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Type 2 diabetes also affects the person’s mental abilities severely and may hamper their ability to perform cognitive functions.
Association of diabetic ketoacidosis and acute pancreatitis: observations in 100 consecutive episodes of DKA. Diabetic ketoacidosis and insulin resistance with subcutaneous terbutaline infusion: a case report. Diabetes is a chronic and life threatening disease that occurs when the pancreas does not produce enough insulin, or when the body cannot effectively use the insulin it produces. Complications from diabetes: cardiovascular diseases, high blood pressure, blindness, kidney disease, etc.
For years, scientists have meticulously researched this complicated disease caused by the destruction of insulin producing islet cells of the pancreas. Type 1: Results from the body's failure to produce insulin, and presently requires the person to inject insulin. Type 2: Results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with an absolute insulin deficiency.
Type 1: Patients with type 1 diabetes usually develop symptoms over a short period of time. The doctors at the Stem Cell Clinic have developed an autologous stem cell transplantation based method for diabetes treatment. It wasn't long before his dad began to experience an achiness in his feet, one of the symptoms of diabetes is often nerve pain. Diabetes can put you at increased risk for other complications, such as skin infections, cataracts, glaucoma, and blindness due to diabetic retinopathy. Nearly 50 percent of African-Americans, who are experiencing diabetic nerve pain, like Kyles' father, are going undiagnosed, despite experiencing dull to severe pain in their hands and feet. Nearly 50 percent of African-Americans, who are experiencing diabetic nerve pain are going undiagnosed.
Because family health history can play a role in an individual's risk for developing type 2 diabetes, Kyles says he now gets screened once a year.
Many of Wall Street's biggest banks have revamped their dining facilities in recent years, adding copious amounts of salad and partnering with local businesses to provide a smorgasbord of organic offerings. Kyles says that although he has a fast paced career, he sees dad a few times a year and they check in by phone regularly. It may cause cerebrovascular disease and vascular cognitive impairment over time.Cerebrovascular disease obstructs blood flow to the brain. DKA is caused by reduced insulin levels, decreased glucose use, and increased gluconeogenesis from elevated counter regulatory hormones, including catecholamines, glucagon, and cortisol. A flowchart for the management of DKA in children and adolescents from the ADA guideline is shown in Figure 2.3 A growing problem is the development of type 2 diabetes in obese children.
Hyperglycemia, or raised blood sugar, is a common effect of uncontrolled diabetes and over time leads to serious damage to many of the body's systems, especially the nerves and blood vessels.
Despite the progress that has been made to alleviate many of the symptoms, there is still a lack of effective therapies.
This method has proven to be effective for diabetes types I and II and is administered via IV Infusion.
The severity of damage increases with duration of exposure of cultured endothelial cells to high glucose.
According to the American Diabetes Association, there are over 2 million blacks living with the disease and nearly half of them don't know they have it. African Americans are more likely to undergo lower extremity amputations due to complications from diabetes. Kyles has teamed up with the American Diabetes Association and Pfizer on the Step On Up initiative to make more people aware of the complications of diabetes such as nerve pain.
But according to a recent study so many people who live with diabetic nerve pain don't discus it with their doctors, even as it becomes more severe. According to Kyles, his father has made the necessary changes to manage his health, including the nerve pain, by taking his medication and by making lifestyle changes, including his diet.
He adds that it is so important to check in with loved ones and talk about health issues like diabetes. Persistent high blood pressure damages and narrows the blood vessels supplying blood to the brain over time, causing this disease.When high blood pressure narrows the vessels, it could also cause a mini-stroke or a major stroke. Intravenous insulin and fluid replacement are the mainstays of therapy, with careful monitoring of potassium levels.
The beta-hydroxybutyrate level may not normalize during the first one to two days of treatment. Blood glucose should be evaluated every one to two hours until the patient is stable, and the blood urea nitrogen, serum creatinine, sodium, potassium, and bicarbonate levels should be monitored every two to six hours depending on the severity of DKA.3 Cardiac monitoring may be warranted for patients with significant electrolyte disturbances. Hyperchloremia is a common but transient finding that usually requires no special treatment.Cerebral edema is a rare but important complication of DKA. Although DKA is less common in these patients than among those with type 1 diabetes, it does occur.
Most patients with DKA will need lifetime insulin therapy after discharge from the hospital. Now, researchers have turned their attention to adult stem cells that appear to be precursors to islet cells that produce insulin. Diabetes treatment with adult stem cells has been very successful with our own patients and is also showing promising results in independent clinical trials. This glucose-induced endothelial cell damage is mitigated by exposure of the endothelial cells to insulin in the presence of high glucose. Diabetes can be a deadly, if left uncontrolled and unmanaged leading to strokes and cardiovascular complications, and kidney failure. It is the most common cause of blindness, and usually occurs in people 40 years of age and above. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue.
Treatment also should be directed at the underlying cause of the DKA, including antibiotics for suspected or identified infection. C-peptide levels may be helpful for determining the type of diabetes and guiding subsequent treatment. There is abundant evidence, including that of author, that insulin treatment prevents diabetes-related microvascular complications including nephropathy and renal failure. The premature death rate for blacks living with diabetes is nearly 30 percent higher than for their white counterparts.
In one study10 of ketoacidosis, amylase was elevated in 21 percent and lipase in 29 percent of patients. Although it is important to monitor urinary output, urinary catheterization is not advised routinely.INPATIENT VS. Even by taking insulin multiple times, glucose level may reach normal level but only for a short time, because endogenous insulin response is insufficient. Infection, insulin omission, and other problems that may have precipitated ketoacidosis should be treated. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol.Abdominal pain may be a symptom of ketoacidosis or part of the inciting cause of DKA, such as appendicitis or cholecystitis. If pancreatitis is suspected, contrast-enhanced computed tomography (CT) may be useful for diagnosis in selected patients. Patients typically improve mentally with initial treatment of DKA, but then suddenly worsen.
Manipulation by oral antidiabetic agents to enhance endogenous insulin release, or increase insulin sensitivity, results in exhaustion of the beta cells, thus changing an easily controllable glycemic state to a pathological uncontrollable glycemic state over the years.
Myocardial infarction is a precipitating cause of diabetic ketoacidosis that is especially important to look for in older patients with diabetes. If the patient has significant hypertriglyceridemia, it can falsely lower glucose and sodium measurements by dilution. Even more troublesome is the lack of established information about the glucose levels that are safe for patients who have diabetes. Treatment of suspected cerebral edema should not be delayed for these tests to be completed. By the term safe glucose level author means a glucose level which is least toxic to microvascular system and not likely to cause neuropathy, foot ulcer, gangrene, sexual dysfunction, and kidney failure. Education to prevent recurrence should be offered to all patients, including how to manage sick days and when to call a physician. In more severe cases, seizures, pupillary changes, and respiratory arrest with brain-stem herniation may occur. To achieve that glucose control is a formidable task for the patients as well as the doctors and nurses.
If dextrose is not given, further ketosis may occur.INSULINAn intravenous insulin drip is the current standard of care for diabetic ketoacidosis, primarily because of the more rapid onset of action.
Thus, on one hand patients must be astute in their care and doctors and nurses must be diligent in implementing and maintaining optimal glucose control in their patients. Studies29 comparing intravenous insulin with subcutaneous or intramuscular insulin have found a quicker decrease in glucose and ketone levels, but no improvement in morbidity and mortality. Both parties must be cohesive to achieve only one goal, which is to keep patients learn to cope with diabetes and thrive.
Randomized clinical trials of glycemic control comparing one insulin against another, or insulin against oral hypoglycemic agents is not ethical.
Although the bicarbonate level typically is low, it may be normal or high in patients with vomiting, diuretic use, or alkali ingestion.
Lispro and aspart (NovoLog) insulin are more expensive and do not work faster than regular insulin when given intravenously.
There were no significant differences in outcomes between the aspart and intravenous insulin regimens. A similar study29 comparing subcutaneous lispro insulin in a medical ward with an intravenous insulin drip in the intensive care unit showed similar outcomes, except for a 40 percent reduction in cost for patients treated in the medical ward.
If the patient is on an insulin pump, it should be stopped, and the patient should be switched to an intravenous infusion.31If an intravenous infusion pump is not available, insulin can be given intramuscularly.

While acute complications reverse with intensive therapy, chronic complications do not necessarily reverse even with intensive therapy.The two serious acute complications are diabetic ketoacidosis and diabetic coma. High uncontrolled sugar level is associated with frequent urination accompanied by excessive loss of body water (dehydration).
Potassium should be started as soon as adequate urine output is confirmed and the potassium level is less than 5 mEq per L.3 Usually 20 to 30 mEq (20 to 30 mmol) of potassium is given for each liter of fluid replacement. All these secondary hormones lead to breakdown of fat and increased release of fatty acids from liver. The byproducts of these fatty acids are acetoacetic acid, which lower blood pH and make the person acidotic. Because there are no studies on patients with a pH level below 6.9, giving bicarbonate as an isotonic solution still is recommended. When the osmotic force in the circulating system increases, water moves away from the above organs into the circulating system to make the balance of the water content between the two spaces.
Liver cells become dry and lead to necrosis with elevated liver enzymes; similarly, heart cells undergo necrosis and lead to heart failure, and kidney cells necrosis leads to acute kidney failure.
Therefore, a diabetic patient with very high glucose levels, if not treated quickly with insulin infusion and fluid therapy, can develop catatrophic events associated with high mortality.2.
In addition to alterations in magnesium metabolism from DKA, many patients with diabetes have taken medications such as diuretics that also may lower magnesium levels.
Symptoms of magnesium deficiency are difficult to recognize and overlap with symptoms caused by deficiencies of calcium, potassium, and sodium. An important question is about the threshold of glucose level above which complications are likely to develop and below which complications are unlikely to develop. Paresthesias, tremor, carpopedal spasm, agitation, seizures, and cardiac dysrhythmias all are reported symptoms.
Checking magnesium levels and correcting low levels should be considered in patients with DKA.
Therefore, a big question is: are glucose particles same or different in someone who is not diabetic versus who is diabetic?Author’s research involving cell culture studies attests to the fact that elevated glucose level, in and of itself, even of similar particles, has something to do with the complications.
Serum sodium is falsely lowered by 1.6 mEq for every 100 mg per dL increase in blood glucose. Hyponatremia needs to be corrected only when the sodium level is still low after adjusting for this effect. Additional cultured cells were treated with glucose of the same concentrations as above and insulin or with glucose, insulin, and heparin.Why are vascular endothelial cells chosen and not other cell types?
There is good evidence in the literature that vascular endothelial cells are most vulnerable to injury by high blood glucose levels (hyperglycemia). The answer is that most cells are able to reduce the transport of glucose inside the cells when they are exposed to high glucose levels, so that their internal glucose concentration remains constant. In contrast, the cells damaged by high glucose concentration are those that cannot retard transport of glucose inside the cells. Thus, in diabetes, endothelial cells and mesangial cells cannot reduce transport of glucose inside the cells in the state of high glucose levels in the blood. In essence, defect in membrane transport of endothelial cells permits excessive amount of glucose to enter inside the cells when glucose level is high. Electron microscopic analysis of glucose-Induced endothelial damage in primary culture (2006).retinopathy, heart attack, foot ulcer, gangrene, or kidney failure. None of the pathways thus far advanced explain damage to all the organs in a unified fashion. Author has proposed a better unified theory, which is ischemia (markedly reduced blood flow), which explains damage to all the organs. This is evident in heart as myocardial fibrosis and cardiomyopathy or atrophic tubules and interstitial fibrosis in kidneys.
Progressive kidney failure is more due to loss of tubules and interstitial fibrosis rather than glomerular sclerosis. Inability to achieve penile erection is clearly due to lack of blood flow through the penile microvasculature. Reduced blood flow can be associated with increased vascular permeability, resulting in exudation of plasma proteins in the free surface outside of the vessels. This is best seen as hemorrhages and exudates in the retina of eyes and as protein leak from kidney glomeruli in diabetes. Reduction of high blood glucose to normal or near normal level with insulin results in mitigation of endothelial damage and repair; and consequently, partial or complete recovery of organ function.
Like this author, other authors have considered that diabetes-specific microvascular disease in the eyes (retina), kidney glomeruli, and vasa nervorum (small vessels surrounding nerves in feet and penis) has similar pathophysiologic features [1].Fundamentally, the worst effects of high glucose level will be felt uniformly in all organs as considered by this author, and other authors [1]. Once again, the uniformly worse effect of high blood glucose is necrosis of vascular endothelial cells, sloughing off of these cells into the capillary lumina forming microthrombi along with cholesterol and platelet deposits and resulting in occlusion of capillaries with slight or no blood flow to the organs.
Hyperglycemia (high glucose level) was induced in rats to find changes in kidney glomeruli in the past. Very subtle changes were found in the kidney glomeruli; no changes were found in the tubules and interstitium. This is the worst pitfall of the utility of experimental studies in live animals in trying to elucidate the pathogenesis of the complications associated with diabetes in humans. On the other hand, cell culture experiments done by the author and the collaborating authors have paved the way in better understanding of the pathogenesis of diabetic complications and how will these complications be adequately prevented.The exact mechanisms of injury to the vascular endothelial cells and tubular epithelial cells caused by high glucose levels are not yet fully elucidated.
Some authors have shown that high blood glucose levels increase oxidative stress and increase the production of reactive oxygen species [2].We have considered that toxic oxygen radicals may be involved in ischemic injury to the organs.
We treated vascular endothelial cells with a potent glutathione inhibitor, buthionine sufoximine for 2 days and 6 days. After 6 days of treatment, endothelial cells had undergone severe necrosis beyond recognition. Thus, this experiment suggests that deficiency of glutathione may be an important mechanism of diabetic microvascular complications [3].Our cell culture studies have helped us to undermine the mechanism of protection against high glucose-induced cellular damage. We treated the cultured endothelial cells with insulin and with insulin and heparin in the presence of high glucose level in the culture medium. This had been shown by my collaborating author [4].There is one mechanism by which heaprin may synergize insulin. We have found that high glucose as well as insulin increases endothelin-1 production in the cultured endothelial cells. Endothelin-1 is a potent vasoconstrictor and can aggravate ischemic injury to the endothelial cells. It is evident in the literature that lowering of high blood glucose level with intensive insulin therapy can prevent diabetic complications [7-10], but no systematic studies were done to unequivocally show that simply by lowering of high glucose level with oral antidiabetic agents, such as glyburide, metformin, or Januvia will prevent diabetic complications. Occasional studies showed that use of metformin alone in Type 2 diabetes reduced the risk of death from myocardial infarction. The most important caveat of Type 2 diabetes is that some of the patients in this type of trial may not have diabetes. Type 2 diabetes was never defined appropriately, such as by 2 h postprandial glucose level or glucose tolerance test. The primary end point was an aggregate of microvascular and macrovascular morbidity and mortality, as separate aggregate scores. Metformin treatment prevented weight gain, improved glycemic control, and reduced insulin requirement but didn’t improve the primary end points. This finding suggests that insulin has a vascular protective effect, which may be independent of simply lowering of glucose [3].
Thus, combining clinical studies with the adjunct of cell culture studies, it is prudent to state that insulin is the cornerstone of therapy for prevention of cellular damage and hence appearance of clinical complications.3.
PREVENTION OF CELLULAR INJURY AND PROTECTION AGAINST CLINICAL COMPLICATIONSBy now the readers have developed a grasp of the fundamentals of diabetes mellitus (DM) and how much damage high glucose causes to the various organs.
Now is the time for the readers to know what we can do to bring down the glucose level and keep that to near normal level, so that anatomical and functional damage to the various organs can be abated. But there is no evidence that keeping the sugar level to normal level will completely prevent the damage (injury) or repair any damage that has already incurred. Further, risk of hypoglycemic reactions is quite high when one attempts to lower the glucose to normal levels. Control of Hyperglycemia and Monitoring of the ControlUtmost attention should be focused to identify and treat DM at the early stage when no complication has surfaced. Aggressive control of hyperglycemia with intensive insulin therapy when complications have already developed, such as; renal failure increases the risk of ireversible hypoglycemia and high mortality.
Technical Pitfalls in Control of HyperglycemiaMost patients check their blood glucose before breakfast and before dinner neither of which provides good information of glycemic control. Few studies have compared the validity of the glucose levels between two-time periods (fasting and 2 hours after a meal) in relation to microvascular or macrovascular complications.
ComplianceA recent report indicates that only 17 percent of Type 2 diabetes patients take insulin.
Another 17 percent of Type 2 diabetes patients take a combination of insulin and oral agents, whereas 54 percent are treated with only oral agents [15]. Despite extensive efforts and more oral drugs available, attempts at reaching and maintaining nearnormal glycemic levels in actual clinical practice have been largely unsuccessful.
The failures are mainly due to lack of diet control and irregularities in taking prescribed doses of insulin. The most difficult part of satisfactory glucose control is refusal of most patients to adhere to a strict diet regimen [15].
In underdeveloped countries, social stigma is even worse making patients feel embarrassed to go to doctors, thus delaying treatment.
Similarly, regular sugar testing, special diet preparation, and long-term treatment program prove to be expensive to many individuals in underdeveloped and developing countries. Controlled diet therapy is difficult in environment of multiple families living together in those countries. Personal or family income is often meager to buy required amount of insulin and diabetes supplies. Fallacy in ClassificationThe worst fallacy in current diabetes care is to ascribe every adult with hyperglycemia automatically as Type 2 diabetes and hence prescribe oral antidiabetic agents and a renin-angiotensin inhibitor drug.
Therapy for DiabetesThe most important therapy for diabetes is obviously replacement therapy, which is insulin. Author does not recommend oral agent(s), because oral agents lower fasting glucose and HbA1c but not 2h PP glucose level, as shown in this patient (Table 1). Discontinuation of metformin and initiation of insulin glargine resulted in control of fasting and 2hPP glucose levels and improvement in renal function. Our experimental studies reinforce the clinical studies in that insulin therapy reverses toxic effects of high glucose on endothelial cells thereby preventing complications [3,6].This is in agreement with a previous report.
A ten year follow up of intensive glucose control in Type 2 diabetes indicates that intensive glucose control starting at the time of diagnosis is associated with a significantly decreased risk of myocardial infarction and death from any cause, in addition to the well-established reduction in the risk of microvascular disease. These findings strengthen the rationale for attaining optimal glycemic control and indicate emergent long-term benefits on cardiovascular risk [16].5.

PRINCIPLES OF INSULIN THERAPYA variety of insulin preparations are available in the market: short-acting, intermediate-acting, and long-acting.
Author recommends sugar testing 2-h after each meal, bed time, and upon waking in middle of night for satisfactory glucose control. Insulin Glargine (Lantus®)A recombinant DNA analog of human insulin, forms microprecipates in subcutaneous tissue, delaying its absorption and prolonging its duration of action. Insulin Detemir (Levemir®)According to pharmaceutical companies, both lantus insulin and insulin detemir have similar onset of action in about 4 hours and reaches its peak in 8 to 9 hours.
There are no data to support or refute that long-acting insulin, such as Lantus or Levemir will be effective for 24 hours in those with normal kidney function.
Because insulin is excreted by the kidneys, thus in diabetes patients with decreased kidney function, insulin excretion will be reduced in proportion to decrease of kidney function. Thus, insulin dosage will be reduced proportionately and will be given at longer intervals such as once a day. Frequent dosing of insulin in patients with decreased kidney function may cause irreversible hypoglycemia and a vegetative life.It is important for the readers to know that Lantus or Levemir taken twice daily after breakfast and dinner (12 hours apart) has made a big difference in attaining satisfactory glucose control among author’s patients in the office and in the hospital.
Here is one such example.A 56 years white female was seen in consultation in February of 2010, for acute elevation of blood glucose and renal insufficiency. On history taking and physical examination, her main problem is bilateral foot ulcer under the heel: one is necrotic looking, and the other not so bad looking. Following are some of the records.In the hospital, she was started on Lantus insulin after breakfast and after dinner (12 hours apart) and aspart insulin on a sliding scale which she followed after discharge. She recorded her sugar one hour after breakfast, lunch, and dinner after discharge from the hospital.
She takes Lantus insulin 20 units after breakfast and 20 units after dinner and aspart insulin on a sliding scale.
A 77 year white - female was first seen by the author in July of 2010 for control of diabetes and renal function with the author’s paradigm of therapy.
She gave a history of diabetes for 12 - 13 years and loss of sensation in the feet suggesting diabetic neuropathy.
Lantus insulin further increased to 35 units after breakfast and dinner which she is taking now. While kidney function could be better if the patient stops taking furosemide, but she feels the need to take the furosemide.
Intermediate-acting insulins are NPH (Neutral Protamine Hagedorn), Humulin N, and Novolin N. All diabetic patients, when they are first seen in author’s office, can be divided into following groups.
The main objective of doing that is to protect kidney function from further deterioration and reduce the risk of entering into dialysis. This is already published by the author [14].An 86 y white male was admitted to the hospital for foot ulcer.
Patients not exposed to insulin therapy, have been treated with multiple oral antidiabetic agents, but find glucose levels going very high.
Before author recommends or starts on insulin therapy, he explains the risks and benefits of insulin therapy. The risks are minimal and mainly slight pain from injections, scarring, and discoloration of the skin from repeated injections. Skin infection from insulin injecttion is rare, if the same syringe with needle is not used more than once and skin is cleaned with alcohol swab before injection. Skin infection, such as furuncles and carbuncles, are common only in those with uncontrolled diabetes and living in unhygienic conditions, as in underdeveloped countries. Author observed huge carboncles in patients with uncontrolled diabetes in Fiji Island.Slight weight gain is a common place with insulin therapy but is not a concern for active individuals.
This dosage is increased at an interval of 4 to 5 weeks until satisfactory glucose control is achieved. The problem with this type of prescription is the insulin effect before post-meal surge, leading to hypoglycemia.
On the other hand, the author recommends taking regular insulin on a sliding scale 1 - 2 hours after meal. However, even in best of circumstances, uncontrolled hyperglycemia could be due to urinary tract infection, flu, or pneumonia, in and of itself, as well as a result of failure to take prescribed doses of insulin due to the illness. Treatment of these incidental conditions along with aggressive insulin therapy help to restore good glycemic control.2) As patients become comfortable with insulin therapy, oral antidiabetic drugs are gradually discontinued, one in each visit after the first visit.
For example, if a patient was taking three different oral antidiabetic agents, all three will be discontinued in three separate consecutive office visits at an interval of six to eight weeks. All author’s patients are treated solely with a combination of long acting and short acting insulins as stated above.3) Frequent office visits to maintain glucose and blood pressure controls Typically, author follows his patients every four to five weeks in the office in order to ascertain glycemic control, blood pressure (BP) control and renal function control. Author’s focus is renal function which serves as the mirror of how well they are managing glycemic and BP controls. Author’s goal is to keep renal function stable at the level they were first seen, or improve but definitely not get worse. Monitoring of Glycemic (Glucose) ControlThere are many ways to monitor day-to-day glucose control.
Traditionally, most patients have done or still do sugar testing at fasting and before each meal. Author recommends checking 1 to 2 hours after each meal, at bedtime, and upon wake up in the middle of night. Although it is generally considered that peaks are harmful, no study was ever done to determine if the valleys are harmless. Author recommends patients to record all glucose readings and bring to office during scheduled visits. It is a tedious job both for the patients and the doctors to keep up with the monitoring of glucose control. Early Morning Glycemic SurgeEarly morning glycemic surge giving rise to fasting hyperglycemia is not uncommon even in the most compliant patients.
This fasting hyperglycemia is a part of early morning hormonal surge, such as high cortisol or epinephrine and noreprinephrine level. Therefore, it is prudent to state that these hormones surge increase blood pressure as well as blood glucose levels. However, the pathways of the interactive role of liver in sustaining hyperglycemia are not yet elucidated. One of the hypoglycemic reactions is waking up in the early morning with perspiration or with an urge to go to bathroom.
They are typically noncompliant, do not follow diet therapy and are inconsistent in taking the insulin.
They are aware of the danger of these glucose levels but apparently don’t care enough to follow the regimen and instruction provided.
He recommends acarbose in combination with insulin in obese and diet noncompliant patients. Acarbose is an alpha-glucosidase inhibitor, which competitively inhibits the alpha-glucosidase enzymes in the gut that digests dietary starch and sucrose. Author starts as 50 mg with breakfast, lunch, and dinner but increases to 100 mg with lunch and dinner to minimize postprandial hyperglycemic surge.
This is caused by undigested carbohydrate reaching the lower bowel, where gases are produced by bacterial flora. In small number of patients, troublesome diarrhea develops, requiring discontinuation of the drug.
A slight increase in liver enzymes may be observed, requiring dosage reduction or discontinuation of the drug.c) Diet Alone Diet control alone works in achieving glycemic control. She was treated with accupril (ACEI) 40 mg tablet daily, hydrochlorothiazide 25 mg daily (which always increases glucose level mimicking diabetes), Lipitor 40 mg daily for hyperlipidemia, and fluoxetine 20 mg daily for depression. She didn’t have any laboratory done except the information that her kidney function was decreased. At best, this patient is prediabetic, but drugs like hydrochlorothiazide can tip off the glycemic control and can cause established diabetes.
Hypoglycemic reactions are more common with short-acting or ultrashort-acting insulins than with long-acting insulins. It has been shown that glyburide appears to cause a higher incidence of hypoglycemia than chlorpropamide, glipizide, or glimepiride.
Most commonly, blood glucose decreases fast and to a very low level when a meal is missed and patients have taken insulin and immediately engaged in a physical activity.The earliest symptoms of hypoglycemia are blurring of vision with inability to read small letters, unsteadiness or feeling weak in standing or walking, feeling loss of balance, or waking up from sleep drenched in sweat.
Difficulty in falling into sleep, feeling nervousness, and feeling excessively hungry are other common symptoms.a. The fastest way to obtain relief is to drink 8 ounces of orange juice with one or two pieces of bread or cookies. Concomitantly with the above, it is imperative not to engage in physical activity for 15 minutes. Apple juice or pineapple juice of same volume is also effective, but relief of symptoms with orange juice is faster than other juices.
Patients with diabetes will learn over the years by trial and error which of the foods will relieve their symptoms most and in a fastest way. Therefore, it is time again to take a low dose of regular insulin to prevent glucose levels rising.
Most importantly, dglucose is Finally, in summary a question may be asked; has author’s paradigm undergone randomized control trial to determine its effectiveness against other therapies for diabetes? Author does not feel it ethical to compare therapies in diabetes with decreased kidney function or other complication in many of them.
Author’s goal is to educate the patients to learn to cope with illness, follow the prescribed therapy and not develop progressive renal failure leading to dialysis.
Similar comments about clinical trials on diabetes therapy have been made by other authors [21].
Most importantly, diabetes care should be individualized and done in an objective fashion, only to reduce the risk of complications. Arguments about evidence-based medicine depending on the results of clinical trials will simply delay effective treatment and increase the risk of developing complications.
Once again, the goal of diabetes therapy is vigilant care by the professsionals to maintain control of postprandial hyperglycemia with insulin therapy which is fundamental to preservation of renal function [14].

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