Published: Thu, 13 Apr 2017 00:00:00 GMT
Last Build Date: Mon, 17 Apr 2017 01:47:38 GMT
2017-04-13We are all well aware of escalating healthcare costs, our ageing population and the challenge of caring for an exponential growth in patients with chronic diseases. In a seminal review Bernard Tyson, CEO of Kaiser Permanente, one of America’s largest providers of integrated healthcare, proposes that the pendulum of healthcare expenditure should be rebalanced from predominantly providing ‘sick care’ to ‘health-care’. Investing in wellness and empowering people to take ownership of their well-being. Medicare payments in 2014 totaled $597, of which 25% of this total was accounted for care given to patients in the last year of their life. We need to invest in expanding the quality of a person’s life within their community.
2017-02-02We thank the authors, Dr Hill and Dr Sayer, for their feedback in response to our article published in QJM: An International Journal of Medicine.1 In principle, we agree with the authors and the recent population-based observational studies2 that chronic use of proton pump inhibitors (PPIs) may adversely affect renal physiology including development and/or progression of chronic kidney disease (CKD). Our earlier work3 applying molecular, cell biological and preclinical models found that PPIs directly inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH); an enzyme that is expressed in different segments of the kidney including proximal tubule, thick ascending limb of the loop of Henle, macula densa, distal convoluted tubule and collecting ducts. Inhibition of renal DDAH enzymatic activity by PPIs is expected to deregulate the endogenous concentration of its substrate asymmetrical dimethylarginine (ADMA); competitive inhibitor of nitric oxide (NO) synthase (NOS). Thus, PPIs could disrupt the DDAH/ADMA/NO homeostasis in the renal system by elevating ADMA levels and suppressing DDAH and NO. Several preclinical and clinical studies indicate that dysfunction of NO, an important molecule in the dilation of afferent and efferent arterioles, is associated with systemic and glomerular hypertension, glomerular ischemia, proteinuria, tubulointerstitial injury, renal fibrosis, progression of CKD and end-stage renal disease (ESRD).4 The studies also report that urinary or dialysate NO is decreased in CKD patients and ESRD patients on peritoneal- or hemo- dialysis. Similarly, elevated ADMA is a major cause of endothelial dysfunction and a predictor of cardiovascular mortality in CKD patients whereas its elimination by hemodialysis in renal failure patients is associated with improved endothelial function. Experimental studies in nephrectomized animals also show that while ADMA is inversely correlated with the number of peritubular and glomerular capillaries, overexpression of DDAH improves creatinine clearance, attenuates tubulointerstitial fibrosis, and reduces urinary protein excretion.
2017-01-16To the editor:
2017-01-10A 46-year-old Japanese man experienced sudden-onset left hand weakness upon waking. He had no history of trauma or heavy manual labor. He had been diagnosed with diabetes mellitus 10 years earlier, but never been treated. Physical examination revealed paralysis in the left flexor pollicis and flexor indicis muscles without muscle atrophy. Although Tinel’s sign was negative, he was unable to form ‘O’ sign by using the index finger and thumb of the left hand, which is known as tear drop sign (Figure 1A, arrowhead). Sensory nerve injury symptoms were absent. His blood glucose, serum hemoglobin A1C, and creatinine levels were 274 mg/dl, 11.1% and 2.1 mg/dl, respectively. He was diagnosed with anterior interosseous nerve syndrome as a part of diabetic mononeuropathy, and intensive insulin therapy was initiated. The patient’s symptoms gradually improved, showing full recovery with a perfect ‘OK’ sign at 8-week follow-up (Figure 1B). Figure 1(A) The patient, on arrival, could not make ‘O’ sign with his left hand, because of acute weakness on his thumb and indexing finger (arrowhead). (B) Eight-week follow-up with glycemic control showed complete recovery of intrinsic muscle of the left hand.
2017-01-06We read with interest the case report by Schattner et al.1 In their clinical picture, bilateral basal ganglia calcification, incidentally found on CT head scan in an elderly diabetic female with vertigo, was deemed to represent Fahr's disease, a neurodegenerative condition characterized by intracerebral calcium deposition. Similar pathology was subsequently detected in her daughter, suggesting a familial form; of note, the son was unaffected. Although the authors mention various associations of basal ganglia calcifications including mitochondrial myopathy, this possibility is dismissed because of a ‘lack of systemic involvement’ in the patient described.
2017-01-06A 43-year-old woman presented with abdominal pain, vomiting and watery diarrhea for 1 day. She had the medical history of breast cancer receiving surgery, adjuvant concurrent chemoradiotherapy and hormone therapy. Upon physical examination, her abdomen was moderately distended with periumbilical tenderness. Bowel sounds were hyperactive. No rebounding pain or muscle guarding was noted, and no masses or organomegaly were palpated. Laboratory examination revealed white blood cell count, 12 000/mm3 (74.4% neutrophils), creatinine 1.74 mg/dl, C-reactive protein, 18.9 mg/l (normal reference, <5 mg/l) and lipase was 513 units/l. Urinalysis showed proteinuria, hematuria and hyaline and granular casts. Contrast enhanced abdominal computed tomography (CT) showed a target sign of the entire small bowel (which indicated diffuse circumferential wall thickening with submucosal edema, Figure 1, arrows) and grade C pancreatitis with peripancreatic region inflammation. There was no image evidence of thrombosis, intestinal perforation or infarction. Additional laboratory test showed positive antinuclear antibody 1:1280, and positive anti-double stranded DNA (anti-dsDNA) antibody 321.7 IU/ml. Based on the clinical and serology criteria, the diagnosis of system lupus erythematous (SLE) associated enteritis, mesenteric vasculitis, lupus nephritis and acute pancreatitis was made. She was treated with methylprednisolone pulse therapy and oral hydroxychloroquine. Her symptoms gradually subsided, and she was discharged uneventfully 6 days after admission. Figure 1Contrast enhanced CT of the abdomen (coronal view) revealed target sign, which indicated diffuse circumferential wall thickening with submucosal edema of the entire small bowel, showing the ‘double halo’ or ‘target,’ sign (arrows).
2017-01-06A 42-year-old woman with history of IgA nephropathy with chronic kidney disease, Stage 5 and hypertension presented with poor appetite, generalized itchy and dysgeusia with decreasing sensation to salt. She denied smoking and betel nuts use. Extra-oral examination revealed petechiae on her back and subconjunctival hemorrhage on her left eye. Intraoral examination revealed the presence of white plaques predominantly involving the lateral borders and dorsal surface of the tongue (Figure 1a), floor of the mouth and buccal mucosae (Figure 1b). The results of blood tests were as follows: white blood cell count of 6.62 × 103/μl; platelet count of 106 × 103/μl; Hemoglobin of 7.4 g/dl, blood urea nitrogen (BUN) of 205 mg/dl and creatinine of 18.9 mg/dl. The virus, fungus and microbiology survey were unremarkable. Pathological report of the lesion was unavailable because the patient declined biopsy. The white lesions almost resolved completely and the taste disturbance improved remarkably after 4 sessions of hemodialysis within 5 days accompanied with lowering of BUN levels. Figure 1(a) Intraoral examination revealed the presence of white plaques predominantly involving the lateral borders and dorsal surface of the tongue. (b) White plaques involving the floor of the mouth and buccal mucosae.
2017-01-06A 72-year-old female presented to emergency room with generalized weakness predominantly in lower limbs. She was apparently normal until 1 week ago after which she developed watery diarrhea, four to six times a day. Stool was non-bloody. There were no associated symptoms such as nausea, vomiting, fever or abdominal pain. Patient denied history of sick contacts, travel and use of laxatives. She had a past medical history of mild persistent bronchial asthma and uses albuterol (inhaler and nebulizer) as needed. Patient looked dehydrated. Her heart rate was 96 beats per minute and blood pressure was 136/76 mm of Hg. Neurological exam and the reminder of physical exam was normal. Because of generalized weakness and dehydration, she was started on intravenous dextrose plus normal saline. Later, she was found to be severely hypokalemic (serum potassium: 2.0 mEq/l, normal: 3–5 mEq/l), and in severe contraction metabolic alkalosis. Electrocardiogram showed normal sinus rhythm with a heart rate of 88 beats per minute and prolonged QT interval (520 ms) (Figure 1A). Corrected QT (QTc) interval was 630 ms. She developed torsade de pointes (Figure 1B) even before receiving potassium replacement. Repeat potassium level was 1.6 mEq/l and magnesium level was normal. She was successfully revived following electrical defibrillation. She received aggressive replacement of potassium intravenously with glucose free solutions. Echocardiography showed mildly decreased left ventricular systolic function (50%). QT prolongation got corrected with potassium replacement. Rapid decrease in serum potassium concentration can lead to life-threatening consequences such as cardiac arrhythmias, severe muscle weakness to frank paralysis and rhabdomyolysis. Mild (<3.5 mEq/l) to moderate hypokalemia (2.5–3.5 mEq/l) is well tolerated in normal healthy people. However, sever hypokalemia (<2.5 mEq/l) in healthy people and even mild hypokalemia in people with cardiac problems could lead to arrhythmias. Potassium homeostasis plays an integral role in maintaining resting membrane potential. Hypokalemia-induced arrhythmogenicity is attributed to prolonged ventricular repolarization, slowed conduction and abnormal pacemaker activity. Prolonged QT interval reflects prolonged cardiac repolarization, which is a pathogenic factor in the genesis of torsade de pointes. Dextrose intravenous fluids stimulate the insulin secretion, causing the shift of extracellular potassium into the cells by activating cell membrane Na+/K+-ATPase pump.1 Our patient had diarrhea for a week, which is one of the important cause for potassium loss from the body. Additionally, use of β-adrenergic agonist (albuterol) and metabolic alkalosis resulting from severe hypokalemia could have contributed to her severe hypokalemia. Hypokalemia is usually associated with hypomagnesaemia. If potassium replacement does not normalize QT interval, we suspect hypomagnesaemia, as magnesium also regulates the Na+/K+-ATPase pump, which prevents intracellular depletion of potassium.2 She had an uneventful hospital course and was discharged home. Figure 1(A) An electrocardiogram showing normal sinus rhythm with a prolonged QT interval of 520 ms. Corrected QT (QTc) interval was 630 ms and (B) an electrocardiogram showing torsade de pointes.
2017-01-06A 63-year-old man presented to the emergency department with a 1-day history of acute onset severe epigastric abdominal pain and nausea several hours after eating raw mackerel at a sushi restaurant. His symptoms persisted, and he was admitted to the hospital on the following day. He had no previous cardiovascular or gastrointestinal problems, and he denied any history of an allergy. His vital signs were normal. On physical examination, he exhibited mild tenderness of his epigastrium without guarding or rebound tenderness. The complete blood examination, including an eosinophil count and blood chemistry, was unremarkable. A simple radiograph showed no abnormality. On the basis of his clinical history, we suspected anisakiasis and we performed endoscopy to find the polypide. The upper gastrointestinal endoscopic examination showed a tortuous polypide with one end burrowed under the mucosal layer of the gastric corpus (Figure 1). Figure 1(A) Endoscopic view of a mobile polypide on corpus mucosa. (B) Endoscopic view of stomach demonstrating biopsy forceps removing Anisakis simplex.
2017-01-06A 58-year-old woman presented to the emergency department with a 4-week history of intermittent cough and progressive dyspnea. She had a history of chronic sinusitis as a child. Physical examination revealed coarse crackles with decreased breathing sounds. Chest radiography showed opaque lumps and dilation of the bronchiolar passages (Figure 1A). High resolution computed tomography (CT) scanning also confirmed diffuse areas of centrilobular nodules with a linear branching pattern (Figure 1B) and sinusitis (Figure 1C). A cold hemagglutination test was strongly positive. Figure 1(A) Chest radiograph are showing bilateral, diffuse, small centrilobular nodules with pulmonary hyperinflation. (B) Lung nodule shadows are extended in a centrilobular fashion, often distributing to small branching linear areas of attenuation, which is called tree-in-bud pattern. (C) CT scans show increased attenuation in the bilateral maxillary sinus.
2017-01-06A 66-year-old man presented to the emergency department with abdominal fullness and constipation for the last 2 weeks. The temperature, pulse, respiratory rate and blood pressure were recorded as 36.1 °C, 105 and 22 breaths per minute and 85/56 mmHg, respectively. Physical examination disclosed distended abdomen without rebounding or knocking pain and decreased bowel sound. Chest radiography revealed linear infiltration in the left lower lung and gas accumulation with an opaque white lesion in the left upper abdomen (Figure 1A). Pneumonia and colonic fecal impaction were suspected initially. Figure 1(A) Chest radiography revealed gas accumulation with an opaque white lesion in the left upper abdomen. (B) Abdominal computed tomography (CT) revealed a large heterogeneous cystic mass with necrotic tissue in the left upper abdomen.
2016-12-26Savvy business leaders always have had an interest in their employees’ health for the same reasons that 98% of large US employers today offer at least one workplace wellness program: Fulfilled and healthy workers are more productive, more engaged in business performance and have fewer absences and fewer health care costs.1
2016-11-01Before the acceptance of neurological criteria for human death in the late 1960s and 1970s leading to Donation after Brain Death (DBD), early organ donation from deceased patients can be characterized as proceeding similar to current protocols for Donation after Circulatory Death (DCD).1 In DCD, death is diagnosed using cardio-respiratory criteria, satisfaction of which confirms that the circulation of the patient has ceased. Whilst these are the same criteria that doctors use to determine whether or not death has occurred in most other environments, in the context of organ donation there is pressure to pronounce death as soon as possible. The reason for this is that the cessation of circulation causes warm ischaemic damage to organs, meaning that their suitability for transplantation rapidly falls (within 20 min, e.g. in the liver).