Prevalence of HIV Viral Load Suppression Among Psychiatric Inpatients with Comorbid Substance Use Disorders.

A consistently suppressed viral load enables HIV (+) patients to live longer, healthier lives and reduces the probability of transmitting the virus. Since the prevalence of HIV is four times higher among those with psychiatric disorders than in the general population, it is likely that this group would also have greater difficulty remaining in care and achieving viral suppression. A secondary data analysis utilizing screening data from the Preventing AIDS Through Health (PATH) for Triples (PFT) Study were examined to assess HIV load suppression among 254 psychiatric inpatients with comorbid substance use disorders in Philadelphia. Viral load results from the past 12 months were obtained from medical records for 63 inpatients identified as HIV (+). The sample was predominately African American (76%), male (56%), and the average age was 43 years. Psychiatric disorders included depression (64%), schizophrenia (21%), and bipolar disorder (13%) with patients reporting use of alcohol (73%), cocaine (64%), cannabis (29%) and opioids (16%) prior to admission. Among this high risk sample of HIV (+) patients, about one-half (52%) achieved viral suppression, with recent opioid users six times more likely to have a detectable viral load than non-opioid users (OR 6.0; CI 1.1-31.7, p = .035). The 52% viral load suppression rate among psychiatric inpatient was higher than expected, given that the CDC's national suppression rate among those diagnosed with HIV in the general population is 58%. However, individuals with mental illness and substance use disorders require constant surveillance, monitoring, and supportive services to achieve viral suppression. Many of those who were virally suppressed were engaged in Philadelphia's extensive treatment network, whereas those who were detectable and enrolled in the PFT intervention were often homeless with unstable psychiatric symptoms and current substance use disorders, particularly opioid abuse.

Patients' revisions of their beliefs about the need for hospitalization.

OBJECTIVE: An influential rationale for involuntary hospitalization is that prospective patients who refuse hospitalization at the time it is offered are likely to change their belief about the necessity of hospitalization after receiving hospital treatment. The authors examine how patients changed their evaluations of psychiatric hospitalization following hospital treatment. METHOD: The authors studied 433 patients who were interviewed about their hospitalization within 2 days of their admission to a psychiatric hospital; 267 of these patients were reinterviewed 4-8 weeks following discharge. RESULTS: When reinterviewed at follow-up, 33 (52%) of 64 patients who said at admission that they did not need hospitalization said that, in retrospect, they believed they had needed it. Only 9 (5%) of 198 patients who said at admission that they needed hospitalization shifted to saying that they had not needed it. CONCLUSIONS: Many of the patients who initially judged that they did not need hospitalization revised their belief after hospital discharge and reported that they had needed hospital treatment. However, perceptions of coercion were stable from admission to follow-up, and patients' attitudes toward hospitalization did not become more positive. Coerced patients did not appear to be grateful for the experience of hospitalization, even if they later concluded that they had needed it.

Primary gallbladder carcinoma: significance of subserosal lesions and results of aggressive surgical treatment and adjuvant chemotherapy.

Advances in methods to diagnose biliary disease have not improved the dismal survival rates reported for primary gallbladder cancer. We analyzed the results of operation in 112 patients with gallbladder cancer. Tumors limited to the gallbladder wall and those that required aggressive surgical therapy and adjuvant chemotherapy for advanced disease were analyzed separately according to the following staging system: tumors that were localized to the mucosa (stage, I, n = 4); tumors that penetrated the muscularis (stage II, n = 4); subserosal tumors (stage III, n = 3); tumors with cystic node involvement (stage IV, n = 13); and tumors that had spread to adjacent organs (stage V, n = 88). Of the 11 patients (10%) with tumor limited to the gallbladder wall (stages I to III), one of five patients (20%) treated with cholecystectomy alone and four of six patients (60%) treated with cholecystectomy and lymphadenectomy (with hepatic wedge resection in three and pancreaticoduodenectomy in one) were alive and tumor free 3 to 6 years after operation. Three patients treated with cholecystectomy alone died of recurrent cancer at 18, 48, and 60 months after operation. Of the 13 patients with cystic node involvement (stage IV), nine were treated by cholecystectomy alone, three with lymphadenectomy, and one with pancreaticoduodenectomy; the cumulative survival rate was only 37% at 6 months, and all patients were dead within 18 months. Of 14 patients with advanced disease (stage V) treated with aggressive surgical therapy, including lymphadenectomy in six patients, hepatic wedge resection in six patients, and right hepatic lobectomy in two patients, the mean survival rate was only 3 months.

Stomach cancer following gastric surgery for benign disease.

The records of 1,079 patients with gastric carcinoma were reviewed. Of these, only 21 (about 2%) had had previous gastric surgery for benign disease, usually peptic ulcer. The average interval between the original gastric surgery and the discovery of stomach cancer was 26.9 years. The symptoms of cancer presentation were not distinguishable from other forms of the postgastrectomy syndrome. Gastric cancer tended to develop in these patients during the sixth decade of life, irrespective of when they had had their original gastric surgery, strongly suggesting an age-related factor. Although it would appear that previous gastric surgery for benign disease is not a major risk factor for the subsequent development of gastric cancer, such a relationship may exist. Patients who have undergone gastrectomy should be followed up carefully for the recurrence of symptoms.

Aberrations in Hollander test response after incomplete vagotomy. Compensating effect of antral resection in the dog.

Acid secretory and serum gastrin responses to 2-deoxy-D-glucose and insulin were compared in gastric fistula dogs before and after partial vagotomy and pyloroplasty or partial vagotomy and antrectomy. The acid response and serum gastrin curve were basically unaltered by partial vagotomy and pyloroplasty. Based on the data presented, the acid response to insulin hypoglycemia appears to be more dependent on the vagal release of antral gastrin than on direct vagal stimulation of the parietal cell. However, acid response to insulin was profoundly suppressed to only 4 per cent of control levels after partial vagotomy and antrectomy. Although acid response to 2-deoxy-D-glucose was also profoundly depressed to 33 per cent of control levels after partial vagotomy and antrectomy, it was seven times greater than that seen with insulin. Serum gastrin response was abolished after antrectomy to either insulin or 2-deoxy-D-glucose. Finally, the question to which we originally addressed ourselves appears to have been answered and, in terms of response to vagal stimulation, antrectomy appears to compensate for incomplete vagal denervation and may lead to aberrations and misinterpretations, raising serious questions as to the validity of the Hollander test in patients who have undergone distal gastric resection.

Gastrin cell populations after highly selective vagotomy in the dog.

Highly selective vagotomy was performed on five dogs. Postoperatively, gastrin cell (G cell) hyperplasia occurred in all dogs. Mean preoperative G cell numbers increased from 350 to 530/cm mucosal length (p less than 0.02). Antral tissue gastrin also increased by 100 per cent (6.7 x 10(6) to 13.7 x 10(6) pg/gm tissue, p less than 0.05). Basal and stimulated serum gastrin were unchanged following highly selective vagotomy. The cause for G cell hyperplasia is not clear, but is probably multifactorial.

Acute effects of ethanol and ethanol plus furosemide on pancreatic capillary blood flow in rats.

The effects of intravenous ethanol and ethanol plus furosemide on pancreatic capillary blood flow (PCBF) were investigated using a laser-Doppler flowmeter. Forty Sprague-Dawley male rats were divided into 4 groups: (1) control, (2) 80% ethanol, (3) 80% ethanol plus furosemide, and (4) furosemide. Mean arterial blood pressure and heart rate were monitored. Levels of serum amylase, calcium, electrolytes, ethanol, and furosemide (groups 3 and 4) were measured, and samples of pancreatic tissue were obtained. The ethanol and furosemide levels were statistically different (p < 0.05). PCBF significantly decreased (p < 0.05) in group 2, increased (p < 0.05) in group 3, and did not differ (p > 0.05) between groups 1 and 4. Histopathologic analysis revealed swollen acini in group 2 and sparse focal necrosis without acinar swelling in group 3. The depressant effect of ethanol on PCBF may be the result of its direct action on pancreatic cells causing edema and capillary compression rather than on primary vascular control mechanisms that adjust blood flow. Furosemide counters this effect.