Renee,
I have no experience with this condition but was intrigued as I know that
the absence of PTHrP (parathyroid hormone related protein) is related to
problems with ductal branching during pregnancy. Here is what I've found in
Medline regarding hypoparathyroidism; surprisingly, it sounds a bit like
diabetes management during lactation only calcium supplementation is the
issue at hand:

~Lisa Marasco
----------------------

J Bone Miner Res. 1990 Jan;5(1):69-75. Related Articles, Links  

Parathyroid hormone is not required for normal milk composition or secretion
or lactation-associated bone loss in normocalcemic rats.

Garner SC, Boass A, Toverud SU.

Department of Pharmacology, University of North Carolina, Chapel Hill
27599-7455.

To determine if parathyroid hormone (PTH) is essential for lactation in
rats, the parathyroid glands were removed surgically during the first week
of lactation and the rats were given a diet containing a high
calcium-phosphorus ratio to maintain a normal serum calcium concentration.
Lactating rats were placed on diet containing 1.2% calcium (Ca) and 0.8,
0.6, or 0.4% phosphorus (P) on day 2 postpartum (PP) and were
parathyroidectomized (PTX) at 4-6 days PP. At 10 days PP serum Ca was 10.5
+/- 0.2 mg/dl (mean +/- SEM) for PTX rats and 10.4 +/- 0.3 mg/dl in
sham-operated lactating rats when the diet contained 0.6% P. When the diet P
was 0.8%, the litters gained little or no weight and serum Ca fell to 6.9
+/- 0.6 mg/dl by day 10 PP in PTX rats compared with 10.2 +/- 0.2 mg/dl in
sham rats. PTX rats fed the diet containing 1.2% Ca and 0.6% P maintained a
normal serum Ca level until at least day 18 PP, but their serum P levels
fell gradually from approximately 5 mg/dl at 10 days to 3 mg/dl at 18 days
PP. In spite of this hypophosphatemia, the litters of PTX and sham rats had
gained the same amount of weight by age 16 days, indicating equal milk
production in the two groups. Milk Ca, P, and total solids were not
significantly different between PTX and sham rats on day 11 PP.(ABSTRACT
TRUNCATED AT 250 WORDS)

---------------------------------------------------

Clin Endocrinol (Oxf). 1987 Jun;26(6):667-74. Related Articles, Links  

Remission of hypoparathyroidism during lactation: evidence for a
physiological role for prolactin in the regulation of vitamin D metabolism.

Cundy T, Haining SA, Guilland-Cumming DF, Butler J, Kanis JA.

Department of Medicine, King's College School of Medicine and Dentistry,
London, UK.

We studied a young woman with surgical hypoparathyroidism who, on her usual
maintenance dose of calcitriol, developed hypercalcaemia 9 d postpartum when
lactation was established. Serum values of 1,25-dihydroxyvitamin D3
(1,25(OH)2D3) values were very high (127 pg/ml). The patient remained
without exogenous calcitriol treatment for 40 d, during which time serum
1,25(OH)2D3 levels remained within the normal range and serum calcium fell
with a half-time of 27 d. The requirements for calcitriol increased to
antepartum levels when lactation had ceased. There was a close negative
correlation between requirements for calcitriol and serum PRL values. After
weaning, an episode of hypercalcaemia was induced by increasing the dose of
calcitriol. On stopping calcitriol the serum 1,25(OH)2D3 fell to low values
(4 pg/ml) within 2 d and serum calcium fell with a half-time of 3 d,
necessitating the early reintroduction of calcitriol. We conclude that in
hypoparathyroidism exogenous vitamin D requirements fall during lactation
because of enhanced endogenous production of 1,25(OH)2D3. The
lactation-associated increase in circulating 1,25(OH)2D3 concentrations thus
results from a parathyroid hormone-independent mechanism, possibly by an
effect of PRL on the 1 alpha-hydroxylase.

-----------------------------------------------
J Reprod Med. 1993 Nov;38(11):914-8. Related Articles, Links  

Reduced calcitriol requirements for treating hypoparathyroidism during
lactation. A case report.

Caplan RH, Wickus GG.

Department of Internal Medicine, Gundersen/Lutheran Medical Center, La
Crosse, Wisconsin.

We reduced the dose of calcitriol from 0.75 to 0.25 microgram/d to maintain
low normal serum calcium levels in a hypoparathyroid woman during lactation.
Calcitriol requirements quickly returned to 0.75 microgram/d when she
discontinued breast-feeding. In her previous pregnancy, failure to reduce
the dose of calcitriol resulted in serious hypercalcemia 11 days after she
began breast-feeding. The changing requirement for calcitriol in our patient
related directly to the falling level of estradiol. Although the cause or
causes of diminished calcitriol requirements in hypoparathyroid women during
lactation remains unclear, increased bone resorption promoted by low plasma
estrogen levels may be an important mechanism. We conclude that the dose of
calcitriol should be reduced during lactation and that both the
hypoparathyroid mother and her infant should be carefully monitored to
detect abnormal serum calcium levels.
--------------------------------------------

Endocrinol Jpn. 1984 Jun;31(3):227-33. Related Articles, Links  

Postpartum resolution of hypocalcemia in a lactating hypoparathyroid
patient.

Rude RK, Haussler MR, Singer FR.

A 24 year old woman with post-surgical hypoparathyroidism was studied during
pregnancy and lactation. During pregnancy the patient required less vitamin
D therapy for control of her hypoparathyroidism and, while lactating,
maintained a normal serum calcium without any supplemental vitamin D. The
serum parathyroid hormone concentration and plasma 1,25 (OH)2 vitamin D
concentration were undetectable and low normal respectively at a time when
the serum calcium concentration was normal and the patient was not on
vitamin D therapy. Urinary calcium excretion was low during this period and
may explain the normalization of the serum calcium. The mechanism by which
the improvement in calcium metabolism occurred is unknown, but may be
secondary to a direct effect of prolactin on calcium homeostasis.

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