture analysis approached 100% for LEAs in the area. Data were collected longitudinally using the standard method of the Global Lower Extremity Amputation Study protocol.RESULTS -Over 5 years there were 454 LEAs (66.3% men) in the South Tees area, of which 223 were diabetes related (49.1%). Among individuals with diabetes, LEA rates went from 564.3 in the first year to 176.0 of 100,000 persons with diabetes in the fifth year. Over the same period, non-DRLEAs increased from 12.3 to 22.8 of 100,000 persons without diabetes. The relative risk of a person with diabetes undergoing an LEA went from being 46 times that of a person without diabetes to 7.7 at the end of the 5 years. The biggest improvement in LEA incidence was seen in the reduction of repeat major DRLEAs.CONCLUSIONS -Our data show that in the South Tees area at a time when major non-DRLEA rates increased, major DRLEA rates have fallen. These diverging trends mark a significant improvement in care for patients with diabetic foot disease as a result of better organized diabetes care.