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PubMed2006

Calcific tendinitis: natural history and association with endocrine disorders.

A retrospective, observational cohort study of 102 consecutive patients (125 shoulders) with calcific tendinitis is presented. Of the patients, 73 (71.6%) were women and 29 (28.4%) were men. Compared with population prevalences, significant levels of endocrine disorders were found. We compared 66 patients (62 women [93.9%] and 4 men [6.1%]; mean age, 50.3 years) (81 shoulders) with associated endocrine disease with 36 patients (11 women [30.6%] and 25 men [69.4%]); mean age, 52.4 years) (44 shoulders) without endocrine disease. The endocrine cohort was significantly younger than the non-endocrine cohort when symptoms started (mean, 40.9 years and 46.9 years, respectively), had significantly longer natural histories (mean, 79.7 months compared with 47.1 months), and had a significantly higher proportion who underwent operative treatment (46.9% compared with 22.7%). Disorders of thyroid and estrogen metabolism may contribute to calcific tendinitis etiology. Classifying calcific tendinitis into type I (idiopathic) and type II (secondary or endocrine-related) aids prognosis and management.

Adult↗
PubMed2000

Aboriginal deaths in Western Australia: 1985-89 and 1990-94.

OBJECTIVE: To examine death data for Aboriginal and non-Aboriginal persons in Western Australia (WA) in 1985-89 and 1990-94. METHODS: Population estimates were provided by the Health Information Centre of the WA Health Department based on data from the Australian Bureau of Statistics (ABS). Death data came from the WA Registrar-General's Office. Standard methods were used to obtain rates and levels of significance. RESULTS: Main causes of deaths among Aboriginal males in 1990-94 were circulatory conditions, respiratory, injury and poisoning, neoplasms and endocrine diseases; in Aboriginal females they were circulatory, neoplasms, endocrine diseases, respiratory diseases, and injury and poisoning. From 1985-89 to 1990-94, the Aboriginal male all-cause age-standardised death rates fell 3% (ns) while the non-Aboriginal male rate fell 11% (p < 0.05). The Aboriginal female all-cause death rate rose 11% (ns) while the non-Aboriginal rate fell 5% (p < 0.05). The all-cause death rate ratio (Aboriginal:non-Aboriginal) changed from 2.4 to 2.6 (males) and 2.5 to 2.9 (females). There was a major increase in deaths from endocrine diseases among Aborigines and non-Aborigines. This increase was proportionally much greater among Aborigines. In non-Aborigines there was a significant decrease in deaths from circulatory diseases (mainly ischaemic heart disease); this did not occur among Aborigines. CONCLUSIONS: Over the study period, Aboriginal health standards, as reflected by death rates, apparently worsened relative to non-Aboriginal standards. IMPLICATIONS: Better health promotion, disease prevention and disease care are required to help achieve acceptable health standards among Aboriginal peoples.

Adolescent↗
PubMed1997

Codon 17 polymorphism of the cytotoxic T lymphocyte antigen 4 gene in Hashimoto's thyroiditis and Addison's disease.

Endocrine autoimmune disorders share susceptibility and resistance factors of the human leukocyte antigen system on the short arm of chromosome 6, but other gene loci also contribute to predisposition and protection. Because the cytotoxic T lymphocyte antigen 4 (CTLA4) alanine-17 encoded by the CTLA4 gene on chromosome 2q33 confers susceptibility to Graves' disease, as well as to type 1 (insulin-dependent) diabetes mellitus, we investigated this dimorphism in the other endocrine autoimmune disorders: Hashimoto's thyroiditis and Addison's disease. We analyzed the CTLA4 exon 1 polymorphism (49 A/G) in 73 patients with Hashimoto's thyroiditis, 76 with Addison's disease, and 466 healthy controls. This dimorphism corresponds to an aminoacid exchange (Thr/Ala) in the leader peptide of the expressed protein. CTLA4 alleles were defined by PCR, single-strand conformational polymorphism analysis, and restriction fragment length polymorphism analysis using BbvI. Patients with Hashimoto's thyroiditis had significantly more Ala alleles than controls, both as homozygotes (22% vs. 15%) and heterozygotes (53% vs. 46%), and less Thr than controls as homozygotes (25% vs. 39%), P < 0.04. The phenotypic frequency for Ala was significantly higher in patients (75%), compared with controls (61%), P < 0.03. Patients with Addison's disease did not differ significantly from controls, but those carrying the suceptibility marker, human leukocyte antigen DQA1*0501, were significantly more CTLA4 Ala17 positive than controls with the same DQA1 allele (P < 0.05). In conclusion, an alanine at codon 17 of CTLA4 confers genetic susceptibility to Hashimoto's thyroiditis, whereas this applies only to the subgroup of DQA1*0501+ patients with Addison's disease.

Abatacept↗
PubMed1996

Identification of 3 beta-hydroxysteroid dehydrogenase as a novel target of steroid cell autoantibodies: association of autoantibodies with endocrine autoimmune disease.

Autoantibodies directed against steroid hormone-producing cells (SCA) detectable by immunofluorescence are typically found in a small proportion of patients with premature ovarian failure (POF) as well as in other endocrine autoimmune diseases. The SCA pattern stains cells in the outer zones of the adrenal cortex, ovary, and testis. To identify the molecular target of SCA, an adrenal complementary DNA expression library was screened using SCA-positive serum, and the steroid enzyme 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) was identified. Only 1 of 48 (2%) patients with idiopathic POF, not pre-selected for the presence of other autoimmune diseases, had SCA by immunofluorescence, whereas 10 of 48 (21%) had anti-3 beta HSD autoantibodies detectable by immunoblot using recombinant human enzyme compared with 6 of 115 (5%) control subjects (P = 0.002). Absorption of SCA-positive serum with recombinant human 3 beta HSD abolished the immunofluorescence pattern. We also examined the prevalence of anti-3 beta HSD autoantibodies in other endocrine autoimmune diseases. Two of 112 (2%) diabetic patients, but none of the thyroid or Addisonian patients, had SCA by immunofluorescence. Twenty-six (23%) diabetic subjects (P < 0.001 vs. controls), 3 of 18 thyroid patients (P > 0.05 vs. controls), and none of 4 Addisonian patients had anti-3 beta HSD autoantibodies. 3 beta HSD is the first steroid cell autoantigen defined at the molecular level to be associated with idiopathic POF occurring in the absence of other polyglandular diseases. Autoantibodies to 3 beta HSD in patients with other organ-specific autoimmune diseases indicate that the enzyme behaves as a typical target of polyendocrine autoimmunity. Anti-3 beta HSD autoantibodies in patients with POF may provide a marker of those subjects whose ovarian failure is autoimmune in origin and, as recent studies suggest, may be salvageable with glucocorticoid treatment.

3-Hydroxysteroid Dehydrogenases↗
PubMed2005

[Hereditary endocrine tumour diseases].

BACKGROUND AND METHOD: The paper reviews inheritable endocrine tumour syndromes based on recent literature and the experience of the authors. RESULTS AND CONCLUSIONS: A number of inheritable endocrine tumour syndromes are caused by mutations in proto-oncogenes or tumour suppressor genes. These include multiple endocrine neoplasia (MEN), familial non-MEN neoplasia, Von Hippel-Lindau's disease and familial medullary thyroid carcinoma, pheochromocytoma and paraganglioma. These conditions are rare, but since inheritance is dominant with a near-complete penetrance, a number of carriers with a high risk of developing tumours are regularly found in the families of affected individuals. Identification of carriers with a high risk of developing tumours gives the opportunity to cure disease manifestations at an early stage and to avoid life-threatening complications. Family members who are not carriers can be excluded from follow up. DNA analyses of the most common disease genes are now performed in genetic laboratories in Norway.

Adrenal Gland Neoplasms↗
PubMed2006

Von Hippel-Lindau disease and endocrine tumour susceptibility.

Von Hippel-Lindau (VHL) disease is a dominantly inherited familial cancer syndrome caused by mutations in the VHL tumour suppressor gene. VHL disease is characterised by marked phenotypic variability and the most common tumours are haemangioblastomas of the retina and central nervous system and clear cell renal cell carcinoma. However, endocrine tumours, most commonly phaeochromocytoma and non-secretory pancreatic islet cell cancers, demonstrate marked interfamilial variations in frequency and are significant causes of morbidity and, sometimes, mortality. Genotype-phenotype correlations have revealed that certain missense mutations are associated with a high risk of phaeochromocytoma but total loss of function mutations are associated with a low risk. Furthermore, rare mutations may predispose to a phaeochromocytoma-only phenotype. Germline VHL mutations may be detected in 5-11% of all phaeochromocytoma cases and mutation analysis of VHL and other phaeochromocytoma susceptibility genes (SDHB, SDHD and RET) should be performed in all cases of familial, multiple or early onset phaeochromocytomas, and considered in other cases. The VHL gene product has a key role in regulating the stability of hypoxia-inducible factors (HIF-1 and HIF-2) such that inactivation of VHL leads to up-regulation of HIF-1 and HIF-2 protein expression and activation of hypoxic gene response pathways. Germline SDHB and SDHD mutations also lead to increased expression of HIF target genes, but it appears that phaeochromocytoma susceptibility in VHL disease cannot be attributed to HIF activation alone. Recently, it has been suggested that an HIF-independent failure of developmental apoptosis is a common feature of all inherited phaeochromocytoma susceptibility syndromes.

Disease Susceptibility↗
PubMed2006

Epigenetics, evolution, endocrine disruption, health, and disease.

Endocrine-disrupting chemicals (EDCs) in the environment have been linked to human health and disease. This is particularly evident in compounds that mimic the effects of estrogens. Exposure to EDCs early in life can increase risk levels of compromised physical and mental health. Epigenetic mechanisms have been implicated in this process. Transgenerational consequences of EDC exposure is also discussed in both a proximate (mechanism) and ultimate (evolution) context as well as recent work suggesting how such transmission might become incorporated into the genome and subject to selection. We suggest a perspective for exploring and ultimately coming to understand diseases that may have environmental or endocrine origins.

Adult↗
PubMed1980

[Experience with CT and adrenal venography in the diagnosis of adrenal disease with endocrine activity (author's transl)].

Report of the result of CT and venography in 12 patients with suspected adrenal disease, venography being combined with selective blood sampling for hormone analysis. In one patient CT showed a 1.6 cm big pheochromocytome in the left adrenal gland, not demonstrated by venography, but proven by analysis of the blood sample. Both methods showed hyperplasia of both adrenals in one patient with Cushing Syndrome with elevated Cortisol levels found in the analysis of the blood smples. Of 3 patients with hyperaldosteronism, venography was able to demonstrate 2 Conn adenomas, not seen on CT; whereas CT showed the third 2 X 1.5 cm big Conn adenoma hidden in an enlarged adrenal gland. Hormone analysis was helpful in 2 of these cases, while in the third it was misleading. The authors believe that both methods should be employed to localise over adrenal disease with endocrine activity.

Adrenal Gland Diseases↗
PubMedDate not supplied

[Autoantibodies in children with vitiligo].

INTRODUCTION: Vitiligo is an acquired, sometimes familial skin depigmentation disorder. In about half of patients it occurs before the age of twenty. The aim of this study was to investigate the incidence and significance of autoantibodies (AT) and associated autoimmune and endocrine diseases in children with vitiligo, in relation to adults with vitiligo and children without vitiligo. MATERIAL AND METHODS: The research was conducted in fifty children with clinically diagnosed vitiligo from 2 to 16 years of age. Children were compared with control groups of children with other skin diseases (aged from 2 to 16) and with adults with vitiligo. Each group comprised 30 patients. A detailed history was obtained and physical examination was performed in each patient to determine presence of autoimmune and endocrine diseases in patients with family history of vitiligo. Routine blood examination, routine urinalysis and stool were performed in all patients. We evaluated the incidence of antinuclear (ANA) and antithyroid antibodies (ATA) in each patient, as well as the incidence of antibodies to gastric parietal cell (APCA), smooth muscle (SMA), cord (ACA) and mitochondrial antigens (AMA) in 38 children with vitiligo and in control groups. RESULTS: Children with vitiligo had positive family history of vitiligo more often compared to children without vitiligo (p<.05). Presence of ANA, ATA, APCA, SMA, ACA and AMA was not considerably increased in children with vitiligo compared with their age group. ANA was more common in adults with vitiligo, in comparison with children with vitiligo (p<0.05). None of the children with vitiligo had an associated autoimmune and endocrine disease in contrast to adults with vitiligo (p<0.05). DISCUSSION AND CONCLUSION: Several studies have shown a significant incidence of positive autoantibodies in children with vitiligo, compared to children without vitiligo. However, in our series, presence of ANA, ATA, APCA, SMA, ACA and AMA was not significantly increased in children with vitiligo, compared with children without vitiligo. Further studies are necessary in this area in order to draw more conclusions. In the previous studies, it has been established that children with vitiligo were generally healthy, whereas adults with vitiligo had an increased incidence of autoimmune and/or endocrine diseases. No studies have shown this association in children with vitiligo. Our results support findings of previous studies.

Adolescent↗
PubMed2002

Endocrine Heart Disease.

With the increasing prevalence of obesity and diabetes mellitus in the United States, associated cardiovascular disease is reaching epidemic proportions with staggering economic and societal impact. Numerous studies have demonstrated the poorer prognosis associated with chronic coronary artery disease and acute coronary syndromes in patients with diabetes compared with nondiabetic patients. Although the therapeutic strategy is largely the same for the two populations, proper management of the diabetic patient with cardiovascular disease must account for the associated metabolic disturbances. Thyroid disease is the next most common endocrine disorder that affects proper function of cardiovascular patients; all patients presenting with coronary artery disease or cardiac arrhythmias should undergo screening with a sensitive thyroid-stimulating hormone assay and appropriate treatment when necessary. Though these areas are the most common points of intersection between the cardiologist and endocrinologist, a thorough understanding of the impacts of each endocrine system on cardiac function is essential to recognize disease entities that often present with a cardiovascular manifestation or affect patients with a primary cardiovascular disease.

Journal Article↗
PubMed1994

[Combined endocrine autoimmune syndrome--incidence, forms of manifestation and clinical significance].

UNLABELLED: In a retrospective case finding study we collected data from patients with polyglandular autoimmune syndrome type II (PGAS Type II) who had been treated in our endocrine outpatient clinic between 1975 and 1989. 31 adult patients (25 females and 6 males) fulfilled the criteria for PGAS Type II (association of autoimmune endocrine disease with at least one other--usually endocrine--autoimmune disease or autoantibodies against another organ). Among these patients, 18 had hypothyroidism due to autoimmune thyroiditis, 8 were hyperthyroid (Graves' disease), and 4 had silent autoimmune thyroiditis (without thyroid dysfunction). Insulin dependent (type I) diabetes mellitus (IDDM) was seen in 11, Addison's disease in 7, primary hypogonadism in 5, vitiligo in 6 and pernicious anemia in 5 cases. The presence of antiparietal cell antibodies was demonstrated in 21 of 30 investigated patients. These patients also showed other evidence of autoimmune gastritis, such as increased gastrin (in 10 out of 13), diminished vitamin B12 levels (6 out of 13), atrophic gastritis (9 out of 9), pernicious anemia (6 out of 30) and funicular myelosis (2 out of 30). CONCLUSION: The most common endocrine diseases in our patient group were autoimmune thyroid diseases (97%) followed by IDDM (35%) and Addison's disease (23%). A high percentage (70%) of our subjects had elevated titers of antiparietal cell antibodies. Polyglandular autoimmune syndrome must be suspected in all patients with autoimmune endocrine disease, especially in the presence of relatives suffering from PGAS. Patients at risk should be screened regularly by measuring thyrotropin (ultrasensitive assay), fasting blood glucose levels, and by checking red blood count and antiparietal cell antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2005

Giessen international workshop on interactions of exocrine and endocrine pancreatic diseases. Castle of Rauischholzhausen of the Justus-Liebig-University, Giessen, Germany. March 18-19, 2005.

The 'Giessen International Workshop on Interactions of Exocrine and Endocrine Pancreatic Diseases' was held on March 18-19, 2005 at the Castle of Rauischolzhausen, Giessen University, Germany. About 50 international clinicians and researchers attended the workshop. It was structured into three sessions: A: Pancreatic Autoimmunity - Interaction Between Exocrine and Endocrine Tissue; B: Diabetes Mellitus - Possible Implications of Exocrine Pancreatic Insufficiency; C: Chronic Pancreatitis - Update on Prevalence, Understanding and Pathophysiological Concepts. Several new aspects of pancreatic diseases were discussed, including new classifications of pancreatitis, new insights into prevalence, pathophysiology and new therapeutical considerations. The meeting resulted in more cooperation and a number of new concepts for clinical study which will provide data for future developments.

Autoimmune Diseases↗
PubMed2001

Latent autoimmune diabetes in adults (LADA) and autoimmune thyroiditis.

Latent autoimmune diabetes in adults (LADA) is characterized by clinical presentation as type 2 diabetes after 25 years of age, initial control achieved with diet or oral hypoglycaemic agents during at least 6 months, presence of autoantibodies (first of all GADA) and some immunogenetic features of diabetes mellitus type 1. In patients with an autoimmune endocrine disease, which could be also autoimmune diabetes, there is a high risk of development of another autoimmune endocrine disorder. The coexistence of two or more autoimmune endocrine diseases is pathognomonic for autoimmune polyglandular syndrome. Autoimmune thyroiditis and type 1 diabetes mellitus are the most common combination of autoimmune endocrine diseases reported. Most studies reported the prevalence of autoimmune thyroiditis in "typical" type 1 adult diabetic subjects about 20 - 40%. Little is known about the prevalence of autoimmune thyroiditis in subjects with LADA. Only a few studies confirmed a high prevalence of thyroid autoantibodies in type 2 diabetic subjects with GADA compared to type 2 diabetic subjects without GADA and compared to non-diabetic population too.

Adult↗