1.
Lactation ketoacidosis: case presentation and literature review.
Al Alawi, AM, Falhammar, H
BMJ case reports. 2018
-
-
Free full text
-
Abstract
A 35-year-old woman presented to the emergency department with a 2 days history of malaise and headache. She was breastfeeding her 5-month old infant and had recently started an altered diet based on reducing carbohydrate amount. Moreover, she had also started exercising 2 weeks prior to her illness. Initial blood tests revealed high anion gap metabolic acidosis and hypoglycaemia (pH 7.13 (normal 7.30-7.40), bicarbonate 9.4 mmol/L (normal 21.0-28.0), anion gap 22.6 mmol/L (normal 8-12), glucose 2.9 mmol/L (normal fasting 3.9-5.8) and ketones 6.4 mmol/L (normal <0.6)). The patient was treated with intravenous dextrose and showed complete resolution of ketoacidosis and hypoglycaemia within 48 hours. She was discharged home and remained well with a balanced diet. After excluding all other the causes of hypoglycaemia and ketoacidosis, the diagnosis of lactation ketoacidosis was made and it was considered triggered by altered diet, exercise and skipping meals. All 11 cases of lactation ketoacidosis which has previously been published are reviewed as well.
2.
Association of Etonogestrel-Releasing Contraceptive Implant with Reduced Weight Gain in an Exclusively Breastfed Infant: Report and Literature Review.
Stuebe, AM, Bryant, AG, Lewis, R, Muddana, A
Breastfeeding medicine : the official journal of the Academy of Breastfeeding Medicine. 2016;(4):203-6
-
-
Free full text
-
Abstract
BACKGROUND Studies have not found that hormonal contraceptive implants adversely affect breastfeeding, but theoretical concerns exist. METHODS We reported a case of reduced weight gain in an exclusively breastfed infant in association with placement of (ENG)-releasing contraceptive implant (Nexplanon) to the FDA Adverse Events Reporting System (FAERS). We further queried reports to FAERS and reviewed published studies of the ENG implant during breastfeeding. RESULTS A breastfeeding mother received an ENG implant at 4 weeks postpartum. Her infant was exclusively breastfeeding. One month after implant placement, the infant had lost 145 g, dropping from the 44th percentile to the 6th percentile for growth. During this period, the mother had not returned to work or decreased frequency of feeding. During a 2-year period of FAERS reports, we found one other report of reduced milk supply following ENG implant placement. Among 108 breastfeeding women studied while using the ENG implant, there was one case of lactation failure. If this were not due to chance, the estimated risk of lactation failure with the ENG implant would be 0.9% (95% confidence interval 0.2-5.1%). CONCLUSION Given uncertainty regarding the true effect of ENG implants on lactation, it seems prudent for providers to counsel each woman about a possible effect on milk supply so that she can monitor her infant for signs of impaired milk transfer. Patient-centered counseling approaches are needed that allow each woman to assess her own individual tolerance of risk of unplanned pregnancy versus possible risk of lactation failure.
3.
Presentation and management of osteoporosis presenting in association with pregnancy or lactation.
Kovacs, CS, Ralston, SH
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA. 2015;(9):2223-41
Abstract
In this review, we summarize our current understanding of the pathophysiology of fragility fractures that occur for the first time during pregnancy and lactation, and provide guidance on appropriate investigations and treatment strategies. Most affected women will have had no prior bone density reading, and so the extent of bone loss that may have occurred during pregnancy or lactation is uncertain. During pregnancy, intestinal calcium absorption doubles in order to meet the fetal demand for calcium, but if maternal intake of calcium is insufficient to meet the combined needs of the mother and baby, the maternal skeleton will undergo resorption during the third trimester. During lactation, several hormonal changes, independent of maternal calcium intake, program a 5-10 % loss of trabecular mineral content in order to provide calcium to milk. After weaning the baby, the maternal skeleton is normally restored to its prior mineral content and strength. This physiological bone resorption during reproduction does not normally cause fractures; instead, women who do fracture are more likely to have additional secondary causes of bone loss and fragility. Transient osteoporosis of the hip may affect one or both femoral heads during pregnancy but it involves localized edema and not skeletal resorption. Case reports have described the use of calcitonin, bisphosphonates, strontium ranelate, teriparatide, vertebroplasty, and kyphoplasty to treat post-partum vertebral fractures. However, the need for such treatments is uncertain given that a progressive increase in bone mass subsequently occurs in most women who present with a fracture during pregnancy or lactation.
4.
Decreased calcitriol requirement during pregnancy and lactation with a window of increased requirement immediately post partum.
Sweeney, LL, Malabanan, AO, Rosen, H
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2010;(3):459-62
Abstract
OBJECTIVE To describe the changes in calcium and calcitriol requirements during pregnancy and lactation in a patient with hypoparathyroidism due to autosomal dominant hypocalcemia. METHODS We summarize the clinical presentation and treatment of the patient and review the pertinent literature. RESULTS Calcitriol requirements disappeared during pregnancy in a 34-year-old woman with autosomal dominant hypoparathyroidism secondary to an activating mutation in the calcium-sensing receptor gene. Within hours after delivery, her serum calcium concentration dropped to 4.7 mg/dL (albumin, 3.2 g/dL), and she required intravenous calcium and reinstitution of calcitriol. When lactation began a few days later, her calcitriol requirement again disappeared. As has occasionally been described in the literature, this patient with hypoparathyroidism required no calcitriol during late pregnancy and lactation to maintain a normal serum calcium level. CONCLUSIONS To our knowledge, this is the first reported case documenting a period of time between pregnancy and lactation when calcitriol requirements reappeared, likely due to a parathyroid hormone-related protein "window" between delivery, when placental production of parathyroid hormone-related protein stops, and lactation, when mammary gland production begins.