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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Due to new methods, including genic recombination, four anti-influenza vaccines are now available: whole inactivated virus vaccine; surface antigen (sub-unit); disrupted virus (split virus); live attenuated virus (used only in the USSR). The safest vaccine at the present time is the split vaccine, as it has been used on large populations (including children) for many years in Japan. Moreover, this is the only vaccine used in the USA on children (over three years of age). Systemic side effects of the split vaccine are exceptional (1 case in 5 million of subjects vaccinated) while local redness or fever are relatively more frequent. The following considerations make vaccination advisable in paediatrics: the increase in number of inpatients with respiratory and other diseases (e.g. febrile convulsions) during influenza epidemics; influenza is a diffuse and highly contagious disease which spreads in the population from children to adults. The split vaccine is not available in Italy, therefore vaccination in our country is limited to children at high risk for influenza related complications. As well as subjects aged over 65, the following children especially need to be vaccinated: patients with chronic disorders of cardiovascular and pulmonary systems (chronic asthma, cystic fibrosis, pulmonary disease due to inhalation) and some metabolic diseases such as diabetes mellitus or Addison's disease.
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PMID:[Anti-influenza vaccination in children]. 391 45

The clinical course of eight boys and six girls with Addison's disease has been reviewed. Adrenal antibodies were found in five boys and five girls, and four children showed clinical evidence of other autoimmune disease (hypoparathyroidism (three); diabetes (one)). The presentation was insidious in 12 children but acute in two. On treatment, linear growth was normal and, with the exception of one girl with theca cell antibodies, pubertal development proceeded normally in the older patients.
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PMID:Clinical presentation, growth, and pubertal development in Addison's disease. 406 44

Long-term ambulatory continuous subcutaneous insulin infusion was undertaken under serial blood-glucose control in nine insulin-dependent diabetics. Before this treatment was started, haemoglobin A1 was increased (more than 13%), diabetic lipoid necrosis was present in three, proliferative diabetic retinopathy in one, treatment-resistant Candida oesophagitis in one and Addison's disease in one. During the total of 630 weeks (range 6-135 weeks) of continuous subcutaneous insulin infusion it was found that (1) the metabolic state of the patients improved significantly, the previously non-responding oesophagitis healed and one of three patients with diabetic lipoid necrosis was markedly improved; (2) the risks of insulin treatment, hypoglycaemia (especially with Addison's disease) and keto-acidosis (for technical reasons) remained; and (3) in long-standing diabetes of type I even good control of blood glucose levels (mean 113 mg/dl) could neither prevent the occurrence of proliferative diabetic retinopathy nor loss of sight.
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PMID:[Continuous subcutaneous insulin infusion: long-term treatment in an unselected group of insulin-dependent diabetics]. 640 20

Selective hypoaldosteronism is defined as diminished production of aldosterone, and sometimes also of 18-hydroxycorticosterone, with otherwise intact adrenal function. A decrease in the secretion of potassium and H+-ions and in the reabsorption of sodium in the distal nephron may result and lead to hyperkalemia, hyperchloremic acidosis, and impaired renal sodium conservation. The form of hypoaldosteronism which occurs in the adult is characterized by the following additional features: the aldosterone deficiency is due in the majority of cases to a decrease in enzymatically active plasma renin ("hyporeninemic hypoaldosteronism"), while various endogenous mechanisms as well as certain drugs (prostaglandin inhibitors, beta-blockers) may contribute. Other disturbances of the renin-angiotensin system (e.g. during treatment with converting-enzyme inhibitors) may rarely be responsible. Abnormalities in adrenal cortical synthesis may sometimes coexist, but proof that adrenal enzymatic defects play a primary pathogenic role in selective hyperaldosteronism in the adult is lacking. Such patients are frequently older (greater than 50 years), and often have diabetes mellitus and/or nephropathy (diabetic, interstitial, or hydronephrosis). Hyperkalemia and acidosis tend particularly to develop in association with mild to moderate impairment of renal function. The differential diagnosis should include other causes of impaired renal potassium secretion (Addison's disease, renal resistance to mineralocorticoids, potassium-sparing diuretics). Moreover, possible extrarenal factors contributing to hyperkalemia (oral potassium intake and redistribution of intracellular/extracellular space, particularly with associated insulin deficiency) should also be considered. For treatment, dietary potassium restriction is recommended as a general step. Replacement with the mineralocorticoid fludrocortisone acetate usually reverses the hyperkalemia and acidosis, but may sometimes induce sodium retention and hypertension. Loop diuretics, potassium-exchanging preparations and/or bicarbonate may also be useful as alternatives or additives.
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PMID:[Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia]. 675 13

Two cases of Addison's disease, two cases of scleroderma, three cases of primary hypothyroidism possibly due to Hashimoto's thyroiditis, three cases of diabetes mellitus, and two cases of ovarian failure and secondary amenorrhoea were diagnosed in a single family. In 44 members of four generations of the family including all the diseased, we have performed HLA typing and measurement of circulating autoantibodies. All diseased patients were older than 12 years, all possessed HLA B8 antigen, and all but two showed specific autoantibodies in their serum. In contrast, none of the family members without HLA B8 developed any of the autoimmune diseases in spite of the fact that in 13 of them some circulating autoantibodies were demonstrable in the serum. It is concluded that genetic factors play an essential role in the development of autoimmunity in the studied family. The individuals acquire circulating autoantibodies as they develop the disease. Environmental factors play a secondary role as evident from the age dependence. HLA typing can become an important diagnostic tool in identifying the individuals at a risk of autoimmune disease. Detection of circulating serum autoantibodies alone correlated poorly with the autoimmune disease.
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PMID:Correlation of the HLA-A1,B8 haplotypes with circulating autoantibodies in a family with increased incidence of autoimmune disease. 698 Dec 77

To establish the frequency and clinical and biochemical characteristics of hyporeninemic hypoaldosteronism (HH), we reviewed 100 consecutive cases of hyperkalemia (potassium content > 5.3 mEq/L). The most common cause was end-stage renal failure (34%). Other causes included overzealous potassium replacement, spironolactone therapy, hemolysis, acute renal failure, acidosis, thrombocytosis, and Addison's disease. Ten of 19 patients with unexplained hyperkalemia showed suppressed renin (0.12 to 1.3 ng/mL/hr) and aldosterone (5.4 to 21.6 ng/dL) responses to furosemide-posture challenge. Cortisol reserve was normal in HH. Fludrocortisone acetate therapy corrected the hyperkalemia. Other features of HH include low serum bicarbonate content, mild renal insufficiency, diabetes, and advanced age. The use of indomethacin and ibuprofen was associated with one case of HH each. Results suggest that HH is an overlooked cause of hyperkalemia, especially in patients whose hyperkalemia is unexplained.
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PMID:Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia. 700 70

The sera from 325 normal individuals, 21 patients with Turner's syndrome, 505 patients with insulin-dependent diabetes mellitus, 15 patients with unexplained ovarian insufficiency, and 37 patients with Addison's disease or serological evidence of adrenal autoimmunity were examined for the presence of gonadal autoantibodies by an indirect immunofluorescent technique using sections of human testis. All 12 patients found to have gonadal autoantibodies also had adrenocortical autoantibodies. These autoantibodies were completely absorbed with powdered adrenal cortex and thus were "steroidal cell" antibodies (SCA), cross-reactive with a cytosolic antigen in the steroid-producing cells of adrenal cortex, placental syncytiotrophoblast, Leydig areas of testis, and theca interna/granulosa layer of ovarian follicles. Sera with SCA had reduced titers of adrenal antibodies after repeated absorptions with gonadal or placental tissues, suggesting that adrenal-specific autoantibodies were also present. Sera from patients with only adrenal antibodies had no significant changes in antibody titers after repeated absorptions with gonadal or placental tissues. In conclusion, all gonadal autoantibodies found were SCA. SCA were only found in patients with adrenal autoimmunity, many of whom had hypogonadism. In other patients or in normal individuals, the existence of SCA or gonadal autoimmunity in the absence of adrenocortical autoantibodies must be rare.
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PMID:Gonadal autoantibodies in patients with hypogonadism and/or Addison's disease. 701 94

A review of 295 patients with autoimmune Addison's disease which occurred as part of a polyglandular autoimmune syndrome is presented. Information of 41 cases was obtained from our clinics and from the examination of medical records, while 254 cases were culled from the literature. We report that autoimmune Addison's disease in association with other autoimmune diseases occurs in at least two distinct types. Addison's disease occurring in Type I polyglandular autoimmune disease (PGA) is associated with chronic mucocutaneous candidiasis and/or acquired hypoparathyroidism. The age of onset is predominately in childhood or in the early adult years. Type I PGA syndrome is also frequently associated with chronic active hepatitis, malabsorption, juvenile onset pernicious anemia, alopecia and primary hypogonadism. Insulin requiring diabetes and/or autoimmune thyroid disease are infrequent. In contrast, Addison's disease in Type II PGA is associated with insulin requiring diabetes and/or autoimmune thyroid disease(s). Although the age of onset of Addison's disease in Type II PGA syndrome is not confined to any age group or any specific sex, it occurs predominately in the middle years of life in females. The associated autoimmune diseases found in Type I disease, such as chronic active hepatitis, etc. (see table II) are rare in Type II PGA disease except for a low frequency of gonadal failure. We provide evidence to support the concept that the Addison's diseases in Type I and II PGA syndromes have different genetic bases, as related to HLA haplotypes, and possibly have different underlying pathogeneses.
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PMID:Two types of autoimmune Addison's disease associated with different polyglandular autoimmune (PGA) syndromes. 702 19

We present a case of left ventricular rupture and formation of a pseudoaneurysm after silent myocardial infarction in a patient with Schmidt syndrome (polyglandular deficiency syndrome including Addison's disease, lymphocytic thyroiditis and diabetes mellitus). This case illustrates the possibility of myocardial rupture without hemodynamic collapse and a possible role of chronic steroid substitution.
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PMID:Silent myocardial rupture in a patient with diabetes and Addison's disease. 755 68

An apparently high frequency of Graves' disease encountered in New Orleans, Louisiana, prompted an investigation for a possible infectious agent that might be triggering the disease in genetically susceptible individuals. We studied 40 patients with Graves' disease, and compared them to the following groups of controls: age and gender matched healthy subjects; patients with multinodular goiter (non-autoimmune thyroid controls); patients with chronic lymphocytic thyroiditis (autoimmune thyroid disease controls) and additional organ or tissue specific autoimmune controls exclusive of thyroid autoimmunity, including patients with Type I diabetes and other endocrine autoimmune complex disorders. Serum antibodies against a prototypic strain of a human intracisternal A-type retroviral particle type 1 (HIAP-1) were detected by a sensitive and specific immunoblotting assay. In 87.5% (35/40) of the Graves' disease patients there was a positive reaction against several HIAP-1-associated proteins, predominantly 97 Kd and 80 Kd, with only 5 showing no reactivity to any. In contrast, 2% (2/105) of sera from normal controls showed positive reactivity. Furthermore, only 10% (1/10) of sera from multinodular goiter control patients and 10% (1/10) of Hashimoto's patients showed reactivity (p < 0.0005). Sera from 3 of 20 (15%) of Type I diabetic patients none of whom had Graves' disease, showed reactivity but there was no reactivity in 9 other patients with one or more of the endocrine autoimmune complex disorders, including Addison's disease, vitiligo, myasthenia gravis and pernicious anemia. In addition we studied two individuals with Graves' disease from each of two families residing outside Louisiana, all of whom were positive for these antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for a retroviral trigger in Graves' disease. 757 70


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