Manifestation Of Hyperparathyroidism Research Articles

A Large Brown Tumor of Mandible as First Manifestation of Hyperparathyroidism

ABSTRACT Brown tumor is a lesion that develops in patients with hyperparathyroidism. It can be described as the terminal stage of bone remodeling process where abnormal bone metabolism takes place. Hyperplasia or adenoma of the parathyroid glands is the main etiology of primary hyperparathyroidism (HPT). Due to overproduction of parathyroid hormone in hyperparathyroidism bone resorption takes place, which appear as cyst-like lesions, commonly known as osteitis fibrosa cystica or brown tumor. Any skeletal bones, including jawbones can be affected in this disorder. Most of the time brown tumor is detected after confirmatory diagnosis of hyperparathyroidism. Presentation of brown tumor as the first manifestation of this disorder is rare. In this present report, a large proliferative growth in left jaw with multilocular radiolucency in 23 years aged female was described as an unusual first manifestation of hyperparathyroidism.

Suspected parathyroid carcinoma: Clinical diagnosis of unique endocrine pathology

Parathyroid carcinoma is an extremely rare malignancy of the endocrine system with an incidence of 0.5 - 5% of patients with hyperparathyroidism worldwide. It typically presents with an indolent course, and manifestations of hyperparathyroidism usually appear well before local invasion

Ectopic pure mediastinal parathyroid adenoma: A case report.

Introduction and importanceThe ectopic parathyroid adenoma is an important cause of refractory and recurrent hyperparathyroidism. The mediastinal location of ectopic parathyroid tissue is reported in up to 20% of cases of ectopic parathyroid adenomas. In around 2% of cases where cervical approach is unfeasible, the mediastinal route imposes a surgical challenge.Case presentationWe describe a case of a twenty-five-year-old male patient with manifestations of hyperparathyroidism. Computed tomography of the chest showed an anterior mediastinal mass. Nuclear scintigraphy detected a functioning parathyroid tissue in the mediastinum. The mass was excised en block with the surrounding adipose tissue using a three-port video-assisted thoracoscopic surgery. The patient showed a full symptomatic and laboratory recovery.Clinical discussionMediastinal parathyroid glands comprise a unique surgical entity with diagnostic and management difficulties.ConclusionMediastinal parathyroid gland is a rare yet important cause of refractory hypercalcemia. The current localization tools improve the thoracoscopic management of MPAs. VATS can provide access and exposure to ectopic parathyroid adenoma with low morbidity.

Primary Hyperparathyroidism: Modern Conception and Clinical Observation

The article is devoted to one of the actual medical and social problems — primary hyperparathyroidism, the late diagnosis of which leads to the development of severe complications and an increased risk of premature death. Unlike developed countries, where 80% of cases are represented by mild forms of the disease, in the Russian Federation this indicator does not exceed 30%, while 70% are manifest forms. Widespread awareness of doctors of various specialties in the diagnosis of parathyroid adenoma is necessary for the timely detection of the disease. The article reflects the main stages of the study of the disease, the pathogenesis of the clinical manifestations of primary hyperparathyroidism, the classic symptoms of which are changes in the target organs of the parathyroid hormone — bone tissue, urinary system and gastrointestinal tract, is considered. Bone disorders are the most common manifestation of hyperparathyroidism and are characterized by increased bone metabolism with a progressive decrease in bone mineral density. Typical changes in the kidneys include nephrolithiasis and nephrocalcinosis, causing the formation of renal failure. Gastrointestinal signs of hyperparathyroidism are erosion and ulcers of the stomach and duodenum, prone to bleeding, recurrent pancreatitis. Diagnosis of the disease is based on laboratory results, characterized by elevated levels of calcium and parathyroid hormone in the blood. Visualization of the paradenomas in most cases is provided by ultrasound and scintigraphy. Removal of parathyroid adenoma is the most effective treatment. A clinical case of a severe form of the disease is presented, indicating an urgent need to take measures to solve the problem of primary hyperparathyroidism.

Primary Hyperparathyroidism: Modern Conception and Clinical Observation

The article is devoted to one of the actual medical and social problems — primary hyperparathyroidism, the late diagnosis of which leads to the development of severe complications and an increased risk of premature death. Unlike developed countries, where 80% of cases are represented by mild forms of the disease, in the Russian Federation this indicator does not exceed 30%, while 70% are manifest forms. Widespread awareness of doctors of various specialties in the diagnosis of parathyroid adenoma is necessary for the timely detection of the disease. The article reflects the main stages of the study of the disease, the pathogenesis of the clinical manifestations of primary hyperparathyroidism, the classic symptoms of which are changes in the target organs of the parathyroid hormone — bone tissue, urinary system and gastrointestinal tract, is considered. Bone disorders are the most common manifestation of hyperparathyroidism and are characterized by increased bone metabolism with a progressive decrease in bone mineral density. Typical changes in the kidneys include nephrolithiasis and nephrocalcinosis, causing the formation of renal failure. Gastrointestinal signs of hyperparathyroidism are erosion and ulcers of the stomach and duodenum, prone to bleeding, recurrent pancreatitis. Diagnosis of the disease is based on laboratory results, characterized by elevated levels of calcium and parathyroid hormone in the blood. Visualization of the paradenomas in most cases is provided by ultrasound and scintigraphy. Removal of parathyroid adenoma is the most effective treatment. A clinical case of a severe form of the disease is presented, indicating an urgent need to take measures to solve the problem of primary hyperparathyroidism.

КАРЦИНОМА ПАРАЩИТОВИДНОЙ ЖЕЛЕЗЫ С ИНТРАТИРЕОИДНЫМ РАСПОЛОЖЕНИЕМ: СЛУЧАЙ ИЗ ПРАКТИКИ

Carcinoma of the parathyroid gland is a rare malignant tumor of the person, which manifests itself clinical syndrome of hyperparathyroidism. The tumor is characterized by structural signs of invasive growth and is characterized by an unfavorable clinical prognosis, often accompanied by metastasis and the formation of relapses. The article provides background information about the incidence of parathyroid carcinoma, the gender and age characteristics of patients with this disease, options for localization of the tumor in the gland itself (typical topic of the neoplasm), in other areas of the neck, thyroid, thymus, and so on. We discuss the features of clinical manifestations of parathyroid carcinoma, among which the most typical are manifestations of hyperparathyroidism and hypercalcemia, and also provide figures for five - and ten-year survival. The article presents the author’s observation of parathyroid carcinoma with an intrathyroid location in a 64-year-old man. After the examination, the patient underwent a cervicotomy with revision of the areas of the typical location of the parathyroid gland in the neck, hemithiroidectomy on the left with a parathyroid tumor incorporated in the thyroid tissue, which was later proved using immunohistochemical research methods. The article details the macroscopic, microscopic, and immunohistochemical characteristics of the operating material. A special feature of the case is a rare atypical intrathyroid localization of parathyroid carcinoma.

Computed tomography diagnosis of primary hyperparathyroidism.

The article presents data on modern approaches to the diagnosis of various manifestations of hyperparathyroidism according to multispiral computed tomography, which do not require morphological verification and ensure the correctness of the diagnostic process. The radiological picture and differential diagnostics of changes from parathyroid glands and bone structures at hyperparathyroidism are described in detail.

Brown Jaw Tumors: challenges and outcomes

Background: Brown tumors are very rare giant cell lesions that arise as a result of hyperparathyroidism, brown tumors rarely affect the mandible and maxilla and its diagnosis and treatment is very challenging and needs a high index of suspicion.Methods: Retrospective chart review of nine cases diagnosed as brown jaw tumors treated in maxillofacial, head and neck surgery unit, department of surgery, Sohag University hospital.Results: They were 9 patients, 3 males and 6 females with a mean age of 43.3 years. Lesions were located in the mandible (4 cases), maxilla (3 cases), both mandible and maxilla (2 cases). The main presentation was a mass lesion. Clinical examination and serum parathormone, serum calcium, serum phosphorus, neck ultrasonography, parathyroid scan was used for diagnosis. Cases did excision with parathyroidectomy. There was no recurrence during a mean follow up period of 9.3 months. All patients had satisfactory results.Conclusions: All cases with osteolytic lesions in mandible or maxilla the possibility of brown tumors should be kept in mind especially if there is any manifestation of hyperparathyroidism. This report will aid in the recognition and treatment of the jaw brown tumors.

The Common Accomplice of Pains, Moans, Groans: Imaging of Brown Tumors Debusted

Brown tumors are focal bone lesions, caused by increased osteoclastic activity and fibroblastic proliferation, encountered in patients with uncontrolled hyperparathyroidism (HPT). They can be located in any part of the skeleton, but are most frequently encountered in the ribs, clavicles, extremities, and pelvic girdle. Clinically significant lesions in the craniofacial bones are rare Brown tumors are focal reactive osteolytic lesions caused by hyperparathyroidism (HPT) and represent the terminal stage of the hyperparathyroidism-dependent bone pathology. Nowadays, the manifestation of hyperparathyroidism with these lesions is extremely rare in developed countries, because of the early detection of the disease, using routine laboratory examination and early treatment of that. These benign lesions present similar radiologic findings as bone metastasis, which makes the diagnosis difficult Brown tumors are focal bone lesions, caused by increased osteoclastic activity and fibroblastic proliferation, encountered in patients with uncontrolled hyperparathyroidism (HPT). They can be located in any part of the skeleton, but are most frequently encountered in the ribs, clavicles, extremities, and pelvic girdle. Clinically significant lesions in the craniofacial bones are rare Brown tumors are focal reactive osteolytic lesions caused by hyperparathyroidism (HTP) and represent the terminal stage of the hyperparathyroidism-dependent bone pathology. Nowadays, the manifestation of hyperparathyroidism with these lesions is extremely rare in developed countries, because of the early detection of the disease, using routine laboratory examination and early treatment of that. These benign lesions present similar radiologic findings as bone metastasis, which makes the diagnosis difficult.

Sex and age modify biochemical and skeletal manifestations of chronic hyperparathyroidism by altering target organ responses to Ca2+ and parathyroid hormone in mice.

We studied mice with or without heterozygous deletion of the Casr in the parathyroid gland (PTG) [(PTG) CaSR(+/-)] to delineate effects of age and sex on manifestations of hyperparathyroidism (HPT). In control mice, aging induced a left-shift in the Ca(2+) /parathyroid hormone (PTH) set point accompanied by increased PTG CaSR expression along with lowered serum Ca(2+) and mildly increased PTH levels, suggesting adaptive responses of PTGs to aging-induced changes in mineral homeostasis. The aging effects on Ca(2+) /PTH set point and CaSR expression were significantly blunted in (PTG) CaSR(+/-) mice, who showed instead progressively elevated PTH levels with age, especially in 12-month-old females. These 12-month-old knockout mice demonstrated resistance to their high PTH levels in that serum 1,25-dihydroxyvitamin D (1,25-D) levels and RNA expression of renal Cyp27b1 and expression of genes involved in Ca(2+) transport in kidney and intestine were unresponsive to the rising PTH levels. Such changes may promote negative Ca(2+) balance, which further exacerbate the HPT. Skeletal responses to HPT were age-, sex-, and site-dependent. In control mice of either sex, trabecular bone in the distal femur decreased whereas cortical bone in the tibiofibular junction increased with age. In male (PTG) CaSR(+/-) mice, anabolic actions of the elevated PTH levels seemed to protect against trabecular bone loss at ≥ 3 months of age at the expense of cortical bone loss. In contrast, HPT produced catabolic effects on trabecular bone and anabolic effects on cortical bone in 3-month-old females; but these effects reversed by 12 months, preserving trabecular bone in aging mice. We demonstrate that the CaSR plays a central role in the adaptive responses of parathyroid function to age-induced changes in mineral metabolism and in target organ responses to calciotropic hormones. Restraining the ability of the PTG to upregulate CaSRs by heterozygous gene deletion contributes to biochemical and skeletal manifestations of HPT, especially in aging females.

A Case of Parathyroid Carcinoma Presenting Hyperparathyroidism that was Clinically Easy to Overlook

Parathyroid carcinoma is very rare in patients with primary hyperparathyroidism, only accounts for 1% to 2% of all cases. It is characterized by higher incidence of renal dysfunction, metabolic bone disease and gastrointestinal symptoms. Although the clinical manifestations of hyperparathyroidism are more severe in patients with parathyroid carcinoma when compared to those with those with parathyroid adenoma, it is difficult to differentiate carcinoma from adenoma without pathologic confirmation. To our knowledge, there have only been a few cases of hyperparathyroidism due to parathyroid carcinomas reported to date. Here, we report a case of 63-year-old woman developing osteoporosis, hypercalcemia and hypophosphatemia due to a parathyroid tumor and was diagnosed with parathyroid carcinoma postoperatively. [Korean Journal of Bone Metabolism, 19(1): 59-65, 2012]

A Case of Brown Tumor of the Mandible Caused by Hyperparathyroidism

Brown tumors are erosive bony lesions caused by the chronic excessive secretion of parathyroid hormone. Since the introduction of routine calcium measurement, the diagnosis of hyperparathyroidism has usually been made in asymptomatic patients, and as a result, brown tumors are rarely observed as an initial manifestation of hyperparathyroidism. The authors report a case of a 32-year-old woman who presented with right cheek swelling. A CT scan showed erosive bone tumors of the mandible. These lesions were finally diagnosed as brown tumors associated with secondary hyperparathyroidism due to chronic renal failure. Brown tumor as a result of hyperparathyroidism is a relatively rare clinical finding in otorhinolaryngology, thus, the authors illustrate this case with a brief review of the literature.

Costal Brown Tumor Detected by Dual-phase Parathyroid Imaging and SPECT-CT in Primary Hyperparathyroidism

A 58-year-old male with primary hyperparathyroidism underwent parathyroid scintigraphy to obtain presurgical localization of a suspected parathyroid adenoma. Increased Tc-99m sestamibi uptake was seen on dual-phase imaging in a focal area corresponding to the right inferior parathyroid. An incidental finding was the intense tracer uptake in the left thorax. Immediate SPECT-CT imaging located the uptake area in the third left rib; it was subsequently demonstrated to represent a brown tumor. Brown tumors, skeletal manifestations of hyperparathyroidism, have been incidentally detected by bone scintig- raphy, more rarely by Tc-99m sestamibi parathyroid scintigraphy.

The Importance of Parathyroid Hormone in Inhibition of Collagen Synthesis and Mitogenesis of Osteoblastic Cell1

Loss of bone substance is a common manifestation of hyperparathyroidism. This suggests that parathyroid hormone (PTH) plays an important role as to bone mass. To investigate the mechanism underlying this change in bone mass, I studied the effects of PTH on collagen synthesis and mitogenesis of UMR-106 rat osteoblastic osteosarcoma cells. PTH inhibits the mitogenesis of UMR-106 rat osteosarcoma cells, the half-maximal concentration being 10(-8) to 10(-7) M, which is similar to the EC50 for cyclic AMP accumulation. Cyclic AMP, whose intracellular concentration was increased by PTH, plays a role in the modulation of mitogenesis, as shown by the comparable inhibitory effects of 8-bromoadenosine-3',5'-cyclic AMP (10(-4) M), forskolin (10(-7) M), and the phosphodiesterase inhibitor, IBMX (10(-5) M). PTH, in a similar concentration range, directly inhibited collagen synthesis. Concurrent with the suppression of collagen synthesis, the amounts of a1(I) and a2(I) collagen mRNA decreased proportionately. The results show that PTH modulates collagen synthesis at the transcriptional level. I concluded that parathyroid hormone inhibits the mitogenesis of osteoblasts as well as collagen synthesis by these cells. The decreases in the number of osteoblasts and the amount of collagen synthesis contribute to the loss of bone substance in hyperparathyroidism.

Can the volume of abnormal parathyroid tissue be predicted by preoperative biochemical measurement?

A strong correlation between the biochemical manifestations of hyperparathyroidism and the volume of abnormal parathyroid tissue could be used to guide the extent of surgical exploration and parathyroid gland resection (i.e., finding a small "adenoma" in a patient with marked hypercalcemia would dictate further exploration). We examined this relationship in patients for whom data were collected prospectively (n = 14) and retrospectively (n = 27). We considered only patients cured after excision of a single gland and glands for which a three-dimensional description or volume of water displacement was available. To exclude artifactually elevated serum concentrations of parathyroid hormone (PTH), PTH values were used only from patients with levels of serum creatinine less than 2 mg/dl. To accommodate different assays, highest preoperative PTH, ionized calcium, and alkaline phosphatase (AP) values were expressed as percent above upper normal limit. There was excellent agreement (r = 0.93, p less than 0.05) between measured and calculated gland volume. In the prospective study (but not in the retrospective study) there was a significant (p less than 0.05) correlation (r = 0.61) between gland volume and highest preoperative total calcium value; however, there was considerable variation in gland size in patients with similar calcium levels. In neither study was there a significant correlation between gland volume and any of the following: calcium, ionized calcium, midregional PTH, carboxyterminal PTH, or intact PTH, alkaline phosphatase, and urine cyclic adenosine monophosphate (AMP). In the prospective study there was a tendency for urine cyclic AMP, ionized calcium, and AP to increase with increasing gland volume (r = 0.42, 0.45, and 0.51, respectively). Preoperative measurements of calcium, PTH, urine cyclic AMP, and AP are too inconsistent to rely on for determining the extent of parathyroid gland resection.

The Many Facets of Secondary Hyperparathyroidism

With the realization of the almost ubiquitous presence of hyperparathyroidism in chronic renal failure, it seems inevitable that the recognition of the spectrum of the symptoms attributed to this condition should expand concomitantly. The usual indications for surgery in secondary hyperparathyroidism are persistent hypercalcemia, symptomatic progressive osteitis fibrosa cystica, and metastatic subcutaneous calcifications.¹We have recently performed subtotal parathyroidectomy on three patients because of manifestations other than the usual ones and wish to report the surgical consequences. A fourth patient is described to demonstrate the therapeutic efficacy of oral phosphate binding antacids for metastatic subcutaneous calcification. One patient suffered from intractable pruritus without manifestations of hyperparathyroidism. The second had acute involuntary muscle contractions associated with hypercalcemia and pruritus. The third developed extensive vascular calcifications associated with the development of angina pectoris and a cardiac murmur. The fourth developed subcutaneous calcification while not taking oral phosphate binders, which interfered with

Less common manifestations of hyperparathyroidism.

Less common manifestations of hyperparathyroidism.

PRIMARY HYPERPARATHYROIDISM ASSOCIATED WITH A CYSTIC LESION IN THE NECK: PROBABLE PARATHYROID CYST

A case of primary hyperparathyroidism is described in which there was clinical and biochemical resolution after a cystic lesion in the superior left lobe of the thyroid gland was surgically removed. On histologic step-section of the cyst an aggregation of epithelial cells was seen in its wall but they could not be definitely identified as parathyroid in origin. Clinical and biochemical evidence is presented which suggests that the lesion was a hyperfunctioning parathyroid cyst. Emphasis is placed on careful historical evaluation regarding manifestations of hyperparathyroidism in patients who have a mass in the anterior neck. Appropriate laboratory investigation in suspected cases may help to document the functional significance of such lesions.

Clinical Experiences of the Lesser Known Manifestations of Hyperparathyroidism

Clinical Experiences of the Lesser Known Manifestations of Hyperparathyroidism

Clinical primary hyperparathyroidism.

Introduction The entity of primary hyperparathyroidism is relatively new. It has been only 33 years (1925) since Mandle 1 first removed a parathyroid adenoma from a patient with osteitis fibrosa generalisata and established a relationship of skeletal disease to parathyroid function. For many years hyperparathyroidism was recognized only by skeletal findings of osteitis fibrosa or von Recklinghausen's disease. It was not until 1929 that Albright, Bauer, Ropes, and Aub 2 showed that the commonest clinical manifestation of hyperparathyroidism was kidney stones. Because of its relatively recent clinical recognition, all of the various manifestations of this disease are not always obvious. At Duke Hospital, 3 over a 25-year period, 17 cases were diagnosed in the first 24 years and 10 cases in the next 1 year. In the past four years we have identified seven cases of hyperparathyroidism resulting from single adenomas and one with multiple adenomas, in which the presenting