[Coma in myxedema--a rare complication of hypothyroidism. Possible iatrogenic factors should be taken into account]. / Myxödem-Koma--eine seltene Komplikation der Hypothyreose. Mögliche iatrogene Auslösefaktoren beachten.

Myxedema coma is the most severe form of hypothyroidism and is characterized by extreme hypothermia, bradycardia, central hypoventilation and hypoxia. Common causes are intercurrent diseases, interruption of thyroid hormone treatment, or an overdose of sleeping pills or sedatives. The diagnosis is usually readily established on the basis of very high serum TSH and low T4 levels. Consideration must also be given to an extra-thyroidal influence on the hormone levels. Intensive care treatment involving intravenous high-dose L-thyroxine and the reversal of hypoxia improve the prognosis of the serious disease.

[Risk of hyperthyroidism in examinations with contrast media]. / Hyperthyreoserisiko bei Kontrastmitteluntersuchungen.

Investigations with contrast media inevitably lead to the patient being exposed to large amounts of iodine. Under certain preconditions this gentails danger for the patient by causing either iodine-induced hyperthyroidism, which is difficult to treat, or even a thyrotoxic crisis. Patients with normal thyroid function and size have only minute changes of thyroid hormones and TSH within the normal range and are not at risk. Patients with unknown hyperthyroidism--independent of the etiological form--and patients with functional autonomy are at risk of exacerbation of pre-existing hyperthyroidism or development of iodine-induced hyperthyroidism. This development depends on two factors: a) the volume of autonomous tissue and b) the quantity of iodine exposure. Besides contrast media, other sources of iodine excess are possible, such as iodine-containing disinfectants, secretolytic agents, antiarrhythmics like amiodarone, eye drops and ointments, geriatrics, skin ointments, toothpaste etc. The development of hyperthyroidism can be prevented by combined treatment with antithyroid drugs and perchlorate in the case of preexisting hyperthyroidism or the urgent clinical suspicion of thyrotoxicosis or with perchlorate alone, when the patients is euthyroid and does not have a large nodular goitre.

[Hypocalcemic crisis. Hypoparathyroidism--non-parathyroid origin--the most frequent form: hyperventilation syndrome]. / Hypokalzämische Krise. Hypoparathyreoidismus - nichtparathyreogene Herkunft - häufigste Form: Hyperventilationssyndrom.

Hypocalcemic crisis presents with the classical symptomatology of tetany plus extrapyramidal symptoms and a disordering of consciousness extending even to coma. It develops when the concentration of ionized serum calcium declines rapidly, and is very rarely found in chronic hypocalcemia. In terms of its etiology, various forms of parathyroid deficiency, and nonparathyrogenic diseases associated with hypocalcemia may be involved. Since in the latter the concentration of albumin is also diminished, and thus ionized calcium decreases to only a small extent, hypocalcemic crisis in these conditions is rare. The most common clinical form is normocalcemic tetany that occurs within the framework of the hyperventilation syndrome. Here, the ionized calcium fraction is temporarily reduced by marked alkalosis. Today, laboratory findings render establishment of the diagnosis simple. Acute therapy takes the form of parenteral calcium administration, and for long-term treatment, vitamin D metabolites, possibly in combination with oral calcium replacement is employed.

[Thyrotoxic crisis. Pitfalls in diagnosis--intensive therapy]. / Die thyreotoxische Krise. Fallstricke in der Diagnostik--Intensivtherapie.

Thyroid storm--a dramatic exacerbation of existing hyperthyroidism of sudden onset associated with hyperthermia, tachycardia and CNS symptomatology--remains a life-threatening disease. On account of an overlapping of the symptoms of precipitating conditions, and complications, e.g. thromboembolism, the clinical diagnosis is not easy, and is often established "too late'. Since an additional role is often played by exposure to iodine, treatment is also rendered more difficult, for antithyroid drugs inhibit only de novo synthesis, but not the secretion of stored thyroxin. Treatment requires the use of thyroid-specific and numerous adjuvant measures, and the patient must be admitted to an intensive care unit with relevant experience.

[Hypercalcemic crisis. Exacerbation of an existing hypercalcemia syndrome]. / Die hyperkalzämische Krise. Entgleisung eines vorbestehenden Hyperkalzämie-Syndroms.

Acute hypercalcemic crisis is the life-threatening exacerbation of an existing hypercalcemia syndrome, which is characterized by additional cerebral symptoms such as clouding of consciousness, somnolence and coma as well as rapid deterioration of renal function. Possible causes are diseases associated with severe hypercalcemia, such as malignant diseases, primary and tertiary hyperparathyroidism, vitamin D poisoning and treatment with calcium, vitamin D and calcium-containing ion exchangers in renal insufficiency. Nowadays the specific diagnosis can usually be established quickly and simply, since only in primary and tertiary hyperparathyroidism are calcium and the intact parathormone elevated. The aim of treatment is to bring about an effective reduction in serum calcium by inhibiting bone resorption and increasing calcium excretion in the urine. Today, the substances calcitonin, biphosphonate, mithramycin (plicamycin) and glucocorticoids, each with a different mode of action, are available. In patients with underlying malignant diseases these substances are used to supplement the treatment of the malignancy, while in hyperparathyroidism they are administered prior to operative parathyroidectomy.

[Recurrent hematemesis and hemobilia in ruptured hepatic artery aneurysm--differential diagnostic aspects of acute, upper gastrointestinal hemorrhage]. / Rezidivierende Hämatemesis und Hämobilie bei perforiertem Leberarterien-aneurysma--ein differentialdiagnostischer Aspekt der akuten, oberen GIB.

Aneurysms of the hepatic artery are mostly localized extra hepatic (80%). Today atherosclerosis is the most prevalent etiology (32%), followed by trauma (22%) and inflammatory lesions (10%). Rupture or perforation of the aneurysm is the initial clinical manifestation (60-80%), and occurs with nearly equal frequency into the peritoneal cavity and into the hepatobiliary tract. Rupture into bile ducts is often responsible for characteristic findings of upper gastrointestinal bleedings with hematemesis. The case of a 38 year-old man is presented and the clinical manifestation, the diagnostic and therapeutic procedures are demonstrated.

Somatostatin receptor scintigraphy and magnetic resonance imaging in recurrent medullary thyroid carcinoma: a comparative study.

In a prospective study, 18 patients with recurrent medullary thyroid carcinoma (MTC) underwent magnetic resonance imaging (MRI) of the neck and mediastinum and somatostatin receptor scintigraphy (SRS) with 111In-labeled pentetreotide. In nine patients with macroscopic MTC, 17 corresponding lesions were found on MRI and SRS; in addition, 13 suspicious lesions were seen on SRS only. Histological confirmation was available for 19 metastatic lesions, showing MRI to be true positive in 13 metastases, SRS in 18. In minimal residual disease (n = 10), MRI and SRS were compared with the histological findings in three patients and with selective venous catheterization (SVC) in seven patients. Corresponding findings on MRI and SVC were seen in one of seven, whereas SRS and SVC showed concordant localization of tumor recurrence in five of seven. Histological examination demonstrated MTC tissue in one of three cases; MRI and SRS were false positive in one of three cases, while in the others the interpretation remained uncertain. In conclusion, SRS is a promising imaging modality for localization of MTC recurrence. MRI provides better spatial resolution and thus facilitates the planning of surgery for macroscopic metastases. In minimal residual disease, SRS turned out to be superior in detecting occult MTC recurrence, confirming SVC findings.

Parathyroid hormone in coronary artery disease--results of a prospective study.

Parathyroid hormone (PTH) influences the calcium metabolism of many different mammalian cell types; indeed, hypertension due to changes in muscle tone is a frequent symptom of hypercalcemic hyperparathyroidism. In a blind study of 81 patients with various forms of heart disease undergoing coronary angiography, the plasma concentrations of the midcarboxyl regional PTH immunoreactivity were determined. PTH concentrations were elevated in 26 of the 56 patients exhibiting organic coronary artery disease (CAD). The plasma PTH levels were highest in those patients with CAD affecting three vessels and in patients with evidence of myocardial infarction. PTH levels were not influenced by previous drug treatments, and did not correlate to stress hormone levels. We propose that increased PTH levels may be a marker for initiation or potentiation of calcium-dependent changes in vascular smooth muscle behavior inducing coronary functional and anatomic lesions typical of CAD.

Androgen and estrogen response to adrenal and gonadal stimulation in idiopathic hemochromatosis: evidence for decreased estrogen formation.

Gonadal function in idiopathic hemochromatosis (IHC) was evaluated by comparing clinical features and levels of sex hormones in 10 male patients with IHC (cirrhosis, 4; fibrosis, 6), 6 male patients with alcoholic cirrhosis (AC) and 10 healthy, age-matched controls. Impotence was present in 9 IHC and all AC patients and was associated with decreased plasma testosterone levels. However, gynecomastia, a feature in all patients with AC, was not present in IHC, and plasma sex hormone binding globulin was normal. Patients with IHC showed significantly lower basal estradiol levels (17.7 +/- 6.3 pg per ml) than did controls (28.5 +/- 8.5 pg per ml), and low LH levels (p less than 0.01), which were insufficiently stimulated by luteinizing hormone releasing hormone (n = 8) as well as a decrease in prolactin concentration (2.9 +/- 1.4 vs. 5.9 +/- 1.9 ng per ml in the controls) suggesting pituitary failure. Synthesizing capacity of sex hormones was determined by adrenocorticotropic hormone and human chorionic gonadotropin administration. Basal and stimulated levels of androstenedione and cortisol indicated normal function of the adrenals in IHC. However after adrenocorticotropic hormone, estrone levels increased to only 16.2 +/- 8.4 pg per ml (controls, 27.3 +/- 4.7 pg per ml; p less than 0.01). Increments of estrone (12.5 +/- 9.2 pg per ml) and estradiol (17.9 +/- 11.6 pg per ml) were also lower in IHC following human chorionic gonadotropin administration than in controls (26.0 +/- 7.2 and 37.5 +/- 11.4 pg per ml, respectively). In contrast, plasma human chorionic gonadotropin raised testosterone levels 3.3-fold in IHC and 2.2-fold in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

[No effect of digitalis on sex and adrenal hormones in healthy subjects and in patients with congestive heart failure]. / Kein Einfluss von Digitalis auf Sexual- und Nebennierenrindenhormone bei gesunden Probanden und bei Patienten mit Herzinsuffizienz.

Digoxin was studied to see whether it impairs adrenal function and feminizes male subjects by changing plasma sexual hormones; both have been reported on previously. In eight healthy male subjects neither estrone (38.7 +/- 7.7 vs 35.4 +/- 3.2 pg/ml) nor estradiol (35.8 +/- 6.4 vs 32.2 +/- 3.9 pg/ml) nor testosterone (6.32 +/- 0.74 vs 6.45 +/- 0.73 ng/ml) were found to be altered by digoxin administration (plasma levels 1.55 +/0- 0.27 ng/ml) lasting 35 days. The same was true of free testosterone (147 +/- 24 vs 142 +/- 19 pg/ml) and free estradiol (657 +/- 77 vs 615 +/- 78 fg/ml). Even maximal stimulation of the adrenal and gonadal glands by adrenocorticotropic hormone (ACTH) and human chorionic gonadotropin (hCG) did not exhibit any digoxin-induced alterations in the synthesizing capacity of steroid hormones, as shown by plasma cortisol (increase from 128 +/- 18 to 389 +/- 18 ng/ml) and testosterone (from 5.96 +/- 0.90 to 10.33 +/- 1.19 ng/ml). Furthermore, seven subjects on digoxin were observed over a period of 150-210 days; they did not show any increase of estrogens. This was also found in three subjects when estrogen levels were elevated initially due to extreme obesity. Also, 35 patients who took beta-methyldigoxin (n = 8), beta-acetyldigoxin (n = 20) and digitoxin (n = 7) from 1 to 9 (mean: 1.9) years demonstrated normal plasma concentrations of gonadal and adrenal steroids, irrespective of duration of application or the digitalis compound.(ABSTRACT TRUNCATED AT 250 WORDS)