Hypokalemic rhabdomyolysis in a patient with a laparoscopic adjustable gastric banding.

Rhabdomyolysis is an acute skeletal muscle disorder characterized by altered integrity of the cell membranes of muscle fiber cells. It can be related to a variety of factors: muscular trauma, muscle enzyme deficiencies, infections, drugs, toxins, alcohol ingestion, endocrinopathies and electrolyte imbalances such as hypokalemia. We report the case of a 46-year-old woman admitted to the Emergency Department for frequent episodes of vomiting associated with food intake in the last two weeks, general muscular weakness and myalgia. Physical examination on admission was unremarkable, except for a symmetrical and dominantly proximal muscular weakness of all four extremities. Blood pressure was 116/70 mmHg with a sinus bradycardia (53 beats/min) on the electrocardiogram. Laboratory tests showed a metabolic alkalosis with marked hypokalemia (K+= 1.9 mEq/l) and elevation of muscular enzymes (myglobin= 993 ng/ml, troponin T= 0,10 ng/ml e CK= 1113 U/l). No symptoms of recurrent rhabdomyolysis were reported, patient denied alcohol consumption and there was not clinical evidence of hyperthyroidism. A iatrogenic etiology could not be excluded for certain because patient was in therapy with lansoprazole (Naranjo algorithm 3/13) but, revealing medical history that she underwent a laparoscopic adjustable gastric banding for the treatment of a severe obesity, we focused our attention on hypokalemia, due to persistent vomiting. Fasting, administration of metoclopramide and infusion of potassium chloride resulted in steady improvement of clinical conditions and normalization of electrolyte imbalance. At the clinical follow-up of three months, after partial deflation of the gastric banding, the patient was asymptomatic with muscular enzymes and potassium levels in the normal range. Authors discuss the pathophysiologic mechanisms of these alterations.

Metformin-induced lactic acidosis in a type 2 diabetic patient with acute renal failure.

Metformin is a biguanide commonly used in type 2 diabetes mellitus (DM). Lactic acidosis, a potentially life-threatening metabolic disorder, may be due to a number of different causes, including metformin therapy. We present a case of a severe metformin-induced lactic acidosis in a patient with type 2 DM, admitted to the emergency department with a history of dehydration due to diarrhoea and complicated by acute renal failure. Patient complained malaise and severe weakness and was tachypneic (Kussmaul's respiration), agitated and confused, with a Glasgow Coma Scale score of 13/15. Heart rate was 75 b/min and blood pressure 110/80 mmHg. The pH was 6.87, HCO3- 3 mmol/l, lactate 15 mmol/l, potassium 6.9 mEq/l. The renal function was markedly impaired with a creatinine of 9.75 mg/dl, and pancreatic enzymes, amylase and lipase, were also increased in absence of abdominal pain. Patient was treated with intravenous fluids, bicarbonate infusion and haemodialysis with bicarbonate buffered replacement fluid. Clinical conditions improved rapidly, with a progressive normalization of the acid-base balance and the other laboratory data. Authors discuss the pathophysiologic mechanisms of these alterations with particular regard to the role played by metformin as potential cause of lactic acidosis.

Hepatitis C-associated osteosclerosis (HCAO): report of a new case with involvement of the OPG/RANKL system.

We report a new case of hepatitis C-associated osteosclerosis (HCAO). The clinical presentation of the patient was an acquired deep severe bone pain with increased serum bone alkaline phosphatase activity (up to 12 times the upper limit of normal), and generalized bone sclerosis, temporally related to the hepatitis C-virus (HCV) infection. We documented in this patient an increase of circulating osteoprotegerin (OPG), and a concentration of circulating receptor activator for nuclear factor-kB ligand (RANKL) below the lower limit of the reference range. The observed abnormalities of the OPG/RANKL system may contribute to the maintenance of the positive balance of bone remodeling that characterizes patients with HCAO.

Low bone density and abnormal bone turnover in patients with atherosclerosis of peripheral vessels.

Patients with vascular calcifications often have low bone mineral density (BMD), but it is still uncertain if osteoporosis and peripheral vascular disease (VD) are interrelated and linked by a common pathomechanism. Moreover, data on bone turnover in patients with advanced atherosclerosis are lacking. We measured BMD by dual-energy X-ray absorptiometry (DXA) and quantitative bone ultrasound (QUS), as well as the serum levels of osteocalcin (OC), bone-specific alkaline phosphatase (BAP), osteoprotegerin (OPG) and its ligand RANKL, and the urinary concentration of the C-terminal telopeptides of type I collagen (CrossLaps), in 36 patient (20 male and 16 female) with serious atherosclerotic involvement of the carotid and/or femoral artery to investigate the underlying mechanism of vascular and osseous disorders. Thirty age-matched and gender matched healthy individuals served as controls. After adjustment for age, BMD was significantly reduced at the lumbar spine in 23/36 (63%) patients (mean T score -1.71+/-1.42) and at the proximal femur in 34/36 (93%) patients (neck mean T score -2.5+/-0.88). Ten patients (27%) had abnormal QUS parameters. Gender and diabetes had no effect on the relationship between vascular calcification and bone density at any site measured. VD subjects had OC and BAP serum levels lower than controls (13.3+/-3.1 vs 27.7+/-3.3 ng/ml, P<0.01, and 8.4+/-2.3 vs 12.5+/-1.4 microg/l, P<0.01, respectively). Urinary CrossLaps excretion was not significantly different in patients with VD and in controls (257.9+/-138.9 vs 272.2+/-79.4 micro g/mmol Cr, respectively). Serum OPG and RANKL levels were similar in patients and in controls (3.5+/-1.07 vs 3.4+/-1.05 pmol/l, and 0.37+/-0.07 vs 0.36+/-0.06 pmol/l, respectively). We proved high occurrence of osteoporosis in VD, with evidence of age and gender independence. Negative bone remodelling balance would be a consequence of reduced bone formation, with no apparent increased activation of the OPG-RANKL system.

Pregnancy-associated changes in bone density and bone turnover in the physiological state: prospective data on sixteen women.

Areal bone mineral density (BMD, g/cm 2) was measured for the total body, lumbar spine and hip with dual-energy x-ray absorptiometry (DXA) before pregnancy and after delivery in sixteen women aged 21 - 35 years. Additional measurements included quantitative ultrasound indices (broadband ultrasound attenuation, BUA, at the calcaneus at baseline and at 16, 26, and 36 weeks of pregnancy, and postpartum) as well as biochemical markers of bone formation and resorption (measured before pregnancy and during pregnancy at 16, 22, 26, 30, 34, and 36 weeks of pregnancy and postpartum). The results of measurements were as follows: 1. Postpartum BMD showed a significant reduction in the total body (- 13.4 %), in the spine (- 9.2 %) and in the hip (-7.8 % at the femoral neck and - 9.2 % at the Ward's triangle) compared to pre-pregnancy values. 2. Biochemical markers of bone resorption increased by 26 weeks. 3. Bone ultrasound measurements that provide information on bone density before delivery did not change throughout pregnancy. A significant reduction of BUA (- 14.5 % compared to baseline) was observed postpartum only. These data would suggest that pregnancy-induced bone loss develops rapidly after the 36 week of pregnancy, possibly via enhanced bone resorption.