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Biomedical subjects

E J Drenick

Publications and source records attributed to E J Drenick.

At least 37 records · Page 2Linked to original sources
PubMed1980

Excessive mortality and causes of death in morbidly obese men.

A group of 200 morbidly obese men (average weight, 143.5 kg; age, 23 to 70 years) were admitted to a weight control program between 1960 and 1977 and were followed up for a mean period of 7 1/2 years. There was complete follow-up until the termination of the study or until death for 185 men. Fifteen men were followed up for fractional periods. Fifty of the 200 died during the course of the study. Life-table techniques, comparing the mortality among the obese with that among men in the general population, demonstrated a 12-fold excess mortality in the obese in the age group 25 to 34 years and a sixfold excess in the age group 35 to 44 years. This ratio diminished with advancing age. Cardiovascular disease was reported as the cause of death more frequently and malignancies less frequently than they were for men in the US general population.

Adult↗
PubMed1980

Cutaneous lesions after intestinal bypass.

Twenty-three of 81 intestinal bypass patients with episodes of bypass enteropathy had papulopustular or nodular skin lesions. Histologic examination of the dermal lesions showed various forms of vasculitis in nine of 14 subjects. In six of 11 patients examined by immunofluorescent microscopy, both the lesions and uninvolved sun-exposed skin areas had immunoglobulin and complement deposits in linear or granular patterns in the dermoepidermal line, giving the appearance of a positive lupus band test. Skin lesions resolved with spontaneous improvement of bypass enteropathy or in response to metronidazole therapy. After the bypass was dismantled, the eruptions disappeared permanently, and previously positive lupus band tests became negative. The skin lesions were frequently observed in association with arthritis, suggesting an immune-complex mechanism, probably originating in "blind loop" bacterial overgrowth.

Fluorescent Antibody Technique↗
PubMed1979

Loss of body nitrogen on fasting.

An analysis of the change in total body nitrogen during fasting shows that it declines exponentially, a small fraction being lost rapidly (t 1/2 of a few days), and the remainder being lost slowly (t 1/2 of many months). The obese faster loses N, and weight, at a slower relative rate than the nonobese; and the ratio of N loss to weight loss during an extended fast is inversely related to body fat content, being about 20 g/kg in the nonobese and about 10 g/kg in those with body fat burdens of 50 kg or more. The loss of body N on a low protein-calorie adequate diet can also be described in exponential terms, and this function allows an estimate to be made of the N requirement.

Adult↗
PubMed1978

Bacterial flora of the small bowel before and after bypass procedure for morbid obesity.

The contents of the proximal jejunum and distal ileum were cultured quantitatively in eight patients who were undergoing intestinal bypass procedure for obesity. Five jejunal specimens were sterile, and three contained low counts of a predominantly aerobic flora. Ileal contents yielded variable but usually higher counts than in the jejunum, and there were similar numbers of anaerobes and aerobes. In three patients in whom a bypass was established, contents of the functioning small bowel showed counts of 10(5.0)-10(7.6) colony-forming units/ml. These counts exceeded the counts in the normal terminal ileum, and the flora qualitatively resembled that of feces. Four specimens from excluded loops revealed colonization with fecal organisms, and the counts ranged between 10(6.4) and 10(9.7) colony-forming units/ml. In jejunoileal bypass both the functioning small bowel and the excluded loop become colonized with colonic flora, a phenomenon that may contribute to some of the side effects of this procedure.

Bacteroides fragilis↗
PubMed1978

Renal damage with intestinal bypass.

Renal function and biopsies were studied in 18 patients, 7 to 108 months after intestinal bypass. Enteropathy was found in 12 and hyperoxaluria in 16. Every biopsy showed a type of focal interstitial nephritis, tubular atrophy, fibrosis, and glomerular hyalinization. Damage ranged from minimal to extensive and renal function from normal to end-stage failure. Tubular injury had resulted partly from oxalate deposits. However, in 10 patients no oxalate crystals were seen. In eight others, most of the damaged areas were remote from crystal deposits. Immunoglobulin M and C3 deposits, found in glomerular capillaries and the messangium in six of 11 specimens, and the presence of circulating immune complexes in five of 10 patients, in addition to the extraintestinal organ involvement, suggested immune complex mesangial injury as one factor in bypass nephropathy. With progressive impairment of renal function, a biopsy appears justified. If damage is significant, the bypass should be dismantled.

Adult↗
PubMed1977

The role of vasopressin and prolactin in abnormal salt and water metabolism of obese patients before and after fasting and during refeeding.

Arginine vasopressin (AVP) and prolactin (PRL) concentrations were measured in the plasma of grossly obese subjects to determine if abnormalities in salt and water homeostasis could be related to these hormones. Acute oral water loads and hypertonic saline infusions were administered during baseline obesity, after prolonged fasting, and after hypocaloric refeeding. Only 64.7%, 46.1%, and 70.1% of a water load was excreted during the respective three stages. Pre-water load plasma AVP levels were normal, but after the water load the obese failed to suppress AVP secretion in a normal fashion; this defect was corrected after fasting and with refeeding. Salt loading resulted in appropriate osmolality and AVP responses. Serum prolactin levels, normal at baseline during all phases, rose slightly after water loading during fasting. Hypertonic.saline produced no changes in prolactin levels in the obese or in the normal controls. In the disordered salt and water metabolism of the obese, persistently high AVP values during water loading appeared to be a factor in the delay of water excretion. In the observed water retentionduring dietary restriction and refeeding, secretion of AVP and PRL did not appear to have a major regulatory function.

Adult↗
PubMed1977

Bypass enteropathy: an inflammatory process in the excluded segment with systemic complications.

Evidence is presented that many of the enteric and systemic manifestations after jejunoileal bypass can be related to an inflammatory process within the bypassed small bowel rather than to the surgically induced sequelae of a short bowel syndrome with malabsorption. Invasion of the excluded segment by fecal flora was associated with a histologically demonstrable inflammatory response of the mucosa. The disorder was of variable severity and duration and occurred in the majority of 28 bypass patients. Progression to a clinical syndrome resembling an acute abdomen occurred in about 15% of the patients. Small bowel ileus and, in some patients, obstruction of the colon were suggested by physical signs and x-ray findings. Surgical exploration in such instances demonstrated an inflammaotry process of the excluded small bowel loops with severe distention of this segment and of the colon, but not organic obstruction. Pneumatosis cystoides intestinalis was a sequal in two patients. Exudative protein loss was documented in the severe cases. Most of the systemic sequelae are comparable to those seen with inflammatory diseases of the bowel such as Crohn's disease. Fever, excessive weight and lean tissue loss, and the involvement of skin, blood vessels, joints and possibly, the liver suggest an immune response as a common factor in the pathogenesis. The clinical improvement with antibiotics such as metronidazole or with restitution of normal bowel continuity indicates that the bacterial flora in the excluded small bowel segment or its byproducts are causally related to the systemic complications. Hyperoxaluria may be primarily the sequela of steatorrhea and not of the inflammatory process.

Adult↗
PubMed1977

Alterations in basal and TRH-stimulated serum levels of thyrotropin, prolactin, and thyroid hormones in starved obese men.

To investigate further the alterations in pituitary-thyroid function seen during starvation, we have measured basal and TRH-stimulated serum levels of thyrotropin (TSH), prolactin (PRL), growth hormone, thyroxine (T4), triiodothyronine (T3), free T4, free T3, and reverse T3 during prolonged fasting in seven obese men. Fasting was associated with a significant decrease in serum (4, (3, and free T3, while there was an increase in serum reverse T3; these values tended to return toward pre-fast levels as the fast continued beyond 3 weeks. No significant changes were seen in basal serum TSH, PRL, growth hormone, or free T4. Although the TSH response to TRH was diminished during fasting, PRL, T4, and T3 responses were unchanged. In addition to transient alterations in the peripheral metabolism of T4, these findings suggest that alterations in the thyroid hormone binding capacity of serum carrier proteins may occur during fasting. The blunted TSH response to TRH despite reduction of serum T3 concentration suggests that subtle alterations in hypothalamic-pituitary function may also occur.

Adult↗
PubMed1977

Therapeutic fasting in morbid obesity.

The weights of 207 morbidly obese patients were reduced via prolonged fasting. Half the patients fasted for close to two months, losing a mean of 28.2 kg; one fourth fasted for less than one month; and the other fourth fasted for more than two months, with a mean 41.4-kg loss. This latter group was heavier initially, and more than 50% attained near-normal weight. Patients with onset of obesity in childhood had the lowest tolerance for fasting and the lowest success rate in attaining normal weight. Over a 7.3-year follow-up period in 121 patients, the reduced weight was maintained for the first 12 to 18 months. Subsequently, regain proceeded equally in all groups irrespective of length of fast, extent of weight loss, or age at onset of obesity. Regain to original weight occurred in 50% within two to three years and only seven patients remained at their reduced weights. Regain to greater than original weight was more common in childhood-onset obesity.

Adult↗
PubMed1976

Bypass enteropathy. Intestinal and systemic manifestations following small-bowel bypass.

Many manifestations following jejunoileal bypass are due to chronic inflammation of the excluded bowel rather than short bowel malabsorption. Diarrhea, abdominal distention, and gas-fluid levels were common diagnostic features of "bypass enteropathy." Exploration showed the bypassed bowel to be dilated, with serosal inflammation and pneumatosis cystoides intestinalis. The bypassed loops contained a fecal flora and the mucosa demonstrated nonspecific chronic inflammatory changes. Exudative protein losses were noted. Systemic complications of bypass enteropathy were similar to other inflammatory diseases of the bowel. Improvement following treatment with metronidazole or after dismantling of the bypass suggested that bacterial byproducts originating in the excluded bowel were causally related.

Arthritis↗
PubMed1975

Pelvic lipomatosis: effect of diet.

Pelvic lipomatosis is a disease of dense infiltration of benign fatty tissue within the confines of the deep bony pelvis. A case is reported of an obese, hypertensive, thirty-nine-year-old black man with the typical clinical and radiographic features of pelvic lipomatosis. Prolonged fasting produced an extensive weight loss and profound resolution of his presenting symptoms, signs, and radiologic abnormalities. Subsequent regain of weight resulted in the reappearance of the disorder, confirming that pelvic lipomatosis may be a disease of accelerated and excessive fat deposition which can be reversed by dietary restriction. The literature pertaining to pelvic lipomatosis is reviewed in detail.

Adult↗
PubMed1975

Evolution of diabetic ketoacidosis in gross obesity.

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.

Adult↗