A 76-year-old man with a history of chronic obstructive pulmonary disease with lung fibrosis, type 2 diabetes mellitus, and chronic kidney disease underwent computed tomography imaging of the chest due to increasing dyspnea. The bones appeared sclerotic, and a bone scan showed diffuse tracer uptake throughout the axial and appendicular skeleton. The prostate showed no features of malignancy on magnetic resonance imaging and prostate-specific antigen was 6.6 μg/L (normal range (NR) 0–5). Serum tryptase levels were mildly elevated at 16 μg/L (NR 2–14) on two occasions. Biochemical investigations showed vitamin D < 14 nmol/L (NR > 50), alkaline phosphatase 665 U/L (NR 30–130), parathyroid hormone 52.8 pmol/L (NR 1.6–7.5), calcium 2.43 mmol/L (NR 2.2–2.6) and phosphate 1.07 mmol/L (NR 0.8–1.5), in keeping with hyperparathyroidism secondary to vitamin D deficiency and chronic kidney disease (creatinine 169 μmol/L and estimated glomerular filtration rate 34 mL/min).

Bone marrow trephine biopsy sections showed areas of active bone resorption by multinucleate osteoclasts forming recesses known as Howship's lacunae (top and bottom left, all histological images hematoxylin and eosin, ×50 objective). In other areas, lamellar bone was being actively laid down by rows of osteoblasts (top center). There was patchy fibrosis at sites of previous bone resorption (bottom center). Notably, there were osteoclasts also visible in the marrow aspirate (top and bottom right, May–Grünwald–Giemsa, ×100 objective). There was no abnormal mast cell population.

These features are typical of hyperparathyroidism where osteoclasts strive to release calcium whilst osteoblasts attempt to repair the trabecular damage. This active bone remodeling with the associated trabecular changes generates the sclerotic radiological appearance of the affected bones. Osteoblasts and osteoclasts normally work together in bone repair, remodeling, and growth but this process is exaggerated under the influence of increased parathyroid hormone whether primary, due to a parathyroid adenoma, or secondary, as a result of vitamin D deficiency or chronic kidney disease. The recognition of the features of bone disorders with associated bone marrow fibrosis is important so that they are not confused with myeloproliferative neoplasms.

一名 76 岁男性，有慢性阻塞性肺疾病伴肺纤维化、2 型糖尿病和慢性肾病病史，由于呼吸困难加重，接受了胸部计算机断层扫描成像。骨骼出现硬化，骨扫描显示整个中轴和附肢骨骼弥漫性示踪剂摄取。前列腺磁共振成像未显示恶性肿瘤特征，前列腺特异性抗原为 6.6 μg/L （正常范围 （NR） 0-5）。血清类胰蛋白酶水平在 16 μg/L （NR 2-14） 时轻度升高。生化调查显示维生素 D < 14 nmol/L （NR > 50）、碱性磷酸酶 665 U/L （NR 30-130）、甲状旁腺激素 52.8 pmol/L （NR 1.6-7.5）、钙 2.43 mmol/L （NR 2.2-2.6） 和磷酸盐 1.07 mmol/L （NR 0.8-1.5），与继发于维生素 D 缺乏和慢性肾病的甲状旁腺功能亢进症一致（肌酐 169 μmol/L 和估计肾小球滤过率 34 mL/min）。

骨髓环钻活检切片显示多核破骨细胞形成称为 Howship 腔隙的隐窝的活动骨吸收区域（左上和左下，所有组织学图像苏木精和伊红，×50 目标）。在其他区域，层状骨被一排排成骨细胞积极铺设（上中）。在先前骨吸收的部位 （底部中心） 有斑片状纤维化。值得注意的是，在骨髓穿刺物中也可见破骨细胞（右上和右下，May-Grünwald-Giemsa，×100 物镜）。没有异常的肥大细胞群。

这些特征是甲状旁腺功能亢进症的典型特征，其中破骨细胞努力释放钙，而成骨细胞试图修复小梁损伤。这种活动性的骨重塑与相关的小梁变化会产生受影响骨骼的硬化放射学外观。成骨细胞和破骨细胞通常在骨骼修复、重塑和生长中协同工作，但在甲状旁腺激素增加的影响下，这个过程被夸大了，无论是原发性的，由于甲状旁腺腺瘤，还是继发性的，由于维生素 D 缺乏或慢性肾病。识别伴有骨髓纤维化的骨骼疾病的特征很重要，这样它们就不会与骨髓增生性肿瘤混淆。