In secondary hyperparathyroidism, a disease outside of the parathyroids causes all of the parathyroid glands to become enlarged and hyperactive. It is usually caused by kidney failure, a problem where the kidney is unable to clean the blood of phosphorus produced by the body and unable to make enough vitamin D (specifically calcitriol, the active form of vitamin D). The build-up of phosphorous leads to low levels of calcium in the blood, which in turn stimulates the parathyroid glands to increase parathyroid hormone (PTH) production which in turn causes them to grow. As the disease progresses, the parathyroid glands no longer respond normally to calcium and Vitamin D. During early secondary hyperparathyroidism, the blood calcium levels are normal or low, but the PTH level is high. As the disease gets worse, some of the treatments for the kidney disease (Vitamin D and calcium-containing phosphate binders) may eventually lead to abnormally high levels of calcium in the blood. High PTH levels can lead to 1) weakening of the bones 2) calciphylaxis (when calcium forms clumps in the skin and leads to ulcers and potentially death of surrounding tissue), 3) cardiovascular complications, 4) abnormal fat and sugar metabolism, 5) itching (pruritis), and 6) low blood counts (anemia).
Figure 7: Calciphylaxis
Other less common causes of secondary hyperparathyroidism are long-term lithium therapy, vitamin D deficiency, gastrointestinal malabsorption syndromes (when the intestines do not absorb vitamins and minerals properly), malnutrition, vitamin D-resistant rickets, or hypermagnesemia (abnormally high blood magnesium levels). 87 Calciphylaxis is uncommon. These painful skin lesions begin as small nodules or plaques with a purplish color, mottling, or livedo reticularis in a stellate pattern. The ulcers grow and parts become necrotic (i.e. the tissue dies). They rarely heal with routine wound care measures.