Clinical_Rounds_in_Endocrinology_Volume_II_-_Pediatric_Endocrinology

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deformities. Therefore, early diagnosis and optimal therapy with oral alkali,
either as bicarbonate or citrate, is recommended. However, citrate is preferred
over bicarbonate as it is better tolerated. The recommended dose is 1–2 mEq/
Kg daily in divided doses in distal RTA and 10–20 mEq/Kg daily in proximal
RTA (higher dose required due to massive urinary loss of bicarbonate). Short-
term administration of potassium, calcitriol, and phosphate may be required
in these patients. Correction of acidosis not only improves hypokalemia and
hypercalciuria but also leads to increased 1,25(OH) 2 D synthesis. Therefore,
long-term use of calcitriol is not required in patients with RTA. In addition, it
may worsen hypercalciuria in patients with distal RTA. Overtreatment with
alkali should be avoided as it may worsen hypokalemia and hypercalciuria.
During follow-up, serum potassium, pH, bicarbonate, and urinary calcium
should be periodically monitored. In addition, renal ultrasonography should
also be performed to detect nephrocalcinosis. The oral alkali preparations
commonly used in the management of RTA are summarized in the table given
below.

Preparation Composition Alkali content Potassium content
Potassium citrate and
citric acid syrup

Each 5 ml contains
Potassium citrate 1100 mg

2 mEq base/ml 5 mEq potassium/
ml
Citric acid 334 mg
Shohl’s solution Each litre contain citric
acid 140 g

1 mEq base/ml −

Hydrated crystalline
sodium citrate 90 g
Sodium bicarbonate
tablets

325 mg/tablet 325 mg tablet
contains 4 mEq


or
650 mg/ tablet 650 mg tablet
contains 8 mEq


  1. What are the endocrine causes of exuberant callus formation?


The exuberant callus formation is the characteristic feature of osteogenesis
imperfecta, glucocorticoid excess (exogenous or endogenous), Charcot’s
arthropathy, renal osteodystrophy, and multiple myeloma. The mechanism of
exuberant callus formation remains elusive. However, unrestrained production
of collagen by the osteoblast in response to poorly mineralized matrix (callus)
possibly explains this phenomenon (Fig. 5.16).

5 Rickets–Osteomalacia

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