Patient with obesity, hypertension and increased HbA1C. In recent studies, Empaglifozin, a highly selective inhibitor of SGLT210, significantly reduces AT, HbA1C and BMI. Glipizide is of the sulfonylurea group. Its use should be avoided in patients with heart disease. Acarbose can interact with beta-blockers, such as those taken by our patient. Sitagliptin has been shown to decrease HbA1C but not HT or BMI.

A 58-year-old man comes for a scheduled check-up for type 2 diabetes mellitus diagnosed 6 years ago. He has a personal history of hypertension, dyslipidemia, ischemic heart disease and pancreatitis of biliary origin. His medication includes lisinopril, metoprolol, metformin, ASA and atorvastatin. Physical examination showed blood pressure 151/93 mmHg, BMI 27.1 kg/m2. Glycated hemoglobin is 8.3%. Which of the following is the most appropriate treatment for this patient?

Reducing global cardiovascular risk in patients with type 2 diabetes mellitus.

Type 2 diabetes mellitus (T2DM) and its complications must be managed by using a comprehensive, or global, approach to treatment. The author describes the case of a white man, aged 51 years, with T2DM that was diagnosed 3 years earlier. The patient was obese and had a history of chronic low back pain. He also had diagnosed hypertension, decreased vibratory sensation in the feet, an S4 atrial gallop, trace ankle edema, degenerative joint disease in the knees, and decreased range of motion in the lumbar spine. Other findings at the patient's initial visit included hyperglycemia, microalbuminuria, and lipid abnormalities. Initial treatment included metformin; a nonsteroidal anti-inflammatory drug (naproxen); a thiazolidinedione (rosiglitazone maleate); a thiazide diuretic (hydrochlorothiazide); an angiotensin-converting enzyme inhibitor (enalapril); and low-dose aspirin. At 6-month follow-up, the patient continued to have elevated glycosylated hemoglobin, hypertension, dyslipidemia, and excess weight. Additional treatment strategies consisted of pioglitazone hydrochloride; metformin in combination with the dipeptidyl peptidase IV inhibitor sitagliptin phosphate; a statin (atorvastatin hydrochloride); and enrollment in a diet and exercise program. Results at 12-month follow-up included a substantial decrease in glycosylated hemoglobin and improved hypertension and dyslipidemia. The patient was successfully treated across the full range of global cardiovascular risk reduction.

[Therapeutic behavior to follow in the following clinical case: treatment of type 2 diabetes].

A 62-year old woman with obesity, high blood pressure and type 2 diabetes mellitus (DM2) was referred to a Vascular Risk Unit of the Internal Medicine Department due to elevated HbA1C (8.1%) in spite of having taken metformin (850 mg/12h) and glipizide (10 mg/12 h) regularly. She tries to exercise daily (walking 30 min) and has lost weight (from 5 to 12 kg) several times, but always regains what she has lost. Furthermore, she monitors her glucose levels in fasting every two weeks and generally has between 120 and 160 mg/dL. Her high blood pressure is being treated with enalapril/HCTZ and she also takes aspirin 100mg/day and simvastatin 20 mg/day. It is seen in her family background that one brother died suddenly at 50 years of age. Her physical examination shows a BMI of 32.4 Kg/m(2), and she has no edemas in the lower limbs. Her BP is 154/82 mmHg and creatinine 0.9 mg/dL. She has no microalbuminuria and her liver function is normal. What treatment do you think would be the more appropriate? 1 - Add glitazones. 2 - Add incretin mimetics (GLP 1/ DPP-4). 3 - Slow acting insulin.

Dyspnea in a 57-Year-Old Man With Recent Viral Illness.

A 57-year-old man presented to the ED with a 1-month history of nonproductive cough and shortness of breath. The patient had been in his usual state of health until 2 months before presentation, when he experienced an episode of nonproductive cough and shortness of breath. He was diagnosed clinically with an upper respiratory tract infection; the symptoms resolved after 7 days with conservative therapy alone. One month later, the nonproductive cough and shortness of breath returned. He was treated with a 5-day course of oral azithromycin without any improvement in his symptoms. On presentation to the ED, he denied fever, chills, night sweats, chest pain, arthralgia, myalgia, or hemoptysis. His medical history was significant for hypertension, poorly controlled type 2 diabetes mellitus, and coronary artery bypass grafting. His medications included aspirin, metoprolol, metformin, and glipizide. He denied any history of tobacco, vaping, or recreational drug use. He worked as a cashier in a departmental store and has been doing so for most of his life.

Dapagliflozin-Induced Acute Pancreatitis: A Case Report and Review of Literature.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are increasingly used as add-on therapy in patients with poorly controlled type 2 diabetes mellitus (T2DM). Although pancreatitis is not a known side effect of SGLT-2 inhibitors, there have been case reports of SGLT-2 inhibitor use being associated with pancreatitis. <iCase Presentation</i. A 51-year-old male with a history of type 2 diabetes, dyslipidemia, and status-post cholecystectomy presented to the emergency room with a four-day history of periumbilical pain radiating to the back. He denied any history of recent alcohol intake or prior episodes of pancreatitis. On physical examination, his abdomen was diffusely tender to palpation without guarding or rebound. Initial labs were notable for a leukocyte count of 9.3 × 10<sup9</sup/L, creatinine level of 0.72 mg/dL, calcium level of 9.5 mg/dL, lipase level of 262 U/L, and triglyceride level of 203 mg/dL. His last HbA1c was 8.5%. CT scan of his abdomen and pelvis showed findings consistent with acute pancreatitis with no biliary ductal dilatation. Careful review of his medications revealed the patient was recently started on dapagliflozin five days prior to admission in addition to his longstanding regimen of insulin detemir, sitagliptin, metformin, and rosuvastatin. His symptoms resolved after discontinuation of sitagliptin and dapagliflozin. A year later, due to increasing HbA1c levels, a decision was made to rechallenge the patient with dapagliflozin, after which he developed another episode of acute pancreatitis. His symptoms resolved upon cessation of dapagliflozin. <iConclusion</i. This case highlights the possible association of SGLT-2 inhibitors and pancreatitis. Patients should be informed about the symptoms of acute pancreatitis and advised to discontinue SGLT-2 inhibitors in case such symptoms occur.

How to prevent and treat pharmacological hypoglycemias.

A 58 year-old woman with type 2 diabetes diagnosed 3 years before came to our clinic. Her treatment was metformin 850 mg every 12 hours and glimepiride 4 mg every 24 hours. After the initiation of glimepiride 9 months before her weight has increased 5 kg, and she suffers frequent hypoglycemias which have affected her while driving. Her BMI is 35.5 kg/m². She has a normal eye fund exam. She has hypertension treated with telmisartán and hidroclorotiazide with adequate control, and also hypercholesterolemia treated with atorvastatine 40 mg every 24 hours. Her blood test shows an HbA1c of 7.0%, normal values of microalbuminuria, total cholesterol 149 mg/dl, HDL cholesterol 52 mg/dl, LDL cholesterol 98 mg/dl and triglycerides 123 mg/dl. Her blood pressure is 129/81 mmHg, there was no orthostatic hypotension, and her peripheral neurological examination shows normal results. In summary, our case is a young woman with type 2 diabetes and obesity, without chronic complications and which has frequent hypoglycaemia. How must this woman be evaluated and treated?

Liraglutide-associated acute pancreatitis.

A case of acute pancreatitis associated with liraglutide is reported. A 53-year-old African-American man (height, 185.4 cm; weight, 108.6 kg) with type 2 diabetes mellitus arrived at the emergency department (ED) with new-onset intolerable abdominal pain in the right upper quadrant and left upper quadrant that had appeared suddenly and lasted two to three hours. He had nausea but no vomiting, with tenderness in the epigastric region. In the ED, his serum amylase concentration was found to be extremely elevated (3,963 units/L), as was his serum lipase concentration (>15,000 units/L). In addition to type 2 diabetes, his medical history included hyperlipidemia, hypertension, peripheral neuropathy, erectile dysfunction, and obesity. His home medications included aspirin 81 mg orally daily, metformin 1000 mg orally every morning and 1500 mg every evening, simvastatin 80 mg orally daily at bedtime, tadalafil 20 mg orally as needed, glimepiride 4 mg orally twice daily, and liraglutide 1.2 mg subcutaneously daily. Two months before his arrival to the ED, the patient's dosage of liraglutide was increased from 0.6 to 1.2 mg subcutaneously daily. Radiographic data were obtained, and acute pancreatitis was diagnosed. Liraglutide was discontinued indefinitely after ruling out elevated triglycerides as the cause of pancreatitis. The patient was initiated on standard therapy for acute pancreatitis and discharged eight days later with complete resolution of symptoms and normal laboratory test values. A 53-year-old man with type 2 diabetes mellitus developed a probable case of liraglutide-induced acute pancreatitis after receiving the drug for approximately two months.

Treating Hispanic patients for type 2 diabetes mellitus: special considerations.

The number of Hispanic people in the United States with diagnosed diabetes mellitus is projected to increase by 107% by 2020. The author presents the case of a 62-year-old obese Hispanic man, with newly diagnosed type 2 diabetes mellitus (T2DM), diabetic peripheral neuropathy, background retinopathy, and diabetic nephropathy. The patient also had diagnosed hypertension, peripheral vascular disease, and hyperlipidemia. The treatment plan for this patient included the following medications: pioglitazone hydrochloride (a thiazolidinedione, 30 mg/d); irbesartan (an angiotensin receptor blocker, 150 mg/d titrated to 300 mg/d); hydrochlorothiazide (an antikaliuretic agent, 12.5 mg/d); and aspirin (325 mg/d). Sitagliptin phosphate (a dipeptidyl peptidase IV inhibitor, 50 mg/d) was added to the treatment regimen to improve glycemic control. Simvastatin (20 mg/d) and niacin (1 g/d) were used for lipid management. Therapy also included a low-protein diet and walking program. At 6-month follow-up, the patient showed substantial improvement in his glycosylated hemoglobin level, lipid profile, blood pressure, creatinine clearance rate, and urine albumin level. There were also improvements in his peripheral vascular disease and diabetic peripheral neuropathy. Furthermore, the patient demonstrated encouraging progress in diet and lifestyle modification and in mental attitude.

Pharmacology_Katzung

A 66-year-old obese Caucasian man presented to an academic Diabetes Center for advice regarding his diabetes treatment. His diabetes was diagnosed 10 years previously on routine testing. He was initially given metformin but when his control deteriorated, the metformin was stopped and insulin treatment initiated. The patient was taking 50 units of insulin glargine and an average of 25 units of insulin aspartate pre-meals. He had never seen a diabetes educator or a dietitian. He was checking his glucose levels 4 times a day. He was smoking half a pack of cigarettes a day. On examination, his weight was 132 kg (BMI 39.5); blood pressure 145/71; and signs of mild peripheral neuropathy were present. Laboratory tests noted an HbA1c value of 8.1%, urine albumin 3007 mg/g creatinine (normal <30), serum creatinine 0.86 mg/dL (0.61–1.24), total choles-terol 128 mg/dL, triglycerides 86 mg/dL, HDL cholesterol 38 mg/dL, and LDL cholesterol 73 mg/dL (on atorvastatin 40 mg daily). How would you

[Management of hyperglycemia in the non-critical hospitalized patients with oral feeding].

A 67-year-old woman with a history of hypertension, hyperlipidemia and 6 years of evolution of type 2 diabetes mellitus presented with fever, purulent sputum and right chest pain. She was on treatment with metformin 850 mg/bid, glimepiride 4 mg/day, candesartan 16 mg/day, atorvastatin 10mg/day and acetylsalicylic acid 100mg/day. Standing out in the physical examination was blood pressure 90/50 mmHg, temperature 38.6 °C, pulse 112/min, respirations 24/min, weight 8 5 kg, height 1.68 m. She had crackling rales in the right lung-base and edema in lower limbs. The blood analysis showed leukocytosis, glucose 348 mg/dl, urea 70 mg/dl, creatinine 1.5mg/dl and HbA1c 8.4%. A chest x-ray revealed condensation in the lower lobe of the right lung. Antibiotic treatment was begun, maintaining an oral diet from admission. What is the best strategy regarding the treatment of this patient's hyperglycemia, its management and what evidence is there on this subject?

[What may cause diabetes].

The case study describes a case of 49-year-old man with morbid obesity since childhood (BMI 40 kg/m2), arterial hypertension (approx. since aged 15, treated since 2004), dyslipidemia (since 2006), type 2 diabetes mellitus (since 2006, on insulin therapy since 2008) and smoking (until 2011, 20 cigarettes a day). 16 types of medication, 8 for hypertension, statin, therapy for diabetes, aspirin, allopurinol. In 2010 (when aged 45) hospitalized in our clinic with dyspnoea and chest pain with a high pressure reading of 180/110 mm Hg (identified symptoms of heart failure with LV ejection fraction of 33 %, in NYHA II functional class, echocardiographically: left atrium: 46 mm, left ventricular chamber size in diastole: 70 mm, interventricular septum: 12 mm, septal hypokinesis, Doppler ultrasonography of lower limb arteries (calcification, diffuse atherosclerotic changes, absent stenosis), CT coronary angiography (significant stenosis of the left coronary artery). Treatment started with 40 mg oral dose of furosemide daily. In May 2011 he was hospitalized with an acute coronary syndrome: acute NSTEMI of the inferior wall (coronarography: 2-vascular problems, implemented PKI, implanted DES - ramus circumflexus, paroxysmal atrial fibrillation, NYHA III functional class, left ventricular ejection fraction: 30 %, pulmonary hypertension). In 2012 renal denervation for resistant hypertension was carried out, carotid stent implanted for stenosis of the carotid artery, presence of diabetic nephropathy (KDOQI stage 3, GF 40 ml/min). In August 2014 admitted to our clinic with pulmonary oedema, cardiogenic shock, acute ischemia of the right calf with peripheral embolisation, presence of atrial flutter, impairment of renal parameters, echocardiographically: left atrium: 55 mm, left ventricle size: 75 mm, akinesis of the septum and posterior wall, occlusion of the right leg arteries (given the patients serious state angio-surgical intervention was contraindicated, vitally indicated leg amputation considered), the patient died after 4 days of hospitalization in an intensive care unit after unsuccessful treatment. A combination of diabetes, hypertension and ischemic heart disease is frequent and prognostically serious. Diabetes increases cardiovascular morbidity and mortality and therefore we should check for diabetes in all cardiovascular patients.

Long-term (18-month) efficacy of atorvastatin therapy in type 2 diabetics at cardiovascular risk.

Dyslipidemia (increased triglyceride and low high-density lipoprotein [HDL] levels, with normal or slightly increased total cholesterol levels) is a common characteristic of type 2 diabetics and a major risk factor for cardiovascular diseases. The aim of this study was to evaluate the long-term efficacy of atorvastatin in a cohort of type 2 diabetics. Participants were divided into 3 groups on the basis of whether they had evidence of myocardial infarction or coronary lesions (group A), a family history of hypercholesterolemia (and/or cardiovascular diseases) and total cholesterol levels constantly above 270 mg/dL in blood samples taken at regular 4-month intervals and previously never at target level (group B), or clinical and/or instrumental (electrocardiogram) evidence of cardiovascular risk (group C). Their mean age was 64 +/- 7 years, known disease duration 0.5 +/- 3 years, body mass index (BMI) 27.7 +/- 1.3 Kg/m2, and haemoglobin A1c 8 +/- 0.6%. Total cholesterol was 256 +/- 24 mg/dL in group A, 298 +/- 25 mg/dL in group B and 244 +/- 31 mg/dL in group C (p < 0.05: group B vs groups A and C). HDL-cholesterol (HDL-C) was 45 +/- 7 mg/dL, triglycerides 225 +/- 20 mg/dL, systolic and diastolic blood pressure (DBP) respectively 144 +/- 7 and 85 +/- 8 mmHg, fibrinogen 330 +/- 23 mg/dL and microalbuminuria 58 +/- 9 mg/L. Eighteen months' atorvastatin treatment (10 mg/day in 106 subjects, 20 mg in 14 subjects, 30 mg in 5 subjects, and 40 mg in 30 subjects) led to a significant decrease in total and low-density lipoprotein (LDL)-cholesterol and triglyceride levels (p < 0.01), with about 86% of the patients achieving target levels, and a significant (p < 0.05) increase in HDL-C. There was a significant decrease in fibrinogen, microalbuminuria and DBP (p < 0.01), without any change in diet, BMI, physical activity or antihypertensive treatment. No new cardiovascular events or hospital admissions due to cardiovascular diseases were recorded during the 18 months of the study. These long-term treatment findings confirm and validate previous medium-term results, and suggest that atorvastatin therapy is effective and safe in the primary and secondary prevention of cardiovascular complications in type 2 diabetes.

InternalMed_Harrison

Diabetes Mellitus: Complications 2428 patients with CHF, thiazolidinediones should not be used (Chap. 418). However, metformin can be used in patients with stable CHF if the renal function is normal. Antiplatelet therapy reduces cardiovascular events in individuals with DM who have CHD and is recommended. Current recommendations by the ADA include the use of aspirin for primary prevention of coronary events in diabetic individuals with an increased 10-year cardiovascular risk >10% (at least one risk factor such as hypertension, smoking, family history, albuminuria, or dyslipidemia in men >50 years or women >60 years of age). ASA is not recommended for primary prevention in those with a 10-year cardiovascular risk <10%. The aspirin dose is the same as in nondiabetic individuals.

Pharmacology_Katzung

Helge Eilers, MD, & Spencer Yost, MD An elderly man with type 2 diabetes mellitus and ischemic pain in the lower extremity is scheduled for femoral-to-popliteal artery bypass surgery. He has a history of hyper-tension and coronary artery disease with symptoms of stable angina. He can walk only half a block before pain in his legs forces him to stop. He has a 50-pack-year smoking history but stopped 2 years ago. Medications include atenolol, atorvastatin, and hydrochlorothiazide. The nurse in the preoperative holding area obtains the following vital signs: temperature 36.8°C (98.2°F), blood pressure 168/100 mm Hg, heart rate 78 bpm, oxygen saturation by pulse oximeter 96% while breathing room air, and pain 5/10 in the right lower leg after walking into the hospital. What anesthetic agents will you choose for his anesthetic plan? Why? Does the choice of anesthetic make a difference?

Pharmacology_Katzung

A 53-year-old woman with a history of knee osteoarthritis, high cholesterol, type 2 diabetes, and hypertension presents with new onset of hot flashes and a question about a dietary supplement. She is obese (body mass index [BMI] 33), does not exercise, and spends a good portion of her work day in a seated position. She eats a low-sugar diet and regularly eats packaged frozen meals for dinner because she doesn’t have time to cook regularly. Her most recent laboratory values include a low-density lipoprotein (LDL) cholesterol that is above goal at 160 mg/dL (goal < 100 mg/dL) and a hemo-globin A1c that is well controlled at 6%. Her blood pressure is high at 160/100 mm Hg. Her prescription medications include simvastatin, metformin, and benazepril. She also takes over-the-counter ibuprofen for occasional knee pain and a multivitamin supplement once daily. She has heard good things about natural products and asks you if taking a garlic supplement daily could help to bring her blood

InternalMed_Harrison

with end-stage renal disease or advanced heart failure). Among the oral hypoglycemic agents, metformin possesses the best evidence base for cardiovascular event reduction. The novel oral hypoglycemic agents tested in sufficiently powered trials, the dipeptidyl peptidase-4 (DPP-4) inhibitors saxagliptin and alogliptin, did not show cardiovascular benefit. Indeed, saxagliptin was associated with a slight increase in heart failure. Diabetic populations appear to derive particular benefit from antihypertensive strategies that block the action of angiotensin II. Thus, the antihypertensive regimen for patients with the metabolic syndrome should include angiotensinconverting enzyme inhibitors or angiotensin receptor blockers when possible. Many of these individuals will require more than one anti-hypertensive agent to reach the 2013 goals for individuals 18 years of age or older with diabetes to achieve a systolic blood pressure of less than 140 mmHg and a diastolic blood pressure of less

Liraglutide

Liraglutide was approved for medical use in the European Union in 2009, and in the United States in 2010. In 2019, it was the 142nd most commonly prescribed medication in the United States, with more than 4million prescriptions. Medical uses Liraglutide is a medication used for the treatment of type 2 diabetes or obesity. Type 2 diabetes Liraglutide improves control of blood glucose. As of 2017 it is unclear if incretin mimetics like liraglutide affect a person's risk of death. In diabetes it is a less preferred agent. It may be used in those in who metformin and another antidiabetic medication such as a sulfonylurea are not sufficient. Obesity Liraglutide may also be used together with diet and exercise for chronic weight management in adult patients. The body mass index (BMI) needs to be greater than 30 kg/m2, or greater than 27 kg/m2 together with high blood pressure, type 2 diabetes mellitus, or dyslipidemia.

Diabetes and osteoporosis: Action of gastrointestinal hormones on the bone.

A 62-year-old woman consulted for evaluation of treatment for her type 2 diabetes diagnosed four years ago. He had been received treatment with metformin 850mg twice, with no chronic associated complications. She had hypertension and dyslipidemia. She was being treated with candesartan/hydrochlorothiazide 32/12.5mg and atorvastatin 40mg. Her weight was 92kg and height 162cm (BMI, 35.1kg/m(2)). The last analysis showed fasting glucose 168mg/dl and glycated hemoglobin 7.5%, Microalbuminuria was negative. Blood pressure and lipid profile were within the therapeutic range. Two years ago she suffered a nontraumatic Colle's fracture in her left arm for which she was taking a daily calcium and vitamin D supplement and weekly alendronate. In summary, this is an obese female patient with type 2 diabetes mellitus and inadequate metabolic control, She also has a history of fragility fracture. How should this patient be evaluated and treated?

A 37-Year-Old Man With Pleuritic Chest Pain.

A 37-year-old man with poorly controlled type 2 diabetes presented with severe right-sided pleuritic chest pain, respiratory splinting, and cough. Two weeks earlier, he had been evaluated at an urgent care for cough and was prescribed a 5-day course of azithromycin for bronchitis. He then presented to our ED reporting mild, right-sided pleuritic chest pain. Vital signs were normal, and his chest radiograph showed a trace right pleural effusion (Fig 1A). He was discharged with naproxen for pleurisy. Three days later, he returned, reporting a dramatic increase in the severity of his pleuritic chest pain and a cough that had become productive of yellow-brown sputum. He denied fever, but endorsed chills and night sweats. His medications included atorvastatin, lisinopril, metformin, and saxagliptin. His parents were from Guam, although he was born and raised in San Diego, CA. He was employed as a social worker and denied any history of cigarette smoking, alcohol, or drug use.

Resolution of Metabolic syndrome with reduction of visceral adipose tissue in a 47 year old patient with Type 2 Diabetes Mellitus.

Metabolic syndrome (MetS), defined as a cluster of metabolic abnormalities including visceral adiposity, insulin resistance, hypertension, and dyslipidemia, now affects more than a third of adults in the United States highlighting the need for effective complementary approaches to current treatments. We present a case report of a 47-year-old man with a history of MetS and poorly controlled Type 2 Diabetes Mellitus (T2D) who completed a 20Lighter program (20L) including a very low calorie diet (VLCD). At the time of enrollment his BMI was 32.7, HbA1c was 9.6%, and prescription medication history included lisinopril, lovastatin, and metformin, glimepiride, and combination sitagliptin/metformin. Fifteen weeks after beginning 20L (6 weeks after program completion) marked reduction of weight, visceral adipose tissue and normalization of HbA1C was seen, and all medications were withdrawn. While longer follow-up is required, this case report shows that a comprehensive program including a relatively short period of nutritionally complete VLCD, followed by gradual return to moderate dietary lifestyle is capable of producing clinically significant improvements in health and quality of life in individuals with MetS and poorly controlled T2D.

Diabetes medication

Sulfonylureas bind strongly to plasma proteins. Sulfonylureas are useful only in type 2 diabetes, as they work by stimulating endogenous release of insulin. They work best with patients over 40 years old who have had diabetes mellitus for under ten years. They cannot be used with type 1 diabetes, or diabetes of pregnancy. They can be safely used with metformin or glitazones. The primary side-effect is hypoglycemia. Typical reductions in glycated hemoglobin (A1C) values for second-generation sulfonylureas are 1.0–2.0%. First-generation agents tolbutamide acetohexamide tolazamide chlorpropamide Second-generation agents glipizide glyburide or glibenclamide glimepiride gliclazide glyclopyramide gliquidone Nonsulfonylurea secretagogues Meglitinides

InternalMed_Harrison

lost 5–7% of their body weight during the 3 years of the study. Studies in Finnish and Chinese populations noted similar efficacy of diet and exercise in preventing or delaying type 2 DM. A number of agents, including α-glucosidase inhibitors, metformin, thiazolidinediones, GLP-1 receptor pathway modifiers, and orlistat, prevent or delay type 2 DM but are not approved for this purpose. Individuals with a strong family history of type 2 DM and individuals with IFG or IGT should be strongly encouraged to maintain a normal BMI and engage in regular physical activity. Pharmacologic therapy for individuals with prediabetes is currently controversial because its cost-effectiveness and safety profile are not known. The ADA has suggested that metformin be considered in individuals with both IFG and IGT who are at very high risk for progression to diabetes (age <60 years, BMI ≥35 kg/m2, family history of diabetes in first-degree relative, and women with a history of GDM). Individuals with IFG,

Hypoglycemia associated with the use of levofloxacin.

A case of hypoglycemia associated with levofloxacin is reported. A 58-year-old Caucasian man was admitted to the hospital for a heart failure (HF) exacerbation with suspected community-acquired pneumonia (CAP). His medical history included HF (left ventricular ejection fraction, 25-35%), hypertension, and type 2 diabetes mellitus. Renal insufficiency was noted during hospitalization, with a serum creatinine concentration of 1.5 mg/dL. The patient's only home medication was a self-reported "sugar pill," later identified as glimepiride. A chest radiograph revealed consolidation in both lung bases and bilateral pleural effusions. Levofloxacin 750 mg was administered orally on hospital day 1 for the treatment of CAP and was ordered to be administered every 48 hours. On hospital day 3, glipizide 10 mg was administered with a sliding-scale regimen of regular insulin in preparation for discharge. On hospital day 4, glipizide 10 mg was given again with the second dose of levofloxacin, 65 hours after the first levofloxacin dose was administered. The patient also received furosemide 40 mg orally twice daily, lisinopril 20 mg orally daily, and metoprolol 25 mg twice daily. The patient was discharged on hospital day 4 and returned to the emergency department early the next morning with a serum glucose concentration of 20 mg/dL. An i.v. infusion of 10% dextrose injection and three ampules of 50% dextrose injection were given to correct his hypoglycemia. Further glipizide doses were not administered. A malnourished 58-year-old man with diabetes developed hypoglycemia after receiving levofloxacin in conjunction with glipizide.

Essential hypertension

Classification A recent classification recommends blood pressure criteria for defining normal blood pressure, prehypertension, hypertension (stages I and II), and isolated systolic hypertension, which is a common occurrence among the elderly. These readings are based on the average of seated blood pressure readings that were properly measured during 2 or more office visits. In individuals older than 50 years, hypertension is considered to be present when a person's blood pressure is consistently at least 140 mmHg systolic or 90 mmHg diastolic. Patients with blood pressures over 130/80 mmHg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment. Resistant hypertension is defined as the failure to reduce blood pressure to the appropriate level after taking a three-drug regimen. Guidelines for treating resistant hypertension have been published in the UK, and US.

[Evaluation of acarbose efficacy and safety for treatment of diabetes mellitus. Testing of observations under general health care conditions].

Acarbose (Glucobay, Bayer) is a competitive inhibitor of intestinal alpha-glucosidases, which use causes inhibition of carbohydrate digestion. The aim of the study was to prospectively observe scheme of acarbose use as well as efficacy and safety of the drug in diabetic patients in general health care. The study was performed in general health care centres all around Poland. 200 physicians were involved, each one was asked to supervise use of acarbose in 3 patients. The whole patients population consisted of 600 persons. The physicians were asked to make records in provided formularies, prior to acarbose use and then after 4 and 8 weeks of the treatment: data from the interview (among others on diabetes type, disease duration, used diet, treatment incl. sulphonylurea or biguanide derivatives); personal data (age, height, weight, etc.); blood glucose level prior to and 2 hours postprandial; glycosuria; basic additional tests; basic lipid tests (total cholesterol, triglycerides); overall score of acarbose use (side effects, withdrawal, physicians and patients opinion on the drug). Fasting glycaemia was the criterion of inclusion into the analysis. Full data on this parameter were obtained in 480 patients (267 female and 213 male, aged 31-88 years). Acarbose was used as the only antidiabetic drug in 34% of the patients, combined with sulphonylurea in 44%, combined with sulphonylurea and biguanide (metformine) in 19% and combined with metformine only in several cases (3%). During the observation, significant weight and BMI loss, 3% reduction average (for both parameters), was observed in the whole studied group. Fasting and 2 hours postprandial glycaemia was markedly improved in the whole studied population (26.8% and 28.1% glucose level reduction, respectively), and particularly in those who was initially qualified into the group of bad diabetes control (29.4% and 32.4% glucose level decrease, respectively). The most favourable effect on glycaemia was observed for acarbose monotherapy (p < 0.005) when compared to combined treatment). No difference was found in glycaemic response referred to the initial body mass index (BMI). Tested lipid parameters improved during 8-week observation: serum cholesterol level decreased by 4.6% in the whole studied population, and by 8.9% in the group of bad diabetes control, respectively. Value differences did not reach, however, presumed statistical significance (p < 0.005). Significant improvement was noted in triglyceride levels: reductions by 17.5% in the whole group and by as much as 26.8% in the sub-group of bad diabetes control (initial level 200 mg/dl). Acarbose observational study performed in the routine treatment conditions confirmed efficacy of the drug in diabetes mellitus, for both--carbohydrate and lipid metabolism. The study showed low significance of side effects and high acceptation of the treatment by the patients and the physicians.

A Patient Loses 18 kg and Type 2 Diabetes Mellitus: The Challenge of Complete Remission.

Type 2 diabetes mellitus (T2DM) in adulthood is strongly related to weight gain and excessive accumulation of pancreatic and hepatic fat. We present a case of a 48-year-old man with diabetes who presented two years prior with poorly controlled T2DM diagnosed more than three years before presentation. He had severe hypertension and marked dyslipidemia. He underwent a complete remission of his diabetes after nonintentionally losing 18 kg (his original weight: 58 kg). The patient had excellent euglycemic measures on no treatment at all for the last two years with healthy blood pressure and lipid profile and a reduced 10-year risk of heart disease and stroke from 11% to 3.3%. This case demonstrates the effect of weight loss on glycemic control and consequent remission in T2DM patients.

[Management of patients with type 2 diabetes. Results in 12 practices of general practitioners].

The care of patients with type 2 diabetes mellitus (2DM) is of great medical and sociopolitical importance. Many such patients are well provided for exclusively within general practice (general practitioners). But evidence based data of this level of medical care has been scarce. Our study reports the experience of the structure and medical management of a population-representative collective of patient with 2DM under the care of general practitioners. Included were all type 2 diabetics seen by 12 general practitioners (from two regions) during the second quarter of 2000. Standardized questionnaires for both patients and doctors provided the basic data on 2DM, other illnesses, symptoms, relevant items on life style and quality of life related to health. Data on patients living in care homes or visited in their home were handled separately. The collective consisted of 1065 patients with 2DM, aged over 40 years. Many of them had associated illnesses: hypertension in 71%, hypercholesteremia in 53%, coronary heart disease in 29%. Mean values of relevant metabolic parameters were: HbA1c 7.1%, total cholesterol 221.4 mg/dl. Many patients were clearly overweight and had other risk factors. Patient compliance, as reported by their doctors, were "very good" or "rather good" in 63%, while "very poor" or "rather poor" in 36%. Patients with 2DM under the care of general practitioners had a high incidence of associated illnesses. The quality of medical care, as measured by relevant metabolic vales, e.g. HbA1c were apparently good. Lipid-lowering drugs and aspirin should be given more widely to decrease cardiovascular events. Primary prevention (especially more exercise and weight loss) and better compliance should be intensified in future.

Successful Management of Type 2 Diabetes with Lifestyle Intervention: A Case Report.

The prevalence of diabetes is growing worldwide. The primary symptom of diabetes mellitus is elevated blood sugar. This is usually treated with lifestyle intervention and drugs according to an algorithm based on glycated hemoglobin (HbA1c) levels. We present the case of a patient who successfully managed his type 2 diabetes solely through lifestyle modification. A 45-year-old businessman with a body mass index of 27 kg/m2 was examined within a secondary prevention program in Austria. His HbA1c was 9.7%-type 2 diabetes mellitus was diagnosed. General recommendations for lifestyle were given and metformin was prescribed. Upon his diagnosis the patient searched for all the information he could get about diabetes and implemented this new knowledge in his everyday life. He had a strong desire to defeat his disease and he wanted to stop using medications. He identified some nutritional ingredients and spices that affected his blood sugar in a positive way. He stopped taking metformin after 4 weeks and handled his diabetes with his personal lifestyle program. Three months after the diagnosis his HbA1c was 6.4%; after 6 months he had an HbA1c of 6.0% without the use of medication. Usually, multiple drug therapy is necessary to handle high blood glucose levels. Our business manager ate as much as before his diagnosis but he modified the contents of his diet so that the lifestyle intervention was not hard for him. General recommendations for lifestyle modification usually include: more exercise, reduced sugar and monosaccharides, and less alcohol and nicotine. With the knowledge of the effects of specific dietary ingredients, it might be possible to modify a regular diet in such a way as to benefit people with type 2 diabetes, to substantially improve quality of life.

[Screening, prevention and early therapy of type 2 diabetics].

For each known diabetic at least one new patient is diagnosed when the 75-g OGTT is used for screening. For early diagnosis in high risk groups, the oral glucose tolerance test is indispensable since ca. 30% of the asymptomatic diabetes cases are identified on the basis of a 2-hour postchallenge glucose value of > 11.1 mmol/l. In controlled studies on persons with IGT, every second diabetes case could be prevented through lifestyle modifications beginning in childhood. Three-year studies showed that the incidence of diabetes could be reduced by about one-third with the medications acarbose, metformin and orlistat. The observation that statins, ACE inhibitors and AT1 blockers also contributed to a reduction of new diabetes cases was made in studies on the prevention of coronary heart diseases.

Early onset type 2 diabetes mellitus in a Saudi child misdiagnosed as type 1 diabetic: A case report.

To report a Saudi young patient with early onset type 2 diabetes, who was misdiagnosed for 6 years as type 1 diabetic. A Saudi male aged 18-year old presented with uncontrolled diabetes. He was diagnosed 6 years earlier to have type 1 diabetes mellitus. He was kept insulin, but he was not compliant to treatment and his blood glucose kept on fluctuating and not controlled. He came to our diabetes center for management of his uncontrolled diabetes. There was no past history of hospitalization. His father was type 2 diabetic. His body mass index was 46.7 kg/m<sup2</sup. His glycosylated hemoglobin (HbA1c) level was 9.9%. Immune dysfunction was evaluated using serum antibody levels of glutamic acid decarboxylase, which proved to be negative (0.7 U/mL), while serum C-peptide level was not low (2.2 ng/mL). Therefore, the patient was diagnosed as early onset type 2 diabetic, not type 1 diabetic. The patient was advised to start physical exercise through daily walking for at least 1 h. The dietitian planned a strict diet plan for him to follow. Insulin injections and Metformin tablets were started. The patient received detailed health education on nature and management of his condition. After 4 months, his body mass index became 39.4 kg/m<sup2</sup and his HbA1c became 6%. Insulin was stopped, and he was advised to continue on metformin, the diet, and daily walking. Two months later, his body mass index was 37.7 kg/m<sup2</sup and his HbA1c became 5.41%. Early onset type 2 diabetes should be suspected among obese children with symptoms of diabetes. Proper health education and patient's compliance to medication, diet, and physical activity are essential for successful management of early onset type 2 diabetes. Moreover, primary care physicians need to be aware that type 2 diabetes is not necessarily adult-onset.

[Long-term intensive glycemic and lipid control ameliorates the carotid intima medial thickness in type 2 diabetes mellitus].

To investigate whether long-term intensive glycemic and lipid control would ameliorate the carotid intima medial thickness (IMT) in patients with type 2 diabetes mellitus (T2DM). IMT was evaluated on B-mode ultrasonography in 116 patients with T2DM. Body mass index (BMI), waist-to-hip ratio (WHR), fasting blood glucose (FBG), 2 hour postprandial glucose (2hPG), hemoglobin A(1)c(HbA(1)c), total cholesterol(TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C),high-density lipoprotein cholesterol (HDL-C) were also measured. Of all the patients 89 were divided randomly into group of intensive glycemic and lipid control and group of conventional treatment and underwent 1 year clinical interview. (1) IMT in patients with T2DM was significantly correlated with age(r = 0.515,P = 0.000) , SBP (r = 0.208, P = 0.025), TC(r = 0.213,P = 0.022), LDL-C(r = 0.253, P = 0.006) and no correlations were found between IMT and BMI,WHR,FBG, 2hPG ,HbA(1)c, TG and HDL-C. In multivariate regression analysis, age (Beta = 0.527, P = 0.000 )and TC(Beta = 0.243, P = 0.002) were significant independent determinants for IMT. (3) After 1 year the change of IMT in the group of intensive glycemic and lipid control was significantly different compared with the group of conventional treatment [(-0.044+/-0.148)mm vs (0.056+/-0.178), P<0.05]. The change of IMT was not significantly associated with the use of Metformin, Sulphonylurea and Aspirin, but significantly associated with the use of statins. The change of IMT in the group using statins was significantly different compared with that in the group without using statins[(-0.053+/-0.153)mm vs (0.042+/-0.165)mm, P <0.05]. Carotid IMT appears to be closely related to age and TC in the patients with T2DM. long-term intensive glycemic control and lipid control could ameliorate the IMT in patients with T2DM. The improvement of IMT may be associated with the use of statin drug.

Diabetes management

A useful test that has usually been done in a laboratory is the measurement of blood HbA1c levels. This is the ratio of glycated hemoglobin in relation to the total hemoglobin. Persistent raised plasma glucose levels cause the proportion of these molecules to go up. This is a test that measures the average amount of diabetic control over a period originally thought to be about 3 months (the average red blood cell lifetime), but more recently thought to be more strongly weighted to the most recent 2 to 4 weeks. In the non-diabetic, the HbA1c level ranges from 4.0 to 6.0%; patients with diabetes mellitus who manage to keep their HbA1c level below 6.5% are considered to have good glycemic control. The HbA1c test is not appropriate if there has been changes to diet or treatment within shorter time periods than 6 weeks or there is disturbance of red cell aging (e.g. recent bleeding or hemolytic anemia) or a hemoglobinopathy (e.g. sickle cell disease). In such cases, the alternative

A 74-year-old woman with diabetes.

Ms M, a 74-year-old woman with type 2 diabetes of 6 years' duration, has a glycated hemoglobin (HbA1C) value of 7.4% despite taking 3 oral antidiabetic medications, as well as coexistent hypertension and abdominal obesity. She has no known microvascular or macrovascular complications of diabetes and is otherwise healthy. She is reluctant to commence insulin treatment as she dislikes the idea of injections and wonders if there are any alternate options if she is to get her HbA(1C) value below 7%. The natural history of type 2 diabetes, reasons why many patients begin requiring insulin over time, rationale for tight glycemic control, and therapeutic options for Ms M are discussed.


Patient with harmful alcohol consumption (60g and female), high fever, hepatic encephalopathy (disorientation, asterixis), very high direct bilirubin, jaundice, painful hepatomegaly, coagulopathy (elevated prothrombin time) and mild elevation of transaminases (less than 5 times the upper limit of normal) suggest acute alcohol hepatitis.

A 50-year-old woman comes to the emergency department with asthenia, anorexia, weight loss, jaundice, fever and abdominal pain. She has no recent history of blood transfusion, risky sexual contacts or addiction to parenteral drugs. Habitual consumption of 60 grams of alcohol per day during the last five years, consumption that has increased during the previous month due to family problems. Temperature 38.5ºC, blood pressure 100/60 mmHg. Physical examination showed temporal and spatial disorientation, malnutrition, asterixis, jaundice and painful hepatomegaly. No ascites or evidence of peritoneal irritation. Laboratory tests include leukocytes 15,000/microliter with 90% polymorphonuclear, red blood cells 3 million/mm3, hemoglobin 10g/dl, mean corpuscular volume 115 fl, bilirubin 15 mg/dl direct predominance, AST (GOT) 300 IU/L, ALT (GPT) 120 IU/L, GGT 635 IU/L, prothrombin time prolongation greater than 50%. What is the most likely diagnosis of the patient's condition?

[Acute pancreatitis and acalculous cholecystitis associated with viral hepatitis A].

We report the case of a 14 year-old male from Lima. He is a student with a history of bronchial asthma since age 4 receives conditional salbutamol, corticosteroids used for asthma attacks (a crisis in 2010, 1 month ago) Refuses surgery or transfusions. He presented with a two weeks for abdominal pain, nausea, fever, and jaundice. Epigastric pain is colicky and radiated back to righ upper quadrant, refers in addition to nausea and fever, for ten days notice jaundice of skin and sclera. On examen he was lucid, with jaundice of skin and mucous membranes. There was no palpable lymph nodes, abdomen with bowel sounds, soft, depressible, liver span of 15cm, positive Murphy, no peritonitis. The laboratory findings showed hemoglobin 13gr, MCV 90, platelets 461.000/mm3, WBC 4320/mm, lymphocytes 1700 (39%). total bilirubin: 8.8, B Direct: 7.6, ALT (alanine aminotransferase): 3016, AST (aspartate aminotransferase): 984, alkaline phosphatase: 250, albumin: 3.34gr%, globulin: 2.8, amylase: 589 (high serum amylase), TP: 17, INR: 1.6, VHA IgM positive. 89 mg glucose, urea 19 mg%, creatinine 0.5 mg Hemoglobin 13gr, MCV 90 Platelet 461000/mm3, WBC 4320/mm, Lymphocytes 1700 (39%). The nuclear magnetic resonance showed hepatomegaly associated with thickening of gallbladder wall without stones up to 11mm inside. No bile duct dilatation, bile duct 4mm, pancreas increased prevalence of body size. Mild splenomegaly and free fluid in the space of Morrison and right flank. Abdominal ultrasound revealed a gallbladder wall thickness (11mm), without stones in his light. Pancreas to increase volume with peripancreatic fluid free perivesicular with a volume of 430 cc. Findings consistent with acute acalculous cholecystitis and acute pancreatitis. CT-scan showed enlarged pancreas with predominance of body and tail with peripancreatic edema; the gallbladder was thickening. We report this case because the extrahepatic manifestations of viral hepatitis A infection are uncommon, specially the associated with acute acalculous cholecystitis and acute pancreatitis simultaneous.

Acute pancreatitis

At admission age in years > 55 years white blood cell count > 16000 cells/mm3 blood glucose > 11.1 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit fall >10% Oxygen (hypoxemia PO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L The criteria for point assignment is that a certain breakpoint be met at any time during that 48 hour period, so that in some situations it can be calculated shortly after admission. It is applicable to both gallstone and alcoholic pancreatitis. Alternatively, pancreatitis can be diagnosed by meeting any of the following:[2] Alternative Ranson score Ranson's score of ≥ 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced CT)

Acute pancreatitis

Glasgow score The Glasgow score is valid for both gallstone and alcohol induced pancreatitis, whereas the Ranson score is only for alcohol induced pancreatitis. If a patient scores 3 or more it indicates severe pancreatitis and the patient should be considered for transfer to ITU. It is scored through the mnemonic, PANCREAS: P - PaO2 <8kPa A - Age >55-years-old N - Neutrophilia: WCC >15x10(9)/L C - Calcium <2 mmol/L R - Renal function: Urea >16 mmol/L E - Enzymes: LDH >600iu/L; AST >200iu/L A - Albumin <32g/L (serum) S - Sugar: blood glucose >10 mmol/L BISAP score Predicts mortality risk in pancreatitis with fewer variables than Ranson's criteria. Data should be taken from the first 24 hours of the patient's evaluation. BUN >25 mg/dL (8.9 mmol/L) Abnormal mental status with a Glasgow coma score <15 Evidence of SIRS (systemic inflammatory response syndrome) Patient age >60 years old Imaging study reveals pleural effusion

Ranson criteria

Acute pancreatitis not secondary to gallstones At admission: Blood glucose > 11.11 mmol/L (> 200 mg/dL) Age > 55 years Serum LDH > 350 IU/L Serum AST > 250 IU/L WBC count > 16000 cells/mm3 Within 48 hours: Serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit decreased by > 10% Oxygen (hypoxemia with PaO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L Acute pancreatitis secondary to gallstones At admission: Glucose > 220 mg/dl Age > 70 years LDH > 400 IU/L AST > 250 IU/ 100 ml WBC count > 18000 cells/mm3 Within 48 hours: Serum calcium < 8 mg/dL Hematocrit decreased by > 10% Base deficit > 4 mEq/L BUN increased by > 2 mg/dL Sequestered fluid > 6L

Grand Rounds: Alcoholic Hepatitis.

A 33-year-old Caucasian male was admitted to hospital with recent onset of jaundice of 2-3 weeks duration. He reported heavy use of alcohol for the last 10 years with the last drink a day prior to the onset of symptoms. At admission, he was alert and oriented to time, place, and person, and was deeply jaundiced. His laboratory profile can be summarised as follows: haemoglobin 12.1 g/dl, white blood cell count 18,700 with 81% neutrophils, serum bilirubin 33 (direct 22) mg/dl, aspartate aminotransferase 147 IU/L, alanine aminotransferase 62 IU/L, alkaline phosphatase 117 IU/L, serum albumin 2.8 gm/dl, serum creatinine 0.6 mg/dl, prothrombin time 18.3 (control 14.5) seconds, and international normalized ratio 1.48. He was diagnosed with severe alcoholic hepatitis (Maddrey discriminant function score of 50) and treated with prednisolone for 28 days with symptomatic and biochemical improvement. His Lille score at seven days was 0.4, and his serum bilirubin had decreased to 3.5 mg/dl at the end of treatment. He was also seen by the addiction team during hospitalisation; he agreed to follow through on recommendations. He was dismissed after completing a three-week inpatient rehabilitation programme but relapsed to alcohol use three months later, and was readmitted with alcohol withdrawal. He was readmitted two months later (about six months from the first episode) for a second episode of severe alcoholic hepatitis. At admission, his model for end-stage liver disease score was 32 and he was treated again with corticosteroids. His Lille score at seven days was 0.6 and steroids were discontinued. The hospital course was complicated by spontaneous bacterial peritonitis and pneumonia with development of acute kidney injury. He continued to worsen, developing multiorgan failure. After a course of one month, the family's preference was for him to receive comfort measures. This scenario raises several questions.

Acute pancreatitis

Practice guidelines state: 2006: "The two tests that are most helpful at admission in distinguishing mild from severe acute pancreatitis are APACHE-II score and serum hematocrit. It is recommended that APACHE-II scores be generated during the first 3 days of hospitalization and thereafter as needed to help in this distinction. It is also recommended that serum hematocrit be obtained at admission, 12 h after admission, and 24 h after admission to help gauge adequacy of fluid resuscitation." 2005: "Immediate assessment should include clinical evaluation, particularly of any cardiovascular, respiratory, and renal compromise, body mass index, chest x ray, and APACHE II score" Ranson score The Ranson score is used to predict the severity of acute pancreatitis. They were introduced in 1974. At admission age in years > 55 years white blood cell count > 16000 cells/mm3 blood glucose > 11.1 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours

Uncertainty of Liver Cirrhosis Diagnosis and Use of Elastography.

A case of severe jaundice in a patient with a long history of alcohol abuse led to a questionable diagnosis of liver cirrhosis. To determine its diagnostic utility in the setting of liver disease, elastography was utilized on our patient to confirm the clinically suspected diagnosis of cirrhosis. A 59-year-old male presented to our emergency department (ED) with two days of progressive jaundice and right upper quadrant (RUQ) pain. The patient admitted to drinking > 500 mL of vodka daily for the last seven years, with his last drink on the morning of admission. Physical exam revealed a man in mild acute distress with severe jaundice and an abdomen diffusely tender to palpation. Two spider angiomas were present on the torso along with caput medusae and mild asterixis. Labs revealed aspartate aminotransferase (AST) 408, alanine aminotransferase (ALT) 69, prothrombin time (PT) 16.3, partial thromboplastin time (PTT) 36, total bilirubin 22.6, and direct bilirubin 19.9 mg/dL. While admitted, total bilirubin rose as high as 31.5 mg/dL. Examination showed a Model for End-Stage Liver Disease (MELD) score of 22 and a Maddrey score of 37. Ultrasound revealed moderate hepatosplenomegaly with no signs of pancreatitis. Based on the patient's history of alcohol abuse paired with physical exam findings and elevated laboratory markers, we were able to diagnose with a high level of suspicion that this patient was suffering from chronic alcoholic liver disease, exacerbated by an acute episode of alcoholic hepatitis, which led to hepatic encephalopathy. Based on these findings, a diagnosis of liver cirrhosis was suspected; however, this diagnosis required further confirmation. We utilized ultrasound elastography to measure the velocity of shear wave transmission in the liver of our patient. A literature review was conducted on the use of elastography for the diagnosis of liver disease, and a significant correlation between the velocity of shear wave transmission and hepatic histological findings was identified. Elastography revealed a mean velocity of shear wave transmission of 1.77 m/s in our patient. This finding is consistent with a Meta-analysis of Histological Data in Viral Hepatitis (METAVIR) score of F = 4, indicating significant fibrosis and confirming the suspected diagnosis of alcohol-induced liver cirrhosis. As a non-invasive and inexpensive diagnostic tool, elastography demonstrates significant potential for clinical utility in patients with liver disease. Clinicians may benefit from the use of elastography in diagnosis, while patients may receive both therapeutic and prognostic benefits secondary to its use. In similar cases with clinical uncertainty, elastography can reliably identify the presence of fibrous tissue in the liver without tissue biopsy, thus aiding in clinical diagnoses and enabling the use of optimal therapeutic regimens for future patients.

Jaundice

Laboratory results for liver panels are frequently compared by the magnitude of their differences, not the pure number, as well as by their ratios. The AST:ALT ratio can be a good indicator of whether the disorder is alcoholic liver damage (above 10), some other form of liver damage (above 1), or hepatitis (less than 1). Bilirubin levels greater than 10 times normal could indicate neoplastic or intrahepatic cholestasis. Levels lower than this tend to indicate hepatocellular causes. AST levels greater than 15 times normal tend to indicate acute hepatocellular damage. Less than this tend to indicate obstructive causes. ALP levels greater than 5 times normal tend to indicate obstruction, while levels greater than 10 times normal can indicate drug (toxin) induced cholestatic hepatitis or cytomegalovirus infection. Both of these conditions can also have ALT and AST greater than 20 times normal. GGT levels greater than 10 times normal typically indicate cholestasis. Levels 5–10

Acute alcoholic hepatitis: a literature review and proposal of treatment.

Severe acute alcoholic hepatitis (AAH) can lead to a clinical picture with a six-month mortality rate in more than 70% of cases. This clinical picture is characterized by: jaundice with a duration of less than three months, jaundice at the first failure event, serum bilirubin greater than 5 mg/dL, ratio AST/ALT>2/1, AST less than 500 IU/L, ALT<300 IU/L, neutrophil leukocytosis and a GGT increase. In addition, encephalopathy, fever, asthenia and coagulopathy may be present. Its onset may also be characterized by portal-hypertension-related complications, particularly bleeding and hepato-renal syndrome. In cases where there is an overlapping of an acute form characterized by an etiological factor other than that of the base hepatopathy, acute on chronic liver failure (ACLF) is obtained. This can result in systemic inflammation response syndrome (SIRS) with a multi-organ systemic involvement. Several indices are used to evaluate the prognosis, in particular Maddrey's discriminant function (mDF) and the model of end stage liver disease (MELD). In our clinical practice, we use the MELD routinely. In cases of ACLF, a consortium organ failure score (CLIF-COFs) is used. Therapy is characterized by abstention in cases of severe forms (mDF>32 and MELD>21); in the absence of contraindications, steroid therapy is possible. In cases of an unresponsive liver, transplantation is premature. In our view, this possibility, after proper selection, must be offered for both prognostic and ethical reasons.

InternalMed_Harrison

Type of Disorder Bilirubin Aminotransferases Alkaline Phosphatase Albumin Prothrombin Time Acute hepatocellular necrosis (viral and drug hepatitis, hepatotoxins, acute heart failure) Alcoholic hepatitis, cirrhosis Infiltrative diseases (tumor, granulomata); partial bile duct obstruction Normal to 86 μmol/L (5 mg/dL) 85% due to indirect fractions Elevated, often >500 IU, ALT > AST Elevated, but usually <300 IU AST:ALT >2 suggests alcoholic hepatitis or cirrhosis Normal to moderate elevation Normal to slight elevation Normal to <3× normal elevation Normal to <3× normal elevation Normal to <3× normal elevation Elevated, often >4× normal elevation Elevated, often >4× normal elevation Fractionate, or confirm liver origin with 5’nucleotidase or γ glutamyl transpeptidase Normal Usually normal. If >5× above control and not corrected by parenteral vitamin K, suggests poor prognosis Fails to correct with parenteral vitamin K Fails to correct with parenteral vitamin K

Surgery_Schwartz

trajectory of a patient, and it can be applied on a daily or more frequent basis. It can also be used in retrospect for audit purposes.Determining EtiologyThe history of alcohol ingestion must be ascertained and preferably confirmed with blood ethanol levels. Gallstones should be investigated by ultrasonography. A gallstone etiology is more likely in females over the age of 50 with an elevation of alkaline phosphatase (>300 iu/L), alanine transferase (>100 iu/L), and amylase (>4000 iu/L). In the absence of gallstones and alcohol, a systematic approach to the identification of another factor will include taking a history of drugs, trauma, ERCP, infection, and measuring serum triglycerides, calcium, and others (see Table 33-4).Fluid ResuscitationFluid therapy to restore and maintain circulating blood volume is the most important intervention in the early management of acute pancreatitis75. However, a recent systematic review has shown that the evidence base for fluid therapy is

Alcoholic liver disease

In people with alcoholic hepatitis, the serum aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio is greater than 2:1. AST and ALT levels are almost always less than 500. The elevated AST to ALT ratio is due to deficiency of pyridoxal phosphate, which is required in the ALT enzyme synthetic pathway. Furthermore, alcohol metabolite–induced injury of hepatic mitochondria results in AST isoenzyme release. Other laboratory findings include red blood cell macrocytosis (mean corpuscular volume > 100) and elevations of serum gamma-glutamyl transferase (GGT), alkaline phosphatase, and bilirubin levels. Folate level is reduced in alcoholic patients due to decreased intestinal absorption, increased bone marrow requirement for folate in the presence of alcohol, and increased urinary loss. The magnitude of leukocytosis (white blood cell depletion) reflects severity of liver injury. Histologic features include Mallory bodies, giant mitochondria, hepatocyte necrosis, and

Cirrhosis

Common causes Alcoholic liver disease (ALD, or alcoholic cirrhosis) develops for 10–20% of individuals who drink heavily for a decade or more. Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates. This injury happens through the formation of acetaldehyde from alcohol, which itself is reactive, but which also leads to the accumulation of other reactive products in the liver. People with ALD may also have concurrent alcoholic hepatitis with fever, hepatomegaly, jaundice, and anorexia. AST and ALT blood levels are both elevated, but at less than 300 IU/liter, with an AST:ALT ratio > 2.0, a value rarely seen in other liver diseases. In the United States, 40% of cirrhosis-related deaths are due to alcohol.

Hepatitis -- Evaluation -- Alcoholic Hepatitis

If patients present with a history of alcohol abuse, typical signs, and symptoms of long-term alcohol abuse, and evidence of liver dysfunction, then usually no further diagnostic workup is required.  If the history is not clear or if patients do not have signs or symptoms of long-term alcohol abuse, then a complete blood count and metabolic panel along with liver function studies can be ordered.  Patients can have moderate anemia with an increase in the mean corpuscular volume (MCV) due to alcohol being a direct bone marrow suppressant.  Patients can also have some degree of leukocytosis with increased neutrophils. The metabolic panel can show hypokalemia and hypomagnesemia due to the effects of malnutrition and vomiting. C-reactive protein can be elevated and has an excellent positive predictive value. Liver enzymes have a characteristic pattern with aspartate aminotransferase (AST) being moderately elevated and alanine aminotransferase (ALT) being either in the reference range or only mildly elevated with the ratio of AST and ALT being greater than 1.  However, the AST/ALT ratio is greater than 1 in patients who have liver cirrhosis of any etiology. Therefore, it is not diagnostic of alcoholic hepatitis in patients with advanced liver disease. Alkaline phosphatase (ALP) is usually only mildly elevated. Gamma-glutamyl transpeptidase (GGTP) is elevated in patients with a history of alcohol use but is not diagnostic of alcoholic hepatitis. Liver biopsy is usually not required but remains a valuable diagnostic option to establish the diagnosis in patients with diagnostic uncertainty and for evaluating the severity of the disease. [45]

Acalculous cholecystitis associated with Hantaan virus: A case report.

Acute acalculous cholecystitis (AAC) still remains one of the most elusive diagnoses and occurs in various conditions. Although AACs caused by viral infections are rare, various viruses have been revealed to cause AAC. Here we present a case in which a man suffered from AAC caused by a Hantaan virus infection. A 35-year-old man was referred to the emergency room for myalgia and fever that began 4 days ago. He suffered oliguria and abdominal pain for 2 days. At the time of his visit to the emergency room, he experienced a fever that spiked up to 38.3℃. An initial blood sample objectified the following pathologic results: white blood cells - 10260/µl; C-reactive protein - 6.76 mg/dl; total bilirubin - 1.7 mg/dl; AST - 90 IU/L; ALT - 233 IU/L. In the computed tomography, bilateral perirenal fluid collections and bilateral flexural effusion were shown and acute hepatopathy and cholecystopathy were also shown. Because there was no definite tenderness around the patient's right upper quadrant from physical examination and his cholecystopathy looked like it was from secondary change according to acute hepatopathy, we decided to perform conservative care without surgical treatment. The following day, in viral antibody test, Hantaan virus antibody was detected. After conservative management, the patient's condition improved and his laboratory findings were stable. The patient was discharged on the 10<supth</sup day at the hospital stay without any symptoms. The Hantaan virus infection should be suspected as a causative agent of AAC, especially when there is abnormal liver function tests and abdominal pain.

Jaundice

Diagnosis Most people presenting with jaundice have various predictable patterns of liver panel abnormalities, though significant variation does exist. The typical liver panel includes blood levels of enzymes found primarily from the liver, such as the aminotransferases (ALT, AST), and alkaline phosphatase (ALP); bilirubin (which causes the jaundice); and protein levels, specifically, total protein and albumin. Other primary lab tests for liver function include gamma glutamyl transpeptidase (GGT) and prothrombin time (PT). No single test can differentiate between various classifications of jaundice. A combination of liver function tests and other physical examination findings is essential to arrive at a diagnosis. Laboratory tests

Alcoholic Hepatitis -- Etiology

While using the terminology alcoholic hepatitis, it is important to understand the difference between alcoholic steatohepatitis (ASH) and alcoholic hepatitis (AH). About 20% to 40% of those who drink alcohol in heavy amounts and have fatty liver eventually develop liver inflammation, which is known as ASH. ASH is a diagnosis based on liver histology, while AH is a clinical diagnosis. The typical features of ASH on liver biopsy are steatosis, hepatocyte ballooning, infiltration of neutrophils, Mallory-Denk hyaline inclusions, and zone 3 perivenular injury with pericellular fibrosis or chicken-wire pattern of fibrosis. AH, on the other hand, is characterized by a history of chronic heavy alcohol consumption until at least 3 to 4 weeks before the onset of jaundice, fever, tachycardia, tachypnea, hepatomegaly, leukocytosis with neutrophilia, and an AST:ALT elevation greater than 1.5:1 with the absolute value of AST/ALT typically never exceeding 500 U/L. AH can occur in patients with any stage of alcoholic liver disease.

Pathology_Robbins

It is estimated that 15 to 20 years of excessive drinking are necessary to develop alcoholic cirrhosis, but alcoholic hepatitis can occur after just weeks or months of alcohol abuse. The onset is typically acute and often follows a bout of particularly heavy drinking. Symptoms and laboratory abnormalities range from minimal to severe. Most patients present with malaise, anorexia, weight loss, upper-abdominal discomfort, tender hepatomegaly, and fever. Typical findings include hyperbilirubinemia, elevated serum alkaline phosphatase levels, and neutrophilic leukocytosis. Serum alanine and aspartate aminotransferases are elevated but usually remain below 500 U/mL. The outlook is unpredictable; each bout of alcoholic hepatitis carries a 10% to 20% risk for death. With repeated bouts, cirrhosis appears in about one-third of patients within a few years.

Ranson Criteria -- Function

The criteria with 11 parameters are used to assess the severity of alcoholic pancreatitis. The 5 parameters on admission are age older than 55 years, WBC count greater than 16,000 cells/cmm, blood glucose greater than 200 mg/dL (11 mmol/L), serum AST greater than 250 IU/L, and serum LDH greater than 350 IU/L. At 48 hours, the remaining 6 parameters are: serum calcium less than 8.0 mg/dL (less than 2.0 mmol/L), hematocrit fall greater than 10%, PaO2 less than 60 mmHg, BUN increased by 5 mg/dL or more (1.8 mmol/L or more) despite intravenous (IV) fluid hydration, base deficit greater than 4 mEq/L, and sequestration of fluids greater than 6 L.

Alcoholic Liver Disease -- History and Physical -- Physical Examination

The clinical definition of alcoholic hepatitis is a syndrome of liver failure where jaundice is a characteristic feature; fever and tender hepatomegaly are often present. The typical presentation age is between 40 and 50 yrs, and it occurs in the setting of heavy alcohol use. Patients often report a history of intake of at least 30 to 50 g alcohol/day though over 100 g/day is common. Patients may be abstinent for weeks before admission. The cardinal sign is the rapid onset of jaundice. Other signs and symptoms include fever, ascites (SAAG greater than 1.1), and proximal muscle loss. Patients presenting with severe alcoholic hepatitis may have encephalopathy. Typically, the liver is enlarged and tender.

Pancreatitis

Late complications include recurrent pancreatitis and the development of pancreatic pseudocysts—collections of pancreatic secretions that have been walled off by scar tissue. These may cause pain, become infected, rupture and bleed, block the bile duct and cause jaundice, or migrate around the abdomen. Acute necrotizing pancreatitis can lead to a pancreatic abscess, a collection of pus caused by necrosis, liquefaction, and infection. This happens in approximately 3% of cases or almost 60% of cases involving more than two pseudocysts and gas in the pancreas. Causes Eighty percent of cases of pancreatitis are caused by alcohol or gallstones. Gallstones are the single most common cause of acute pancreatitis. Alcohol is the single most common cause of chronic pancreatitis. Triglyceride levels greater than 1000 mg/dL (11.29 mmol/L) is another cause.

Jaundice

or cytomegalovirus infection. Both of these conditions can also have ALT and AST greater than 20 times normal. GGT levels greater than 10 times normal typically indicate cholestasis. Levels 5–10 times tend to indicate viral hepatitis. Levels less than 5 times normal tend to indicate drug toxicity. Acute hepatitis typically has ALT and AST levels rising 20–30 times normal (above 1000) and may remain significantly elevated for several weeks. Acetaminophen toxicity can result in ALT and AST levels greater than 50 times normal.

InternalMed_Harrison

Even in affluent locales, ~20% of patients have an alcohol use disorder. These men and women can be identified by asking questions about alcohol problems and noting laboratory test results that can reflect regular consumption of six to eight or more drinks per day. The two blood tests with ≥60% sensitivity and specificity for heavy alcohol consumption are γ-glutamyl transferase (GGT) (>35 U) and carbohydrate-deficient transferrin (CDT) (>20 U/L or >2.6%); the combination of the two is likely to be more accurate than either alone. The values for these serologic markers are likely to return toward normal within several weeks of abstinence. Other useful blood tests include high-normal MCVs (≥91 μm3) and serum uric acid (>416 mol/L, or 7 mg/dL).

[Alcoholic hepatitis: clinical, laboratorial and histological study of 50 cases].

The clinical, laboratorial and histological aspects of 50 cases of alcoholic hepatitis were analysed, as well as the follow-up of 24 patients. The mean age of the 50 patients was 42,9 years (range: 25 to 65 years); 44 were males. The beginning of the symptomatology was insidious in great number of cases. The hepatomegaly was most habitual clinical signal (92% of cases). The jaundice was observed in 58% of the cases. Twenty six per cent of the patients had not manifestation of advanced hepatopaty at the moment of diagnosis. The most constant laboratorial alteration (except the increase of gama-glutamil-transpeptidase, dosed in rare cases) was the increase of SGOT (94%). Histological examination showed necrosis and inflammatory exudate in all cases; steatosis in 98%; Mallory bodies in 78%; fibrosis in 84%; cirrhosis in 44%. In the group of patients that came to the obit at the first internation, jaundice, digestive bleeding, encephalopathy, infection, leucocitosis and decreased prothrombin activity. The follow-up of 24 cases (3 months to 5 years) showed aggravation of illness and frequent evolution to cirrhosis in patient that maintained the alcohol ingestion.

[Utility of investigations by family physician of some biological parameters in chronic alcoholism].

To assess some biological alterations induced by chronic alcohol consumption and its correlation with the ingestion period and severity of consumption. The study was carried out on a series of 98 individuals (age range 20 to 80 years), followed up for alcohol consumption; 45 age-matched persons which did not consume alcohol served as controls. In both series the following parameters were assessed: blood count, mean erythrocyte volume (MEV), platelet count (PC), mean platelet volume (MPV), gamma-glutamyl-transferase (GGT), alanine and aspartate transaminases (ALT, AST). The male/female distribution was 0.98; the average amount of alcohol consumed the last five years: within accepted limits (66.32%), moderate (16.32%), increased (17.36%). The results (average values) revealed, compared to the controls, an increase in MEV from 90.312 to 97.125 I3, normal values for PC and MPV, higher levels of AST and ALT, especially in the heavy drinkers, and a significant increase of GGT level. Chronic alcohol consumption induces the appearance of important alterations of some biological parameters, in correlation with the consumption period and alcohol amount. A systematic assessment of all of these biological parameters, carried out by the family physician, may be a useful tool in the early detection of severe alterations caused by excessive alcohol consumption.

Pancreatitis

This can be remembered using the mnemonic PANCREAS: PO2 oxygen < 60 mmHg or 7.9 kPa Age > 55 Neutrophilia white blood cells > 15,000/µlitre Calcium < 2 mmol/litre Renal function (BUN) > 16 mmol/litre Enzymes lactate dehydrogenase (LDH) > 600iu/litre aspartate transaminase (AST) > 200iu/litre Albumin < 32g/litre Sugar glucose > 10 mmol/litre The BISAP score (blood urea nitrogen level >25 mg/dl (8.9 mmol/L), impaired mental status, systemic inflammatory response syndrome, age over 60 years, pleural effusion) has been validated as similar to other prognostic scoring systems. Epidemiology Globally the incidence of acute pancreatitis is 5 to 35 cases per 100,000 people. The incidence of chronic pancreatitis is 4–8 per 100,000 with a prevalence of 26–42 cases per 100,000. In 2013 pancreatitis resulted in 123,000 deaths up from 83,000 deaths in 1990. Society and culture Economics

Cases from the Osler Medical Service at Johns Hopkins University.

A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen. On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. Urinalysis revealed an elevated specific gravity and numerous muddy granular casts. Hepatitis A, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm. What is the diagnosis?

[The role and importance of biochemical markers in diagnosis of alcoholic acute pancreatitis].

Alcoholic acute pancreatitis occurs in 10% of alcoholics, who take more than 80 g alcohol daily. Different biochemical markers are used to diagnose acute pancreatitis, and some of them may help in establishing etiology of acute pancreatitis. This study is a prospective review of 21 patients. All patients were hospitalized at the Department for Gastroenterology and Hepatology or at the Department for Surgery of the Clinical Centre of Nif in the period from August 1st 2009 to March 1st 2010 with diagnosis of acute alcoholic pancreatitis. Detailed anamnesis, clinical examination, biochemical analyses and ultrasonography of the upper abdomen were done in all patients. All patients provided data on alcohol abuse. The analysis of the corresponding biochemical parameters revealed a statistically significant correlation between the following values: serum amylase and serum lipase (R = 0.964674; p < 0.001), cholesterol and triglycerides (R = 0.93789; p < 0.001), total and direct bilirubin (R = 0.857899; p < 0.001) and between aspartate aminotransferase and alanine aminotransferase (R = 0.824461, p < 0.001) in patients with alcoholic acute pancreatitis. In addition, there was a statistically significant correlation between the values of serum amylase and urinary amylase (R = 0.582742, p < 0.001). The analysis of biochemical markers showed that some of them were significant for beforehand diagnosis of alcoholic acute pancreatitis, which is in accordance with other studies. Some biochemical parameters can be potential predictors of alcoholic acute pancreatitis (lipase/amylase ratio > 2, greater ratio of aspartate aminotransferase/alanine aminotransferase, enhanced triglycerides and values of mean corpuscular volume.

Theiler's disease

Lab tests The most characteristic feature are elevated levels of gamma glutamyl transferase (100–300 IU/L), aspartate transaminase (>1000 IU/L) and sorbitol dehydrogenase, with AST levels > 4000 IU/L indicating a poor prognosis. High levels of unconjugated and total bilirubin, and serum bile acids, can be seen. Moderate to severe acidosis, leukocytosis, polycythaemia, increased creatine kinase and hyperammonemia may be present, and hemolysis can occur at the end stage. The prothrombin time (PT) and partial thromboplastin time (PTT) is often prolonged. Subclinical horses may only show elevated liver enzymes without any other clinical signs. Horses are rarely hypoglycemic, but blood glucose monitoring is ideal to indicate which horses may be benefited by glucose treatment. Differential diagnosis This is quite extensive and includes acute infectious hepatitis acute mycotoxicosis acute pyrrolizidine toxicosis haemolytic disease hepatotoxins

[Acute alcoholic hepatitis and death of cirrhotic patients].

Alcoholic hepatitis (AH) seems to be less frequent and to play a lesser role in the death of cirrhotic patients than previously acknowledged. The purpose of this work was: 1) to study the cause of death of cirrhotic patients 2) to determine the prevalence of AH among these patients and 3) to describe the clinical and laboratory features of cirrhotic patients with AH. The data were collected from a series of 107 necropsies in cirrhotic patients without hepatocellular carcinoma. The statistical analyses were carried out with an IRIS 80 computer. Severe liver failure with jaundice and encephalopathy, hemorrhage and uncontrolled infection with septic shock represented 84 p. 100 of the causes of death in patients with cirrhosis. Seventy-nine out of 107 patients (74 p. 100) had no AH (group 1), and 28 (26 p. 100) had AH (group 2): AH was mild in 15 cases and severe in 13 cases. All patients with AH died from a complication directly related to their liver disease while 21.5 p. 100 of patients without AH died from a complication not related to cirrhosis. The clinical and laboratory features of the patients without AH and cirrhosis differed from those of patients without AH by: a more frequent presence of fever (p less than 0.01), the absence of important weight loss (p less than 0.001), the total absence of abstinence (p less than 0.05), a higher value of ASAT/ALAT ratio, of serum levels of total bilirubin (p less than 0.01) and conjugated bilirubin (p less than 0.05), gamma glutamyl transpeptidase (p less than 0.001) and total cholesterol (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholic Hepatitis -- Etiology

The National Institute on Alcohol Abuse and Alcoholism (NIAAA), Alcoholic Hepatitis Consortia defines alcoholic hepatitis to include the following: The onset of jaundice within 60 days of heavy alcohol consumption (more than 50 g/day) for a minimum of 6 months Serum bilirubin more than 3 mg/dL Elevated aspartate aminotransferase (AST) to 50 U/L to 400 U/L AST:ALT (alanine aminotransferase) ratio of more than 1.5 No other cause of acute hepatitis

Rare but Lethal Hepatopathy-Sickle Cell Intrahepatic Cholestasis and Management Strategies.

Sickle cell disease can affect the liver by way of the disease process, including sickling in hepatic sinusoids, as well as its treatment, including repeated blood transfusions leading to hemosiderosis and hepatitis. Sickle cell intrahepatic cholestasis (SCIC) is an extreme variant of sickle cell hepatopathy, and is associated with high fatality. We present the case of a 31-year-old man with past medical history of sickle cell disease and cholecystectomy who was admitted with uncomplicated vaso occlusive crisis and during the hospital stay developed fever, upper abdominal pain, and jaundice. There was an accelerated rise in total bilirubin to 50 mg/dL, direct bilirubin 38 mg/dL, and Cr 3.0 mg/dL. Hb was 6.4 g/dL, reticulocyte count 16%, ALT 40 IU/L, AST 155 IU/L, ALP 320 IU/L, and LDH 475 IU/L. Hepatitis panel was negative and MRCP showed normal caliber of the common bile duct, with no obstruction. Exchange transfusion of 9 units of packed red blood cells led to great improvement in his condition. SCIC, unlike the other sickle cell hepatopathies, requires urgent and vigorous exchange transfusion. Renal impairment in SCIC has not been well studied but usually is reversible with the hepatic impairment, as in this case. Unresolved renal impairment requires dialysis and is associated with poor outcome. There is limited data on use of hydroxyurea to prevent SCIC, and liver transplant is associated with high mortality. A timely diagnosis of SCIC and appropriate management is life-saving.