Challenges faced by physicians when discussing the Type 2 diabetes diagnosis with patients: insights from a cross-national study (IntroDia® ).

AIMS: To investigate physicians' recalled experiences of their conversations with patients at diagnosis of Type 2 diabetes, because physician-patient communication at that time may influence the patient's subsequent self-care and outcomes. METHODS: As part of a large cross-national study of physician-patient communication during early treatment of Type 2 diabetes (IntroDia® ), we conducted a cross-sectional survey of physicians treating people with Type 2 diabetes in 26 countries across Africa, Asia, Europe, Latin America, the Middle East, North America and Oceania. The survey battery was designed to evaluate physician experiences during diagnosis conversations as well as physician empathy (measured using the Jefferson Scale of Physician Empathy). RESULTS: A total of 6753 of 9247 eligible physicians completed the IntroDia® survey (response rate 73.0%). Most respondents (87.5%) agreed that the conversation at diagnosis of Type 2 diabetes impacts the patient's acceptance of the condition and self-care. However, almost all physicians (98.9%) reported challenges during this conversation. Exploratory factor analysis revealed two related yet distinct types of challenges (r = 0.64, P < 0.0001) associated with either patients (eight challenges, α = 0.87) or the situation itself at diagnosis (four challenges, α = 0.72). There was a significant inverse association between physician empathy and overall challenge burden, as well as between empathy and each of the two types of challenges (all P < 0.0001). Study limitations include reliance on accurate physician recall and inability to assign causality to observed associations. CONCLUSIONS: Globally, most physicians indicated that conversations with patients at diagnosis of Type 2 diabetes strongly influence patient self-care. Higher physician empathy was associated with fewer challenges during the diagnosis conversation.

Etiologies, periocular manifestations and surgeries for congenital and childhood acquired facial nerve palsy.

AIM: To report periocular surgeries performed for patients with congenital and childhood acquired facial nerve palsy (FNP). METHODS: A retrospective case series of pediatric patients who presented with FNP over the last 34 years, was conducted at two tertiary eye hospitals in Riyadh. Data were collected from electronic charts, hospital records and external photos. Main outcome measures were visual acuity, lagophthalmos, eyelid abnormalities, Bell's phenomena, exposure keratopathy, and corneal scar; in these cases, periocular surgeries were required. RESULTS: Among the 90 recruited subjects; the mean age of onset was 4.8±5.4 years old (range, 0.01 to 17.76 years). Traumatic and congenital causes of FNP were the most common, representing over 80% of the cases. Seventy-one patients developed lagophthalmos, 26 with severe exposure that resulted in scarring. Thirty-six (40%) cases had associated strabismus. Lower lid retraction was the most common eyelid abnormality noted in 23 cases, followed by entropion in 16 and ectropion in 6 cases. Temporary tarsorrhaphy was performed in three patients (3.3%), while 18 patients (20%) needed permanent tarsorrhaphy. Gold weight implants were placed in 17 patients (18.9%). Lower lid retraction repair was performed in twelve patients (13.3%). Five patients (5.6%) underwent lower eyelid entropion repair, and three patients (3.3%) underwent lower eyelid ectropion repair. CONCLUSIONS: Lagophthalmos is the most common finding in children presenting with FNP and needs to be managed early to prevent permanent visual loss. Compared to adults, children may present with a different spectrum of eyelid abnormalities, with lower lid retraction and entropion being the most common eyelid malpositions.

Metabolic effects of the nocturnal rise in cortisol on carbohydrate metabolism in normal humans.

Glucocorticoid concentrations vary throughout the day. To determine whether an increase in cortisol similar to that present during sleep is of physiologic significance in humans, we studied the disposition of a mixed meal when the nocturnal rise in cortisol was mimicked or prevented using metyrapone plus either a variable or constant hydrocortisone infusion. When glucose concentrations were matched with a glucose infusion, hepatic glucose release (2.6 +/- 0.2 vs. 1.5 +/- 0.4 nmol/kg per 6 h) was higher (P < 0.05) while glucose disappearance (5.9 +/- 0.3 vs. 7.3 +/- 0.9 mmol/kg per 6 h) and forearm arteriovenous glucose difference (64 +/- 24 vs. 231 +/- 62 mmol/dl per 6 h) were lower (P < 0.05) during the variable than basal infusion. The greater hepatic response during the variable cortisol infusion was mediated (at least in part) by inhibition of insulin and stimulation of glucagon secretion as reflected by lower (P < 0.05) C-peptide (0.29 +/- 0.01 vs. 0.38 +/- 0.04 mmol/liter per 6 h) and higher (P < 0.05) glucagon (42.7 +/- 2.0 vs. 39.3 +/- 1.8 ng/ml per 6 h) concentrations. In contrast, the decreased rates of glucose uptake appeared to result from a state of "physiologic" insulin resistance. The variable cortisol infusion also increased (P < 0.05) postprandial palmitate appearance as well as palmitate, beta-hydroxybutyrate, and alanine concentrations, suggesting stimulation of lipolysis, ketogenesis, and proteolysis. We conclude that the circadian variation in cortisol concentration is of physiologic significance in normal humans.

Effects of a change in the pattern of insulin delivery on carbohydrate tolerance in diabetic and nondiabetic humans in the presence of differing degrees of insulin resistance.

While it is well established that people with non-insulin dependent diabetes mellitus have defects in both insulin secretion and action, the relative contribution of each to glucose intolerance is not known. Therefore, nondiabetic (lean and obese) and non-insulin dependent diabetes mellitus subjects were studied on two occasions. On each occasion, insulin secretion was inhibited with somatostatin and glucose was infused in a pattern and amount that mimicked the systemic delivery rate normally observed after ingestion of 50 g of glucose. Insulin also was infused so as to mimic postprandial insulin profiles observed in separate groups of diabetic and nondiabetic subjects after food ingestion. Glucose turnover was measured using the isotope dilution method. A delayed pattern of insulin delivery (i.e., a "diabetic" insulin profile) led to higher (P < 0.05) glucose concentrations in all groups; however, the effects were transient, resulting in only a modest increase in the integrated glycemic responses. An isolated defect in insulin action had little effect on peak glucose concentration; however, it prolonged the duration of hyperglycemia, leading to a 2.5-4.2-fold increase (P < 0.05) in the integrated glycemic response. A combined defect in the pattern of insulin secretion and action was additive rather than synergistic. Both defects caused hyperglycemia by altering suppression of endogenous glucose release and stimulation of glucose disposal. Whereas obese diabetic and nondiabetic subjects had comparable defects in glucose clearance, non-insulin dependent diabetes mellitus subjects also had defects in hepatic insulin action. Thus, abnormalities in the pattern of insulin secretion and action alone or in combination impair glucose tolerance. An isolated defect in insulin action has a more pronounced and prolonged effect than does an isolated change in the pattern of insulin secretion. Hepatic and extrahepatic insulin resistance results in marked and sustained hyperglycemia.

The effects of non-insulin-dependent diabetes mellitus on the kinetics of onset of insulin action in hepatic and extrahepatic tissues.

The mechanism(s) of insulin resistance in non-insulin-dependent diabetes mellitus remains ill defined. The current studies sought to determine whether non-insulin-dependent diabetes mellitus is associated with (a) a delay in the rate of onset of insulin action, (b) impaired hepatic and extrahepatic kinetic responses to insulin, and (c) an alteration in the contribution of gluconeogenesis to hepatic glucose release. To answer these questions, glucose disappearance, glucose release, and the rate of incorporation of 14CO2 into glucose were measured during 0.5 and 1.0 mU/kg-1 per min-1 insulin infusions while glucose was clamped at approximately 95 mg/dl in diabetic and nondiabetic subjects. The absolute rate of disappearance was lower (P < 0.05) and the rate of increase slower (P < 0.05) in diabetic than nondiabetic subjects during both insulin infusions. In contrast, the rate of suppression of glucose release in response to a change in insulin did not differ in the diabetic and nondiabetic subjects during either the low (slope 30-240 min:0.02 +/- 0.01 vs 0.02 +/- 0.01) or high (0.02 +/- 0.00 vs 0.02 +/- 0.00) insulin infusions. However, the hepatic response to insulin was not entirely normal in the diabetic subjects. Both glucose release and the proportion of systemic glucose being derived from 14CO2 (an index of gluconeogenesis) was inappropriately high for the prevailing insulin concentration in the diabetic subjects. Thus non-insulin-dependent diabetes mellitus slows the rate-limiting step in insulin action in muscle but not liver and alters the relative contribution of gluconeogenesis and glycogenolysis to hepatic glucose release.

Assessment of insulin action and glucose effectiveness in diabetic and nondiabetic humans.

Insulin concentrations in humans continuously change and typically increase only when glucose also increases such as with eating. In this setting, it is not known whether the severity of hepatic and extrahepatic insulin resistance is comparable and whether the ability of glucose to regulate its own uptake and release is defective in non-insulin-dependent diabetes mellitus (NIDDM). To address this question, NIDDM and nondiabetic subjects were studied when glucose concentrations were clamped at either 5 mM (euglycemia) or varied so as to mimic the glucose concentrations observed in nondiabetic humans after food ingestion (hyperglycemia). Insulin was infused so as to simulate a "nondiabetic" postprandial profile. During euglycemia, insulin increased glucose disposal in nondiabetic but not diabetic subjects indicating marked extrahepatic resistance. In contrast, insulin-induced suppression of glucose release was only minimally less (P < 0.05) in diabetic than nondiabetic subjects (-1.06 +/- 0.09 vs. -1.47 +/- 0.21 nmol.kg-1 per 4 h). Hyperglycemia substantially enhanced disposal in both groups. Glucose effectiveness measured as the magnitude of enhancement of disposal (0.59 +/- 0.18 vs. 0.62 +/- 0.17 nmollkg-1 per 4 h) and suppression of release (-0.36 +/- 0.12 vs. -0.14 +/- 0.12 nmol.kg-1 per 4 h) did not differ in the diabetic and nondiabetic subjects. In conclusion, when assessed in the presence of a physiological insulin profile, people with NIDDM demonstrate: (a) profound extrahepatic insulin resistance, (b) modest hepatic insulin resistance, and (c) normal ability of glucose to stimulate its own uptake and suppress its own release.

Impaired basal glucose effectiveness in NIDDM: contribution of defects in glucose disappearance and production, measured using an optimized minimal model independent protocol.

People with NIDDM are resistant to insulin. The present studies sought to determine whether the ability of glucose to regulate its own metabolism in the presence of basal insulin concentrations is impaired. To address this question, basal insulin concentrations were maintained constant with an exogenous insulin infusion, while endogenous hormone secretion was inhibited by somatostatin. The integrated glycemic response above baseline during identical prandial glucose infusions was greater (1,411 +/- 94 vs. 938 +/- 45 mmol/l per 5 h; P < 0.01) in the diabetic subjects than in the nondiabetic subjects, indicating a decrease in net glucose effectiveness. [6-3H]glucose also was infused to determine whether the decrease in net glucose effectiveness was due to a decrease in the ability of glucose to stimulate its own uptake and/or to suppress its own production. Despite identical rates of tracer infusion, the increment in plasma concentration of [6-3H]glucose was higher (4.50 +/- 0.29 vs. 3.16 +/- 0.21 x 10(5) dpm/ml per 5 h; P < 0.05) in the diabetic subjects than in the nondiabetic subjects. This was due to both a decrease (P < 0.05) in the ability of glucose to stimulate its own disappearance via mass action and to a greater (P < 0.01) inhibitory effect of glucose on its own clearance. The increase in glucose concentration resulted in prompt and comparable suppression of endogenous glucose production in both groups. Under these optimized conditions, indexes of glucose effectiveness calculated with both the "cold" and "hot" minimal models also were lower (P < 0.05) in the diabetic subjects than in the nondiabetic subjects and were highly correlated (r = 0.94-0.99; P < 0.001) with the indexes of glucose effectiveness calculated from the increments above baseline of glucose and [6-3H]glucose concentration. We conclude that the ability of glucose to regulate its own metabolism in the presence of basal insulin concentrations is abnormal in people with NIDDM.

Microalbuminuria in patients with NIDDM: an overview.

We have come a long way in our understanding of the epidemiology, pathophysiology, and clinical significance of albuminuria in patients with NIDDM. However, substantial gaps remain to be defined. NIDDM nephropathy is a serious and increasingly burdensome disease for both the diabetic individual and the society at large. Onset of microalbuminuria, an early but common manifestation of NIDDM nephropathy, marks an ominous turn for the NIDDM patient, in whom its development forecasts a grave cardiovascular outcome. Interception of albuminuria with antihypertensive agents such as ACE inhibitors in otherwise healthy NIDDM subjects holds a significant promise but must first await further investigation.

The role of growth hormone in the development of diabetic retinopathy.

OBJECTIVE: To determine the role of growth hormone (GH) in the development of diabetic retinopathy. RESEARCH DESIGN AND METHODS: Medical records of 1,423 patients who had undergone insulin tolerance tests (1976-1991) at the Mayo Clinic were examined, and diabetic subjects were identified as either GH-deficient (GH increment after hypoglycemia < 5 micrograms/L and peak < 10 micrograms/L) or GH-sufficient. Prevalence of retinopathy was determined in these cases and in a cohort group of diabetic subjects selected to match the GH-deficient cases. These control patients (32 cases) were selected from medical records of individuals who had received medical care at Mayo during the same interval but who had not undergone insulin tolerance testing. RESULTS: Twenty-four patients with diabetes were identified, of whom 16 were GH-deficient and 8 GH-sufficient. Despite comparable age, duration of diabetes, and metabolic control, the prevalence of diabetic retinopathy in the GH-deficient group (2 of 16; 12.5%) was less (P < 0.05) than that observed in the GH-sufficient group (5 of 8; 62.5%). Prevalence in the GH-deficient group also was lower than that observed in the cohort control group (15 of 32, 47%). CONCLUSIONS: These data strongly suggest that GH contributes to the development of diabetic retinopathy in humans.

Effects of insulin on plasma magnesium in noninsulin-dependent diabetes mellitus: evidence for insulin resistance.

Insulin influences both glucose metabolism and magnesium homeostasis in humans. The present studies sought to determine whether insulin-induced stimulation of magnesium uptake is impaired in noninsulin-dependent diabetes mellitus (NIDDM) and enhanced by acute hyperglycemia. To do so, we measured plasma magnesium concentrations in diabetic and nondiabetic subjects on two occasions: once when glucose concentrations were maintained constant and once when glucose concentrations were varied to mimic a postprandial pattern. The same amount of insulin was infused on both occasions in a manner that reproduced the systemic insulin concentrations normally observed after glucose ingestion. During the prandial insulin infusion, the decrement in the plasma magnesium concentration was lower (P < 0.05) in the diabetic patients than that in the nondiabetic subjects during both the euglycemic (4.1 +/- 0.9 vs. 7.8 +/- 1.3 mmol/L.4 h) and hyperglycemic (1.7 +/- 1.1 vs. 6.6 +/- 1.4 mmol/L.4 h) studies. Glucose disappearance also was lower (P < 0.05) in the diabetic patients than that in the nondiabetic subjects, and the insulin-induced decrement in plasma magnesium was correlated (P < 0.01) with glucose disappearance. On the other hand, despite higher (P < 0.05) rates of disappearance in the hyperglycemic than euglycemic experiments, the decrement in plasma magnesium did not differ in either group on either occasion. We conclude that insulin resistance in subjects with NIDDM impairs the ability of insulin to stimulate magnesium as well as glucose uptake.

Prevalence of microalbuminuria in Saudi Arabians with non-insulin-dependent diabetes mellitus: a clinic-based study.

Prevalence of diabetic nephropathy varies in different racial groups, being especially high in communities that have abandoned an active traditional living and embraced a modern but sedentary life-style. As a new and rapidly developing country, Saudi Arabia has witnessed impressive changes in socio-economic growth and development and concurrently, a disturbing trend in non-insulin-dependent diabetes mellitus (NIDDM). These observations therefore prompted us to investigate the prevalence of microalbuminuria among Saudi Arabians with NIDDM. Two hundred and eleven patients attending a large Diabetic Clinic in Riyadh were screened for microalbuminuria (30-300 mg/24 h). Twenty-seven subjects had clinical proteinuria (dipstick-positive) and were excluded, leaving 184 cases for analysis. Seventy-six subjects (76/184, 41.3%) had microalbuminuria. These subjects had higher fasting plasma glucose concentrations (P = 0.002) and greater body mass index (P = 0.049) than subjects with normal albumin excretion rate (< 30 mg/24 h). There were no significant differences between subjects with and without microalbuminuria with regards to fasting total plasma cholesterol and triglycerides concentrations, frequency of hypertension, duration of diabetes or type of therapy for diabetes. In multivariate analysis, glycaemia (P < 0.005) and years since diagnosis of diabetes (P = 0.05) remained independently associated with albumin excretion rate. We conclude that microalbuminuria is exceedingly common in a clinic-based population of Saudi Arabians with NIDDM and its presence is closely related to glycaemic control. Whether the prevalence of microalbuminuria is truly increased in the diabetic population at large in Saudi Arabia must now await further population-based studies.

Diabetes care in the wake of the United Kingdom Prospective Diabetes Study.

Full text is available as a scanned copy of the original print version.

The diagnosis of diabetes mellitus. A contest between 3 points!

A major debate is currently taking place on the world diabetes scene on the merits of fasting versus 2-hour postprandial glucose concentrations as a reference point for the diagnosis of diabetes. Other time points of the oral glucose tolerance test on the other hand, seem to attract little attention. In Saudi Arabia however, we have been intrigued by the scale and severity of hyperglycemia observed at one-hour following glucose load. Plasma glucose concentration one-hour postprandially is strikingly abnormal amongst native Saudis and interestingly, is associated with insulin resistance and features of syndrome X. Such observations have prompted us to call into question the wisdom of current practices, namely of excluding the one-hour plasma glucose concentration in the diagnosis of diabetes. In the proceeding article therefore, we describe in detail our local observations and debate the wider scientific and historical issues surrounding the place of one-hour glucose concentration as a potentially useful diagnostic point in the detection and classification of glucose intolerance.

Obesity and overweight in type II diabetes mellitus patients in Saudi Arabia.

Full text is available as a scanned copy of the original print version.

The size of the pancreas in diabetes mellitus.

To determine whether there was an association between the size of the pancreas and the type of diabetes, ultrasonography of the pancreas was performed on 57 diabetic patients: 14 with Type 1 (insulin-dependent) diabetes, 10 insulin-treated and 33 tablet-treated patients with Type 2 (non-insulin-dependent) diabetes, and 19 non-diabetic subjects. The pancreas of patients with Type 1 diabetes was markedly smaller (p < 0.0001) than the pancreas in non-diabetic subjects. The pancreas of patients with Type 2 diabetes was more moderate in size: larger (p < 0.001) than that of Type 1 diabetic patients but smaller (p < 0.5) than the pancreas of the control group. Pancreatic size of patients with Type 2 diabetes was also related to basal insulin secretion with insulin-deficient patients (low or undetectable C-peptide) having smaller (p < 0.05) pancreases than those with normal insulin secretion. There was no difference in the size of the pancreas in the different treatment groups of Type 2 diabetic patients. Pancreatic size did not correlate with age, body mass index or the duration of diabetes. We conclude that the pancreas is a smaller organ in patients with diabetes mellitus and that the decrement in size is maximal in insulin-dependent/insulin-deficient subjects. Ultrasonography, therefore, can potentially serve to discriminate between the different types of diabetes.

Diabetic hyperosmolar non-ketotic decompensation.

To assess whether the outcome of hyperosmolar non-ketotic decompensation has changed in the past 20 years with modern medical management, a retrospective study analysis was performed of all patients presenting with the syndrome to a large teaching hospital during the period 1982 to 1986. Twenty-two patients were identified of whom 68 per cent had no previous history of diabetes mellitus. The immediate mortality rate (within 72 h of presentation) was 36 per cent (eight of 22), the overall mortality rate was 41 per cent (nine of 22) and vascular thromboembolism was common. A comparison was made of the early deaths (n = 8) and survivors (n = 14) in an attempt to identify favourable prognostic factors. The two groups could not be distinguished either by clinical or laboratory variables at presentation nor by treatment regimen; however there was a significant delay in establishing the diagnosis in some of the patients who died. Our results indicate there has been no improvement in the outcome of the hyperosmolar non-ketotic decompensation syndrome in the last two decades and that a high index of suspicion is required to identify patients presenting with this condition.

Unusual causes of calf swelling--2. Rhabdomyolysis mimicking deep vein thrombosis.

A 55 year old woman with pain and swelling of the leg was heparinized on the basis of a clinically diagnosed ilio-femoral deep vein thrombosis (DVT). Subsequent investigation showed her to have extensive rhabdomyolysis of the leg. Rhabdomyolysis can mimic the appearance of deep vein thrombosis and this case further illustrates the importance of venography in the assessment of the swollen leg.