Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153690 (bone metastases)
 6,382 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case histories of the 49 patients who died in a series of 165 patients admitted to the Medical Unit between 1958 and 1984 with polyarteritis nodosa (PAN) were reviewed. The causes of death of the 29 men and 20 women, mean age 51.44 +/- 7.4 years, were classified into 6 groups. Infection accounted for 26.5% (13/49) of deaths, the initial site of infection being pulmonary, complicated by septicaemia in 6 cases. Cardiovascular events were responsible for death in 24.4% (11/49): terminal cardiac failure (4 cases), myocardial infarction (1 case), ventricular tachycardia (1 case), stroke (1 case), pulmonary embolism (2 cases), fulminant hemoptysis (1 case). Gastrointestinal complications were the cause of death in 16.3% (8/49): ischemic necrosis (5 cases), acute pancreatitis (2 cases), oesophageal ulceration (1 case). Renal failure was observed in 10.2% (5/49), all occurring before 1972: acute renal failure (3 cases), chronic renal failure (2 cases). Cancer was the cause of death in 10.2% (5/49): primary bronchial carcinoma (2 cases), laryngeal carcinoma (1 case), carcinoma of the vulva (1 case), bone metastases (1 case). Finally, 14.2% (7/49) could not be classified in the preceding groups. Sudden death occurred in 3 patients, shock in 1 patient, multivisceral PAN in 2 patients and anaphylactic shock in 1 patient. Three of the 12 patients who had post-mortem studies had signs of progressive vasculitis. The results are compared with other reports in the literature and the pathogenic mechanisms are discussed. The infections and cardiovascular deaths occurred early or late and were not related to the state of the activity of the vasculitis. Immunosuppressive treatment seems to play an important role in their pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Causes of death in systemic vasculitis of polyarteritis nodosa. Analysis of a series of 165 patients]. 290 28

Etidronate is an oral bisphosphonate compound that is known to reduce bone resorption through the inhibition of osteoclastic activity. The efficacy of etidronate for involutional (postmenopausal and senile) and glucocorticoid-induced osteoporosis, as well as that for other skeletal diseases, was reviewed in Japanese patients. Cyclical etidronate treatment (200 mg or 400mg/day for 2 weeks about every 3 months) increases the lumbar bone mineral density (BMD) in patients with involutional osteoporosis and prevents incident vertebral fractures in patients with glucocorticoid-induced osteoporosis. The losses of the lumbar BMD in patients with liver cirrhosis and the metacarpal BMD in hemiplegic patients after stroke are prevented, and the lumbar BMD is possibly increased, preventing fragile fractures in adult patients with osteogenesis imperfecta type I. Furthermore, proximal bone resorption around the femoral stem is reduced and some complications may be prevented in patients who undergo cementless total hip arthroplasty. Oral etidronate treatment may also help to transiently relieve metastatic cancer bone pain followed by a decrease in abnormally raised bone resorption in patients with painful bone metastases from primary cancer sites, such as the lung, breast and prostate. Thus, oral etidronate treatment is suggested to be efficacious for osteoporosis, as well as other skeletal diseases associated with increased bone resorption, in Japanese patients. Randomized controlled trials needed to be conducted on a large number of patients to confirm these effects.
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PMID:Efficacy of oral etidronate for skeletal diseases in Japan. 1598 1

We report a rare presentation of a 66-year-old female with diffuse metastatic adenocarcinoma of unknown primary involving liver, lymphatic system and bone metastases. The neoplastic cells were positive for CK7 and OC125, while negative for CK20, thyroid transcription factor 1, CDX2, BRST-2, chromogranin, synaptophysin, estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2/neu). Fluorescence in situ hybridization showed no amplification of the HER2/neu gene. Molecular profiling reported a breast cancer origin with a very high confidence score of 98%. The absence of immunohistochemistry staining for ER, PR, and HER2/neu further classified her cancer as triple-negative breast cancer. Additional studies revealed high expression levels of topoisomerase (Topo) I, androgen receptor, and ribonucleoside-diphosphate reductase large subunit; the results were negative for thymidylate synthase, Topo II-a and O6-methylguanine-DNA methyltransferase. The patient was initially treated with a combination regimen of cisplatin and etoposide, and she experienced a rapid resolution of cancer-related symptoms. Unfortunately, her therapy was complicated by a cerebrovascular accident (CVA), which was thought to be related to cisplatin and high serum mucin. After recovery from the CVA, the patient was successfully treated with second-line chemotherapy based on her tumor expression profile. We highlight the role of molecular profiling in the diagnosis and management of this patient and the implication of personalized chemotherapy in this challenging disease.
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PMID:Occult breast cancer presenting as metastatic adenocarcinoma of unknown primary: clinical presentation, immunohistochemistry, and molecular analysis. 2237 71

A 62-year-old female patient with metastatic renal cell carcinoma under third-line treatment with pazopanib for 8 weeks suddenly developed severe headaches, grand mal seizures and paresis of the left arm in combination with gait instability as well as nausea and vomiting during her vacation abroad. The emergency physician measured systolic blood pressure values over 300 mm Hg and suspected a stroke. The CT imaging without contrast agent in a local hospital did not show any pathologic findings despite bone metastases. The colleagues suspected cerebral metastases or meningeosis carcinomatosa and referred the patient to our department for further diagnostics and treatment planning. An MRI scan ruled out the suspected cerebral metastases or meningeosis carcinomatosa, but showed signs of reversible posterior leukoencephalopathy syndrome (RPLS) in the form of band-like hyperintensities as a sign of cytotoxic edema in the gray and white matter of the left parietal lobe. The patient then reported that similar blood pressure values had been measured shortly after the start of a first-line therapy with sunitinib, so that we discontinued the current treatment with pazopanib. Within 6 days the neurologic symptoms vanished and the patient was discharged. An intermittent hypertension persisted. A follow-up MRI 3 weeks later showed an RPLS-typical cortical infarction in the affected area. RPLS should be considered as the actual reason for neurologic findings in hypertensive patients with known metastatic cancers under tyrosine kinase inhibitor therapy.
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PMID:Posterior reversible leukoencephalopathy syndrome associated with pazopanib. 2362 62

A 65-year-old man with disseminated bone metastases of prostate cancer was referred for Ga-PSMA-HBED-CC-PET/CT (short PSMA-PET/CT) to exclude visceral metastases before treatment of bone metastases with Ra-dichloride. Apart from disseminated bone metastases, PSMA-PET/CT revealed a focal cerebral tracer uptake in the right frontal lobe highly suspicious for cerebral spread. According to patient history, a cerebral infarction occurred 14 days before PSMA imaging in corresponding localization confirmed by MRI scanning. This case demonstrates the possibility of false-positive finding of cerebral metastases in PSMA-PET early after stroke.
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PMID:Subacute Stroke Mimicking Cerebral Metastasis in 68Ga-PSMA-HBED-CC PET/CT. 2735 52