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Michael J Komar - One of the best experts on this subject based on the ideXlab platform.

  • Clinical Observations Hypercalcemia and Peptic Ulcer Disease–Related Milk-Alkali Syndrome
    2016
    Co-Authors: Matthew B. Grundfast, Do Christopher, D. Still, Michael J Komar
    Abstract:

    ABSTRACT: Milk-Alkali Syndrome was considered “extinct ” by 1985 because of the advent of non-Alkaline ulcer medications (ie, histamine-2 receptor blockers and proton pump inhibitors). At that time, it was thought to cause 1 % of hypercalcemia, which occurred when one ingested a sufficient quantity of calcium and Alkali together. This case emphasizes the importance of consid-ering this Syndrome in patients who self-medicate for control of symptoms related to gastroesophageal reflux and peptic ulcer disease and for those using calcium supplementation for prevention or treatment of osteopo-rosis. A 59-year-old male presented to our institution complaining of weakness for 1 week, difficulty ambulating for 4 days, nausea and emesis for 2 days, slurred speech, and an episode of coffee ground emesis. He had anorexia for 2 weeks, and was able to take only liquids, because solid food caused him a “sour stomach. ” He had a past medical history of peptic ulcer disease, tuberculosis with partial pneu-monectomy, chronic obstructive pulmonary disease, tobacco abuse, and chronic lower back pain. Medica-tions included alprazolam 0.5 mg orally at bedtime, propoxyphene 100 mg/acetaminophen 650 mg 1 cap-sule orally every 4 hours as needed, 5 enteric-coated aspirin (325 mg) tablets daily, and 15 to 25 Rolaid

  • hypercalcemia and peptic ulcer disease related Milk Alkali Syndrome
    Nutrition in Clinical Practice, 2003
    Co-Authors: Matthew B. Grundfast, Christopher D. Still, Michael J Komar
    Abstract:

    Milk-Alkali Syndrome was considered "extinct" by 1985 because of the advent of non-Alkaline ulcer medications (ie, histamine-2 receptor blockers and proton pump inhibitors). At that time, it was thought to cause <1% of hypercalcemia, which occurred when one ingested a sufficient quantity of calcium and Alkali together. This case emphasizes the importance of considering this Syndrome in patients who self-medicate for control of symptoms related to gastroesophageal reflux and peptic ulcer disease and for those using calcium supplementation for prevention or treatment of osteoporosis.

  • Hypercalcemia and peptic ulcer disease-related Milk-Alkali Syndrome.
    Nutrition in Clinical Practice, 2003
    Co-Authors: Matthew B. Grundfast, Christopher D. Still, Michael J Komar
    Abstract:

    Milk-Alkali Syndrome was considered "extinct" by 1985 because of the advent of non-Alkaline ulcer medications (ie, histamine-2 receptor blockers and proton pump inhibitors). At that time, it was thought to cause

Matthew B. Grundfast - One of the best experts on this subject based on the ideXlab platform.

  • Clinical Observations Hypercalcemia and Peptic Ulcer Disease–Related Milk-Alkali Syndrome
    2016
    Co-Authors: Matthew B. Grundfast, Do Christopher, D. Still, Michael J Komar
    Abstract:

    ABSTRACT: Milk-Alkali Syndrome was considered “extinct ” by 1985 because of the advent of non-Alkaline ulcer medications (ie, histamine-2 receptor blockers and proton pump inhibitors). At that time, it was thought to cause 1 % of hypercalcemia, which occurred when one ingested a sufficient quantity of calcium and Alkali together. This case emphasizes the importance of consid-ering this Syndrome in patients who self-medicate for control of symptoms related to gastroesophageal reflux and peptic ulcer disease and for those using calcium supplementation for prevention or treatment of osteopo-rosis. A 59-year-old male presented to our institution complaining of weakness for 1 week, difficulty ambulating for 4 days, nausea and emesis for 2 days, slurred speech, and an episode of coffee ground emesis. He had anorexia for 2 weeks, and was able to take only liquids, because solid food caused him a “sour stomach. ” He had a past medical history of peptic ulcer disease, tuberculosis with partial pneu-monectomy, chronic obstructive pulmonary disease, tobacco abuse, and chronic lower back pain. Medica-tions included alprazolam 0.5 mg orally at bedtime, propoxyphene 100 mg/acetaminophen 650 mg 1 cap-sule orally every 4 hours as needed, 5 enteric-coated aspirin (325 mg) tablets daily, and 15 to 25 Rolaid

  • hypercalcemia and peptic ulcer disease related Milk Alkali Syndrome
    Nutrition in Clinical Practice, 2003
    Co-Authors: Matthew B. Grundfast, Christopher D. Still, Michael J Komar
    Abstract:

    Milk-Alkali Syndrome was considered "extinct" by 1985 because of the advent of non-Alkaline ulcer medications (ie, histamine-2 receptor blockers and proton pump inhibitors). At that time, it was thought to cause <1% of hypercalcemia, which occurred when one ingested a sufficient quantity of calcium and Alkali together. This case emphasizes the importance of considering this Syndrome in patients who self-medicate for control of symptoms related to gastroesophageal reflux and peptic ulcer disease and for those using calcium supplementation for prevention or treatment of osteoporosis.

  • Hypercalcemia and peptic ulcer disease-related Milk-Alkali Syndrome.
    Nutrition in Clinical Practice, 2003
    Co-Authors: Matthew B. Grundfast, Christopher D. Still, Michael J Komar
    Abstract:

    Milk-Alkali Syndrome was considered "extinct" by 1985 because of the advent of non-Alkaline ulcer medications (ie, histamine-2 receptor blockers and proton pump inhibitors). At that time, it was thought to cause

Christopher D. Still - One of the best experts on this subject based on the ideXlab platform.

  • hypercalcemia and peptic ulcer disease related Milk Alkali Syndrome
    Nutrition in Clinical Practice, 2003
    Co-Authors: Matthew B. Grundfast, Christopher D. Still, Michael J Komar
    Abstract:

    Milk-Alkali Syndrome was considered "extinct" by 1985 because of the advent of non-Alkaline ulcer medications (ie, histamine-2 receptor blockers and proton pump inhibitors). At that time, it was thought to cause <1% of hypercalcemia, which occurred when one ingested a sufficient quantity of calcium and Alkali together. This case emphasizes the importance of considering this Syndrome in patients who self-medicate for control of symptoms related to gastroesophageal reflux and peptic ulcer disease and for those using calcium supplementation for prevention or treatment of osteoporosis.

  • Hypercalcemia and peptic ulcer disease-related Milk-Alkali Syndrome.
    Nutrition in Clinical Practice, 2003
    Co-Authors: Matthew B. Grundfast, Christopher D. Still, Michael J Komar
    Abstract:

    Milk-Alkali Syndrome was considered "extinct" by 1985 because of the advent of non-Alkaline ulcer medications (ie, histamine-2 receptor blockers and proton pump inhibitors). At that time, it was thought to cause

Philip R. Orlander - One of the best experts on this subject based on the ideXlab platform.

  • Milk Alkali Syndrome is a major cause of hypercalcaemia among non end stage renal disease non esrd inpatients
    Clinical Endocrinology, 2005
    Co-Authors: Michalis K. Picolos, Victor R. Lavis, Philip R. Orlander
    Abstract:

    Summary Objective  Milk–Alkali Syndrome, once a common cause of hypercalcaemia, is now considered rare. Our aim was to estimate the prevalence of Milk–Alkali Syndrome among hypercalcaemic, non-end-stage renal disease (non-ESRD) inpatients of a University Hospital and identify patients’ and Syndrome characteristics. Design and patients  In this retrospective chart review study, we identified patients hospitalized with possible hypercalcaemia between November 1998 and October 2003 by a computer search of admission, discharge and consultation diagnoses. Patients with renal transplantation, stage 5 chronic kidney disease (CKD-5) and those admitted for parathyroidectomy were excluded. The remaining patients’ charts were reviewed for confirmation of hypercalcaemia and identification of the cause. In patients with Milk–Alkali Syndrome, additional historical, clinical, laboratory and imaging data were collected. Results  We identified 125 patients with hypercalcaemia, 11 (8·8%) of whom had Milk–Alkali Syndrome, 42 (33·6%) had malignancy and 37 (29·6%) hyperparathyroidism. Thirty-five patients had severe hypercalcaemia, defined as corrected serum calcium  3·5 mmol/l. Malignancy accounted for 13 of those patients (37·1%) and Milk–Alkali for nine (25·7%). Conditions prevalent among the Milk–Alkali inpatients were female gender, hypertension, chronic kidney disease, osteoporosis, upper gastrointestinal diseases, diuretic treatment and vitamin D derivative supplementation. Five of the patients with Milk–Alkali Syndrome were treated with bisphosphonates and all five developed hypocalcaemia, compared to one of the five who received conventional treatment (P = 0·047). Conclusion  Milk–Alkali was the third leading cause of hypercalcaemia of any degree and the second cause of severe hypercalcaemia among inpatients without ESRD. In Milk–Alkali Syndrome, treatment with bisphosphonates contributes to post-treatment hypocalcaemia.

  • Milk–Alkali Syndrome is a major cause of hypercalcaemia among non‐end‐stage renal disease (non‐ESRD) inpatients
    Clinical Endocrinology, 2005
    Co-Authors: Michalis K. Picolos, Victor R. Lavis, Philip R. Orlander
    Abstract:

    Summary Objective  Milk–Alkali Syndrome, once a common cause of hypercalcaemia, is now considered rare. Our aim was to estimate the prevalence of Milk–Alkali Syndrome among hypercalcaemic, non-end-stage renal disease (non-ESRD) inpatients of a University Hospital and identify patients’ and Syndrome characteristics. Design and patients  In this retrospective chart review study, we identified patients hospitalized with possible hypercalcaemia between November 1998 and October 2003 by a computer search of admission, discharge and consultation diagnoses. Patients with renal transplantation, stage 5 chronic kidney disease (CKD-5) and those admitted for parathyroidectomy were excluded. The remaining patients’ charts were reviewed for confirmation of hypercalcaemia and identification of the cause. In patients with Milk–Alkali Syndrome, additional historical, clinical, laboratory and imaging data were collected. Results  We identified 125 patients with hypercalcaemia, 11 (8·8%) of whom had Milk–Alkali Syndrome, 42 (33·6%) had malignancy and 37 (29·6%) hyperparathyroidism. Thirty-five patients had severe hypercalcaemia, defined as corrected serum calcium  3·5 mmol/l. Malignancy accounted for 13 of those patients (37·1%) and Milk–Alkali for nine (25·7%). Conditions prevalent among the Milk–Alkali inpatients were female gender, hypertension, chronic kidney disease, osteoporosis, upper gastrointestinal diseases, diuretic treatment and vitamin D derivative supplementation. Five of the patients with Milk–Alkali Syndrome were treated with bisphosphonates and all five developed hypocalcaemia, compared to one of the five who received conventional treatment (P = 0·047). Conclusion  Milk–Alkali was the third leading cause of hypercalcaemia of any degree and the second cause of severe hypercalcaemia among inpatients without ESRD. In Milk–Alkali Syndrome, treatment with bisphosphonates contributes to post-treatment hypocalcaemia.

  • CALCIUM CARBONATE TOXICITY: THE UPDATED Milk-Alkali Syndrome; REPORT OF 3 CASES AND REVIEW OF THE LITERATURE
    Endocrine Practice, 2005
    Co-Authors: Michalis K. Picolos, Philip R. Orlander
    Abstract:

    Objective: To describe 3 patients with calcium carbonate-induced hypercalcemia and gain insights into the cause and management of the Milk-Alkali Syndrome. Methods: We report the clinical and laboratory data in 3 patients who presented with severe hypercalcemia (corrected serum calcium ³ 14 mg/dL) and review the pertinent literature on Milk-Alkali Syndrome. Results: The 3 patients had acute renal insufficiency, relative metabolic alkalosis, and low parathyroid hormone (PTH), PTH-related peptide, and 1,25-dihydroxyvitamin D concentrations. No malignant lesion was found. Treatment included aggressive hydration and varied amounts of furosemide. The 2 patients with the higher serum calcium concentrations received pamidronate intravenously (60 and 30 mg, respectively), which caused severe hypocalcemia. Of the 3 patients, 2 were ingesting acceptable doses of elemental calcium (1 g and 2 g daily, respectively) in the form of calcium carbonate. In addition to our highlighted cases, we review the history, classifi...

Michalis K. Picolos - One of the best experts on this subject based on the ideXlab platform.

  • Milk Alkali Syndrome is a major cause of hypercalcaemia among non end stage renal disease non esrd inpatients
    Clinical Endocrinology, 2005
    Co-Authors: Michalis K. Picolos, Victor R. Lavis, Philip R. Orlander
    Abstract:

    Summary Objective  Milk–Alkali Syndrome, once a common cause of hypercalcaemia, is now considered rare. Our aim was to estimate the prevalence of Milk–Alkali Syndrome among hypercalcaemic, non-end-stage renal disease (non-ESRD) inpatients of a University Hospital and identify patients’ and Syndrome characteristics. Design and patients  In this retrospective chart review study, we identified patients hospitalized with possible hypercalcaemia between November 1998 and October 2003 by a computer search of admission, discharge and consultation diagnoses. Patients with renal transplantation, stage 5 chronic kidney disease (CKD-5) and those admitted for parathyroidectomy were excluded. The remaining patients’ charts were reviewed for confirmation of hypercalcaemia and identification of the cause. In patients with Milk–Alkali Syndrome, additional historical, clinical, laboratory and imaging data were collected. Results  We identified 125 patients with hypercalcaemia, 11 (8·8%) of whom had Milk–Alkali Syndrome, 42 (33·6%) had malignancy and 37 (29·6%) hyperparathyroidism. Thirty-five patients had severe hypercalcaemia, defined as corrected serum calcium  3·5 mmol/l. Malignancy accounted for 13 of those patients (37·1%) and Milk–Alkali for nine (25·7%). Conditions prevalent among the Milk–Alkali inpatients were female gender, hypertension, chronic kidney disease, osteoporosis, upper gastrointestinal diseases, diuretic treatment and vitamin D derivative supplementation. Five of the patients with Milk–Alkali Syndrome were treated with bisphosphonates and all five developed hypocalcaemia, compared to one of the five who received conventional treatment (P = 0·047). Conclusion  Milk–Alkali was the third leading cause of hypercalcaemia of any degree and the second cause of severe hypercalcaemia among inpatients without ESRD. In Milk–Alkali Syndrome, treatment with bisphosphonates contributes to post-treatment hypocalcaemia.

  • Milk–Alkali Syndrome is a major cause of hypercalcaemia among non‐end‐stage renal disease (non‐ESRD) inpatients
    Clinical Endocrinology, 2005
    Co-Authors: Michalis K. Picolos, Victor R. Lavis, Philip R. Orlander
    Abstract:

    Summary Objective  Milk–Alkali Syndrome, once a common cause of hypercalcaemia, is now considered rare. Our aim was to estimate the prevalence of Milk–Alkali Syndrome among hypercalcaemic, non-end-stage renal disease (non-ESRD) inpatients of a University Hospital and identify patients’ and Syndrome characteristics. Design and patients  In this retrospective chart review study, we identified patients hospitalized with possible hypercalcaemia between November 1998 and October 2003 by a computer search of admission, discharge and consultation diagnoses. Patients with renal transplantation, stage 5 chronic kidney disease (CKD-5) and those admitted for parathyroidectomy were excluded. The remaining patients’ charts were reviewed for confirmation of hypercalcaemia and identification of the cause. In patients with Milk–Alkali Syndrome, additional historical, clinical, laboratory and imaging data were collected. Results  We identified 125 patients with hypercalcaemia, 11 (8·8%) of whom had Milk–Alkali Syndrome, 42 (33·6%) had malignancy and 37 (29·6%) hyperparathyroidism. Thirty-five patients had severe hypercalcaemia, defined as corrected serum calcium  3·5 mmol/l. Malignancy accounted for 13 of those patients (37·1%) and Milk–Alkali for nine (25·7%). Conditions prevalent among the Milk–Alkali inpatients were female gender, hypertension, chronic kidney disease, osteoporosis, upper gastrointestinal diseases, diuretic treatment and vitamin D derivative supplementation. Five of the patients with Milk–Alkali Syndrome were treated with bisphosphonates and all five developed hypocalcaemia, compared to one of the five who received conventional treatment (P = 0·047). Conclusion  Milk–Alkali was the third leading cause of hypercalcaemia of any degree and the second cause of severe hypercalcaemia among inpatients without ESRD. In Milk–Alkali Syndrome, treatment with bisphosphonates contributes to post-treatment hypocalcaemia.

  • CALCIUM CARBONATE TOXICITY: THE UPDATED Milk-Alkali Syndrome; REPORT OF 3 CASES AND REVIEW OF THE LITERATURE
    Endocrine Practice, 2005
    Co-Authors: Michalis K. Picolos, Philip R. Orlander
    Abstract:

    Objective: To describe 3 patients with calcium carbonate-induced hypercalcemia and gain insights into the cause and management of the Milk-Alkali Syndrome. Methods: We report the clinical and laboratory data in 3 patients who presented with severe hypercalcemia (corrected serum calcium ³ 14 mg/dL) and review the pertinent literature on Milk-Alkali Syndrome. Results: The 3 patients had acute renal insufficiency, relative metabolic alkalosis, and low parathyroid hormone (PTH), PTH-related peptide, and 1,25-dihydroxyvitamin D concentrations. No malignant lesion was found. Treatment included aggressive hydration and varied amounts of furosemide. The 2 patients with the higher serum calcium concentrations received pamidronate intravenously (60 and 30 mg, respectively), which caused severe hypocalcemia. Of the 3 patients, 2 were ingesting acceptable doses of elemental calcium (1 g and 2 g daily, respectively) in the form of calcium carbonate. In addition to our highlighted cases, we review the history, classifi...

  • Milk-Alkali Syndrome in pregnancy.
    Obstetrics & Gynecology, 2004
    Co-Authors: Michalis K. Picolos, Charles R. Sims, Joan M. Mastrobattista, Mary A. Carroll, Victor R. Lavis
    Abstract:

    BACKGROUND:Severe hypercalcemia, a potentially life-threatening medical emergency, is rare in pregnancy.CASE:We report a 32-year-old woman presenting early in the second trimester with severe hypercalcemia (total calcium 22mg/dL), alkalosis, and acute renal insufficiency resulting from excessive ing