Diagnosis and Treatment > Investigation > Bone scintigraphy
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General Surgery, Mount Druitt Hospital, Mount Druitt, New South Wales, Australia
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Summary
In most developed countries, breast carcinoma is the most common malignancy in women and while thyroid cancer is less common, its incidence is almost three to five times greater in women than in men. Since 1966, studies have demonstrated an association between thyroid and breast cancer and despite these studies, the mechanism/s by which they are related, remains unclear. We present a case of a 56-year-old lady who initially presented in 2014 with a screen detected left breast carcinoma but was subsequently found to have occult metastatic thyroid cancer to the axilla, diagnosed from a sentinel node biopsy from the primary breast procedure. The patient underwent a left mastectomy, left axillary dissection and total thyroidectomy followed by three courses of radioactive iodine ablation. Despite this, her thyroglobulin level continued to increase, which was secondary to a metastatic thyroid cancer parasternal metastasis. Breast and thyroid cancer presents metachronously or synchronously more often than by chance. With improving mortality in primary cancers, such as breast and differentiated thyroid cancer, it is likely that as clinicians, we will continue to encounter this association in practice.
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There has been a long-standing observation of an association between breast and thyroid cancer although the exact mechanism of this association remains unclear.
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Our patient presented with thyroid cancer with an incidental diagnosis from a sentinel node biopsy during her primary breast operation for breast cancer and was also found to have a parasternal distant bony metastasis.
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Thyroid axillary metastases are generally rare.
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The interesting nature in which this patient’s metastatic thyroid carcinoma behaved more like a breast carcinoma highlights a correlation between these two cancers.
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With improving mortality in these primary cancers, clinicians are likely to encounter this association in clinical practice.
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Systemic therapy for metastatic breast and thyroid cancers differ and therefore a clear diagnosis of metastasis is crucial.
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Summary
Brown tumors are osteoclastic, benign lesions characterized by fibrotic stroma, intense vascularization and multinucleated giant cells. They are the terminal expression of the bone remodelling process occurring in advanced hyperparathyroidism. Nowadays, due to earlier diagnosis, primary hyperparathyroidism keeps few of the classical manifestations and brown tumors are definitely unexpected. Thus, it may happen that they are misdiagnosed as primary or metastatic bone cancer. Besides bone imaging, endocrine evaluation including measurement of serum parathyroid hormone and calcium (Ca) levels supports the pathologist to address the diagnosis. Herein, a case of multiple large brown tumors misdiagnosed as a non-treatable osteosarcoma is described, with special regards to diagnostic work-up. After selective parathyroidectomy, treatment with denosumab was initiated and a regular follow-up was established. The central role of multidisciplinary approach involving pathologist, endocrinologist and oncologist in the diagnostic and therapeutic work-up is reported. In our opinion, the discussion of this case would be functional especially for clinicians and pathologists not used to the differential diagnosis in uncommon bone disorders.
Learning points:
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Brown tumors develop during the remodelling process of bone in advanced and long-lasting primary or secondary hyperparathyroidism.
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Although rare, they should be considered during the challenging diagnostic work-up of giant cell lesions.
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Coexistence of high parathyroid hormone levels and hypercalcemia in primary hyperparathyroidism is crucial for the diagnosis.
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A detailed imaging study includes bone X-ray, bone scintiscan and total body CT; to rule out bone malignancy, evaluation of bone lesion biopsy should include immunostaining for neoplastic markers as H3G34W and Ki67 index.
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If primary hyperparathyroidism is confirmed, selective parathyroidectomy is the first-line treatment.
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In advanced bone disease, treatment with denosumab should be considered, ensuring a strict control of Ca levels.
Endocrinology, Rheumatology/Immunology, Klinikum Südstadt Rostock, Rostock, Germany
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Endocrinology, Rheumatology/Immunology, Klinikum Südstadt Rostock, Rostock, Germany
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Summary
Tumor-induced osteomalacia (TIO) is caused by the hormone fibroblast growth factor 23 (FGF-23). It is mainly produced in the tissue of mesenchymal tumors. Patients with TIO frequently suffer from a chronic decompensated pain syndrome and/or muscle weakness with postural deformity. Despite the severity of the disease, the diagnosis is frequently established late. In some cases, it takes several years to establish the condition. This case report concerning a 68-year old woman demonstrates the selective blood sampling for FGF-23 as path-breaking diagnostics to confirm the diagnosis of a neuroendocrine tumor.
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Tumor-induced osteomalacia is a rare condition compared to other paraneoplastic syndromes.
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It causes complex symptoms such as progressive reduction of physical capacity, exhaustion, fatigue, a decompensated pain syndrome of the musculoskeletal system and fractures of several bones.
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Elevated serum levels of FGF-23 implicate massive phosphate elimination and resulting hypophosphatemia.
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The diagnosis is often established over a period of several years because the localization of small FGF-23-producing tumors is complicated.
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It is the combination of MRI and selective blood sampling for FGF-23 which permits reliable identification of tumors causing TIO and leads to accurate localization.
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In a patient with generalized pain and reduced physical capacity, osteological parameters such as phosphate, 25-OH vitamin D3 and 1,25-(OH)2D3, as well as bone-specific alkaline phosphatase levels in serum should be determined. Hypophosphatemia should always lead to further diagnostic investigations aiming at the detection of an FGF-23-producing tumor.
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Summary
Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome characterized by renal phosphate wasting leading to hypophosphatemia due to excessive actions of fibroblast growth factor 23 (FGF23) produced by the tumors. Although the best way of curing TIO is complete resection, it is usually difficult to detect the culprit tumors by general radiological modalities owing to the size and location of the tumors. We report a case of TIO in which the identification of the tumor by conventional imaging studies was difficult. Nonetheless, a diagnosis was made possible by effective use of multiple modalities. We initially suspected that the tumor existed in the right dorsal aspect of the scapula by 68Ga-DOTATOC positron emission tomography/computed tomography (68Ga-DOTATOC-PET/CT) and supported the result by systemic venous sampling (SVS). The tumor could also be visualized by 3T-magnetic resonance imaging (MRI), although it was not detected by 1.5T-MRI, and eventually be resected completely. In cases of TIO, a stepwise approach of 68Ga-DOTATOC-PET/CT, SVS and 3T-MRI can be effective for confirmation of diagnosis.
Learning points:
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TIO shows impaired bone metabolism due to excessive actions of FGF23 produced by the tumor. The causative tumors are seldom detected by physical examinations and conventional radiological modalities.
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In TIO cases, in which the localization of the culprit tumors is difficult, 68Ga-DOTATOC-PET/CT should be performed as a screening of localization and thereafter SVS should be conducted to support the result of the somatostatin receptor (SSTR) imaging leading to increased diagnosability.
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When the culprit tumors cannot be visualized by conventional imaging studies, using high-field MRI at 3T and comparing it to the opposite side are useful after the tumor site was determined.
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Summary
Thyroid cancer with cranial metastasis in a pregnant woman is very rare. In the literature, most cases are diagnosed early from neurogenic signs or symptomatic thyroid gland. Pregnancy also contributes to a hesitation toward early surgical and medical treatments. We reported a scalp tumor in a physically healthy 37-year-old pregnant female with a follicular thyroid carcinoma (FTC) with lung, bone and cranial metastasis in initial presentation. Silent neurogenic and physical examinations make an early diagnosis very challenging. Resection of scalp and intracranial tumor, a thyroidectomy, post-operative radioactive iodine therapy and tyrosine kinase inhibitors were employed as treatment. The scalp tumor was confirmed as a metastatic follicular thyroid carcinoma via positive immunoreactivity for thyroglobulin and thyroid transcription factor 1 in tumor cells. Blood examination revealed an elevated thyroglobulin level (>5335 ng/mL). The patient was discharged without any neurological deficit. An asymptomatic scalp tumor in a pregnant woman with a normal thyroid disease history needs differential diagnosis from intracranial origin. Rapid progression and an elevated thyroglobulin level are the indicators that further image study is needed. Aggressive surgical excision of resectable thyroid gland and metastatic tumor are essential for a longer survival rate. There is nothing to indicate that a post-partum operation will worsen prognosis.
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Summary
Skeletal manifestations of primary hyperparathyroidism (pHPT) include brown tumors (BT), which are osteoclastic focal lesions often localized in the jaws. Brown tumors are a rare manifestation of pHTP in Europe and USA; however, they are frequent in developing countries, probably related to vitamin D deficiency and longer duration and severity of disease. In the majority of cases, the removal of the parathyroid adenoma is enough for the bone to remineralize, but other cases require surgery. Hyperparathyroidism in MEN1 develops early, and is multiglandular and the timing of surgery remains questionable. To our knowledge, there are no reports of BT in MEN 1 patients. We present a 29-year-old woman with MEN 1 who developed a brown tumor of the jaw 24 months after getting pregnant, while breastfeeding. Serum corrected calcium remained under 2.7 during gestation, and at that point reached a maximum of 2.82 mmol/L. Concomitant PTH was 196 pg/mL, vitamin D 13.7 ng/mL and alkaline phosphatase 150 IU/L. Bone mineral density showed osteopenia on spine and femoral neck (both T-scores = −1.6). Total parathyroidectomy was performed within two weeks, with a failed glandular graft autotransplantation, leading to permanent hypoparathyroidism. Two months after removal of parathyroid glands, the jaw tumor did not shrink; thus, finally it was successfully excised. We hypothesize that higher vitamin D and mineral requirements during maternity may have triggered an accelerated bone resorption followed by appearance of the jaw BT. We suggest to treat pHPT before planning a pregnancy in MEN1 women or otherwise supplement with vitamin D, although this approach may precipitate severe hypercalcemia.
Learning points:
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Brown tumors of the jaw can develop in MEN 1 patients with primary hyperparathyroidism at a young age (less than 30 years).
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Pregnancy and lactation might trigger brown tumors by increasing mineral and vitamin D requirements.
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Early parathyroidectomy is advisable in MEN 1 patients with primary hyperparathyroidism, at least before planning a pregnancy.
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Standard bone mineral density does not correlate with the risk of appearance of a brown tumor.
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Removal of parathyroid glands does not always lead to the shrinkage of the brown tumor, and surgical excision may be necessary.
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Summary
Hepatitis C-associated osteosclerosis (HCAO), a very rare disorder in which an extremely rapid bone turnover occurs and results in osteosclerosis, was acknowledged in 1990s as a new clinical entity with the unique bone disorder and definite link to chronic type C hepatitis, although the pathogenesis still remains unknown. Affected patients suffer from excruciating deep bone pains. We report the 19th case of HCAO with diagnosis confirmed by bone biopsy, and treated initially with a bisphosphonate, next with corticosteroids and finally with direct acting antivirals (DAA: sofosbuvir and ribavirin) for HCV infection. Risedronate, 17.5 mg/day for 38 days, did not improve the patient’s symptoms or extremely elevated levels of bone markers, which indicated hyper-bone-formation and coexisting hyper-bone-resorption in the patient. Next, intravenous methylprednisolone pulse therapy followed by high-dose oral administration of prednisolone evidently improved them. DAA therapy initiated after steroid therapy successfully achieved sustained virological response, but no additional therapeutic effect on them was observed. Our results strongly suggested that the underlying immunological alteration is the crucial key to clarify the pathogenesis of HCAO. Bone mineral density of lumbar vertebrae of the patient was increased by 14% in four-month period of observation. Clarification of the mechanisms that develop osteosclerosis in HCAO might lead to a new therapeutic perspective for osteoporosis.
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HCAO is an extremely rare bone disorder, which occurs exclusively in patients affected with HCV, of which only 18 cases have been reported since 1992 and pathogenesis still remains unclear.
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Pathophysiology of HCAO is highly accelerated rates of both bone formation and bone resorption, with higher rate of formation than that of resorption, which occur in general skeletal leading to the diffuse osteosclerosis with severe bone pains.
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Steroid therapy including intravenous pulse administration in our patient evidently ameliorated his bone pains and reduced elevated values of bone markers. This was the first successful treatment for HCAO among cases reported so far and seemed to propose a key to solve the question for its pathogenesis.
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The speed of increase in the bone mineral content of the patient was very high, suggesting that clarification of the mechanism(s) might lead to the development of a novel therapy for osteoporosis.
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Summary
Paget's disease is a chronic and progressive disorder of bone characterized by focal areas of excessive osteoclastic resorption accompanied by a secondary increase in the osteoblastic activity. Paget's disease of bone (PBD) is a rare endocrine disease especially among Africans and Asians. Hence the detection of a case in a middle-aged Nigerian is of interest. We present the case of a 62-year-old Nigerian man in apparent good health who was found to have a markedly elevated serum total alkaline phosphatase (ALP) of 1179 U/l (reference range, 40–115 U/l) 4 years ago during a routine medical check-up in the USA. He had no history suggestive of PDB and also had no known family history of bone disease. Examination findings were not remarkable except for a relatively large head. A repeat ALP in our centre was 902 U/l (reference range, 40–120 U/l). Cranial CT scan showed diffuse cranial vault thickening consistent with Paget's disease which was confirmed by Tc-99m hydroxymethylene diphosphonate. He was placed on 40 mg alendronate tablets daily for 6 months. The patient has remained asymptomatic and has been in continuing biochemical remission during the 3-year follow-up period. The most recent ALP result is 88 U/l (reference range, 30–132 U/l) in April 2015.
Learning points
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Serum total alkaline phosphatase remains a sensitive marker of bone turnover and an isolated increase above the upper limit of normal warrants more intense scrutiny in form of investigations targeted at excluding PD.
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Paget's disease is very rare but can occur in the Africans as seen in this Nigerian man and most patients are asymptomatic.
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Asymptomatic patients can benefit from treatment if disease is active, polyostotic or the lesions are located in bones with future risk of complications such as long bones, vertebrae and skull.
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Bisphosphonates are still the mainstay of treatment and alendronate is a useful therapeutic option for treatment.
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Summary
A man underwent total thyroidectomy for goiter when he was 62 years old. The pathology report informed on a 5.5 cm oncocytic follicular adenoma and a 3.5 mm papillary microcarcinoma. Due to the papillary tumor, he was treated with ablative radioiodine therapy and suppressive doses of levothyroxine. After uneventful follow-up for 9 years, increased levels of serum thyroglobulin were detected. Further imaging studies including a whole body scan (WBS) after an empirical dose of 200 mCi 131I were negative. Two years later, a 99mTc SestaMIBI WBS and a 2-[18F]-fluoro-2-deoxy-d-glucose positron-emission tomography showed a well-delimited focal uptake in the right femur. A bone biopsy of the lesion demonstrated metastasis of follicular thyroid carcinoma. Retrospective histological reexamination of available material from the primary oncocytic thyroid tumor failed to reveal definitive traits of malignancy.
Learning points
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Oncocytic follicular thyroid tumors are a relatively uncommon variant of follicular thyroid neoplasms mostly composed of distinctive large oxyphilic cells (Hürthle cells).
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Criteria for the distinction between benign and malignant oncocytic neoplasms are not different from those used in the diagnosis of ordinary follicular tumors.
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Some cases of apparently benign oncocytic neoplasms have been found to develop malignant behavior.
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Search to rule out vascular and capsular invasion should be particularly exhaustive in histological assessment of oncocytic thyroid tumors.
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Even so, long-term surveillance remains appropriate for patients with large apparently benign oncocytic tumors.
