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Today, intensified conventional insulin therapy (ICT) is the standard treatment for type 1 diabetes, but patients with type 2 diabetes younger than 70 also profit it. Within an international framework too, the DCCT study has confirmed the usefulness of intensified insulin therapy. Factors that have a decisive influence on the success of such treatment are the choice of a suitable insulin, its dose, site of injection, and prandial adaptation. The various possibilities of carrying out ICT are discussed.

In 12 healthy volunteers the gastro-duodenal damaging effects of Ossiplex retard tid, Mono-Tridin tid and Ossin bid were investigated in a randomised, single blind cross-over study. Prior to the start of the three therapeutic phases subjects underwent endoscopic examination to exclude gastro-duodenal mucosa lesions. On day 14 of therapy 2 hours after the application of the last fluoride dose subjects underwent endoscopy again. The 14 days administration of Ossiplex retard, Mono-Tridin und Ossin led to gastro-duodenal mucosa lesion scores of 0.42 +/- 0.26; 1.50 +/- 0.54 and 2.08 +/- 0.71 (mean +/- SEM) respectively. These differences were statistically significant when comparing Ossiplex retard vs Ossin (p less than 0.05), but not Ossiplex retard vs Mono-Tridin. Regarding the number and the severity of lesions the differences between the gastro-duodenal mucosa damaging potency of the three fluoride preparations were also evident. With Ossiplex retard only in three subjects petechiae (n = 1) and antral erythemas (n = 2) were observed. Under Mono-Tridin and Ossin, however, a higher grade of lesions i.e. erosions and an ulcer were seen endoscopically. This study shows that the slow release fluoride preparation Ossiplex retard demonstrates a lower gastro-duodenal mucosa damaging potency when compared to the other fluorides Ossin and Mono-Tridin. There was no relationship between serum fluoride concentrations and the grade of gastro-duodenal mucosa lesions.

In a crossover design in random order 12 healthy male volunteers were given either beta-acetyldigoxin (Novodigal, CAS 5511-98-8) tablets, oral solution or i.v. application at a digoxin equivalent dose of 0.284 mg. To reach steady state each preparation was given for 10 days on a once-daily schedule. On days 8, 9 and 10 of each observation period blood was sampled to determine trough concentrations of digoxin in steady state. In addition, on day 10 blood was collected repeatedly at appropriate time intervals and urine was sampled concomitantly for 24 h. Trough values during steady state and 24 h AUC were used to calculate digoxin bioavailability for tablets and oral solution. From trough values, the mean bioavailability for beta-acetyldigoxin tablets was 91.2% (range 73.1-118.1) and for solution 93.8% (range 65.7-114.8). Using the AUCs 0-24 h at steady state bioavailability was calculated 77.7% for the tablets and 84.5% for the solution. Since trough values in steady state represent the body burden of digoxin which is supposed responsible for the therapeutic effect, trough values should be given priority for the determination of digoxin bioavailability from beta-acetyldigoxin tablets and solution. All formulations were well tolerated. No clinically relevant side effects were observed.

Forms of coping with diabetes were determined on the basis of self-ratings of emotions (depressive, sad, angry, anxious) and responses on a 30-item "stages of grief" questionnaire by 52 inpatients aged between 25 and 50 (diabetes duration 1 to 35 years) at the beginning of a 12 day diabetes education program. Psychometric qualities of the instruments were evaluated. To test empirically the notion of grief stages in coping with diabetes, the frequency of emphasis on one or more emotional areas or stages of grief was determined and tested to ascertain whether various conditions occurred more frequently than was expected by chance. Results indicated that shortly after diabetes manifestation scores on protest and depression with respect to diabetes were elevated. The majority of cases could not be assigned to a single emotion or stage of grief but displayed negative emotional reactions in different content areas simultaneously. Consequently the concept of grief stages for coping with diabetes as well as recommendations based on this concept are questioned.

Acid Suppression Profile of Hydrotalcite in Man. In this randomized, double blind, placebo-controlled cross-over study, the effect of hydrotalcite (CAS 12304-65-3, Talcid), 2 tablets qid (neutralizing capacity 122 mmol) on intragastric 24-h acidity was investigated. 12 healthy male and female volunteers were administered hydrotalcite, 2 tablets qid, or placebo on 2 study days, in each case at 10, 15, 20 and 23 h. Daytime (8-22 h) and nighttime (23-7 h) intragastric H+ concentrations (mmol/l) were significantly reduced by hydrotalcite compared with placebo. The following inhibiton rates were obtained: daytime 37.4%, nighttime 31.5% (p less than 0.05). During the 2-h periods immediately after oral application of hydrotalcite or placebo inhibition rates of up to 65% were observed. These results suggest that hydrotalcite may have also antiulcer activity like other antacids which are used in the treatment of peptic ulcer disease in low daily neutralizing capacities (120-280 mmol/die).

In this open controlled clinical trial the lipid-lowering effect, the tolerance and clinical safety of the new hydrophilic HMG-CoA reductase inhibitor pravastatin and cholestyramine were compared in the treatment of 45 patients with primary hypercholesterolaemia over a period of 16 weeks. Following a dietary lead-in of six weeks, patients were randomized at a ratio of 3:2 to receive either pravastatin 10 mg b.i.d. or cholestyramine 8 g b.i.d. The dose of pravastatin was increased to 40 mg per day after eight weeks of treatment and after 16 weeks cholestyramine 8 g b.i.d. was added. Two thirds of the patients in the cholestyramine group were switched to gemfibrocil 900 mg. At the end of the 48 week treatment period the mean reduction rates of total cholesterol, LDL-cholesterol and triglycerides for the pravastatin combination compared to cholestyramine (in brackets values for gemfibrocil) were -30, -35 and -17% versus -17 (-19), -25 (-22) and +27 (-24)%. Pravastatin lead to an increase of the HDL concentration of approximately 8%, gemfibrocil to approximately 13%, whilst cholestyramine alone did not change this lipid fraction. The reduction of total cholesterol and LDL-cholesterol was associated with a decrease in the apolipoprotein B concentration. However, the apolipoprotein AI and AII levels remained unchanged. Due to the absence of clinically relevant side effects and laboratory abnormalities coupled with the excellent compliance in this study, pravastatin proved to be a convincing therapeutic alternative to cholestyramine and gemfibrocil. The combination therapy of pravastatin and cholestyramine offers a potentially highly efficacious and safe therapeutic regimen for the future.

In a prospective study, 100 patients who underwent general surgical or urological operations under spinal anesthesia were examined to determine whether there was a relation between the anesthesia and postoperative hearing loss. Audiograms were performed preoperatively and as the 1st, 2nd, 3rd, and 5th postoperative days. It was found that 16 patients had impairment of hearing. The average ages of these patients were similar to those of the total population. The hearing loss was typical: only the frequencies between 125 and 2000 Hz were affected. It began on the 2nd day after spinal anesthesia and disappeared within 3 days without special therapy. The cause of this typical hearing loss after spinal anesthesia is a drop in cerebrospinal fluid pressure transmitted to the perilymph via the cochlear aqueduct. The change in the endoperilymphatic pressure difference results in a change in the oscillation of the basilar membrane. Because 16% of patients may suffer hearing loss after spinal anesthesia, it seems reasonable from a medicolegal point of view to explain the possibility of defective hearing to the patient.

In a large percentage of cases, diabetes mellitus leads to hyperlipidemia. In addition to the diabetes-related secondary hyperlipidemias, all types of primary disturbances of lipid metabolism can also be observed in diabetics. Depending upon the degree of severity and type of metabolic disorder presenting, not only suitable dietetic treatment, but also the various lipid-lowering drugs, fibrates, nicotinic acid, probucol, cholestyramine and the HMG-CoA reductase inhibitors should be introduced into therapy. As in all groups with an elevated coronary risk, strict management of the lipid levels is mandatory in diabetics, too.

12 healthy volunteers participated in this single-blind, randomized, cross-over study. All subjects were given Piroxicam 20 mg mane on three different 14 days treatment periods in the presense of Nizatidine 150 or 300 mg bid and placebo respectively. Only subjects without endoscopically revealed gastroduodenal lesions were enrolled into the study. Endoscopy was repeated at day 14 of therapy. Between treatment periods a 2 weeks wash out phase was interposed. The gastroduodenal lesion score was the following: score 0 = no injury, score 1 = erythema, score 2 = less than or equal to 9 lesions, score 3 = greater than or equal to 10 lesions (petechiae/erosions), score 4 = ulcer. The mean lesion score with Piroxicam averaged 1.5 +/- 0.35 (+/- SEM) when placebo was coadministered. The mucosal lesion scores were reduced to 0.17 +/- 0.08 and 0.42 +/- 0.19 (+/- SEM) when Nizatidine 150 or 300 mg bid was given concurrently. This protection afforded by Nizatidine was significant when compared with placebo (p less than 0.01). The difference between the two Nizatidine doses, however, did not reach statistical significance. Our data suggest that Nizatidine markedly improves the gastroduodenal tolerability of Piroxicam.

At the Radiological Hospital of the Heidelberg University, one patient with a local recurrence of an esthesioneuroblastoma situated on the left-hand side of the skull base was treated between February 11 and March 18, 1986, by an afterloading contact therapy with curative intent. After preceding surgery and percutaneous radiotherapy, repeated local recurrences and locoregional lymph node metastases had occurred. The contact therapy was performed after adjusting an individual face mask in which the afterloading probe was placed and brought into its position in the tumor region. The irradiation scheme was based on the transformation of the source coordinates form the stereoscopic X-ray localization system into the coordinate system of the computed tomogram by means of X-ray tight reference points. The irradiation planning by computed tomography allows to optimize the arrangement of sources within the tumor region. The principles of the method as well as the treatment result are presented.

In a randomized, double-blind, placebo-controlled, comparative cross-over study, we studied the effect of four H2-receptor antagonists on intragastric 24-hour acidity, nocturnal volume and acid output. Ten healthy male volunteers were administered 300 mg or 150 mg nizatidine, 800 mg cimetidine, 300 mg ranitidine, 40 mg famotidine, or placebo on several days, in each case at 9:000 PM. Nocturnal intragastric H+ concentration (mmol/l) (11:00 PM to 7:00 AM) was significantly reduced by all H2 blockers compared with placebo. We obtained the following inhibition rates: Cimetidine 67%; ranitidine 95%; famotidine 89%; nizatidine 80% (300 mg) and 69% (150 mg). Nocturnal acid (mmol/l) and volume output (ml/h) were also significantly (compared with placebo) inhibited by all four H2-receptor antagonists. Inhibition of nocturnal acid secretion was almost identical on nizatidine 300 mg nocte, ranitidine 300 mg nocte, famotidine 40 mg nocte, and cimetidine 800 mg nocte. Nizatidine 300 mg nocte and 150 mg nocte exclusively reduced acid secretion at night, without an aftereffect into the following day (8:00 AM to 6:00 PM). These results suggest that the clinical efficacy of these H2-receptor antagonists is identical with respect to healing peptic ulcer disease and providing freedom from pain. It is generally accepted today that gastric acid inhibitors used in the treatment of peptic ulcer disease should interfere with daytime gastric acid secretion as little as possible, particularly since the acid protects the stomach from bacteria ingested with the food during the day.

Urocanic acid was measured by means of high-performance liquid chromatography (HPLC) in the stratum corneum of a 3.5-year-old child suffering from hidroa vacciniformia. Compared to ten healthy children of equal age, the urocanic acid content of the stratum corneum was reduced significantly. In addition, there was an elevated level of some amino acids in the urine, particularly that of histidine and methylhistidine, which seems to be a very important finding. Urocanic acid acts as a natural sun protective agent, and the results are discussed with this in mind. It was not possible to elicit hidroa vacciniformia lesions in the patient by UV-A, as described by others.

Tumor growth in a 72-year-old male patient with malignant haemangiopericytoma in the left hemithorax could be followed radiologically for 4 years before symptoms of recurrent hypoglycaemia appeared. The endogenous insulin level in serum was maximally and serum IGF-1 and IGF-2 markedly reduced. An intravenous arginine load test showed a normal stimulation capacity of the pancreatic glucagon secretion but not that of insulin. After resection of the tumor, blood sugar metabolism was completely normalised. The insulin level, IGF-1 and IGF-2 in serum returned to normal.

Today histamine-H2-receptor antagonists are the most intensively investigated drugs in the therapy of acid related diseases. They are characterized by a clear mechanism of action, a convenient application form, a high tolerability, a low incidence of side effects, and a large therapeutic window. The single nocturnal dosage regimen of H2-blockers follows the concept to reduce substantially night time acidity only, which is believed to play a decisive pathogenetic role in peptic ulcer disease, while during day time physiological acid secretion remains unaffected. The clinical efficacy of this application form has been well documented in the healing and symptomatic relief of acute peptic ulcers. However, about 30% of patients still suffer from ulcer pain after a 2 weeks treatment period. A more flexible dosage regimen, which is more adapted to the ulcer symptoms of the patient will probably lead to even better clinical results.

The chemical structure of etintidine differs from that of cimetidine by the addition of an ethinyl group to the terminal methyl group of the side chain. We investigated the influence of etintidine 300 or 400 mg b.d. and of etintidine 300 or 600 mg nocte, cimetidine 800 mg nocte versus placebo in two different double-blind randomized cross-over studies on 24-h intragastric acidity and nocturnal volume and acid secretion (12:00 midnight to 6:00 a.m.) in 12 and 8 healthy male volunteers, respectively. 5-10 ml of gastric contents were aspirated hourly via a nasogastric tube. The pH of the samples was determined using a glass electrode. The results were expressed in terms of H+-activity (mmol/l). Etintidine 300 or 400 mg b.d. reduced day- and nighttime acidity by 53 and 60% or 41 and 41%, respectively. Nocturnal acid secretion (mmol/l) was inhibited by 38 and 42%, resp. Etintidine 300 or 600 mg nocte and cimetidine 800 mg nocte (9:00 p.m.) lowered nocturnal intragastric acidity by 69, 84 and 79%, resp. Daytime inhibition was not observed. Our results suggest, that 1. etintidine 300 and 400 mg b.d. are equipotent in promoting peptic ulcer healing and 2. that this new imidazole H2-receptor antagonist is also effective in a single bedtime dose.

A multicenter, double-blind, randomized controlled study was conducted in 314 duodenal ulcer patients to compare the efficacy and safety of the antimuscarinics telenzepine and pirenzepine in the treatment of duodenal ulcer. Patients received telenzepine 3 mg (156) once-daily at bedtime or 50 mg pirenzepine (158) two times daily for 2 weeks. If ulcerous lesions persisted treatment was extended to 4 weeks. Efficacy was assessed by relief of ulcer pain and endoscopic findings of ulcer healing. Safety was determined on the basis of side effects and results of laboratory tests. The 2- and 4-week healing rates achieved with telenzepine were 21.1 and 67.3%, respectively, and with pirenzepine they were 20.0 an 69.0%, respectively; the differences in healing rates for the two drugs were not statistically significant. Similarly both drugs provided satisfactory relief of pain. The incidence of untoward effects was 24.5% with telenzepine and 29.7% with pirenzepine, dryness of mouth being most prominent (20.4 vs. 19.3%). With telenzepine blurred vision was reported in a significantly lower rate compared to pirenzepine (0.7 vs. 4.2%, p less than 0.05). Clinically relevant abnormal laboratory tests were not observed. The present study shows for the first time that the newly developed antimuscarinic drug telenzepine is in a single nocturnal dosage regimen (3 mg nocte) as effective as pirenzepine (50 mg bid) in the treatment of duodenal ulcer.

A study of 27 patients (18 males and 9 females; median age 57 [35-70] years) with hypercholesterolaemia examined the lipid-reducing effect, clinical reliability and tolerance of lovastatin, an HMG-CoA-reductase inhibitor, given in a single evening dose. After a four-week period on placebo and a lipid-reducing diet the patients received 20 mg lovastatin for four weeks. If, at the end of this period, total cholesterol levels were still above 200 mg/dl, the dose was increased to 40 mg, after a further four weeks to 80 mg. After a three-month treatment period total cholesterol concentration in lovastatin-treated patients was 28% lower than in the placebo group (289.4 +/- 42.2 vs 208.0 +/- 39.9 mg/dl; P less than 0.0001). LDL-cholesterol concentration had fallen by 40% (215.1 +/- 44.4 vs 130.1 +/- 24.7 mg/dl; P less than 0.0001), while plasma triglyceride concentrations had fallen by 15% (166.3 +/- 71.8 vs 141.8 +/- 69.8 mg/dl; P less than 0.01). At the same time, HDL-cholesterol levels had risen by 12% (42.9 +/- 12.4 vs 47.9 +/- 18.2 mg/dl; P less than 0.01). These results confirm the marked lipid-reducing effect of lovastatin.

In a 41-year-old patient administration of 5 g parathion led to respiratory failure and unconsciousness. Ventilatory support and antidote therapy were initiated early. However, only extensive gastric lavage and lowering of the plasma concentration by hemoperfusion with activated carbon resulted in the crucial elimination of the poison. Antidote and supportive measures may overcome the hazards of cholinesterase-inhibition, but not the direct toxic effect on the cardiovascular system which is currently regarded as the predominant cause of death.