Treatment of hypocalcemia  


— Hypocalcemia is also related to a spectrum of clinical manifestations, starting from few if any symptoms if the hypocalcemia is mild and/or chronic, to severe life-threatening symptoms if it’s severe and/or acute. Thus, the management of hypocalcemia depends upon the severity of symptoms. In patients with acute symptomatic hypocalcemia, intravenous calcium gluconate is that the preferred therapy, whereas chronic hypocalcemia is treated with oral calcium and viosterol supplements. The treatment of hypocalcemia are reviewed here. The etiology, clinical manifestations, and diagnostic approach to hypocalcemia are reviewed separately.


— Calcium in serum is absolute to proteins, principally albumin. As a result, total serum calcium concentrations in patients with low or high albumen levels might not accurately reflect the physiologically important ionized (or free) calcium concentration. As an example, in patients with hypoalbuminemia, total serum calcium concentration is also low when serum ionized calcium is normal. The serum total calcium concentration falls approximately 0.8 mg/dL for each 1 g/dL reduction within the albumin concentration. Thus, in patients with hypoalbuminemia or hyperalbuminemia, the measured serum calcium concentration should be corrected for the abnormality in albumin or for traditional units If there’s uncertainty whether the corrected serum calcium is reflective of the ionized calcium, and if a laboratory known to live ionized calcium reliably is obtainable, some authorities opt to measure the ionized calcium directly. Direct measurement of the ionized calcium concentration might be considered in patients with symptoms of hypocalcemia within the setting of a traditional total calcium concentration. Symptomatic hypocalcemia with normal total calcium but low ionized calcium can occasionally occur in patients with acute alkalosis thanks to increased binding of calcium to albumin. In patients with asymptomatic hypocalcemia, it’s important to verify with repeat measurement (ionized calcium or total serum calcium corrected for albumin) that there’s a real decrease within the calcium concentration.


— The treatment of hypocalcemia varies with its severity and therefore the underlying cause. The severity of symptoms (paresthesias, carpopedal spasm, tetany, seizures) and signs (Chvostek’s or Trousseau’s signs, bradycardia, impaired cardiac contractility, and prolongation of the QT interval) depends upon absolutely the level of calcium, furthermore because the rate of decrease. Patients with acute hypocalcemia are symptomatic at serum calcium values that might not cause symptoms in patients with chronic hypocalcemia (eg, hypoparathyroidism). Clinical manifestations also vary with other factors like the arterial pH and therefore the reason for hypocalcemia. There are few studies examining the optimal treatment of hypocalcemia. Most recommendations are based upon accepted practice or clinical experience We recommend intravenous calcium for symptomatic patients (carpopedal spasm, tetany, seizures), for patients with a chronic QT interval, and for asymptomatic patients with an acute decrease in serum corrected calcium to ≤7.5 mg/dL (1.9 mmol/L). For those with milder symptoms of neuromuscular irritability (paresthesias) and corrected calcium concentrations greater than 7.5 mg/dL, oral calcium supplementation may be initiated. If symptoms don’t improve with oral supplementation, we recommend switching to intravenous calcium. When vitamin D deficiency or hypoparathyroidism is that the reason for hypocalcemia, administration of calcium alone is typically only transiently effective. Long-term management requires the addition of cholecarciferol. Recombinant human internal secretion is approved for the treatment of osteoporosis but isn’t yet standard look after hypoparathyroidism due to high cost and also the necessity for subcutaneous administration. Intravenous calcium — Intravenous calcium is indicated for acutely symptomatic patients, as can occur when there’s a rapid and progressive reduction in serum calcium (eg, acute hypoparathyroidism following post-radical neck dissection for head and neck cancer). it’s also indicated for asymptomatic hypocalcemia in several other settings. These include patients with acute decreases in serum calcium to ≤7.5 mg/dL (1.9 mmol/L) who may develop serious complications if untreated, and patients with milder degrees of hypocalcemia or with chronic hypocalcemia (due to hypoparathyroidism) who become unable to require or absorb oral supplements, as may occur after complex surgical procedures requiring prolonged recuperation. Intravenous calcium isn’t warranted as initial therapy for asymptomatic hypocalcemia in patients with impaired renal function in whom correction of hyperphosphatemia and of low circulating 1,25-dihyroxyvitamin D are usually the first goals Initially, intravenous calcium (1 to 2 g of calcium gluconate , adore 90 to 180 mg elemental calcium, in 50 mL of 5 percent dextrose) is infused over 10 to twenty minutes. The calcium mustn’t tend earlier, due to the chance of great cardiac dysfunction, including systolic arrest This dose of calcium gluconate will raise the serum calcium concentration for less than two or three hours; as a result, it should be followed by a slow infusion of calcium in patients with persistent hypocalcemia. Either 10 percent calcium gluconate (90 mg of elemental calcium per 10 mL) or 10 percent salt (270 mg of elemental calcium per 10 mL) is wont to prepare the infusion solution. Calcium gluconate is sometimes preferred because it’s less likely to cause tissue necrosis if extravasated. An intravenous solution containing 1 mg/mL of elemental calcium is ready by adding 11 g of calcium gluconate (equivalent to 990 mg elemental calcium) to normal saline or 5 percent dextrose water to produce a final volume of 1000 mL. This solution is run at an initial infusion rate of fifty mL/hour (equivalent to 50 mg/hour).

The dose are often adjusted to take care of the serum calcium concentration at the lower end of the traditional range (with the serum calcium corrected for any abnormalities in albumin as noted above). Patients typically require 0.5 to 1.5 mg/kg of elemental calcium per hour. The infusion should be prepared with the subsequent considerations

: • The calcium should be diluted in dextrose and water or saline because concentrated calcium solutions are irritating to veins.

  • The intravenous solution shouldn’t contain bicarbonate or phosphate, which might form insoluble calcium salts. If these anions are needed, another intravenous line (in another limb) should be used. Intravenous calcium should be continued until the patient is receiving a good regimen of oral calcium and vitamin D. Calcitriol, in a very dose of 0.25 to 0.5 mcg twice daily, is that the preferred preparation of ergocalciferol for patients with severe acute hypocalcemia thanks to its rapid onset of action (hours Concurrent hypomagnesemia  — Hypomagnesemia could be a common explanation for hypocalcemia, both by inducing resistance to hormone (PTH) and by diminishing its secretion. In patients with hypomagnesemia, hypocalcemia is difficult to correct without first normalizing the serum magnesium concentration. Thus, if the serum magnesium concentration is low, 2 g (16 meq) of sulphate should be infused as a ten percent solution over 10 to twenty minutes, followed by 1 gram (8 meq) in 100 mL of fluid per hour. Magnesium repletion should be continued as long because the serum magnesium concentration is a smaller amount than 0.8 meq/L (1 mg/dL or 0.4 mmol/L). More careful monitoring is required in patients who have impaired renal function who would be at greater risk of developing hypermagnesemia. Persistent hypomagnesemia, as occurs in some patients with ongoing gastrointestinal (eg, malabsorption) or renal losses, requires supplementation with oral magnesium, typically 300 to 400 mg daily divided into three doses. Oral calcium — Oral calcium supplementation is preferred for patients with milder degrees of acute hypocalcemia (serum corrected calcium concentration of seven.5 to 8.0 mg/dL [1.9 to 2.0 mmol/L] or a serum ionized calcium concentration above 3.0 to 3.2 mg/dL [0.8 mmol/L]) or for chronic hypocalcemia. Such patients are typically asymptomatic or at the most mildly symptomatic (eg, oral paresthesias). they will be treated initially with 1500 to 2000 mg of elemental calcium given as carbonate or calcium citrate daily, in divided doses. As an example, carbonate is 40 percent elemental calcium, so 1250 mg of carbonate contains 500 mg of elemental calcium. The dose of elemental calcium is listed on most supplement labels. The role of oral calcium as a phosphate binder in patients with chronic nephrosis is presented elsewhere. additionally to calcium, patients with ergocalciferol deficiency or hypoparathyroidism require D supplementation, which frequently permits a lower dose of calcium supplementation. viosterol and metabolites  — Several preparations of ergocalciferol are available for the treatment of hypocalcemia thanks to hypoparathyroidism or viosterol deficiency. The role of calciferol therapy in patients with chronic renal disorder is discussed separately. viosterol requirements vary considerably from patient to patient and therefore the correct dose in any given patient is primarily determined by trial and error. Because PTH is required for the renal conversion of calcidiol (25-hydroxyvitamin D) to the active metabolite calcitriol (1,25-dihydroxyvitamin D), patients with hypoparathyroidism are preferably treated with calcitriol. The initial dose of calcitriol is often 0.25 to 0.5 mcg twice daily. the varied preparations differ in onset of action, duration of action, and cost. the most important side effects are hypercalcemia and hypercalciuria, which, if chronic, can cause nephrolithiasis, nephrocalcinosis, and nephropathy Hypercalciuria is that the earliest sign of toxicity and may develop within the absence of hypercalcemia; it’s presumably to occur in patients with hypoparathyroidism since internal secretion stimulates renal calcium reabsorption. However, in patients with ergocalciferol deficiency, enhanced intestinal absorption of calcium with fat-soluble vitamin therapy and also the resulting increases in serum calcium may additionally reduce PTH concentrations, potentially leading to hypercalciuria before hypercalcemia occurs. Thus, both serum and urinary calcium should be measured frequently (two-week intervals) initially so every six months to 1 year once a stable dose is achieved. Hypercalciuria and, if present, hypercalcemia usually resolve in a very few days after cessation of therapy in patients treated with calcitriol. In contrast, recovery is slower (as long as two to a few weeks thanks to storage in fat) in patients treated with viosterol, but are often accelerated by a brief course of glucocorticoid therapy. Vitamin D — ergocalciferol deficiency is often treated with ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3). ergocalciferol is obtainable in several doses for oral administration. In some countries (not within the United States), it’s is also available for parenteral administration the foremost advantage of fat-soluble vitamin is its low cost, which is approximately 20 percent that of the ergocalciferol metabolites. Disadvantages include the need for hepatic and renal metabolism and slow onset and long duration of action. It must lean daily for several weeks before the complete effect becomes evident and hypercalcemia, should it occur, can persist for 2 to a few weeks after it’s discontinued. Calcitriol — Calcitriol (1,25-dihydroxyvitamin D, Rocaltrol) is most useful in diseases within which its renal synthesis is impaired, like nephropathy or hypoparathyroidism. it’s the foremost active metabolite of fat-soluble vitamin. the benefits of calcitriol include lack unavoidably for endogenous activation, rapid onset of action (hours), and a biologic half-life of about four to 6 hours. While hypercalcemia is more common during treatment with calcitriol than with viosterol, cessation of treatment is followed by resolution of hypercalcemia in a very few days instead of some weeks Other vitamin D analogues   — fat-soluble vitamin metabolites may be wont to treat hypocalcemia, particularly when there’s abnormal viosterol metabolism (renal or liver disease). The recommended preparation and dose vary with the clinical condition.
  • • Alfacalcidol (1-alpha-hydroxyvitamin D3) could be a synthetic analog of calciferol that’s converted within the liver to the active metabolite 1,25-dihydroxyvitamin D. just like calcitriol, it’s a rapid onset of action and comparatively short half-life. Although it’s not available within the us, it’s utilized in other countries for the treatment of hypocalcemia related to hypoparathyroidism and as a treatment adjunct in chronic renal disorder.
  • • Dihydrotachysterol is that the functional equivalent of 1-hydroxyvitamin D, in this only 25-hydroxylation within the liver is required to make the active drug. As a result, dihydrotachysterol is effective in patients in whom renal 1-hydroxylation is impaired, like those with chronic nephropathy. it’s a rapid onset of action and a comparatively short duration of action, so toxicity resolves in a very few days.
  • • Calcidiol (25-hydroxyvitamin D) doesn’t require hepatic 25-hydroxylation, and is therefore most useful in patients with disease. Its action is more rapid and not as prolonged as that of cholecarciferol, but slower in onset and more prolonged than that of calcitriol.


— Hypoparathyroidism occurs when there’s abnormal endocrine gland development, destruction of the parathyroid glands (autoimmune, surgical), altered regulation of hormone (PTH) production, or impaired PTH action. Most patients with hypoparathyroidism require lifelong calcium and vitamin D supplementation. An exception is that the occurrence of transient hypoparathyroidism after thyroidectomy or parathyroidectomy. The goals of therapy in patients with hypoparathyroidism are to alleviate symptoms and to lift and maintain the serum calcium concentration within the low-normal range, eg, 8.0 to 8.5 mg/dL (2.0 to 2.1 mmol/L). Attainment of upper values isn’t necessary and is sometimes limited by the event of hypercalciuria because of the loss of renal calcium retaining effects of PTH. The initial dose of oral calcium should be 1.0 to 1.5 g of elemental calcium daily, in divided doses Although carbonate is commonly used (it is that the least expensive), it should be less well-absorbed in older patients and people who have achlorhydria. These patients could be treated with another preparation, like calcium citrate . Although a range of viosterol preparations will be wont to treat hypoparathyroidism calcitriol is commonly thought to be the treatment of choice A typical starting dose is 0.25 mcg twice daily, with weekly dose increments to realize a low-normal serum calcium. Many patients require up to 2 mcg daily. Monitoring of urinary and serum calcium and serum phosphate are required weekly initially, until a stable serum calcium concentration (at the low end of the conventional range) is reached. Thereafter, monitoring at three- to six-month intervals is sufficient Preventing hypercalciuria  — a rise in urinary calcium excretion could be a predictable consequence of raising the serum calcium in patients with hypoparathyroidism These patients lack the conventional stimulatory effect of PTH on renal tubular calcium reabsorption and so excrete more calcium than normal subjects at the identical serum calcium concentration. Thus, completely correcting hypocalcemia may cause hypercalciuria, which may produce nephrolithiasis, nephrocalcinosis, and possible chronic nephropathy To prevent these complications, urinary calcium excretion should be measured periodically and therefore the dose of calcium and calciferol reduced if it’s elevated (≥300 mg in 24 hours). Some patients with hypoparathyroidism require a thiazide diuretic (25 to 100 mg daily), with or without dietary sodium restriction, to decrease urinary calcium excretion A thiazide is usually added when the 24-hour urinary calcium approaches 250 mg In patients who develop thiazide-induced hypokalemia, potassium supplementation is important. The mechanism by which both PTH and thiazides enhance distal calcium reabsorption is reviewed elsewhere. Recombinant human PTH  — The administration of recombinant internal secretion (PTH), which is obtainable for the treatment of osteoporosis, holds promise as a treatment for hypoparathyroidism. Subcutaneous administration of PTH 1-34 and PTH 1-84 are investigated, as illustrated by the following:

  • In two randomized trials from the identical group, subcutaneous administration of synthetic PTH 1-34 controlled hypocalcemia with a lower risk of hypercalciuria in comparison with calcitriol (all subjects received oral calcium supplementation) Twice-daily administration of PTH 1-34 provided better metabolic control and allowed a discount in total daily PTH dose (46 versus 97 mcg daily) Similar findings were noted during a trial comparing once- versus twice-daily PTH administration in 14 children with chronic hypoparathyroidism (total daily dose 25 versus 58 mcg

In an open label study of PTH 1-84 (100 mcg every other day) in 30 hypoparathyroid patients, PTH 1-84 significantly reduced supplemental calcium and calcitriol requirements without altering serum and urinary calcium concentrations Bone mineral density significantly increased within the lumbar spine (2.9 percent) and decreased within the distal one-third radius (2.4 percent). Recombinant human PTH may additionally improve abnormal skeletal properties in hypoparathyroidism. in a very histomorphometric analysis of paired iliac crest biopsy samples from 30 patients with primary hypoparathyroidism, PTH treatment of hypoparathyroidism was related to a rise within the remodeling rate in both trabecular and cortical compartments with tunneling resorption within the trabecular compartments These findings suggest that PTH restores bone metabolism to levels more typical of euparathyroid individuals. Recombinant human PTH isn’t yet approved to be used in hypoparathyroidism, primarily since the long-term safety of this dose (relative to its skeletal effects) has not been established, particularly in growing children who is also at greater risk of osteosarcoma. additionally, recombinant PTH is way costlier than standard therapy with calcitriol and calcium. Thyroidectomy or parathyroidectomy — Hypocalcemia could be a common problem after total or near-total thyroidectomy and partial or total parathyroidectomy in patients with primary hyperparathyroidism. As an example, hypoparathyroidism is that the most frequent complication of near-total thyroidectomy. Transient hypoparathyroidism occurs in up to twenty percent of patients after surgery for thyroid cancer and permanent hypoparathyroidism occurs in 0.8 to 3.0 percent of patients after total thyroidectomy, particularly when the goiter is extensive and anatomic landmarks are displaced and obscured. The management of post-thyroidectomy hypoparathyroidism is reviewed elsewhere. vitamin D deficient patients undergoing parathyroidectomy are at increased risk for developing postoperative hypocalcemia and hungry bone syndrome [ 21 ]. Hungry bone syndrome most frequently occurs in hyperparathyroid patients who developed bone disease preoperatively because of a chronic increase in bone resorption induced by high levels of PTH (osteitis fibrosa). In these patients, calcium is avidly obsessed by the demineralized bone after surgery, and calcium supplementation is required to take care of a standard serum calcium concentration. vitamin D deficient postparathyroidectomy patients may require prolonged, massive calcium and D therapy thanks to hungry bone syndrome. Hypoparathyroidism during pregnancy   — Special care should be taken within the management of girls with hypoparathyroidism during pregnancy and following delivery. There are conflicting data on whether calcitriol requirements fall or don’t fall during pregnancy On the opposite hand, there’s uniform agreement that calcitriol requirements decrease during lactation Serum concentrations of 1,25-dihyroxyvitamin D (calcitriol) double during a traditional pregnancy. However, intact PTH concentrations remain low-to-normal, suggesting that PTH doesn’t mediate the late partum rise in 1,25-dihydroxyvitamin D (1,25D) production. the rise in serum 1,25D is also regulated by other pregnancy hormones, which are normal in hypoparathyroid women, like PTH-related protein (PTHrP), prolactin, estrogen, and placental hormone Thus, serum calcium concentrations should be measured frequently during late pregnancy and lactation in women with hypoparathyroidism who may have an increase in serum calcium, requiring a decrease in calcitriol dose If the calcitriol dose isn’t reduced, the mix of elevated serum 1,25D and PTHrP can result in increases in intestinal absorption and bone resorption and hypercalcemia [ 28 ]. the necessity for calcitriol will return to antepartum levels with cessation of lactation.

Autosomal dominant hypocalcemia

— Autosomal dominant hypocalcemia could be a rare disorder caused by an activating mutation within the calcium-sensing receptor (CaSR). Increased activity of this receptor within the renal tubules ends up in normal or high urinary calcium excretion despite hypocalcemia; raising the patient’s serum calcium concentrations with cholecarciferol may result in additional hypercalciuria, nephrocalcinosis, and renal disorder. Fortunately, most patients with this disorder have few if any symptoms of hypocalcemia and frequently require little or no therapy. When approved, recombinant human parathormone , which reinforces calcium absorption within the tubules, could also be an alternate if therapy is required. It can raise the serum calcium concentration during this disorder with a coffee risk of exacerbating hypercalciuria. Alternatively, calcilytics, a category of medication in development that inhibit the CaSR, may provide a useful therapeutic approach within the future.

cholecarciferol deficiency

— Nutritional cholecarciferol deficiency is often treated with 50,000 international units of vitamin D2 or D3 weekly for 6 to eight weeks. Chronic renal disorder   — Few patients with chronic nephropathy have symptomatic hypocalcemia. Such patients are often treated with oral calcium to bind intestinal phosphate and to stop bone disease instead of hypocalcemia in and of itself. The addition of a vigorous sort of viosterol is required in a number of these patients. These issues are discussed very well elsewhere Hypercatabolic state — Unless they’re symptomatic from hypocalcemia (eg, tetany or cardiac arrhythmia), patients with acute hypocalcemia and hyperphosphatemia thanks to a hypercatabolic state like the tumor lysis syndrome or massive trauma mustn’t be treated with calcium until the hyperphosphatemia is corrected to stop calcium-phosphate precipitation. Hemodialysis is commonly indicated in such patients who have symptomatic hypocalcemia.

  • Pseudohypoparathyroidism  — Pseudohypoparathyroidism (PHP) refers to a bunch of heterogeneous disorders defined by targeted organ (kidney and, perhaps, bone) unresponsiveness to PTH . it’s characterized by hypocalcemia, hyperphosphatemia, and in contrast to hypoparathyroidism, elevated instead of reduced PTH concentrations. The clinical manifestations and diagnosis of this disorder are reviewed elsewhere The long-term treatment of hypocalcemia in adults with pseudohypoparathyroidism is analogous to the treatment of hypocalcemia caused by other kinds of hypoparathyroidism. However, patients with pseudohypoparathyroidism infrequently develop hypercalciuria with calcium and fat-soluble vitamin therapy Therefore, the goal of treatment with calcium and ergocalciferol is to keep up normocalcemia (rather than low-normal serum calcium as for other types of hypoparathyroidism). A typical starting dose of calcitriol is 0.25 mcg twice daily. The dose should be increased weekly to realize a standard serum calcium. Many patients require up to 2 mcg daily Approximately 1 to 2 gm of elemental calcium daily (in divided doses) is usually recommended. Patients with pseudohypoparathyroidism can also require screening for other endocrinopathies, particularly hypothyroidism and hypogonadism.


— UpToDate offers two varieties of patient education materials, “The Basics” and “Beyond the fundamentals.” the fundamentals patient education pieces are written in plain language, at the 5 th to six th grade reading level, and that they answer the four or five key questions a patient may need a few given condition. These articles are best for patients who desire a general overview and preferring short, easy-to-read materials. Beyond the fundamentals patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the ten th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to the current topic. We encourage you to print or e-mail these topics to your patients. (You also can locate patient education articles on a range of subjects by searching on “patient info” and also the keyword(s) of interest.) SUMMARY and proposals Calcium   — The treatment of hypocalcemia varies with its severity and also the underlying cause.

  • Patients with hypocalcemia who are severely symptomatic (carpopedal spasm, tetany, seizures, decreased cardiac function, or prolonged QT interval) require rapid correction of calcium levels with IV calcium therapy. We also suggest IV calcium therapy in asymptomatic patients with an acute decrease in serum corrected calcium to ≤7.5 mg/dL (1.9 mmol/L) Intravenous calcium isn’t warranted as initial therapy for asymptomatic hypocalcemia in patients with impaired renal function in whom correction of hyperphosphatemia and of low circulating 1,25-dihyroxyvitamin D are usually the first goals.
  • For those with milder symptoms of neuromuscular irritability (paresthesias) and corrected serum calcium concentrations greater than 7.5 mg/dL (1.9 mmol/L), initial treatment with oral calcium supplementation is sufficient. If symptoms don’t improve with oral supplementation, intravenous calcium infusion is required.
  • To effectively treat hypocalcemia in patients with concurrent magnesium deficiency, hypomagnesemia should be corrected first. Vitamin D

— When hypoparathyroidism (transient or permanent) or fat-soluble vitamin deficiency are the explanation for hypocalcemia, administration of intravenous calcium is merely transiently effective (as long because the infusion continues), and oral calcium might not be absorbed. In these cases, successful management requires the addition of D, which frequently permits a lower dose of calcium supplementation.

  • For the initial management of patients with hypoparathyroidism, we recommend cholecarciferol supplementation additionally to calcium ). Calcitriol is that the viosterol metabolite of choice because it doesn’t require renal activation, it’s a rapid onset of action (hours), and a shorter half-life. Other acceptable options include alfacalcidol, calciferol (ergocalciferol or cholecalciferol), or dihydrotachysterol
  • In individuals with hypocalcemia thanks to cholecarciferol deficiency, we recommend cholecarciferol repletion Nutritional deficiency (25OHD <20 ng/mL [50 nmol/L]) requires initial treatment with 50,000 units of vitamin D2 or D3 orally once per week for 6 to eight weeks, then 800 to 1000 international units of vitamin D3 daily thereafter. Permanent hypoparathyroidism
  • In patients with permanent hypoparathyroidism, the goals of therapy are to alleviate symptoms, to lift and maintain the serum calcium concentration within the low-normal range (eg, 8.0 to 8.5 mg/dL [2.0 to 2.1 mmol/L]), and to avoid hypercalciuria (maintain 24-hour urinary calcium below 300 mg
  • All patients with permanent hypoparathyroidism require adequate calcium intake (1.0 to 1.5 g elemental calcium daily).
  • Along with calcium supplementation, we recommend calcitriol instead of recombinant human parathormone (PTH) The long-term safety of PTH has not been established. additionally, recombinant PTH is far dearer than standard therapy with calcitriol. However, in patients with refractory hypercalciuria, PTH could be a reasonable option.
  • The initial treatment of hypercalciuria in patients with hypoparathyroidism is reducing the dose of calcium and fat-soluble vitamin. Some patients would require the addition of thiazide diuretics.

Diabetes Mellitus

Diabetes Mellitus

Diabetes Mellitus (DM) is a chronic medical condition that affects the patient’s ability to use energy in food (sugar) There are three main types of diabetes: Type 1 DM, Type 2 DM, and Gestational diabetes, which is the only type of diabetes that can be cured. Diabetes is classified as a complex case requiring daily care, because neglect leads to serious complications that affect the quality of life of the patient, and can reduce life expectancy.

How diabetes affects the body

The body of the diabetic cannot maintain normal levels of glucose in the blood, which is a form of sugar that represents the main source of energy in the body. In a normal body, insulin is produced in the process of converting food to energy in the natural body, but is not produced in diabetic patients or produced at levels that do not meet the body needs.


In diabetes patients

Foods like bread and fruits are not converted into glucose, and insulin hormone that is made by the pancreas is not produced, so blood sugar levels rise. This leads to the need for insulin injections to control the energy metabolism in the body and convert it into glucose.




Types of diabetes

Type 1 DM

The immune system attacks the pancreas with antibodies, so the damaged pancreas cannot produce insulin, which is a genetic condition. However, it can be caused by a defect in the pancreatic beta cells, which produce insulin. The treatment of this type involves the taking insulin injections.

Type 2 DM

This is the most common type, accounting for 95% of diabetes cases in adults. About twenty-six million American adults have been diagnosed with this type of diabetes, which also affects children and adolescents. This type is often more moderate than type I, despite its serious side effects that may affect small blood vessels feeding the kidneys, nerves, and eyes. The pancreas is producing very little insulin and does not meet the body needs. It is worth mentioning that the second type of diabetes is a acquired not genetic, especially in the obese people who have a 20% increase in the probability of developing the disease.

Gestational Diabetes

This type of diabetes occurs at the mid-point of pregnancy or at the end of it because of the high levels of sugar in the body of mother due to transport of excess sugar from the fetus to mother through the placenta. According to the U.S. National Health Institute, the prevalence of diabetes among pregnant women is up to 10%. This condition must be controlled and treated as it affects both the mother and the fetus. It can be converted to type 2 diabetes after birth.



Diabetes complications

Prescribed doses of insulin must be maintained at the appropriate time daily, because neglect leads to serious complications.

They are: Blindness, renal failure, heart attacks, and strokes up to four times more than healthy people. Effects on the patient’s mental and physical health, as well as depression, anxiety and psychiatric disorder increasing by 30%.