Percutaneous endoscopic gastrostomy. Do surgeons and gastroenterologists get the same results?

Numerous investigators have reported the safety, cost effectiveness, and low morbidity and mortality of percutaneous endoscopic gastrostomy (PEG) but not studies compare the results of gastroenterologists and surgeons performing PEG. In a retrospective review of PEG performed at our institution, morbidity and mortality were compared between these two groups. The procedure was performed by either the surgical service (n = 49) or gastroenterology service (n = 51). One hundred PEGs were successfully placed in 92 patients. Three placement failures occurred in the gastroenterology group. Major complications were defined as conditions requiring operative intervention or resulting in death. Minor complications, using a defined list (13 different complications), were those not serious or life-threatening, which were managed medically or resolved without treatment. Twenty-nine minor (17 patients) complications and 3 major (3 patients) complications occurred in the gastroenterology group. Thirteen minor (11 patients) complications and 4 major (4 patients) complications occurred in the surgery group. Overall 30-day mortality was 14 per cent (13 patients), two of which were probably procedure-related in the gastroenterology group. In both groups, there was no difference in the numbers of patients who had complications (P greater than 0.05). The complication rate (numbers of complications/number of patients) doubled in the gastroenterology group compared with the surgery group for minor (P less than 0.04) and total complications (minor and major--P less than 0.06). Since PEG is a procedure frequently performed by gastroenterologists, it is imperative that surgeons, particularly those not performing endoscopy, be aware of the potential morbidity associated with PEG.     

Apomorphine disrupts the inhibition of acoustic startle induced by weak prepulses in rats

Separate experiments conducted in two different laboratories assessed the importance of the prepulse intensity in the ability of apomorphine to reduce prepulse inhibition of acoustic startle responses. Rats were presented with noise bursts alone or noise bursts 100 ms after presentation of prepulse stimuli ranging from 70 to 85 or 90 dB. Throughout testing, the background noise was maintained at 65 dB. In both laboratories, apomorphine markedly decreased the absolute magnitude of prepulse inhibition when the prepulse stimuli were no more than 10 dB above the background. With more intense prepulse stimuli, apomorphine had no significant effect on prepulse inhibition. Hence, apomorphine does not interfere with the inhibitory process which actually mediates prepulse inhibition, but appears to affect the detectability of the prepulse.     

Is maintenance antiparkinsonian treatment necessary?

The authors designed a three-phase prospective trial in which only those patients who developed an acute, neuroleptic-induced extrapyramidal side effect (EPSE) received benztropine (BZ) at 2 mg i.m. and then 1 mg p.o. b.i.d. for 2 days after their symptoms were rated for severity and type (Preparatory Phase 1). They were then randomly assigned under double-blind conditions to continue BZ or be switched to placebo for 8 days (Experimental Phase 2). Finally in Phase 3 (Followup), all patients continued on placebo in a single-blind design until Day 30. If the patient re-experienced an acute EPSE that was of sufficient severity to require immediate BZ administration, he or she was rated, treated, and then dropped from the study. EPSE scores and dropout rates did not differ in Phase 2 between the placebo- and BZ-treated groups. Implications for the continuation, cessation, or intermittent use of antiparkinsonian (AP) drugs are discussed.     

Metaplastic cystitis complicated with Von Brunn nests, cystitis cystica, and intestinal type of glandular metaplasia

It is well documented that under certain stimuli the bladder epithelium can undergo metaplasia. The origin of glandular epithelium, which may be found in the bladder, is somewhat controversial. Endoscopic and histopathologic features of an eighty-one-year-old white man with proliferative metaplastic cystitis are presented. This case demonstrates that glandular differentiation was due to progressive cystitis rather than congenital intestinal rest.     

Treatment of acute graft-versus-host disease with a nonmitogenic anti-CD3 monoclonal antibody.

Treatment with the monoclonal antibody OKT3 specific for the CD3 complex associated with the T cell antigen receptor can reverse acute rejection of human renal allografts. However, efficacy of anti-CD3 antibodies for treatment of patients with acute graft-versus-host disease after marrow transplantation has not been established. The dose-limiting side effects resulting from T cell activation induced by some anti-CD3 antibodies in vivo have discouraged their use for this application. We now report a phase I-II study of GVHD treatment with the anti-CD3 antibody BC3, a monoclonal murine IgG2b that, unlike OKT3, does not activate T cells. Fourteen patients were treated with BC3 after progression of acute GVHD despite treatment with cyclosporine and corticosteroids, and three patients received BC3 as primary treatment for GVHD. BC3 was administered at a dose of 0.1 or 0.2 mg/kg/day for seven or eight days. Five patients achieved complete resolution of GVHD, eight patients had partial improvement, two patients had no change, and two patients had progression of GVHD on therapy. Responses were sustained in 8 of 13 patients. Mild chills, fever, hypertension, and chest discomfort occurred in various combinations following 6 of 17 (35%) initial infusions of BC3 and following 4 of 99 (4%) subsequent infusions. In each instance it was possible to continue BC3 therapy without adjusting the dose or treatment schedule. In each patient treated, the absolute count of peripheral blood lymphocytes decreased transiently but returned to baseline within 22 hr after the first infusion. Circulating T cells had surface CD3 molecules saturated by the infused antibody in all but one patient. Four patients survived longer than one year after treatment with antibody BC3, and 13 patients died of infection or organ failure. Administration of the nonmitogenic anti-CD3 antibody BC3 was associated with improvement in the clinical manifestations of GVHD with minimal acute toxicity. Efficacy of antibody treatment did not depend on depletion of circulating T cells. Therefore, antibody BC3 may be achieving therapeutic immunosuppression by modulating T cell function. Controlled studies in patients treated earlier in the course of GVHD should determine whether antibody BC3 can improve survival.     

Screening for Depression in Patients with Chronic Illness

Why should depression screening be conducted in chronically ill populations? Depression is a disabling illness and is very common among patients who have chronic illnesses. Despite its high prevalence in this patient population, depression often goes unrecognized. Having a plan for a population-based screening program for depression can not only identify patients who are at risk of depression, but can also help to foster early treatment and enhanced care for these patients. This article provides an overview of commonly-used depression screening tools and presents an example of how this might be carried out in a healthcare organization.     

T lymphocytes expressing HECA-452 epitope are present in cutaneous acute graft-versus-host disease and erythema multiforme, but not in acute graft-versus-host disease in gut organs.

Lymphocytes in formalin-fixed skin biopsies from patients with cutaneous acute graft-versus-host disease (aGVHD) were studied with HECA-452 (an antibody recognizing lymphocytes with skin-homing properties) and a panel of antibodies recognizing pan-B (L26 [CD20]), pan-T (L60 [CD43] and A6 [CD45RA]), and T-helper subset (OPD4) antigens in paraffin sections. Biopsies from patients with erythema multiforme (EM) were similarly studied for comparison. In both conditions, T lymphocytes stained by OPD4 were predominantly confined to the dermis, whereas those stained by HECA-452 were concentrated in the epidermis; however, there was considerable variation between cases, and overlap between findings in the dermis and epidermis. Lymphocytes similarly studied in paraffin sections of liver, salivary gland, and gut affected by aGVHD were essentially unreactive with HECA-452, although they were largely stained by pan-T markers and showed some comparable reactivity with OPD4. The findings suggest that aGVHD of the skin is mediated by a different set of lymphocytes than in gut organs, and may have a similar immunologic mechanism to EM.     

Nocturnal growth hormone secretion in schizophrenic patients and healthy subjects.

Plasma growth hormone concentrations were measured at hourly intervals between 10 p.m. and 8 a.m. the next morning in 15 drug-free chronic schizophrenic male inpatients and 14 healthy males. Growth hormone secretion was significantly lower in the patients as compared with the controls. Growth hormone release peaked around 1 a.m. in the controls, but a growth hormone peak was absent in the patient group. Increased dopamine activity, increased serotonin activity, or both could explain the absence of a nocturnal growth hormone surge in the schizophrenic patients.