Temporomandibular joint reconstruction after failed teflon-proplast implant: case report and literature review.

Multiple reports document that a foreign-body giant cell reaction forms around Proplast-Teflon temporomandibular joint (TMJ) implants. This results in destruction of surrounding bone and instability of the implants. This case presents a patient whose Proplast-Teflon TMJ implants became displaced into her middle cranial fossa. The staged reconstruction of this patient is described, including removal of the TMJ implants, reconstruction of the defect, concomitant orthodontic treatment and final reconstruction with TMJ Concepts. This process involved a multidisciplinary approach between several medical and dental specialties. At her 3-year follow up, the patient had a stable postoperative result.

Effect of glucagon on net splanchnic cyclic AMP production in normal and diabetic men.

Glucagon activates hepatic adenylate cyclase, thereby increasing acutely the liver content of cyclic AMP (cAMP) as well as the release of cAMP into the hepatic vein. Insulin, on the other hand, antagonizes this glucagon-mediated cAMP production, thus providing a hypothetical mechanism through which insulin might correct some of the metabolic abnormalities of diabetes. To study this hormonal interaction in man, net splanchnic cAMP production (NScAMPP) was investigated in normal and insulin-dependent diabetic men under basal conditions and in response to intravenous glucagon, 50 ng/kg/min for 2 h. In normals (n=19), basal hepatic vein cAMP concentration was 23.6+/-1.1 nM and NScAMPP was 1.7+/-0.6 nmol/min. Glucagon stimulated NScAMPP in four normal subjects to a peak of 99.6+/-43 nmol/min at 25 min with a subsequent fall to 12.4+/-5.1 nmol/min by 90 min despite continuing glucagon infusion. Endogenous insulin secretion was stimulated as indicated by rising levels of immunoreactive insulin and C-peptide (connecting peptide) immunoreactivity, raising the possibility that endogenous insulin might be responsible for the fall in NScAMPP that followed the initial spike. In the diabetics (n=8), basal hepatic vein cAMP concentration was 24.7+/-1.2 nM and NScAMPP was undetectable. Glucagon stimulated NScAMPP in five diabetics to a peak of 169.9+/-42.6 with a subsequent fall to 17.4+/-3.9 nmol/min by 90 min even though endogenous insulin secretion was not stimulated (no rise in C-peptide immunoreactivity). Although the mean increase in NScAMPP was greater in the diabetics, the two groups did not differ significantly.Conclusions. In normal resting man the liver is a significant source of circulating cAMP. Diabetics do not release abnormally large amounts of hepatic cAMP under basal conditions. Glucagon markedly enhances hepatic cAMP release with a spike-decline pattern in both normal and diabetic men. The decline in hepatic cAMP release despite continuing glucagon stimulation is due to factors other than a stimulation of insulin secretion.

Effects of glucagon on lipolysis and ketogenesis in normal and diabetic men.

The effect of glucagon (50 ng/kg/min) on arterial glycerol concentration and net splanchnic production of total ketones and glucose was studied after an overnight fast in four normal and five insulin-dependent diabetic men. Brachial artery and hepatic vein catheters were inserted and splanchnic blood flow determined using indocyanine green. The glucagon infusion resulted in a mean circulating plasma level of 4,420 pg/ml. In the normal subjects, the glucagon infusion resulted in stimulation of insulin secretion indicated by rising levels of immunoreactive insulin and C-peptide immunoreactivity. Arterial glycerol concentration (an index of lipolysis) declined markedly and net splanchnic total ketone production was virtually abolished. In contrast, the diabetic subjects secreted no insulin (no rise in C-peptide immunoreactivity) in response to glucagon. Arterial glycerol and net splanchnic total ketone production in these subjects rose significantly (P=<0.05) when compared with the results in four diabetics who received a saline infusion after undergoing the same catheterization procedure.Net splanchnic glucose production rose markedly during glucagon stimulation in the normals and diabetics despite the marked rise in insulin in the normals. Thus, the same level of circulating insulin which markedly suppressed lipolysis and ketogenesis in the normals failed to inhibit the glucagon-mediated increase in net splanchnic glucose production. It is concluded (a) that glucagon at high concentration is capable of stimulating lipolysis and ketogenesis in insulin-deficient diabetic man; (b) that insulin, mole for mole, has more antilipolytic activity in man than glucagon has lipolytic activity; and (c) that glucagon, on a molar basis, has greater stimulatory activity than insulin has inhibitory activity on hepatic glucose release.

Transient stimulatory effect of sustained hyperglucagonemia on splanchnic glucose production in normal and diabetic man.

Insulin can modulate glucagon-stimulated hepatic glucose production and is considered to be the major factor acting in vivo to exert a couterregulatory action to glucagon. The insulin-dependent diabetic, therefore, might be especially vulnerable to enhanced hepatic glucose production promoted by glucagon. To investigate this hypothesis, low-dose glucagon infusions were administered to normal and diabetic men to compare the effects of glucagon on net splanchnic glucose production (NSGP). Four normal and three insulin-dependent, ketosis-prone, hyperglycemic diabetic men (insulin withheld for 24 hours) underwent brachial-artery-hepatic-vein catheterization. Each received a 90-minute glucagon infusion at 5 ng/kg./min. Glucagon levels rose four-to-fivefold in both groups, plateauing at 300-600 pg./ml. In the normals, NSGP rose from 92+/-12 to 211+/-31 mg./min. at 15 minutes and returned to basal levels by 45 minutes. Insulin measured in the hepatic vein rose from 19+/-6 to 33+/-11 muU/.ml., while plasma glucose rose 17 mg./dl. In the insulin-dependent diabetics, NSGP rose from 78+/-24 to a peak of 221+/-33 mg./min. at 30 minutes and then fell sharply to 113+/-15 mg./min. at 60 minutes despite continuing hyperglucagonemia. Plasma glucose in the diabetics rose 21 mg./dl. These data suggest a mechanism that acts to rapidly diminish glucagon-induced hepatic glucose production in diabetic man but does not appear to be mediated by increased insulin secretion.

Diuretic regimens in essential hypertension. A comparison of hypokalemic effects, BP control, and cost.

Intolerable side effects and hypokalemia during thiazide treatment of hypertension frequently necessitate a change in diuretic regimen. The hypokalemic effects, effectiveness in controlling BP, and cost of several alternate diuretic regimens were evaluated. Prevalences of serum K+ values less than 3.5 mEq/L were as follows for the various regimens: hydrochlorothiazide, 50 mg daily, 11.0% (n = 500); chlorthalidone, 25 mg daily, 8.1% (n = 37); triamterene, 100 mg, plus hydrochlorothiazide, 50 mg daily, 5.3% (n = 357); hydrochlorothiazide, 25 mg daily, 2.2% (n = 183); and furosemide, 40 mg daily, 3.5% (n = 284). In paired studies comparing hydrochlorothiazide with alternate diuretic regimens, potassium conservation was comparable with furosemide, the triamterene/hydrochlorothiazide combination, the spironolactone/hydrochlorothiazide combination, and adding potassium, 37 mEq daily. All alternate diuretic regimens were as effective as hydrochlorothiazide in controlling BP. Furosemide reduced serum glucose and calcium levels compared with hydrochlorothiazide. When these factors and costs are considered, furosemide appears to be the most cost-effective alternative in patients with hypertension in whom intolerable side effects or hypokalemia develops while taking hydrochlorothiazide.

Urinary estriols: are they of value in normoglycemic diabetic pregnancy?

The purpose of the study was to assess the value of 24-h urinary estriols in the management of diabetic pregnancies. Twenty-seven pregnant diabetic patients (White's class B through R) received insulin dosages twice daily as a combination of NPH and regular insulin. Laboratory and home monitored blood glucose was maintained within the range of 70-150 mg/dl. From 32 wk onward daily 24-h urinary estriols, weekly fetal heart rate monitoring, and, when indicated, amniotic fluid lecithin/sphingomyelin ratio were used to evaluate fetal well-being. Fetal heart rate and amniotic fluid testing were of value while urinary estriols failed to be useful in management or timing of delivery. We conclude that when third-trimester normoglycemia is maintained in pregnant diabetic patients, one obviates the need for the costly and odious task of daily urine estriol measurements.

Acute tolbutamide administration alone or combined with insulin enhances glucose uptake in the perfused rat hindlimb.

We examined the effects of acute administration of tolbutamide on glucose uptake in the non-cyclically perfused rat hindlimb. During the hour of study, 500 microunits boluses of insulin were given every ten min in the presence or absence of 3 X 10(-3)M tolbutamide. Tolbutamide by itself increased glucose uptake; however at no time was this increase significantly different from that seen in the group which received insulin alone. After 42 min of perfusion, the insulin-stimulated uptake was 26% and the tolbutamide was 20% greater than control (1.90 +/- 0.08, 1.80 +/- 0.06, and 1.50 +/- 0.05 mumol/min/100 g respectively). After 20 min of perfusion, the increase in glucose uptake seen with the combination of insulin + tolbutamide was significantly greater than that obtained with either tolbutamide or insulin alone. At the termination of perfusion, the glucose uptake with the combined treatment was 59% greater than control, 35% greater than tolbutamide, and 19% greater than insulin alone (2.67 +/- 0.10, vrs. 1.68 +/- 0.07 vrs. 1.97 +/- 0.07 vrs. 2.16 +/- 0.07 mumol/min/100 g). These results demonstrate not only a direct effect of tolbutamide, but also a potentiation of insulin-stimulated glucose uptake in the rat hindlimb. Therefore, tolbutamide has extra-pancreatic effects which probably contribute to the hypoglycemic action of this sulfonylurea.

Dose-related influence of indomethacin on parathyroid hormone-stimulated adenosine 3',5'-monophosphate release from the perfused rat hindlimb.

We examined the effect of indomethacin (INDO) on PTH-stimulated cAMP release from the perfused rat hindlimb. Since this preparation has not been used previously to study the effects of PTH, we first determined the dose-response curve for cAMP release in response to the 1-34 fragment of synthetic bovine PTH. cAMP release peaked 3-6 min after the PTH bolus and declined gradually toward baseline, even with sustained PTH infusion. The rate of cAMP release was directly related to the PTH dose. The lowest PTH priming dose that provoked a significant increase in cAMP release was 0.6 IU. Maximal cAMP release, occurring in response to a PTH priming dose of 30 IU, was 3- to 4-fold greater than baseline. PTH caused no increase in cAMP release from or the cAMP content of isolated skeletal muscle in vitro, suggesting that cAMP released from the hindlimb in response to PTH is derived solely from bone. PTH-stimulated cAMP release was unaltered by pretreatment of the intact rat with 2 mg/kg INDO, a dose that blocks prostaglandin synthesis. In contrast, PTH-stimulated cAMP release was significantly attenuated by pretreatment with 75 mg/kg INDO. The effect was not dependent on the addition of drug to the perfusate and was not altered by thyroparathyroidectomy at the time of INDO administration. We conclude that 1) the perfused rat hindlimb can be used to examine PTH effects on bone; 2) 2 mg/kg INDO has no effect on PTH-stimulated cAMP release from the perfused rat hindlimb; and 3) INDO in high doses blunts PTH activation of adenylate cyclase.

Insulin-glucagon interaction in controlling splanchnic glucose production in normal man.

The interaction of glucagon and insulin in controlling hepatic glucose production in man has been inferred from studies of immunoreactive glucagon and insulin. This study directly examines the interaction of glucagon and insulin in controlling net splanching glucose production (NSGP) in eight normal men. Glucagon was infused iv at 5 ng/kg/min for 15 min and resultant arterial glucagon levels (1.3 X 10(-10) M) did not exceed the physiologic portal range. In four normal men NSGP increased 2.3-fold by 5 min and remained elevated for 15 min. There was no change in arterial insulin concentration. To study the effect of exogenous insulin on this glucagon-induced increase in NSGP, insulin was infused at 10 mU/kg/min in four normal men to achieve arterial immunoreactive insulin concentrations of 1500 muU/ml (1 X 10(-8) M). Blood glucose was stabilized by glucose infusions. During insulin and glucose administration, NSGP was suppressed and net splanchnic glucose uptake occurred. After 40 min of insulin and glucose pretreatment, a 5 ng/kg/min glucagon infusion resulted in no increase in NSGP (arterial insulin: glucagon molar ratio of approximately 100). In two subjects the glucagon infusion rate was then increased to 15 ng/kg/min (arterial insulin: glucagon molar ratio of approximately 33), resulting in stimulation of NSGP. These studies provide evidence that insulin in high concentration can suppress glucagon-stimulated NSGP in normal man.

Effect of diet composition on metabolic adaptations to hypocaloric nutrition: comparison of high carbohydrate and high fat isocaloric diets.

The metabolic consequences of two hypocaloric diets were assessed in 10 obese men. The study, performed on a metabolic ward, compared the response of these men to two cholesterol-free liquid formula diets of differing composition (10 kcal/kg per day, 70% carbohydrate, 20% protein, 10% fat versus 70% fat, 20% protein, 10% carbohydrate) but identical in calories. These were administered for 14 days in a random order and each diet was preceded by a 7-day control weight maintenance diet (30 kcal/kg per day, 40% carbohydrate, 20% protein, 40% fat). The low calorie diets were well tolerated by the men and effected similar losses of nonaqueous body weight. Fasting glucose and insulin decreased significantly in these men after they ingested either weight loss diet for 14 days, but the change in each parameter was greater for high fat as compared to high carbohydrate (15% versus 7% and 67% versus 35%, respectively, P less than 0.01). In contrast, fasting glucagon concentration decreased in these subjects to a greater extent in response to the high carbohydrate diet (35% versus 16%, P less than 0.01). This adaptive response thus resulted in a 50% fall in insulin:glucagon molar ratio for high fat and no change for high carbohydrate weight loss. Despite these hormonal alterations no change in glucose tolerance was observed. Fasting serum triglyceride and cholesterol levels declined in these subjects to a greater extent following the high fat compared to the high carbohydrate regimen (45% versus 28%, P less than 0.01 and 8% versus 3%, not significant, respectively). These changes reflected decrements in very low density lipoproteins alone. Despite similar increments in free fatty acid levels, (350% versus 270%, not significant) serum ketone body (beta-hydroxybutyrate and acetoacetate) concentrations increased 7-fold on the high fat diet compared to the high carbohydrate diet, P less than 0.001. The hyperketonemia of these men in response to the high fat, low calorie diet suggested the occurrence of a shift in hepatic free fatty acid metabolism toward ketogenesis rather than triglyceride synthesis. The associated decrease in the insulin: glucagon molar ratio raised the question of a possible role for these hormones in the adaptation.

Endocrine and metabolic alterations with food and water deprivation.

Two healthy men were evaluated before and after a 56-day raft voyage to determine endocrine and metabolic status immediately after and during the recovery phase after long-term caloric, protein, and water deprivation. Daily intake during the trip consisted of no protein, 300 ml water, and for the first 40 days, 300 kcal glucose. The subjects lost weight from 84.1 to 58.1 and 78.3 to 57.7 kg, respectively. Significant variations included: 1) decreased excretion and loss of diurnal pattern of 17-hydroxycorticoids with normal serum corticoid levels and variation; 2) decreased serum testosterone levels and concomitant low follicle stimulating hormone and low normal luteinizing hormone levels; 3) decreased urinary 17-ketosteroid levels; 4) low plasma insulin levels with normal serum glucose concentrations; 5) increased triglyceride content in the 1.006 less than d less than 1.063 lipoproteins during fasting with a marked increase in high density lipoprotein cholesterol upon refeeding. The percent content of the R-serine (C-I) apoprotein among the soluble apoproteins of very low density lipoproteins diminished markedly during the fast; 6) abnormal liver function immediately after fasting with increased abnormality after the 2 weeks of refeeding and return to normal by 6 weeks; 7) normal fat and xylose absorption, normal estradiol, estrone and prolactin levels, and renal function studies.

Effect of sulfonylurea therapy and plasma glucose levels on hemoglobin A1c in type II diabetes mellitus.

It is well known that hemoglobin A1c reflects plasma glucose concentrations in patients with diabetes mellitus. To examine hemoglobin A1c and plasma glucose relationships in sulfonylurea-treated patients, 25 patients with well-controlled type II diabetes (fasting plasma glucose 128 +/- 6 mg/dl, hemoglobin A1c 7.6 +/- 0.5 percent) were evaluated in a double-blind study. This study was divided into two phases (periods I and II). During period I each patient was given a diet plus a placebo and was followed every two weeks until the mean of two consecutive plasma glucose determinations was more than 50 mg/dl above the initial plasma glucose concentration obtained while the patient was taking sulfonylurea. At that point each patient was switched in a double-blind fashion to either diet plus a placebo or diet plus tolazamide. Fasting plasma glucose concentrations increased to 178 +/- 9 mg/dl (p less than 0.005) for all patients by week 2 of period I. The increase in hemoglobin A1c concentration was seen to lag behind the increasing fasting plasma glucose concentration by four to six weeks. Fasting plasma glucose and hemoglobin A1c concentrations returned to values indistinguishable from initial values in patients who were given tolazamide and who responded to it. A positive correlation was noted when the hemoglobin A1c concentration was compared with the fasting plasma glucose concentration measured four to six weeks previously.

A head impact model of early axonal injury in the sheep.

Axonal injury (AI), one of the principal determinants of clinical outcome after head injury, may evolve over several hours after injury, raising the future possibility of therapeutic intervention during this period. A new head impact model of AI in sheep was developed to examine pathological and physiological changes in the brain resulting from a graded traumatic insult. In this preliminary study 10 anesthetized and ventilated Merino ewes were used. Head injury was produced by impact from a humane stunner to the temporal region of an unrestrained head. Eight sheep were studied for 1, 2, 4, or 6 h after impact. Two sham animals (no impact, 6 h survival) were also examined. Arterial blood pressure, intracranial pressure, and cerebral blood flow were monitored continuously. A physiological index of injury severity was calculated by weighting the percentage shift from preinjury values for each monitored parameter over the first hour after injury. Immunostaining with amyloid precursor protein (APP) was used as a marker of axonal damage and the distribution of APP positive axons was recorded according to a sector scoring method (APPS). Widespread AI was identified in 7 of the 8 impacted animals, around cerebral contusions and in hemispheric white matter, central gray matter, brain stem, and cerebellum, and was detected as early as 1 h after injury. The degree of axonal injury (APPS) correlated well with an index of physiological response to injury (r = 0.83, p = 0.005).

Effects of pharmacologic hyperglucagonemia on plasma amino acid concentrations in normal and diabetic man.

Four normal and five insulin dependent diabetic men received a 2 h pharmacologic glucagon infusion (50 ng/kg/min) resulting in plasma glucagon levels (4400 pg/ml) similar to those seen in glucagonoma patients. In normal subjects in whom plasma insulin concentrations rose significantly (239 uU/ml) and the blood level of 15 of the 18 amino acids measured fell significantly. In contrast, in the diabetic men who secreted no insulin in response to glucagon (no rise in C-peptide levels), only 10 of 18 amino acid levels fell significantly. The branched chain amino acids valine, leucine and isoleucine, as well as tyrosine and phenylalanine were among the 8 amino acids which showed no change in response to glucagon in the diabetics. Thus, glucagon appears to have no acute affect on branched chain amino acid levels in man.

Hemoglobin A1 correlates with the ratio of low-to high-density-lipoprotein cholesterol in normal weight type II diabetics.

Because cardiovascular risk correlates with serum low density lipoprotein (LDL) cholesterol and is inverse with high density lipoprotein (HDL) cholesterol, the LDL-HDL cholesterol ratio has been advocated as a sensitive index of relative cardiovascular risk. In 50 normal weight insulin-treated Type II diabetic subjects, mean LDL-HDL ratios were significantly higher than for controls. In diabetic women, the LDL-HDL cholesterol ratio correlated with hemoglobin A1 better than any of the lipids or lipoprotein cholesterol fractions. When 8 poorly controlled diabetics were treated with insulin, the LDL-HDL ratio changed more significantly than did its component fractions, and the fall in LDL-HDL ratio paralleled the fall in hemoglobin A1.

Insulin therapy for gestational diabetes.

Seventy-two patient with gestational diabetes were randomly treated with insulin (20 units NPH and 10 units regular) and diabetic diet, diet alone, or neither. Of the 27 patients treated with insulin and diet, 2 (7%) had babies weighing more than 8 1/2 pounds. Of the 11 patients treated with diet alone, 4 (36.4%) had babies weighing more than 8 1/2 pounds. Of the 34 patients treated with neither diet nor insulin, 17 (50%) had babies weighing more than 8 1/2 pounds. These data support the hypothesis that treatment of the gestational diabetic with insulin will reduce the incidence of fetal macrosomia.

Radio frequency (13.56 MHz) energy enhances recovery from mild hypothermia.

The rate of warming after hypothermia depends on the method of rewarming. This study compared the effectiveness of radio frequency (RF) energy against hot (41 degrees C) water immersion (HW) and an insulated cocoon (IC) for rewarming hypothermic men. Six men fasted overnight and were rewarmed for 1 h after attaining a 0.5 degree C reduction in rectal temperature (Tre). Tre and esophageal (Tes) temperature were recorded every 5 min with nonmetallic thermal probes. The base-line value for Tre and Tes just before rewarming was subtracted from each 5 min Tre and Tes during rewarming to give delta Tre and delta Tes. The 12 delta Tes values were averaged for each individual and were compared using analysis of variance. The average delta Tes for RF (1.15 +/- 0.22 degrees C/h) was faster (P less than 0.001) than either IC (0.37 +/- 0.16 degrees C/h) or HW (0.18 +/- 0.09 degree C/h). The present study shows the superiority of RF energy for rewarming mildly hypothermic men.

Adrenergic responses to cognitive activity in a cold environment.

Adrenergic responses during physical stress such as cold exposure have been reported to differ from those responses observed during cognitive activity. Both the separate and the combined effects of cold and cognitive activity on catecholamine activity were examined in six male subjects. Alterations in plasma epinephrine and norepinephrine showed different patterns as a function of exposure to a 4 degrees C cold environment, a cognitive performance assessment battery (PAB), and the two conditions combined. Plasma epinephrine was not altered by exposure to cold and only slightly increased by PAB performance when given at 23 degrees C. However, epinephrine was substantially elevated by exposure to combined cold and PAB. Heart rate changes paralleled observed changes in epinephrine. Norepinephrine release was predominantly increased by cold exposure and was not altered by PAB performance.

Improved glucose control in nonhospitalized pregnant diabetic patients.

Methods for management of diabetic pregnancy in the outpatient setting require strict glucose control. To assess the effect of diet and injection of short and intermediate acting insulin on glucose, diabetic patients tested their urine daily for glucose and had biweekly serum glucose tests. A brief metabolic ward study in 9 diabetic patients during the third trimester yielded hourly glucose determinations. These results defined the range of serum glucose over a 24-hour period. Glucose data on 6 normal third trimester women also came from hourly glucose values. Glucose results of normal and diabetic subjects were similar. A 16th subject with diabetic eye, renal, and foot complications is included as a case report to illustrate management technics. Infants of the diabetic women had no perinatal mortality, morbidity, or macrosomia and thus differ from an earlier study where glucose was not strictly controlled. The data suggest hospitalization can be short and low perinatal morbidity and mortality are possible with this outpatient method of management of the pregnant diabetic patient.

Serum lipid changes after estrogen therapy in prostatic carcinoma.

A study of serum lipid fraction changes in 15 estrogen-treated patients with carcinoma of the prostate is conducted. Estrogen therapy is known to be associated with cardiovascular complications. certain serum lipid fraction changes, particularly elevated low-density lipoprotein (LDL) and decreased high-density lipoprotein (HDL), are known to increase the risk of cardiovascular diseases. In our study, decrease in total cholesterol, increase in triglycerides, decreased LDL, and LDL/HDL ratio in combination with elevated HDL fraction suggest that the lipid changes are not the mediators of above complications.