Spinal Cοrd Compression Secondary to Brοwn Tumοr as First Manifestation of Primary Hyperparathyroidism.

BACKGROUND: Brown tumors (BTs) represent the typical nonmalignant lesions of hyperparathyroidism. Mandibles, ribs, and large bones are the most usual localization of BT. The diagnosis of these tumors requires biological and radiologic assessments. Their treatment is essentially based on parathyroidectomy. CASE DESCRIPTION: The present case report describes a patient with primary hyperparathyroidism who developed a cervical BT revealed by slow spinal compression. CONCLUSIONS: The brown tumor, when localized at the level of the spine, can be life-threatening and must be managed as soon as possible.

Management challenges with brown tumor of primary hyperparathyroidism masked by severe vitamin D deficiency: a case report.

BACKGROUND: Hyperparathyroidism is a disease characterized by excessive secretion of parathyroid hormone, the hormone responsible for calcium and phosphate homeostasis in the body. It can be of three types: primary, secondary, or tertiary. It is essential to bear in mind that in any one patient more than one type of hyperparathyroidism may be found, which may create perplexity regarding the etiology of the case. Hyperparathyroidism can become apparent early in its course when a patient presents with symptoms of abdominal pain, recurrent renal calculi, repeated fractures, or behavior changes. It is generally accepted that bone involvement is a late manifestation of primary hyperparathyroidism. It is imperative to consider that some patients, such as our patient described in this report, may be previously asymptomatic clinically and on the basis of laboratory findings and present with only late skeletal manifestations. Brown tumors are one of the mimickers of lytic lesions of the jaw and need to be ruled out early in the course of management. Researchers in several studies published in high-impact journals have recommended the use of high-dose vitamin D as safe in patients with primary hyperparathyroidism without the risk of raising calcium levels significantly. In our patient, we observed considerable hypercalcemia after high-dose vitamin D therapy, and we propose exercising discretion with the use of high-dose therapies. CASE PRESENTATION: We report a case of a 21-year-old Arab woman with a brown tumor who presented with hypocalcaemia. She presented with a mixed picture of primary hyperparathyroidism and severe vitamin D deficiency. CONCLUSIONS: Brown tumors, although thought to be a forgotten entity with the advent of early screening for hypercalcemia, is still prevalent, as a handful of patients may present late in the disease course with no early markers, such as in our patient. We emphasize using a holistic approach for early diagnosis and adopting a restricted attitude to treating these benign entities, especially in the context of cosmesis for sensitive locations such as the face. In addition, we express caution in using daily supplementation with a high vitamin D dose to improve vitamin D status and decrease parathyroid hormone.

Musculoskeletal manifestations of primary hyperparathyroidism.

Primary hyperparathyroidism (PHPT) can be associated with a variety of musculoskeletal complaints, which occasionally can be the leading or presenting manifestation. In this paper, we describe the musculoskeletal manifestations observed in patients with primary hyperparathyroidism. Medical record reviews of a select population of 74 patients with primary hyperparathyroidism are seen in a rheumatology practice. Bone manifestations included back pain in 11 patients (15.2 %), generalized bone pain in 7 patients (9.7 %), rib cage/chest pain in 6 (8.3 %), pseudoclubbing in 3, and a giant cell tumor of the mandible in 2 (2.3 %) patients. Articular manifestations such as chondrocalcinosis with or without apatite deposition disease were seen in 13 (17.7 %), arthralgias in 11 (15.2 %), and non-specific synovitis in 7 (9.7 %). Muscle weakness was observed in six patients (8.3 %) and myalgias in three (4.6 %). Less common manifestations such as Achilles tendon rupture, Jaccoud-like arthropathy, sacral insufficiency fracture, arthritis associated with fever of unknown origin (FUO), meningitis, cervical cord compression, and persistent headache were observed in single patients. Musculoskeletal findings are still a frequent and important presentation in patients with primary hyperparathyroidism seen in rheumatology practice. Some of these manifestations can be quite unusual and may represent diagnostic dilemmas to the practicing rheumatologist and/or endocrinologist.

Facial disfigurement due to osteitis fibrosa cystica or brown tumor from secondary hyperparathyroidism in patients on dialysis: A systematic review and an illustrative case report.

Osteitis fibrosa cystica (OFC) is the most frequent type of osseous change in renal osteodystrophy affecting the majority of dialysis patients. Brown tumors are a severe form of OFC. The involvement of the craniofacial skeleton causing facial disfigurement in patients on dialysis appears to be limited to case reports. After searching PubMed, we performed a systematic review of 127 cases with a severe form of OFC resulting in a facial disfigurement to understand possible determinants for this condition. We found that since the first published case in 1974, and after a peak in 1996, there appears to be an increase in published reported cases. Only 27.6% of these cases were published in nephrology journals. The most common region for reported cases was North America. Mean age of these patients was 31.2 years with a mean dialysis duration of 7 years. Almost 67% were women, and almost all were on hemodialysis. The disease tended to most commonly localize to the maxilla (73.2%) and mandible (57.5%). As part of the treatment, 59% of patients had a parathyroidectomy. More than one-third (35.4%) had symptomatic improvement at follow-up. Mean follow-up was 1.6 years. Clinicians should be aware of this clinical presentation of a severe form of OFC and/or brown tumors. Timely diagnosis and intervention may help to prevent or decrease destructive bone changes and reduce negative psychological consequences of facial disfigurement.

[Brown tumor of the jaws]. / Tumore bruno dei mascellari.

Brown tumour is one of the forms in which fibrous-cystic osteitis, which represents the terminal stage of the bone remodelling processes during primary or secondary hyperparathyroidism, is manifested. For years brown tumour was regarded as a typical lesion of primary hyperparathyroidism, but cases of brown tumours in patients with hyperparathyroidism secondary to renal failure were increasingly often reported in the literature. From an epidemiological point of view, the frequency of brown tumours in patients with renal insufficiency is extremely variable, as is the bone site affected. Several bone segments can be affected at once, but the ethmoid and frontal sinus are rarely reported. Symptoms are caused by the considerable dimensions of the brown tumour and its localisation: in the jawbones it may present sometimes painful, hard and clearly palpable swellings; if large, the tumour may deform the appearance of the bone segments affected or alter the function of the masticatory apparatus. In other cases, there is a complete absence of clinical symptoms and diagnosis may be totally coincidental during the radiological examinations. In histological terms, brown tumours are made up by a cell population consisting of rounded or spindle-like mononucleate elements, mixed with a certain number of plurinucleate giant cells, resembling osteoclastic cells, among which recent haemorrhagic infiltrates and hemosiderin deposits (hence the brown colour) are often found. The aim of this study was to report three cases from a population of 107 patients undergoing haemodialysis at the Turin University Centre. In conclusion, the localisation of maxillary brown tumours appears to prefer a young, female population; brown tumours are rarely an early sign of hyperparathyroidism in haemodialysis patients, but they often appear in conditions of advanced hyperparathyroidism which have escaped medical control either owing to unsuitable therapy or scant patient compliance; they are rapidly evolving lesions whose regression may be very slow or not occur even after total parathyroidectomy; the severity of the lesion caused by a brown tumour may lead to evident osteolysis in the maxillofacial district, thus suggesting the need for early and regular radiological screening; in the event of lesions which are already present, from the authors' point of view, the choice of treatment must be oriented towards parathyroidectomy.

[Bone pain, polydipsia, polyuria]. / Knochenschmerzen, Polydipsie, Polyurie.

This 20 year old man suffered increasingly from multifocal bone- and back pain over the last 6 months. Painful weakness of the left leg with dysesthesia of the 4th and 5th toe, a weight loss of 15 kg and polydipsia and pollakiuria had developed. The clinical workup disclosed hard tumors in the right mandible and tibia, a waddling gait with bilateral sign of Trendelenburg, reduced muscular force in the left leg with missing achilles tendon reflex and a loss of sensibility in the distal S1 segment, epigastric tenderness on pressure and hypertension with a value of 160/100 mmHg. X-rays revealed multiple cystic bone lesions at all sites. Hypercalcemia and massively elevated parathyroid hormone were measured. Since the parathyroids were enlarged on sonography, primary hyperthyroidism with fibrosing osteitis v. Recklinghausen was diagnosed.

[Morpho-functional imaging in a patient with hyperparathyroidism and multifocal maxillary brown tumor]. / Imagerie morphologique et fonctionnelle des tumeurs brunes. À propos d'un cas de localisation maxillo-mandibulaire.

INTRODUCTION: Brown tumors are uncommon osteolytic lesions directly related to the increased osteoclastic activity due to hyperparathyroidism. CASE REPORT: A 37-year-old woman presented with hypercalcemia related to primary hyperparathyroidism. Multiple and bilateral maxillary osteolytic lesions showing intense fluorodesoxyglucose (FDG) uptake were noted in a positron emission tomography computed tomography (PET-CT). Diagnosis of maxillary brown tumors was discussed and confirmed by both orthopantomogram and magnetic resonance imaging. Left inferior parathyroid adenoma was detected by both cervical ultrasonography and parathyroid scintigraphy, and then surgically treated with consequent improvement of hyperparathyroidism. CONCLUSION: Our case emphasizes the necessity of a multidisciplinary diagnostic approach to optimize the interpretation of the available imaging, especially in unusual and unrecognized pathology as brown tumors.

[Brown tumors of upper and lower jaws in Recklinghausen neurofibromatosis. A case report]. / Tumori brune ale maxilarului si mandibulei in neurofibromatoza Recklinghausen. Observatii pe marginea unui caz.

We report the case of a 41-year-old patient who presented multiple cafe au lait spots and exophytic tumors of the upper jaw, causing facial asymmetry and masticatory impairment. Physical examination and paraclinical investigations established the diagnosis of NF1 (type 1 neurofibromatosis) associated with brown tumors in jaws and left nasal bone, caused by a primary hyperparathyroidism (Oxyphilic adenoma). The parathyroidectomy determines brown tumors regression and sclerosis with no dependence on their localization.

[Brown tumor of the upper jaw. Surgical-rehabilitation problems]. / Tumore bruno del mascellare superiore. Problemi chirurgico-riabilitativi.

The Authors describe etiology, pathogenesis and main clinical aspects of brown tumors in patients with chronic renal failure. Then, by presenting two cases of patients with secondary hyperparathyroidism and brown tumors of upper maxillary bone, they report the measures to be applied for the surgical treatment and prosthetic management of these patients. In both cases the patients have been undergone a radical resection of a brown tumor of the palate. After maxillectomy have been successfully applied at first an interim obturator prosthesis and then, approximately three months later the definitive obturator prosthesis.

Sphenoid sinus brown tumor, a mass lesion of occipital bone and hypercalcemia: an unusual presentation of primary hyperparathyroidism.

Brown tumor is a focal lesion of the bone caused by primary or, less commonly, secondary or tertiary hyperparathyroidism (HPT). While the mandible is the most frequently involved bone in the head and neck region, atypical involvement of the cranium in the area of the sphenoid sinus is exceedingly rare. In the literature, a unique case of brown tumor of the sphenoid sinus was reported in a patient with primary HPT. We present a case of sphenoid sinus and occipital bone brown tumor associated with primary HPT. A 47-yr-old woman presented a 2-yr history of headaches, dizziness, diffuse body and articular pain, fatigue, and a 6-month history of intermittent nausea and vomiting, polydipsia, and polyuria. Magnetic resonance imaging (MRI) demonstrated an expansive mass lesion in the sphenoid sinus with erosion of the sellar floor and medial wall of the right orbit, and expansion in the medulla of bone. Examination of biopsy specimens obtained from sphenoid sinus mass confirmed the diagnosis of brown tumor. The biochemical laboratory studies showed elevation of parathyroid hormone and confirmed the diagnosis of primary HPT. Excision of a parathyroid adenoma affected the metabolic status into normalizing. At the follow-up of 12 months postoperatively, the size of sphenoid sinus brown tumor decreased and the mass of occipital bone disappeared. In conclusion, this is a first report of primary HPT masquerading as a destructive fibrous sphenoid sinus brown tumor associated with a mass lesion of occipital bone and hypercalcemia in the literature.

Concomitant osteitis fibrosa cystica and ameloblastoma of the mandible.

A patient with a multiloculated cystic lesion of the mandible, and clinical as well as biological features of hyperparathyroidism is presented. This association suggesting the diagnosis of brown tumor was actually due to an ameloblastoma of the mandible. Such a concomitant association of an ameloblastoma with symptomatic hyperparathyroidism has never been reported to our knowledge.