It is known that chromium is an inhaled carcinogen and an important risk factor in the development of lung carcinoma.The authors used a microscopic X-ray fluorescence analyzer with transmitted X-ray mapping imaging (Horiba, Kyoto, Japan) to measure the accumulation of chromium in 10 resected lung tissue specimens and 90 biopsy specimens from chromate workers.The maximum chromium accumulation (mean +/- standard deviation) in 10 resected lung tissue specimens was 197 +/- 238 counts per second (cps)/mili ampere (mA) (range, 4-649 cps/mA). Chromium accumulation was scattered in six tissue specimens and diffuse in one specimen. Chromium accumulation in the proximal bronchi was less than in the bronchioles or subpleural regions of the lung. Chromium accumulation was detectable in 63 (70%) of 90 biopsy specimens, and the mean accumulation was 6.5 +/- 9.2 cps/mA (range, 0-46.5 cps/mA). Chromium detected in bronchial tissue specimens was deposited in the bronchial stroma but not in the epithelium. The maximum chromium accumulations in dysplasic (n = 3), squamous metaplastic (n = 10), and normal bronchial epithelia (n = 9) in chromate workers and in normal bronchial epithelia (n = 3) in non-chromate workers were 20.2 +/- 5.4, 18.3 +/- 12.2, 13.2 +/- 13.4, and 3.0 +/- 1.8 cps/mA, respectively. The amount of chromium accumulation significantly increased according to the progression of malignant change of the bronchial epithelium (P = 0.003).Previous studies found that lung carcinoma with chromate exposure exhibited a variety of genetic abnormalities. Considering genetic aberrations and chromium accumulation in these premalignant lesions is useful for elucidating the process of carcinogenesis in chromium-induced lung carcinoma.
Summary Background A subset of familial isolated primary hyperparathyroidism (FIHP) is a variant of hyperparathyroidism–jaw tumour syndrome (HPT‐JT). Aim/patients and methods We investigated the involvement of the HRPT2 , MEN1 and CASR genes in 11 provisional FIHP families and two HPT‐JT families. Results Germline mutations of HRPT2 were found in two of the 11 FIHP families and one of the two HPT‐JT families. One FIHP family with parathyroid carcinoma and atypical adenomas and another FIHP family with cystic parathyroid adenoma had novel frameshift mutations of 518–521del and 62–66del, respectively. In a patient with HPT‐JT, a de novo germline mutation of 39delC was detected. Novel somatic HRPT2 mutations of 70–73del and 95–102del were found in two of five parathyroid tumours in a family with a 518–521del mutation. Biallelic inactivation of HRPT2 by a combination of germline and somatic mutation was confirmed in the parathyroid tumours. The finding that two families diagnosed with FIHP carried HRPT2 mutations suggests that they have occult HPT‐JT. In the remaining 10 families, one family had a missense MEN1 mutation. No mutations of CASR were detected. Conclusion Our results confirm the need to test for HRPT2 in FIHP families, especially those with parathyroid carcinomas, atypical adenomas or adenomas with cystic change.
A 71-year-old woman was admitted to the hospital because of a fever and back pain on April 12, 1995. There were previous histories of undergoing artificial pneumothorax for pulmonary tuberculousis when she was 28 years old, and paracentesis for pyothorax 2 years before. The tumor detected by CT and MRI was situated in contact with pyothorax and extended to the liver. Only necrotic tissue was found by the percutaneous needle biopsy of the tumor. The extirpation of the tumor was performed on August 5, 1995. It was contact with pyothorax and invaded diaphragma and right lobe of the liver. Removed mass measured 8.0×7.5×6.0cm in size and showed solid growth with extensive central necrosis. Microscopically, it was non-Hodgkin malignant Lymphoma, diffuse, large cell, B cell type.
