ABSTRACT
OBJECTIVE: Hypoparathyroidism is a disorder in which parathyroid hormone is deficient in the circulation due most often to immunological destruction of the parathyroids or to their surgical removal. The objective of this work was to define the abnormalities in skeletal microstructure as well as to establish the potential efficacy of PTH(1-84) replacement in this disorder. SUBJECTS AND METHODS: Standard histomorphometric and µCT analyses were performed on iliac crest bone biopsies obtained from patients with hypoparathyroidism. Participants were treated with PTH(1-84) for two years. RESULTS: Bone density was increased and skeletal features reflected the low turnover state with greater BV/TV, Tb. Wi and Ct. Wi as well as suppressed MS and BFR/BS as compared to controls. With PTH(1-84), bone turnover and bone mineral density increased in the lumbar spine. Requirements for calcium and vitamin D fell while serum and urinary calcium concentrations did not change. CONCLUSION: Abnormal microstructure of the skeleton in hypoparathyroidism reflects the absence of PTH. Replacement therapy with PTH has the potential to correct these abnormalities as well as to reduce the requirements for calcium and vitamin D.
OBJETIVO: O hipoparatiroidismo é uma doença em que há diminuição dos níveis circulantes do paratormônio, em geral, causada por destruição autoimune ou exerese cirúrgica. O objetivo deste estudo foi descrever as anormalidades microestrutrurais esqueléticas, como também o potencial terapêutico do uso do PTH(1-84). SUJEITOS E MÉTODOS: Histomorfometria padrão e análise de micro-CT foram realizadas em biópsias de crista ilíaca de indivíduos com hipoparatiroidismo. Os participantes foram tratados com PTH(1-84) por dois anos. RESULTADOS: A densidade óssea aumentou e os achados esqueléticos refletiram o estado de baixa remodelação óssea com maior BV/TV, Tb Wi e CT Wi, como também supressão de MS e BFR/BS quando comparado com o grupo controle. Com o uso de PTH(1-84), a remodelação óssea aumentou e a densidade óssea aumentou na coluna lombar. As necessidades de cálcio e vitamina D diminuíram e a calciúria não mudou. CONCLUSÃO: A microestrutura esquelética anormal no hipoparatiroidismo reflete a ausência do PTH. A terapia de reposição com PTH tem o potencial de reverter essas anormalidades, como também reduzir as necessidades de cálcio e vitamina D.
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Bone and Bones/ultrastructure , Calcium/therapeutic use , Hormone Replacement Therapy , Hypoparathyroidism/drug therapy , Parathyroid Hormone/therapeutic use , Vitamin D/therapeutic use , Biopsy , Bone Density Conservation Agents/therapeutic use , Bone Density/drug effects , Bone and Bones/drug effects , Case-Control Studies , Calcium/analysis , Hypoparathyroidism/pathology , Image Processing, Computer-Assisted , Spine/drug effects , Vitamin D/analysis , X-Ray MicrotomographyABSTRACT
Physiological intracranial calcification occurs in about 0.3-1.5% of cases. It is asymptomatic and detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Such parkinsonism does not respond to drugs containing levodopa. Infections [toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS] give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, serum concentration of calcium, phosphorus, and parathyroid hormone [PTH] is suggested to be determined in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism
Subject(s)
Humans , Male , Calcinosis/diagnosis , Basal Ganglia/pathology , Hypoparathyroidism/pathology , Tomography, Spiral Computed , Cerebellum/pathologyABSTRACT
En este artículo se revisan las complicaciones de la cirugía tiroidea con especial énfasis en la lesión de nervio recurrente, hipoparatiroidismo transitorio y permanente, sangrado post operatorio y la lesión de nervio laringeo superior. Se mencionan los factores de riesgo que predisponen a complicaciones quirúrgicas insistiendo en la necesidad de una técnica operatoria cuidadosa que extreme los cuidados en la hemostasia, realice una exacta localización y preservación de los nervios recurrentes y una correcta identificación del mayor número posible de glándulas paratiroides ejerciendo una manipulación depurada y cuidadosa de estas estructuras. El uso de drenajes en el lecho operatorio de la tiroidectomía es controvertido, razón por la cual se comentan los pro y contras del uso rutinario. Se concluye que la experiencia del cirujano y una técnica quirúrgica meticulosa son los factores más determinantes de la morbilidad de esta cirugía.