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Piero et al: Asian Journal of Biomedical and Pharmaceutical Sciences 500mg robaxin for sale kidney spasms after stent removal; 4(40) 2014 discount robaxin 500 mg without prescription muscle relaxant list by strength,1-7 buy 500mg robaxin back spasms 8 weeks pregnant. Insulin is a pancreatic hormone amounts of urine produced by diabetics attracted flies responsible for blood glucose level regulation. The traditional way of diagnosing diabetes hormone binds to its receptor sites on peripheral side of mellitus in ancient Chinese was by observing whether the cell membranes. Insulin ages, the European doctors tested for diabetes by stimulates catabolism on glucose into pyruvate through tasting the urine themselves, a scene occasionally glycolysis. These metabolic events Diabetes mellitus has been known since antiquity, its are antagonistic to metabolic events triggered by the treatments were known since the Middle Ages, and the hormone glucagon. When glucose levels are at or below elucidation of its pathogenesis occurred mainly in the threshold, glucose stays in the blood instead of entering 20th century. The discovery of the The body attempts to arrest hyperglycemia, by drawing role of the pancreas in diabetes was made by Joseph water out of the cells and into the bloodstream. This is why that upon complete removal of the pancreas from dogs, diabetics present with constant thirst, drinking large the dogs exhibited all the signs and symptoms of amounts of water, and polyuria as the cells try to get rid diabetes and died shortly afterwards. This subsequently leads to Edward Albert Sharpey-Schafer of Edinburgh in glucosuria (Piero, 2006). Scotland suggested that diabetics lacked a single As hyperglycemia prolongs, the body cells are devoid of chemical which was normally produced by the glucose due to the lack of insulin. Name of this chemical was later proposed to seek alternative mobilizable energy sources. The fats are not fuel sources for the red blood Best repeated the work of Von Mering and Minkowski cells, kidney cortex and the brain. The red blood cells but went a step further and managed to show that they lack mitochondria in which beta-oxidation pathway could reverse the induced diabetes in dogs by giving rests. The fatty acids cannot pass the blood-brain them an extract from the pancreatic islets of barrier. This was a step forward in acetyl-CoA arising from catabolism of fatty acids is elucidation of the endocrine role of pancreas in diverted to ketogenesis to generate ketone bodies, metabolism and existence of insulin (Banting et al. These ketone bodies are also passed in from bovine pancreases at the University of Toronto in the urine, thereby leading to ketonuria, which Canada, thereby leading to the availability of an characterizes diabetes mellitus. Build up of ketone effective treatment of diabetes mellitus, with the first bodies in the blood produces ketosis. A combination of diabetes was made by Sir Harold Percival (Harry) ketosis and acidosis lead to a condition called Himsworth in 1935 (Himsworth, 1936). If left untreated, ketoacidosis leads to Following these discoveries, other landmark discoveries coma and death (Belinda, 2004). Insulin output under Insulin exhibits a multitude of effects in many tissues, basal condition approximates 0. The effects of insulin on carbohydrate clearing the postprandial glucose load (Ginsberg et al. The insulin production is directly across muscle and adipocyte cell membranes, proportional to the amount of sugar (carbohydrate) regulation of hepatic glycogen synthesis, and inhibition consumed. The more sugar one consumes, the more of glycogenolysis and gluconeogenesis (Piero, 2006). Incorporation of fatty acids from over-production of insulin will eventually exhaust that circulating triglyceride into adipose triglyceride and capacity and the cells will cease to operate (Robert, lipid synthesis are stimulated by insulin; lipolysis is 2002). Insulin deficiency plays a central role in all Insulin initiates its physiological effects by binding to a forms of diabetes because it is the major hormone that high affinity specific receptor located on the plasma enables cells (primarily muscle and fat cells) to uptake membrane. Insulin makes it possible binding capacity and the biological activity of insulin for most body tissues to remove glucose from the blood are maximal at a plasma insulin concentration of 20 to for use as fuel, for conversion to other needed 30 U/ml. Furthermore, insulin is also process, and reaction of the disulfide bonds is not the major regulatory signal for glycogenesis in the involved. As a Stimulation of intracellular Potassium transport is one consequence of the widespread prevalence of diabetes of the well-known effects of insulin (Steiner, 1977). Magnesium is to identify and develop more effective remedies to involved in the activation of many intracellular improve the quality of life of those affected by the enzymes. The result is accumulation of of diabetes mellitus underlies autoimmune destruction Magnesium intracellularly with activation of critical of the pancreatic beta cells leading to insulin deficiency intracellular enzymes. Following an overnight fast, the and biosignalling derangements that are consequent to 8. Defective insulin Asian Journal of Biomedical and Pharmaceutical Sciences, all rights reserved. Stunted growth and susceptibility to in type 2 diabetics in relation to the degree of opportunistic infections may also be associated with hyperglycemia present. Uncontrolled diabetes mellitus fasting hyperglycemia in a given patient with non- leads to hyperglycemia with ketoacidosis as well as the insulin-dependent diabetes mellitus is closely related to nonketotic hyperosmolar syndrome. Long-term the degree of impaired pancreatic beta-cell metabolic complications of diabetes mellitus include responsiveness to glucose. Meta-analyses demonstrate that cardiovascular, peripheral arterial and cerebrovascular lifestyle interventions, including diet and physical disease. Hypertension and abnormalities of lipoprotein activity, led to a 63% reduction in diabetes incidence in metabolism also accompany uncontrolled diabetes those at high risk. The levels are maintained by sustenance of balance between dietary management of diabetes mellitus is a hepatic glucose production and glucose utilization by complement of lifestyle management. Dietary gluconeogenesis and promotes glucose catabolism by management aims at optimal metabolic control by the skeletal muscles. In type which positively correlates with fasting plasma glucose 2 diabetes, the dietary objective is for improved concentration. Between gluconeogenesis and glycemic and lipid levels and weight loss as appropriate glycogenolysis, gluconeogenesis appears to be (Piero et al. Unnecessary glucose output can be have been in use to aid in maintenance of blood glucose ameliorated by inhibition of glycogenolysis and/or level at the requisite threshhold in diabetics through gluconeogenesis from endogenous precursors. Sulfonylureas Stimulation of intrahepatic disposal of neoformed and the nonsulfonylurea secretagogues establish glucose contributes to autoregulation. Metformin works by decreasing is closely related to the degree of fasting hyperglycemia hepatic gluconeogenesis while at times also increasing but in a curvilinear fashion. Decreased insulin secretion peripheral glucose mobilization and disposal (Curtis, and defective cellular insulin action also compromises 2007). Synthetic insulin injections are also a therapy efficient glucose uptake by peripheral tissues. Management interventions hypoglycemic agents available to manage type 2 improve islet function and raise plasma insulin levels, diabetes, 5% to 10% of the population with diabetes experience secondary failure. This bottleneck can be Asian Journal of Biomedical and Pharmaceutical Sciences, all rights reserved. Secondary failure arises as a apparently bedeviled by side effects, need to be result of deteriorating beta cell function, poor optimized to mitigate these demerits. A major drawback intended goal of lowering the glycemic index in associated with hypoglycemic agents is that they are diabetics. The strategy was turn to phytodrugs to avoid the adverse effects based on the premise that non-insulin producing cells associated with conventional hypoglycemic agents.
Infectious Diarrhea Microbes cause diarrhea either directly by invasion of gut mucosa or indirectly through elaboration of different types of toxins: Secretory enterotoxins buy robaxin 500mg with visa muscle relaxant menstrual cramps, cytotoxins and inflammatory mediators discount robaxin 500mg amex zyprexa spasms. I) Secretory toxin induced diarrhea Patients seldom have fever or major systemic symptoms discount robaxin 500mg visa muscle relaxer kidney pain. Examples: a) Vibrio cholerae produces enterotoxins which stimulate adenylate cyclase which results in massive intestinal secretion. Examples: a) Shigella dysenterae produces Shiga toxin which causes destructive colitis. Common causes include : Acute shigellosis Feaco-orally transmitted, as few as 10 - 100 bacteria are enough to cause diarrhea Initially multiplies in the small intestine causing secretary diarrhea. Acute Salmonellosis Transmitted by ingestion of contaminated meat, dairy or poultry products. This is in marked contrast to the 3 - 4 wks febrile illness caused by Salmonella typhi and paratyphi, which are not usually associated with diarrhea. Campylobacter jejuni It may be responsible for up to 10% of acute diarrhea world wide. Norwalk and Rota viruses Invade and damage villous epithelial cells Cause diarrhea by interfering with absorption through selective destruction of absorptive villous tip cells with sparing of secretary crypt cells. Cysts or trophozoites can be identified in the stool, and treatment should be given in both cases. They may cause voluminous life threatening diarrheal diseases in patients with acquired immunodeficiency syndrome. Evaluation of a patient with diarrhea Careful interview of patients with diarrhea contributes in etiologic diagnosis, evaluation of severity of illness, and in designing treatment and preventive measures. Thus, the history should include Duration of illness: if the diarrhea lasts for 2 - 4 wks, acute diarrheal diseases are said to exist. However, if it lasts for more than 4 wks, consider chronic diarrheal diseases and infectious causes are unlikely. Bloody diarrhea is usually inflammatory or ischemic in origin and caused by invasive organisms, ulcerative colitis, or neoplasms Volume of diarrhea Large volume diarrhea indicates small bowel or proximal colonic diseases Scanty, frequent stools associated with urgency suggest left colon or rectal diseases Any association with specific meal? If diarrhea is associated with intake of Fat it is due to fatty intolerance Sweet diet it is due to osmotic diarrhea Milk and milk products - it is due to lactase deficiency Is there history of drug intake? Laxatives Chemotherapeutic agents 7) Presence of underlying diseases (like diabetes mellitus) or systemic symptoms Physical examination: Assess severity of dehydration, Wight loss and other associated signs in patient with chronic diarrhea. Diagnosis: Laboratory tests: 1) Culture and sensitivity testing to detect a pathogenic bacterial strains. Proctosigmoidoscopy: to exclude of confirm the diagnosis of inflammatory bowel diseases. Rehydration In patients with massive diarrhea and vomiting with hypotension intravenous fluids like Ringers lactate or Normal saline should be given in adequate amount. Antimicrobial therapy Antibiotics: Most acute infectious diarrheal diseases do not require antibiotic therapy because majority of them are self limited and viral in nature. In immunocompromized patients continue maintenance dose of the same drug three times a week. Anemia Learning objectives: At the end of this topic the student we be able to:- 1. Evaluate cases of anemia with appropriate history, physical examination and proper laboratory studies 4. Anemia: General approach a) Definition Functional definition: A significant reduction in red cell mass and a corresponding decrease in the 02 carrying capacity of the blood. For instance; 389 Internal Medicine Hgb or Hematocrite could be falsely elevated ( plasma volume) e. Clinical approach to the Patients with anemia Anemia is a manifestation of an underlying pathological condition. Multifactorial : a combination of these History: Accurate history provides information crucial to the diagnosis of the underlying cause. Cardiovascular adjustment Increased in cardiac output occurs at Hgb level of 7-8 gm% : the increased in cardiac output coupled with modest tachycardia creates a hyperdynamic state and hence systolic ejection murmur Peripheral vascular resistance decreases there by facilitating tissue perfusion; clinically is evidenced by wide pulse pressure. Local changes in tissue perfusion: Redistribution of blood flow to vital organs at the expense of reduced blood flow to less vital organs. Reduction of mixed venous O2 tension to increases the arteriovenous O2 difference O2 extraction at peripheral tissues 393 Internal Medicine Individuals tend to survive at extremely low hemoglobin levels (even as low as 3 gm %) due to these compensatory mechanisms. Therapeutic considerations and indications In the management of anemic patients carefully remember the following points Identify and correct the cause of anemia Administration of Hematinines such as Iron, Vit B12 or folate without correct diagnosis of the cause of anemia is an unacceptable practice in the treatment of anemia Therapeutic modalities include: Iron, folate, Vit. Identify possible reasons for inadequate response to therapy and indications for parenteral iron administration 8. Iron deficiency anemia Hypo chromic microcytic cells Etiologies of Iron deficnecy Anemia 1. Increased demands Prematurity in newborns Rapid growth ( as in adolescent ) growth spurt Pregnancy 3. Poor diet Contributory factor in many countries but rarely sole cause Clinical manifestation: Is insidious in onset and progressive in course Patients often present with nonspecific symptoms mentioned above with/without some specific symptoms. Inadequate response may imply Continuing hemorrhage non compliance to therapy Wrong diagnosis Mixed deficiency associated folate or vit. Inability or unwillingness to take orally Iron-dextran complex or iron sorbitol citrate can be used Intra-muscularly or intra-venous route. Correction of reversible contributors (iron, folate, cobalamine supplements if necessary) C) Sideroblastic anemia: Refractory anemia with hypochromia with marrow iron Many pathological ring sideroblasts are found in the bone marrow Is caused by defect in hem synthesis Classification: Hereditary (sex linked recessive trait) Acquired 399 Internal Medicine o Primary :Myelodysplasia o Secondary : - Malignant diseases of the marrow - Drugs e. Macrocytic Anemia Learning objectives: at the end of the student will be able to:- 1. Understand the management of Megaloblastic anemia and asses response to therapy properly Megaloblastic Anemia and other Macrocytic Anemia Pathogenesis: Its a descriptive morphologic term in which maturation of the nucleus is delayed relative to that of cytoplasm. Abnormalities of vitamin B12 or folate metabolism, transcobalamine deficiency, antifolate-drugs 4. B12 deficiency 1) Nutritional: especially in vegans 2) Malabsorption a) Gastric causes i) Adult (addisonian) pernicious anemia ii) Congenital lack or abnormality of intrinsic factor iii) Total or partial gastrectomy b) Intestinal causes i) Intestinal stagnant loop syndrome, jejunal diverticulosis, blind loop, stricture etc. Vit B12 Deficiency: is treated with Hydroxocobalamine which is given parentraly Dose: Initial dose: 6 x 1000 g over 2-3 weeks and Maintenance : 1000 g every 3 months Prophylactic therapy is indicated in patients with Total gastrectomy and Ileal resection 2. Folate deficiency: is treated with Folic acid preparation which is given orally Dose: 5 mg Po daily Prophylactic therapy is indicated in pregnancy, sever hemolytic anemia, in patients with dialysis, and premature newborns 3. Additional measures: Correct underlying cause Antibiotics for bacterial over growth and treatment of fish tapeworm Response to therapy Feeling of general well being is restored in 48 hrs Reticulocytosis begins in 3-4 days and peaks in 7-10 days. Leukemias Learning Objective: At the end of this unit the student will be able to 1) Define leukemia 2) Classify the different types of leukemias 3) Describe the possible etiologies and epidemiology of leukemia. Cell of origin : there are two types of leukemias Lymphoid leukemias Myeloid leukemias 2. But studies have demonstrated that both genetics and environmental factors are important in the causation of these diseases. Genetics There is a greatly increased incidence of leukemia in the identical twin of patients with leukemia. Environmental factors like Ionizing radiation: The relation between acute leukemia and ionizing radiation, has been established in those having occupational radiation exposure, patients receiving radiotherapy and Japanese survivors of atomic bomb explosions.
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The duodenum is predominately retroperitoneal and comprises the cap discount robaxin 500mg without a prescription muscle relaxant mechanism, the descending and the distal portions purchase 500mg robaxin with mastercard muscle relaxant exercises. This point is relatively constant and marks a change from the prominent rugal folds of the gastric body to the smoother discount robaxin online mastercard spasms film, less-prominent folds of the antrum. The stomach and duodenum lie in close proximity to a number of impor- tant anatomic structures. Anterosuperiorly are the left diaphragm and left lobe of the liver, while the body and tail of the pancreas lie posteriorly. Laterally to the left are: the hilum of the left kidney, the left adrenal gland and, above that, the spleen. These organs form the stomach bed and are separated from it by the lesser omentum and the lesser sac. The parasympathetic supply con- tracts the stomach, relaxes the pylorus and stimulates acid, pepsin and mucus secretion, whereas sympathetic stimulation constricts the blood supply and reduces gastric motor activity and secretion while the pylorus is contracted. Functions of the Stomach The food bolus exits the lower esophageal sphincter through the cardiac orifice, the opening that connects the cardia region of the stomach to the esophagus. Vagal reflexes initiated by the cephalic phase of eating inhibit contractile activity in the proximal stomach and the entry of food into the stomach promotes relaxation of the cardia of the stomach. When relaxed and empty, the adult human stomach has a near empty volume, but it normally expands to hold about 1 L of food and liquid. The stomach temporarily stores the swallowed food and liquid until it is passed to the intestines. The release of ghrelin is stimulated by fasting and is suppressed by the ingestion of food. Ghrelin stimulates gastric emptying and acts via the central nervous system to stimulate appetite. The stomach mixes up food and digestive juice and macerates the mixture into a semiliquid state, called chyme. Acid Secretion The thick layers of gastric mucosa secrete gastric juice, which contains two key substances involved in digestion: hydrochloric acid and pepsin. Parietal cells contain secretory channels called canaliculi from which the gastric acid is secreted into the lumen of the stomach. Chloride and hydrogen ions are secreted separately from + the cytoplasm of parietal cells and mixed in the canaliculi. Cl- and K ions are transported into the lumen of the cannaliculus by conductance channels. The frequency (3 cycles per minute [cpm]) and propagation velocity (approximately 14 mm/second) of the gastric peristaltic waves are controlled by the slow wave, which leads the contraction from the proximal corpus to the distal antrum, as shown at electrodes A through D. Peristaltic contractions occur three times per minute, the frequency of the gastric slow wave. In contrast to visceral sensations, somatic nerves such as from the skin carry sensory information via A-delta and C fibers through the dorsal root ganglia and into the dorsal horn and then through dorsal columns and spinothalamic tracts to cortical areas of somatic representation. Sleisenger & Fordtrans gastrointestinal and liver disease: Pathophysiology/Diagnosis/Management 2006: page 1007. Dumping syndrome is a frequent compilation of esophageal, gastric or bariatric surgery. The early postprandial phase results from the rapid emptying of the stomach including larger than normal food particles, with the osmotic shift of fluid into the duodenal lumen plus the distention of the human releasing gastrointestinal and pancreatic hormones. These hormones cause the gastrointestinal and vascular symptoms of the early dumping syndrome. The rapid and early absorption of nutrients causes prompt secretion of insulin, and the late dumping syndrome characterized by reactive hypoglycaemia (Tack et al. A modified oral glucose tolerance test may be used to establish the reactive hypoglycaemia. The dumping syndrome does not always respond to dietary maneuvers, and pectin or guar gum may be needed to slow gastric emptying, a carbose to slow starch digestion and reduce pos-prandial reactive hypoglycaemia, or in extreme cases somatostatin injections may be given to slow gastric emptying and to slow sugar absorption. There are numerous centrally acting drugs used for the treatment First Principles of Gastroenterology and Hepatology A. Some persons with severe, intractable gastroparesis, such as may occur with severe type I diabetes, may improve with near-total gastrectomy and Roux-en-Y anastomosis. Slowed gastric emptying and delayed small intestinal transit occur in persons with cirrhosis. If intractable symptoms persist, acupuncture (P6 point) or gastric electrical stimulation may be of limited benefit. Unfortunately, nausea and vomiting is common during pregnancy, particularily during the first trimester. Curiosly, vitamin b6 (thiamine), soda crackers, and ginger are often helpful (Table 4). Non-pharmaceutical options (Dietary and lifestyle modifications) for the treatment of nausea and vomiting during pregnancy o Avoidance of precipitating factors o Frequent, small meals high in carbohydrate and low in fat o Vitamin B6 (thiamine) o Ginger o Stimulation of P6 acupuncture point o Treat dehydration, electrolyte disturbances o Correct malnutrition o Soda crackers (unproven benefit) Avoid offending foods/beverages Modified from: Keller J, et al. Nature Clinical Practice Gastroenterology & Hepatology 2006; 3(5): page 258; and printed with permission: Keller J, et al. Factors that slow the rate of gastric emptying rate Gastric Neuromuscular o Tachygastria o Decreased fundic accommodation o Increased fundic accommodation o Antral hypomotility o Pylorospasm o Antroduodenal dyscoordination First Principles of Gastroenterology and Hepatology A. The volume of the meal alters the rate of gastric emptying in proportion to the volume of the meal. Hypergastrinemia From our appreciation of the numerous ways in which acid secretion may be turned on or off, it is straight-forward to work out the causes of hypergastrinemia, and those mechanisms of hypergastrinemia which would be associated with increased gastric acid secretion, and might lead to severe peptic ulcer disease (Table 8 and 9) Table 8. Causes of hypergastrinemia With acid hypersecretion With variable acid secretion With acid hyposecretion Gastrinoma Hyperthyroidism Atrophic gastritis Isolated retained gastric antrum Chronic renal failure Pernicious anemia Antral G-cell hyperplasia Pheochromocytoma Gastric cancer Massive small bowel resection Postvagotomy and pyloroplasty Pyloric outlet obstruction Hyperparathyroidism First Principles of Gastroenterology and Hepatology A. There are many possible explanations for an elevated serum gastrin concentration (Table 9). It is one of the most common complaints bringing patients to consult their family physician. Dyspepsia is a symptom or symptoms, and when the person presents, their symptom is not diagnosed, so this is called uninvestigated dyspepsia. Lifestyle factors such as smoking, excess alcohol intake, stress and a high fat diet could precipitate dyspeptic symptoms. Commonly Used Terms to be Distinguished Dyspepsia - A symptoms or symptoms, with no known diagnosis because the symptom has not be investigated. When the patient presents with (uninvestigated) dyspepsia, there are several approaches which may be taken (Table 2). Safe -Continuing or recurrent symptoms and cost-effective compared with may frustrate patients and endoscopy clinician -Possible reduced risk of later ulcer development o H. Shaffer 102 In Canada, the recommended approach to the patient with undiagnosed dyspepsia is The Hand. Terms used to describe Dyspepsia History and physical examination First exclude non-gastrointestinal sources of pain or discomfort in the upper abdomen, e. Long-term healthcare costs are estimated to be approximately the same regardless of which investigative approach is followed. A 20% decline in IgG serology titer over 6 months correlates with successful eradication of H.
The success rate of vaginal penetration was assessed in two trials of mild to 306 moderate (study a) and severe patients (study b) purchase robaxin overnight muscle relaxant half life. In the first trial discount robaxin 500mg otc muscle relaxant end of life, men allocated to nitroglycerine ointment compared with placebo reported more adverse events (frequent burning at the application site: 12 robaxin 500 mg without a prescription muscle relaxant otc usa. In the second trial, men allocated to nitroglycerine plaster had more frequent headache (35. In addition, 6 percent of men allocated to nitroglycerine withdrew from therapy due to adverse events (severe pain) versus 0 percent of placebo subjects. One trial (n=132 participants) compared the 313 efficacy and harms of nitroglycerine ointment to minoxidil. Men assigned to received nitroglycerine ointment group reported more frequent side effects than did men in the minoxidil group, including more frequent burning at the application 313 site (12. Topical Aminophylline plus Isosorbide dinitrate plus Co-dergocrine versus Placebo. Two crossover trials compared the efficacy and harms of Aminophylline plus Isosorbide dinitrate 312,314 plus Co-dergocrine versus placebo. None of the patients had prolonged erection or priapism, clinically significant cardiovascular adverse events (such as postural dizziness), headache, or pain at site of 314 312 application. In the second trial, men assigned to the active treatment reported that they experienced erections adequate for intercourse after 3. All successful applications for both the active treatment and placebo 312 groups occurred in a single participant. One crossover trial (n=132) compared the efficacy and harms of 313 minoxidil to placebo. Compared with placebo, men allocated to minoxidil reported more frequent burning at the application site (6 versus 0 percent). No hypotension was reported by either the minoxidil or placebo-treated participants. One trial (n=80) compared the efficacy and 144 harms of topical sildenafil to oral sildenafil. In men assigned to receive topical sildenafil, four (10 percent) reported mild headache. In those assigned to receive oral sildenafil, two participants (5 percent) developed severe headache, one participant (3 percent) reported disturbed visual function, and one participant (3 percent) experienced severe dyspepsia. Quantitative Synthesis No meta-analysis could be performed because of substantial degree of clinical heterogeneity across the trials with regard to patient characteristics, interventions, and the assessed outcomes. Overview of Trials 322,323,326 Three trials used crossover, and the remaining 17 used parallel design. Treatment 319,321,323,330 316 duration in several trials was 6 months and in one trial 12 months. Racial characteristics were reported in only three trials with the majority of the subjects being Caucasians. While trials generally enrolled men with hypogonadism and/or andropause, the specific sexual dysfunction and testosterone entrance criteria across trials varied widely. With respect to 145,323,326 testosterone, all but three trials mandated that participants have levels below a specified threshold. Five trials studied testosterone in combination with a 5,77,145,231 phosphodiesterase inhibitor. Two other trials studied a cream combining testosterone, 322,329 isosorbide dinitrate and co-dergocrine. Several trials 231 reported that adverse effects were absent or were negligible and without a difference in 77,145,319 frequency between treatment groups. In one open label trial outcomes for efficacy and 324 harms were compared between oral testosterone and no treatment. Subjects were excluded from the trial if they had prostate abnormality or any illness considered likely to impair sexual function. The outcomes for efficacy and harms associated with the 316,319 use of oral testosterone versus placebo were compared in two trials. In the first trial, the difference in the occurrence of adverse events between the two treatment groups was not statistically significant. In the second trial, 86 percent and 93 percent of men in the testosterone and placebo group, respectively, reported that their 316 erections were less strong at 12 weeks of the followup. One trial evaluated and compared the efficacy and harms between oral testosterone alone and oral testosterone combined 145 with sildenafil. These men were randomized to 2 months of treatment with either oral testosterone undecanoate alone (120 mg/d) or oral testosterone undecanoate (120 mg/d) plus sildenafil (50-100 mg). Patients with prostate hypertrophy, prostate cancer, and mammary carcinoma were excluded. The study reported that apart from mild headache occurring in three patients taking 145 sildenafil 100 mg, no serious adverse events were observed. One trial evaluated and compared the efficacy and harms for oral testosterone versus propionyl-L 319 carnitine plus acetyl-L-carnitine. Results comparing testosterone and propionyl-L-carnitine plus acetyl-L-carnitine are reported here. The occurrence of adverse events was not statistically significantly different between the two treatment groups. The corresponding median score in those assigned to the propionyl-L carnitine plus acetyl-L-carnitine group changed from 8 (range 522) to 24 (range 829) (within group difference: p <0. One trial evaluated and compared the efficacy and harms outcomes of oral testosterone plus sildenafil compared with sildenafil 93 145 alone. The men were randomized to receive a 2-month treatment with either oral testosterone undecanoate (120 mg daily) plus sildenafil (50-100 mg) or sildenafil alone. Apart from mild headaches occurring in three patients taking sildenafil 100 mg, no serious adverse events were observed. The active treatment arms each lasted for at least 6 months, while the placebo treatment lasted for 2 months. Patients with major disorders, a history of substance abuse, obesity, or major psychopathology were excluded from the trial. Patients with psychiatric disorders or abnormal prostate exam result (men aged > 50 years) were excluded. In the third trial, men who received testosterone were more likely to report acne (testosterone: 20. Differences between men in the testosterone and placebo groups with respect to the occurrence of irritability (17. In the first trial, weekly frequency of erections in the testosterone and placebo treatment groups were 7. There was no difference in the degree of erection during 94 sex with partner (scale 16, with = none and 6 = full), with a mean score of 5. The weekly frequency of erection was not different between the two groups of testosterone and human chorionic gonadotropin treatment (7. The efficacy and harms of gel testosterone versus placebo 317 were compared in one trial In this trial, 406 hypogonadal men (total T <300 ng/dL) aged 20 80 years (mean age: 58 years) reporting one or more symptoms of low testosterone deficiency (i. One participant from the group treated with 50 mg gel testosterone, five in the group treated with 100 mg gel testosterone, and none treated with placebo withdrew due to an adverse event.