Bone marrow necrosis.

BACKGROUND: In the medical community, little is known regarding bone marrow necrosis (BMN) as a clinicopathologic entity, although to the authors' knowledge it was described for the first time more than 50 years ago. To identify the rate of prevalence, the symptoms and signs, the underlying disease associations, and the usefulness of diagnostic procedures, an extensive literature search was made. METHODS: Only cases identified as extensive necrosis and diagnosed during life were selected. Two hundred forty cases met these criteria. RESULTS: Bone pain (75%) and fever (68.5%) were the most important symptoms, whereas anemia (91%) and thrombocytopenia (78%), associated with a leukoerythroblastic picture (51%), were the most frequent hematologic abnormalities. Nearly 50% of patients showed elevated lactate dehydrogenase and alkaline phosphatase levels. In 90% of the patients an underlying malignancy was identified. CONCLUSIONS: Bone marrow necrosis is caused by hypoxemia after failure of the microcirculation. Given the high rate of malignancy as an underlying disease association, an extensive search for neoplastic disease is justified whenever BMN is diagnosed. Pancytopenia and embolic processes are major complications that should be managed with supportive measures until effective treatment of the underlying disease has been administered. When necrosis resolves, repopulation of the bone marrow cavity with normal hematopoiesis is observed.

A radioimmunoassay for murine thyroglobulin in serum: age-related increase of serum thyroglobulin levels in AKR/J mice.

Possible regulation of the synthesis of murine thyroglobulin (mTg) and a possible role for the major histocompatibility complex in this process were evaluated in 18 inbred strains of mice. A double antibody RIA was first developed to measure mTg in serum. The isolated mTG was labeled with 131I since 125I rapidly degraded the mTg molecule. The sensitivity of this mTg assay allowed detection of 15-20 ng/ml. Specificity was demonstrated by the minimal cross-reactivity with rat Tg (0.008%) and the total lack of cross-reactivity with human Tg. There was no correlation between H-2 haplotype and serum mTg levels. In five strains of mice with the H-2k haplotype, mTg levels varied from 30 +/- 2 to 48 +/- 11 ng/ml (mean +/- SD); however, only aged AKR/J mice (H-2k) exceeded this range (196 +/- 27 ng/ml). Strains with other haplotypes (a, b, d, g, q, v) demonstrated a similar range of mTg levels, but none had this age-related increase in mTg levels. The high levels of mTg were not caused by a decrease in the half-life of this protein and probably not caused by virus-induced alterations in the thyroid economy. Thyroids from the AKR/J mice, however, had larger follicles and flatter epithelia compared to thyroids from other strains. These studies suggest that AKR/J mice may represent a useful animal model for the study of goitrogenesis.