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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients are described in whom arthritis following intestinal bypass surgery for obesity was associated with the presence of circulating immune complexes (CLC) and HLA B27. The arthritis was characteristically intermittent and controlled by low dose prednisone, indomethacin, and tetracycline therapy. The findings suggest that immune complexes play a role in the pathogenesis of arthritis associated with condition, and that perhaps the association with HLA B27 may predispose to the development of this complication.
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PMID:Intestinal bypass arthritis: association with circulating immune complexes and HLA B27. 14 52

Sixteen insulin dependent diabetic patients (age at onset less than 35 years) and their families were tissue typed for HLA antigens. Glucose tolerance of relatives was also tested. Among diabetic patients two HLA antigens were found with increased frequency: B8 (31 percent, control 15 percent) and Bw35 (38 percent, control 23 percent). Among normal relatives B8 and Bw35 had the same frequency as the control group. Bw15 frequency was not increased in either group. In relatives, no correlation between HLA antigens (B8 or Bw35) and abnormal glucose tolerance, obesity and over-weight at birth was found. Present data confirm previous reports of high B8 frequency in early onset diabetic patients, but fail to demonstrate a raised frequency of abnormal glucose tolerance among relatives bearing B8 (or, in our cases, Bw35). B8 may be considered a genetic indicator for susceptibility to juvenile diabetes. On the basis of present results in families, however non genetic factors clearly also play a determinant role. Furthermore, that diabetogenesis arises from a link between Ir-genes and HLA-B8 antigen should only be considered a suggestive hypothesis.
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PMID:HLA antigens and insulin dependent diabetes mellitus. A family study. 41 51

Human arterial hypertension is likely a multifactorial trait resulting from multiple measurable monogenes, blended polygenes, shared family environment, and individual environment. Familial aggregation of hypertension and familial correlation of blood pressure appears to be more due to genes than to shared family environment. Total genetic heritability of 80% with some recessive major gene effects have been found for several traits associated with hypertension including urinary kallikrein excretion, intraerythrocytic sodium, and sodium-lithium countertransport. Other interesting factors regarding hypertension genetics include: non-modulation of the renin angiotensin system, intralymphocytic sodium, ionized calcium, and several genetic markers such as haptoglobin, HLA, and MNS blood type. Probably the most clinically useful information regarding the genetics of hypertension is evolving in several studies reporting a strong association of hypertension with dyslipidemia, diabetes, and obesity.
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PMID:Genetics of hypertension: what we know and don't know. 220 56

The majority of patients with diabetes mellitus can be classified as suffering from either Type 1 or Type 2 diabetes. The pathogenetic pathways for these two categories of diabetes appear to be distinct and separate. Both forms of diabetes have a genetic as well as environmental component in their pathogenesis. Type 1 diabetes has a weaker genetic link; its association with HLA antigens is well established. Type 2 diabetes has a stronger genetic association but the exact gene or genes responsible is unknown. The environmental trigger in Type 1 diabetes may be a viral infection while urbanisation, obesity, physical inactivity and stress may trigger the development of Type 2 diabetes. Type 1 diabetes is a chronic autoimmune disease where beta cell destruction may occur over a number of years before clinical diabetes is diagnosed. Type 2 diabetes is the result of an interplay of relative insulin deficiency or a defect in insulin release together with insulin resistance. Hyperglycaemia perpetuates the problem of beta cell defect and insulin resistance. The understanding of pathogenesis of diabetes is the key to prevention and treatment of diabetes mellitus.
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PMID:Pathogenesis of type 1 and type 2 diabetes mellitus. 222 10

Hyperglycemia and other metabolic derangements resulting from absolute or functional deficiency of insulin are accompanied by typical signs and symptoms of diabetes. The clinical signs and the findings of hyperglycemia over 200 mg/dl should establish a diagnosis of diabetes mellitus. An oral glucose tolerance test (O-GTT) is rarely necessary for diagnosis of diabetes in a child. A small proportion of children, however, present less severe symptoms, and may require an O-GTT. Approximately 14% of IDDM children were in coma at diagnosis in Tokyo, and 11 onset deaths (0.94%) were observed among the 1172 newly diagnosed IDDM cases in Japan. A significant decline in the onset mortality, however, has been observed in the past 20 years in Japan in association with the improvement of early management of childhood diabetes. The clinical distinction of IDDM from NIDDM is often difficult in diabetic children of Oriental origin without obesity. Japanese IDDM can be divided into two forms, abrupt and slow onset forms, but they may be essentially the same disease. There was no difference in the frequency of being tested positive for circulating ICA between the two groups of the patients. But a difference in the frequency of HLA DR4 and DRW9 was noticed between the two groups. Clinical features of 107 children with NIDDM were studied and about 75% of these cases were obese. All of them can be detected by routine urinalysis for glucose. Diet and exercise therapy in most of the newly diagnosed patients resulted in remission but some of them may require insulin or an oral hypoglycemic agent to get better glycemic control.
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PMID:Initial signs and diagnosis of diabetes--special considerations of Oriental patients. 263 91

The importance of genetic factors in the aetiology of NIDDM has been underlined by study of family pedigrees and identical twin pairs. Although in some isolated populations and a tiny minority of Western families inheritance follows an autosomal dominant pattern, a polygenic mode of transmission predominates in Europe and North America. No genetic markers have been identified despite intensive study of the HLA system and gene polymorphisms. Environmental factors appear to play some role, but examination of the evidence for an aetiological effect of the commonly assumed factors, diet and obesity, suggests that they exert no direct effect. However, it is likely that these factors together with physical inactivity could modulate the speed of progression to symptomatic disease. Both beta cell dysfunction and tissue insulin insensitivity are important in producing the syndrome of NIDDM. Insulin insensitivity is present from very early in the time course of the syndrome, but it is clear that the disease cannot develop in the absence of beta cell dysfunction. The recent discovery of islet associated amyloid is exciting as it represents a major step in tracing the pathogenesis of NIDDM backwards towards genetic and non-genetic aetiological influences.
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PMID:Aetiology of non-insulin dependent diabetes. 267 75

The relationship between the HLA system and non-insulin-dependent diabetes mellitus (NIDDM) in South African Indians, a migrant Indian group, was evaluated by testing HLA-A, -B, and -C antigens in 184 patients and 1444 control subjects and HLA-DR antigens in 104 patients and 330 control subjects. There was a significant increase in the frequency of HLA-Bw61 in patients compared with control subjects (27.7 vs. 18%, P = .00155), although the degree of association was not very strong (relative risk 1.7). A similar association has been noted in Fiji Indians, another migrant Indian group. However, no relationship could be established at the DR locus. It is suggested that the relatively high frequency of the Bw61 allele in South African Indians could, in the presence of some environmental factor like obesity, confer increased susceptibility to NIDDM.
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PMID:HLA class I and II antigens in South African Indians with NIDDM. 338 81

In this report, we present an analysis of glucose and insulin responses during oral glucose tolerance tests in 369 siblings of Type 1 diabetic patients. All have been HLA typed at the A, B and C loci. Though most had normal glucose tolerance by National Diabetes Data Group criteria (92% of the males and 95% of the females), siblings who shared both HLA haplotypes with the diabetic patient in the family had higher mean 3-hour glucose areas than those who shared one or neither HLA haplotype (p less than 0.01). This difference was more marked in males and older siblings. Insulin concentrations did not differ significantly between the two groups except that, for those aged less than 16 years, the group sharing both haplotypes had lower fasting insulin concentrations (p = 0.05); for 16-29 year olds, the corresponding group had marginally higher 3-hour insulin areas than the remainder of siblings (p = 0.17). Little association with specific haplotypes (A1B8 or A2B15) was seen. Multivariate analyses, adjusting for age and obesity, eliminated the 3-h glucose difference in females by HLA sharing status (p = 0.37) although in males it remained significant (p less than 0.001). Failure to account for age, sex and obesity may explain some of the conflicts in the reported literature. The glucose tolerance differences seen by HLA haplotype sharing status did not correlate with the presence of anti-islet cell antibodies. These results are consistent with the hypothesis that the HLA identical siblings, particularly males, have different (i.e. worse) glucose tolerance than their haploidentical and non-HLA identical siblings.
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PMID:Glucose tolerance in siblings of type 1 diabetic patients: relationship to HLA status. 351 42

To elucidate the relationship between endometrial carcinoma and the constitution, HLA antigen typing (A-locus, 13; B-locus, 20; C-locus, 6; DR-locus, 9) was investigated in 74 patients with endometrial carcinoma. A significant increase in two HLA antigens, Cw7 and DRw8, was demonstrated, but there was no intimate correlation between Cw7 or DRw8 and the three complications commonly associated with endometrial carcinoma--diabetes mellitus, obesity, and hypertensive disease. On the basis of these results, a new classification of endometrial carcinoma was proposed as follows: type A is positive Cw7 or DRw8 group; type B is negative for Cw7 and DRw8 and positive for the complications mentioned; type C is negative for Cw7 and DRw8, negative for the complications mentioned, and positive for DR 5; type D is a non-A, non-B, and non-C type.
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PMID:Human leukocyte antigen associated with endometrial carcinoma with a new classification of endometrial carcinoma based on its etiology. 361 92

Three adult sisters with previously unrecognized Prader-Willi syndrome (PWS) demonstrated the six diagnostic features of this congenital condition: neonatal hypotonia, hypomentia, hypogonadism, obesity, short stature, and dysmorphism. Detailed endocrine investigations were performed, including ovarian biopsy in the propositus. HLA genotype A2 was present in each patient. The normal high-resolution prometaphase karyotypes indicated heterogeneity; the absence of the deletion 15q12 frequently found in patients with sporadic PWS distinguished this sibship as representing a possible autosomal recessive type of PWS. Current evidence suggests that the diagnosis of PWS may be often overlooked. Increased clinical awareness of the features of PWS should result in prompt diagnosis and optimal management of affected patients, together with increased understanding of this enigmatic condition.
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PMID:Familial Prader-Willi syndrome. 382 55


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