1/42. New technique of parathyroidectomy to prevent parathyromatosis and hypoparathyroidism.A 54-year-old woman with end-stage renal disease and on haemodialysis for 4 years developed severe secondary hyperparathyroidism and was operated upon. The two upper and the largest lower parathyroid glands were resected. The right lower gland was dissected from the lower pole of the thyroid and, by gently pulling upwards, the lateral walls were dissected using electrocautery. The lower aspect of the gland maintained the blood supply through small mediastinal and thymic vessels of the neopedicle, which allowed its mobilization to a more superficial plane. Because of the large size of the gland, the part opposite to the neopedicle was resected and the cutting surface was sealed with fibrin adhesive. Pre-thyroidal muscles were reapproximated and the remnant of the parathyroid gland was pulled out through a small hole in the inferior part of the midline and sutured with fine silk to the muscle. The gland was therefore placed in a subcutaneous position in the lowest part of the operative field just above the sternal border. The postoperative course was uneventful and, 8 months after surgery, the patient maintains a normal parathyroid function.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
2/42. hypoparathyroidism secondary to Riedel's thyroiditis. A case report and a review of the literature.Riedel's thyroiditis is a rare condition in which the thyroid gland is replaced by fibrous tissue. fibrosis in various distant sites is a possible concomitant event. We report a case of Riedel's thyroiditis complicated by mediastinal fibrosis, a tumefactive fibro-inflammatory lesion of the neck and primary hypothyroidism. A review of the literature in which only 8 previous cases of hypoparathyroidism secondary to Riedel's thyroiditis have been recounted concludes the report.- - - - - - - - - - ranking = 0.16666666666667keywords = gland (Clic here for more details about this article) |
3/42. digeorge syndrome with Graves' disease: A case report.digeorge syndrome (DGS) is characterized by aplasia or hypoplasia of the thymus and parathyroid glands, cardiac defects and anomaly face. This syndrome is usually associated with hypocalcemia resulting from hypoparathyroidism. In most cases the initial symptom is tetany caused by hypocalcemia within 24-48 hours after birth, with symptoms by immune abnormality appearing later. We report a woman who passed with no symptoms before age 18 and was diagnosed digeorge syndrome by tetany with developing auto-immune thyroid disease (Graves' disease). She had surgery for intraventricular septal defect at age 3, hypoparathyroidism, decrease of T cells in peripheral blood and the deletion of the 22nd chromosome long arm (22q11.2). It is supposed that abnormalities of immune function of this case are not complete as indicated by complicating of Graves' disease, and contributing to her long-term survival.- - - - - - - - - - ranking = 0.16666666666667keywords = gland (Clic here for more details about this article) |
4/42. Idiopathic hypoparathyroidism with intracranial calcifications and dominant skin manifestations.Presented here is an unusual case of a 41-year-old man with idiopathic hypoparathyroidism strongly connected with dermatological, ophthalmological and neurological disorders. Since the age of 4 he had been treated ineffectively for mycosis resulting in complete baldness and atrophic nail plate changes. At the age of 35 he was diagnosed with idiopathic hypoparathyroidism. He underwent surgery twice due to bilateral cataract. CT scans of the head demonstrated numerous symmetrically located calcifications in both frontal lobes, subcortical nuclei, the paraventricular region, brain fornix, and both cerebellar hemispheres. The neuropsychological examination demonstrated the occurrence of psychosensory disorders under the form of hallucinations accompanied by a sense of fear and anxiety. It seems essential to investigate the parathyroid gland for any sign of pathology, especially amongst patients with severe dermatological and/or neuropsychological symptoms. early diagnosis and treatment of patients with hypoparathyroidism may prevent the development of many serious complications or at least result in marked improvement of neurological manifestations.- - - - - - - - - - ranking = 0.16666666666667keywords = gland (Clic here for more details about this article) |
5/42. growth hormone deficiency in autoimmune polyglandular disease type 1.This is a case report of 2 patients who were diagnosed to have autoimmune polyglandular disease type 1. Both developed mucocutaneous candidiasis, hypoparathyroidism, vitiligo, and adrenocortical insufficiency. Both were noticed to have subnormal linear growth velocity and delayed bone age. Both showed subnormal stimulated serum growth hormone values indicating growth hormone deficiency. The first case showed favorable response to growth hormone therapy.- - - - - - - - - - ranking = 0.83333333333333keywords = gland (Clic here for more details about this article) |
6/42. Rapid increase in bone mineral density in a child with osteoporosis and autoimmune hypoparathyroidism treated with PTH 1-34.We describe a 16-year-old girl with autoimmune polyglandular syndrome type 1 including hypoparathyroidism, who had osteoporosis that improved rapidly with parathyroid hormone replacement therapy. patients with hypoparathyroidism usually have high bone mass. Our patient developed vertebral compression fractures at age 10, shortly after hypoparathyroidism was diagnosed. She continued to have low lumbar bone mass until age 16, when a dual energy x-ray absorptiometry (DEXA) revealed a Z score of - 2.2 SD. Several factors including decreased physical activity, total body magnesium depletion, and intermittent ketoconazole and short-term prednisone treatment, may have contributed to the development and progression of osteoporosis. Therapy with synthetic human parathyroid hormone (PTH) 1-34 rapidly normalized lumbar bone mass, as assessed by DEXA.- - - - - - - - - - ranking = 0.16666666666667keywords = gland (Clic here for more details about this article) |
7/42. hypoparathyroidism associated with aneurysm of the left subclavian artery (Kommerell's diverticulum) in an adult patient with a chromosome 22q11.2 deletion.hypoparathyroidism may either be acquired or of congenital origin. From the latter group, which represents a minority of cases, agenesis or hypoplasia of the parathyroid glands resulting in symptomatic hypocalcemia in the newborn or infant frequently is caused by a microdeletion of chromosome 22q11.2. We describe a man in whom hypoparathyroidism was first diagnosed at the age of 59 years. The endocrine disorder was found to be associated with this chromosome imbalance and also with an aneurysm of the left subclavian artery (Kommerell's diverticulum) compressing the esophagus and trachea. Given the potential implication for genetic counseling, a 22q11.2 deletion should be considered in the differential diagnosis of adult patients with hypoparathyroidism of unknown origin and should be searched for by appropriate molecular cytogenetic technique.- - - - - - - - - - ranking = 0.16666666666667keywords = gland (Clic here for more details about this article) |
8/42. Familial isolated hypoparathyroidism caused by a mutation in the gene for the transcription factor GCMB.hypoparathyroidism is characterized by hypocalcemia, hyperphosphatemia, and absent or markedly reduced circulating concentrations of parathyroid hormone. The transcription factor GCMB is predominantly, if not exclusively, expressed in parathyroid cells and is critical for development of the parathyroid glands in mice. Thus, in the present study we examined the GCMB gene, mapped to 6p23-24, as a candidate for isolated hypoparathyroidism. We defined the boundaries of the five exons of the human GCMB gene and then identified a large intragenic mutation in the GCMB genes of the proband of an extensive kindred with isolated hypoparathyroidism. Her parents and several other unaffected relatives were heterozygous for the mutation. Despite an absence of any history of consanguinity, microsatellite analysis showed shared genotypes that flanked the GCMB gene over a span of 5 cM, suggesting that both of the proband's GCMB alleles had been derived from a single common ancestor. Analysis of additional, unrelated cases did not disclose the same mutation. We conclude that homozygous loss of function of the GCMB gene impairs normal parathyroid gland embryology and is responsible for isolated hypoparathyroidism in a subset of patients with this disease.- - - - - - - - - - ranking = 0.33333333333333keywords = gland (Clic here for more details about this article) |
9/42. Isolated adrenocorticotropic hormone deficiency presenting with hypercalcemia in a patient on long-term hemodialysis.The authors report on a 44-year-old female hemodialysis (HD) patient who presented with hypercalcemia secondary to isolated adrenocorticotropic hormone (ACTH) deficiency. She had been suffering from nausea and abdominal pain caused by recurrent esophageal ulcer. blood calcium (Ca) adjusted for serum albumin concentration was increased to 14.9 mg/dL (3.72 mmol/L) concurrently with fever and hypotension. Serum intact parathyroid hormone (PTH)-related peptide was not elevated, but serum intact PTH and 1,25-(OH)2 vitamin D3 were decreased to 31 pg/mL (ng/L) and 8.1 pg/mL (2.6 pmol/L), respectively. Endocrinologic examination found that plasma ACTH was reduced below 5.0 pg/mL (0.22 pmol/L). A single ACTH stimulation normally increased blood cortisol, whereas a single corticotropin-releasing hormone injection failed to increase plasma ACTH and cortisol. Pituitary magnetic resonance imaging disclosed no enlargement of pituitary gland. Circulating bone formation and absorption markers were not elevated. blood Ca was normalized shortly after pamidronate disodium administration without glucocorticoid supplementation. This case suggested that secondary adrenal insufficiency caused by isolated ACTH deficiency could be an occult cause of severe hypercalcemia in HD subjects.- - - - - - - - - - ranking = 0.16666666666667keywords = gland (Clic here for more details about this article) |
10/42. erythropoietin-deficient anemia associated with autoimmune polyglandular syndrome type I.Autoimmune polyglandular syndrome type I (APS1), a relatively common disorder in some populations, is frequently associated with adrenal insufficiency, hypoparathyroidism, and other endocrine and skin abnormalities. We describe an 18-year-old male with APS1, as documented by genotyping, who presented with hypoparathyroidism and a normocytic, hypoproliferative, isolated anemia. An extensive hematological work-up revealed a low serum erythropoietin, without any other hematological abnormalities. His renal function was normal, and he did not have many of the laboratory or clinical findings associated with an anemia of chronic disease. His anemia was responsive to superphysiologic doses of erythropoietin. We thus suggest that erythropoietin deficiency may be one of the endocrine abnormalities associated with APS1, and clinicians should be cognizant of the association of treatable anemia in patients with APS1.- - - - - - - - - - ranking = 0.83333333333333keywords = gland (Clic here for more details about this article) |
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