Hypothalamic-pituitary-adrenal axis activity in depressive illness. Its relationship to classification

Serum cortisol response to the 1-mg overnight dexamethasone suppression test was studied in 221 depressed patients and 109 nondepressed psychiatric controls. Nonsuppression distinguished patients with primary unipolar depression (65/146) from patients with secondary unipolar depression (0/42) and nondepressed controls (0/109). Furthermore, nonsuppression distinguished the three familial subtypes of primary unipolar depressive illness: familial pure depressive disease (FPDD; 38/50 patients), sporadic depressive disease (SDD; 24/55 patients), and depression spectrum disease (3/41 patients). Moderate elevations in baseline serum cortisol levels were found in FPDD, SDD, and bipolar depression. Medication did not affect the results. The data suggest that the depressive syndrome is composed of separate illnesses, each of which has a distinctive pattern of hypothalamic-pituitary-adrenal axis activity during the depressed state as well as a specific clinical and familial psychiatric history.     

Catecholamine-induced muscle weakness

Infusions of epinephrine or levarterenol bitartrate into a rabbit nerve-muscle preparation decreased the force of the evoked twitch of anterior tibial and gastrocnemius-soleus muscles. The adverse effect of the catecholamines was not directly on skeletal muscle. The alpha-receptor blocking drug phenoxybenzamine hydrochloride prevented the adverse effect of the catecholamines if it was given prior to catecholamine infusions and unmasked a weak augmentation of twitch tension. Taken with the finding of abnormal accumulation of catecholamine in human dystrophic muscles, the production of an experimental myopathy resembling human dystrophy by the monoamine oxidase inhibitor pargyline hydrochloride, and the finding of excessive levels of catecholamines in the tissues and urine of dystrophic animals, these experiments support the hypothesis that catecholamines could play a pathogenetic role in some dystrophic diseases of muscle.     

Preliminary study of the in vivo motion in the canine shoulder

An instrumented spatial linkage was used to measure the total motion in a canine shoulder as the dog was engaged in a variety of activities, including walking on a level carousel track, as well as over a hurdle, up and down a step, and up and down a ramp placed on the same track. For each activity, the motion data were analyzed, using 2 procedures. First, the linkage data and the joint contour data were combined by computer, and the motion was represented by a series of sequential computer drawings showing the scapular and humeral articular surfaces in their proper relative positions for selected increments of time during the various activities described. As an alternate but approximate method for describing the relative humeral-scapular motion, rotations about 3 mutually perpendicular axes through the average center of the shoulder joint were determined.     

Is colostomy closure a hazardous procedure? A comparison of elemental diet and routine bowel preparation

Morbidity after closure of a colostomy is low if a simple antiseptic technique of intraperitoneal closure is used. In 26 patients there was no example of major wound sepsis and only 2 faecal fistulas both of which rapidly closed spontaneously. A randomized study of preoperative bowel preparation incorporating an elemental diet showed no apparent advantage for this method using our criteria for assessment.     

Pancreatitis and severe metabolic abnormalities due to phenformin therapy

Two elderly diabetic patients with abdominal pain were demonstrated to have complications of phenformin hydrochloride therapy. The first developed severe lactic acidosis treated with sodium bicarbonate given intravenously and followed by rebound alkalosis. The second showed severe acidosis (specimens for lactate determination were unfortunately unsatisfactory for analysis) and similar alkalotic rebound after therapy. She then developed severe pancreatitis, proved at operation, no cause for which other than phenformin was apparent. Poor renal and hepatic function predispose to these conditions by increasing serum phenformin levels and by decreasing urinary excretion of its metabolites. The acidosis should be treated judiciously with sodium bicarbonate administered intravenously. A rebound alkalosis, ensuring as the accumulated lactate is metabolized, is best treated by potassium chloride and ammonium chloride given intravenously. The mechanism by which phenformin causes pancreatitis is unknown, but termination of therapy causes cessation of the pancreatitis.