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Wheeless' Textbook of Orthopaedics
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Hyperparathyroidism


- See:
      - Renal Osteodystrophy:
      - Remodeling of Bone

- Discussion:
    - caused by excessive production of parathyroid hormone which leads to hypercalcemia, recurrent nephrolithiasis, pancreatitis, peptic ulcers, and mental changes;
    - incidence of approx 5 /10,000 pts per year;
    - usually affects adults over 50 yrs & occurs more commonly in females;
    - causes:
           - in most cases is due to single parathyroid adenoma (80% of patients);
           - malignant tumor: occurs in about 1% of patients with hyperparathyroidism;
                 - occurs often in association w/ multiple endocrine neoplasia syndrome, and rarely to parathyroid carcinoma;
                 - hyperparathyoidism is sometimes seen in renal cell carcinoma and squamous cell carcinoma;
    - diff dx:
           - occult tumor;
           - multiple myeloma (often associated w/ hypercalcemia);
    - classification:
           - primary defect of the parathyroid gland w/ hypersecretion of PTH as seen w/ adenoma's of the parathyroid gland;
           - secondaray causes arise from conditions that produces abnormally low ionic plasma Ca levels and thereby stimulates production of PTH (see renal disease: effects on bone):
           - tertiary conditions in which PTH secretion has become autonomous after prolonged stimulation of gland owing to secondary parathyroidism;
    - references:
           - Primary hyperparathyroidism: incidence, morbidity, and potential economic impact in a community.  Heath H III, Hodgson SF, Kennedy MA. N Engl J Med 1980;302:189-93.                      
           - Pathology of the parathyroids in hyperparathyroidism: discussion of recent advances in the anatomy and pathology of the parathyroid glands.  Roth SI. Arch Pathol 1962;73:495-510.        
           - Recent advances in parathyroid gland pathology.  Roth SI. Am J Med 1971;50:612-22.                                                    
           - Primary hyperparathyroidism: changing patterns in presentation and treatment decisions in the eighties.  Rao DS.  Henry Ford Hosp Med J 1985;33:194-7.                                                    


- Labratory Diagnosis of Hyperparathyroidism

- Histology of Hyperparthyroidism:

- Radiology of HyperParaThyroidism: Chondrocalcinosis


- Clinical Presentation:
    - General:
         - recurrent nephrolithiasis, peptic ulcers, mental changes which has led to the phrase: stones, bones, and groans;"
               - lethargy, somnolence, and polydipsia are also nonspecific findings;
    - Bone:
         - PTH mobilizes bone and phosphate;
         - releases osteocytic perilacunaar stores (fast)
         - increases osteocytic number and activity (slow)
         - activates & increases number of osteoclasts, which leads to osteomalacia and more acutely, releases Ca & Phos;
         - causes diffuse bone pain and tenderness;
         - stimulate bone remodeling, w/ increase in number of BMU;
         - brown tumor;
         - chondrocalcinosis and calcific periarthritis are common (ossification of soft tissue);
         - fractures secondary to diffuse skeletal osteoporosis;
         - references:
                - Fractures of the femoral neck in elderly patients with hyperparathyroidism.
                - Joint lesions of hyperparathyroidism.  Bywaters EGL, Dixon ASJ, Scott JT. Ann Rheum Dis 1963;22:171-87.                      
                - Osteosclerosis in primary hyperparathyroidism.  Genant HK, Baron JM, Straus FH II, Paloyan E, Jowsey J. Am J Med 1975;59:104-13.                                                  
                - Hyperparathyroidism: tumor of the parathyroid glands associated with osteitis fibrosa.  Wilder RM. Endocrinology 1929;13:231-44.                                                          
                - Parathyroid hormone and bone. Reeve J, Zanelli JM. Clin Sci 1986;71:231-8.                                                           
                - A case of multiple skeletal lesions of brown tumors, mimicking carcinoma metastases 
    - Kidney:
         - increases resorption of calcium;
         - increases excretion of phosphate;
         - stimulates 1,25 (OH)2 vit D3 (calcitriol) production;
         - common occurrence of renal calculi (in untreated cases, calculi sometimes caused renal failure);
         - increase renal phosphate excretion by decreasing renal tubular reabsorption of phosphate;
    - Gut:
         - increases absorption thru vitamin D;
         - acting at level of gut (w/ vit D) to incr absorption of calcium;
         - gastric ulcers (seen in 25% of patients) & pancreatitis are common;
         - pancreatic calcifications;
    - Neuromuscular:
         - proximal weakness, easy fatigability, and atrophy of muscles;
    - Pyschiatric:
         - individuals w/ serum Ca level of > than 12 mg/dl (2.99 mm/lit) (see hypercalcemia) have mental aberrations, confusion, and dementia;
         - references:
               - Neuropsychologic deficits associated with primary hyperparathyroidism. Numann PJ, Torppa AJ, Blumetti AE. Surgery 1984;96:1119-23.


- Treatment:
         - non operative treatment includes adequate calcium intake and avoidance of Vit D;
               - w/ vague constitutional symptoms that such as fatigue, weakness, and/or constipation associated w/ mild hypercalcemia then surgery is not indicated;
         - note that in most patients w/ primary hyperparathyroidism there is little if any disease progression;
         - among asymptomatic patients, approximately 25 % will have progressive disease, which can be measured as a signficant decrease in bone mass over a decade;
         - operative treatment indications:
               - surgical treatment is indicated when clinical symptoms occur along with laboratory or radiographic abnormalities;
               - clinical findings:
                      - osteitis fibrosa cystica
                      - nephrolithiasis
                      - classic neuromuscular symptoms (proximal muscle weakness, atrophy, hyperreflexia, and gait disturbances);
                      - hyperparathyroid crisis (a discrete episode of life-threatening hypercalcemia);
               - laboratory and radiographic data;
                       - serum calcium concentration of greater than 12 mg per deciliter (3 mmol per liter)
                       - marked hypercalciuria (urinary calcium excretion, greater than 400 mg per day [10 mmol per day])
                       - markedly reduced cortical bone density (z score for the distal third of the radius, less than -2;
                               - z score reflects standard deviation from mean for sex-matched and age-matched reference population), an unexplained reduction in creatinine clearance,





Fractures of the femoral neck in elderly patients with hyperparathyroidism.

Joint lesions of hyperparathyroidism.  Bywaters EGL, Dixon ASJ, Scott JT. Ann Rheum Dis 1963;22:171-87.                      

Osteosclerosis in primary hyperparathyroidism.  Genant HK, Baron JM, Straus FH II, Paloyan E, Jowsey J.  Am J Med 1975;59:104-13.                                                  

Hyperparathyroidism: tumor of the parathyroid glands associated with osteitis fibrosa.  Wilder RM. Endocrinology 1929;13:231-44.                                                          

Parathyroid hormone and bone.  Reeve J, Zanelli JM. Clin Sci 1986;71:231-8.                                                          

A 10-Year Prospective Study of Primary Hyperparathyroidism with or without Parathyroid Surgery
     The New England Journal of Medicine -- October 21, 1999 -- Vol. 341, No. 17
     Shonni J. Silverberg, Elizabeth Shane, Thomas P. Jacobs, Ethel Siris, John P. Bilezikian









Original Text by Clifford R. Wheeless, III, MD.

Last updated by Clifford R. Wheeless, III, MD on Sunday, January 27, 2008 7:57 pm