Calcium Alkali Thiazide Syndrome: What We Need to Know.

Depending on each institution's laboratory test, mean serum calcium levels range between 8.8 and 10.8 mg/dL and hypercalcemia is defined as two standard deviations above the mean. According to recent epidemiological studies, 90% of cases of hypercalcemia are due to hyperparathyroidism or malignancy. Milk Alkali syndrome (MAS) also known as Calcium Alkali syndrome (CAS) is the third biggest cause of hypercalcemia, but its incidence seems to be higher than previously thought. Here we present a case of Calcium Alkali Thiazide syndrome (CATS) in a 57-year-old female who was on calcium and vitamin D supplements (after parathyroidectomy) while also taking thiazide diuretic for hypertension. She was brought to the ED with nausea, vomiting, confusion, difficulty walking along with numbness in extremities. She had parathyroidectomy three weeks ago. During history taking, patient reported intake of calcium carbonate 1 g three times daily, calcitriol 0.5 mcg twice daily, cholecalciferol (vitamin D3) 10,000 units once daily, chlorthalidone 25 mg once daily and irbesartan 300 mg once daily. At admission, her calcium level was 23 mg/dL, ionized calcium 12.03 mg/dL, pH was 7.59 and HCO3 was 33. She was in renal failure with creatinine of 1.9 mg/dL (baseline 0.8 mg/dL). Her parathyroid hormone (PTH) level was 0. A diagnosis of CATS was made. She was treated with intravenous fluids and furosemide and discharged home on hospital day 5 after her calcium and creatinine levels normalized. A triad of hypercalcemia, acute kidney injury and metabolic alkalosis comprises MAS. Traditional MAS was caused by "Sippy diet" (containing milk and alkali) used for the treatment of peptic ulcer disease. Over the decades, the same triad of symptoms occurred in patients using excess calcium and vitamin D, hence changing the name to CAS. A subset of patients at risk for CAS also use thiazide diuretics for hypertension, making them more vulnerable to hypercalcemia and acute kidney injury. In such subset of patients, it is preferable to use the term CATS rather than MAS or CAS.

Autologous stem cell transplantation with in vivo purged progenitor cells shows long-term efficacy in relapsed/refractory follicular lymphoma.

High-dose chemotherapy with autologous stem cell transplantation (ASCT) has been shown effective in the control of relapsed/refractory follicular lymphoma. We evaluate the long-term outcome of patients with relapsed or refractory follicular lymphoma treated with ASCT with in vivo purged progenitors cells. We report the long-term results of a prospective multicenter phase 2 trial on 124 relapsed/refractory follicular lymphoma patients treated with a program of anthracycline-based debulking chemotherapy, immunochemotherapy, mobilization of in vivo purged PBSC followed by ASCT. Median age was 52 years; 14% of patients had grade 3A histology. Debulking chemotherapy produced CR in 16% and PR in 71%, while 13% of patients progressed. After rituximab, cyclophosphamide, vincristine, prednisone (R-COP), CR was obtained in 60% and PR in 35%; 118 patients successfully mobilized PBSC and 117 proceeded to ASCT. The harvest in all the 32 molecularly informative patients was bcl-2 negative. TRM was 0%. The 5-year PFS was 54% and the 5-year OS was 83%. After a median f-up of 6.7 years (range 1.5-13.6), 54% are still in CR. These data show that prolonged PFS is achievable in relapsed/refractory patients with high dose autologous transplantation of in vivo purged progenitor cells.

Invasive fungal infections in lymphoproliferative disorders: a monocentric retrospective experience.

Invasive fungal infections (IFIs) seem to be a relevant cause of morbidity and mortality in patients with chronic lymphoproliferative disorders. We studied retrospectively the epidemiology, clinical manifestations and outcome of invasive fungal infections in 42 patients with lymphoproliferative diseases, treated between January 2004 and February 2012 for probable or proven IFI. In our entire population (1355 patients) of chronic lymphoproliferative malignancies, the incidence of probable/proven IFI was 3% (molds 2.3%, yeasts 0.5%, mixed infections 0.2%). Eight patients developed a yeast infection documented by blood cultures in seven cases and by the microscopic observation of Candida spp. in the vitreum after vitrectomy in one case. Among molds we diagnosed three proven infections by histologic evidence of Aspergillus spp. (n = 2) and Mucor (n = 1) in the lung and 28 probable mycoses. Three mixed infections from both molds and yeasts were also observed. Twenty-two cases showed positivity of galactomannan antigen in the serum (n = 16), in bronchoalveolar lavage (BAL) fluid (n = 4) or in both (n = 2). Cultures were positive in 11 cases. The overall rate of response to therapy was 64%. Fungal-attributable mortality rate was 17%, with a significant difference between molds and yeasts (16% vs. 25%, p = 0.03). At univariate analysis, the only risk factors related to mortality were severe and prolonged neutropenia (p = 0.003) and age (p = 0.03). Among molds, the rapid start of antifungals was probably partially responsible, together with new drugs, for the reduction of mortality, despite the severe immunosuppression of these patients.