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CASE STUDY; Hyperparathyroidism
Requirements; APA, two references, single page, American peer review articles or websites dated no later then 2009.
Mrs. F is a 65 year old female, who is a new client, retired, and denies complaints. She has a history of bipolar disorder, hypertension, GERD. She presents her old lab records that shows a low albumin 3 g/dL (normal range: 3.5-5.5 g/dL), and a borderline high calcium of 10.2 mg/dL (normal range: 8.4-10.2 mg/dL). Her current medications are: chlorthalidone, lithium, and pantoprazole.
A study in the Endocrine Journal (1995) found that lithium creates an increased risk of hypercalcemia by affecting the calcium metabolism but does not seem to affect the level of serum parathyroid hormone (PTH) (Kotmatsu et al., 1995). In 2010, another study found that patients who are taking lithium also have a risk of hyperparathyroidism. (Pomerantz, J. M. (2010). Hyperparathyroidism resulting from lithium treatment remains under-recognized. Drug Benefit Trends, 22, 62-63. Chlorthalidone, a blood pressure medication, excretes sodium and potassium and increases water removal through the kidneys, and in the presence of lithium can have increased side effects. Chlorthalidone lowers calcium excretion in urine but increases it in stool due to causing a lower calcium intestinal absorption (Bushinsky, D. A., Favus, M. J., & Coe, F. L. (1984).
The provider changed the medications from chlorthalidone to amlodipine, and the psychiatrist was consulted and changed lithium to lamotrigine. The family history does not have endocrine disorders. A dual energy x-ray absorptiometry (DXA) was ordered, and at the 3-month follow-up the DXA screen for osteoporosis had a T score result of -3.0 distal radius. According to the International Society For Clinical Densitometry (2010), osteoporosis is diagnosed in men who are 50 years old and older and postmenopausal women when the T-score is -2.5 or less for lumbar spine, femoral neck or total hip or 33% in the radius. The laboratory results at this time were albumin 3 g/dL and calcium 10.8 mg/dl the same as the first visit, but the 43-hour urinary calcium is very high at 800 mg (400 mg is normal). Creatinine is low at 0.5 mg/dL (normal range: 0.7-1.3 mg/dL for men, 0.6-1.1 mg/dL for women). PTH is high at 65 pg/ml (normal range: 14-64).
There are three principal hormones in calcium metabolism: the parathyroid hormone located in the parathyroid that are 4 tiny glands on the posterior side of the thyroid gland; calcitonin from the thyroid gland and vitamin D (cholecalciferol) made by sunlight and processes in the skin or from oral supplements. In nearly all cases (over 80%) a benign parathyroid tumor will cause hyperparathyroidism where PTH hormone is in excess and creates hypercalcemia (Buttaro et al, 2013). Other hormones related to calcium metabolism are estrogens, corticosterioids, glucagon, somatotropin, thyroxine ( Vet Book – need to find another resource…
Each age group have rates of bone resorption (calcium leaving the bone) and formation, where elderly usually have bone loss and in negative bone balance (formation < resportion), children are in positive bone balance (formation > resorption) and teens are neutral bone balance (formation = resorption) (Peacock, 2010).
Although this case study does not mention the patient as a smoker of cigarettes, smoking negatively affects calcium metabolism, as well as the function of the pituitary, adrenal, thyroid, ovarian, testicular, and insulin, and increases the risk of osteoporosis to mention a few of the health risks (Kapoor, & Jones, 2005). An abnormal high parathyroid hormone (PTH) level results in excess removal of calcium is taken from the bones resulting in osteoporosis.
The serum calcium is corrected by albumin, because 50% of calcium is bound to protein, the result is corrected by increasing albumin, and the calcium concentration changes 0.8 mg/dL for every 1.0 g/dL of plasma albumin. The formula to estimate plasma calcium level is:
Corrected [Ca] = Total [Ca} + (0.8 x [4.5 – albumin level]) (Skugor, & Milas, 2009).
The state of acidosis or alkalosis will change the binding of calcium to albumin, in acidosis binding of calcium to albumin is decreased and in alkalosis it is increased.
The normal range of total serum calcium is 5.2-10.4 mg/dL (or ionized calcium 2.60-1.30 mmol/L) and the classification of hypercalcemia are:
- Mild: total serum calcium 10.5-12 mg/dL (or ionized calcium 5.6-8 mg/dL)
- Moderate: total serum calcium 11.5-18.0 mg/dL (or ionized calcium 2.88-4.51 mmol/L)
- Severe: total serum calcium > 18.0 mg/dL and hemodialysis may be needed (Lewis III, 2016).
Patients with hypercalcemia present with clinical manifestations such as:
Table 1: Clinical Manifestations of Hypercalcemia
Symptoms and Signs Associated Conditions
- Depression Organic brain syndromes
- Cognitive dysfunction
- Polyuria Nephrolithiasis
- Polydipsia Nephrogenic diabetes insipidus
- Nocturia Renal insufficiency
Renal tubular acidosis
- Short QT Interval Hypertension
- Constipation Peptic ulcer disease
- Anorexia Acute pancreatitis
- Abdominal pain
- Muscle weakness Osteopenia, osteoporosis
- Aches, pains Gout, pseudogout
- Fractures Chondrocalcinosis
Hypercalcemic crisis (Skugor, & Milas, 2009).
The differential diagnosis with hypercalcemia should be considered early and narrowed down, examples being:
- Parathyroid hormone-related
o Primary hyperparathyroidism
- Sporadic, familial, associated with multiple endocrine neoplasia I or II
o Tertiary hyperparathyroidism
- Associated with chronic renal failure or vitamin D deficiency
- Vitamin D-related
o Vitamin D intoxication
- Usually 25-hydroxyvitamin D2in over-the-counter supplements
o Granulomatous disease sarcoidosis, berylliosis, tuberculosis
o Hodgkin’s lymphoma
o Humoral hypercalcemia of malignancy (mediated by PTHrP)
o Tumors (solid) especially of lung, head, and neck squamous cancers, renal cell tumors
o Local osteolysis (mediated by cytokines), multiple myeloma, breast cancer
- Miscellaneous causes
o Endocrine disorders
o Genetic disorders
Evaluating hypercalcemia is best demonstrated by the following table:
Clinical Manifestations of Hypercalcemia
- Renal “stones”
- Nephrogenic diabetes insipidus
- Skeleton “bones”
- Bone pain
- Osteitis firosa cystica in hyperparathyroidism (subperiosteal resorption, bone cysts)
- Gastrointestinal “abdominal moans”
- Nausea, vomiting
- Anorexia, weight loss
- Abdominal pain
- Peptic ulcer disease
- Neuromuscular “psychic groans”
- Impaired concentration and memory
- Confusion, stupor, coma
- Lethargy and fatigue
- Muscle weakness
- Corneal calcification (band keratopathy)
- Shortened QT interval on electrocardiogram
- Cardiac arrhythmias
- Vascular calcification
o Keratitis, conjunctivitis (Pomerantz, 2010).
Guidelines from the Fourth International Workshop (2014), for the management of asymptomatic primary hyperparathyroidism (PHPT) may or may not require surgery, whereas when symptoms present parathyroidectomy surgery is recommended (Bilezikian, Khan, Potts, Jr., 2009). To evaluate, the recommendation is:
- a biochemistry panel of phosphate, calcium, alkaline phosphatase, creatinine, and BUN, 25(OH)D and
- PTH by second or third immunoassay
- Urine 24-h for creatinine, creatinine clearance, and calcium
- Stone risk profile. Bone mass density by DXA of lumbar and vertebral spine, hip, and distal 1/3 radius.
- Stone risk profile
- Abdominal imaging by x-ray, ultrasound, or CT scan
o TBS by DXA
o Bone turnover markers (bone-specific alkaline phosphatase activity, osteocalcin, P1NP [select one]; serum CTX, urinary NTX [select one]_
o Fractional excretion fo calcium on timed urine sample
o DNA testing if genetic basis for PHPT is suspected (Bilezikian, Khan, Potts, Jr., 2009).
For asymptomatic PHPT patients, a biochemistry panel monitoring is done those who don’t meet surgical guidelines or who decline surgery. Monitoring is done with dual-energy x-ray absorptiometry measuring bone mass density (BMD) every 2 years or yearly with clinical judgment when a patient has comorbidities. Limitation of intake of calcium creates more disease complications, therefore intake is the same as in non-PHPT patients. Supplementation of vitamin D 800-1000 IU daily is prescribed to reach serum levels of greater than 20 ng/dl (50 nmol/liter) of 25-hydroxyvitamin D. monitor serum calcium yearly or twice a year, BMD yearly whereas some may only need evaluation every 2 years. Biophosphonate increases BMD, and alendronate has the best evidence of lumbar spine BMD and stable serum calcium and PTH results, whereas cinacalcet is beneficial in reducing serum calcium to normal limits but only a reduces a modest amount of PTH. A third of patients after monitoring 25 years, may have kidney stones, BMD loss, and/or increased hypercalcemia.
The management of hypercalcemia is shown and explained in Table 5 below:
Pharmacologic Options for the Treatment of Hypercalcemia
|AGENT||MODE OF ACTION||INDICATION IN HYPERCALCEMIA||CAUTIONS|
|Normal saline 2 to 4 L IV daily for 1 to 3 days||Enhances filtration and excretion of Ca++||Severe↑Ca++ > 14 mg per dL (3.5 mmol per L)Moderate↑Ca++with symptoms||May exacerbate heart failure in elderly patientsLowers Ca++ by 1 to 3 mg per dL (0.25 to 0.75 mmol per L)|
|Furosemide (Lasix) 10 to 20 mg IV as necessary||Inhibits calcium resorption in the distal renal tubule||Following aggressive rehydration||↓K+, dehydration if used before intravascular volume is restored|
|BisphosphonatesPamidronate (Aredia), 60 to 90 mg IV over 4 hoursZoledronic acid (Zometa), 4 mg IV over 15 minutes||Inhibits osteoclast action and bone resorption||Hypercalcemia of malignancy||Nephrotoxicity, ↓Ca++, ↓PO4, rebound↑Ca++ in hyperparathyroidismMaximal effects at 72 hours|
|Calcitonin (Calcimar or Miacalcin) 4 to 8 IU per kg IM or SQ every 6 hours for 24 hours||Inhibits bone resorption, augments Ca++excretion||Initial treatment (after rehydration) in severe/Ca++||Rebound↑Ca++ after 24 hours, vomiting, cramps, flushingRapid↑Ca++ within 2 to 6 hours|
|GlucocorticoidsHydrocortisone, 200 mg IV daily for 3 days||Inhibits vitamin D conversion to calcitriol||Vitamin D intoxication, hematologic malignancies, granulomatous disease||Immune suppression, myopathy|
|Plicamycin (Mithracin), 25 mcg per kg per day IV over 6 hours for 3 to 8 doses||Cytotoxic to osteoclasts||Rarely used in severe↑Ca++||Marrow, hepatic, renal toxicity|
|Gallium nitrate (Ganite) 100 to 200 mg per m2 IV over 24 hours for 5 days||Inhibits osteoclast action||Rarely used in severe↑Ca++||Renal and marrow toxicity|
IV = intravenously; Ca++ = calcium;/ = increase; ¬ = decrease; K+ = potassium; PO4 = phosphate radical; IM = intramuscularly; SQ = subcutaneously. (Carroll, & Schade, 2003).
Fuller Albright wrote a book entitled: Parathyroid Glands and Metabolic Bone Disease, in 19?? He was born January 12, 1900 in Buffalo, New York, and d/t his father’s wealth attended a school founded by his father, excelled academically and attended Harvard College, went to the Army for World War I when the influenza pandemic broke out. He contracted Parkinson’s disease in his 30’s. He graduated from Harvard Medical School as Alpha Omega Alpha and intern/resident at Massachusetts General Hospital, researched mineral metabolism with Read Ellsworth until the partner died in 1937of tuberculosis. Studied in Vienna (1928-1929) with D. Jacob Erdheim, pathologist, who was known to have had found the parathyroid glands and calcium metabolism relationship (1906) and in addition, osteomalacia and compensatory hyperplasia of parathyroid gland. In 1929 at Massachusetts General Hospital he continued clinical research where patients were studied, urine/fecal collections and biochemical tests with special diet intake. Hyperparathyroidism (Primary) was reported first and treated in 1934 by Fuller Albright, hyperparathyroidism secondary to renal disease and the development of hyperparathyroidism described in 1937, pseudohypoparathyroidism with Albright Hereditary Osteodystrophy described in 1942, and many other disorders with some disorders named after Albright (Kleeman, Levine, & Felsenfeld, 2009). An abnormal high parathyroid hormone (PTH) level will remove calcium from the bones resulting in osteoporosis.
Bilezikian, J. P., Khan, A. A., Potts, Jr., J. T. (2009). Guidelines for the management of asymptomatic primary
hyperparathyroidism: Summary statement from the third international workshop. The Journal of Clinical Endocrinology
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67(9):1959-1966. Retrieved from http://www.aafp.org/afp/2003/0501/p1959.html#afp20030501p1959-t3
Kleeman, C. R., Levine, B., S., & Felsenfeld, A., J. (2009). Fuller Albright: The consummate clinical investigator. Clinical
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Kotmatsu, M., Shimizu, H., Tsuruta, T., Kato, M., Fushimi, T., Inoue, K., & Kuroda, T. (1995, October). Effect of lithium
on serum calcium level and parathyroid function in manic-depressive patients. Endocrine Journal, 42(5), 691-695.
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