Frequency and factors influencing portal hypertensive gastropathy and duodenopathy in cirrhotic portal hypertension

Portal hypertensive gastropathy and duodenopathy are distinct clinical and endoscopic entities. Data on factors influencing the development of these lesions are still emerging. Data on portal hypertensive duodenopathy are scarce. We prospectively studied 230 patients with liver cirrhosis and oesophageal varices attending the liver clinic of the Sanjay Gandhi Post Graduate Institute of Medical Sciences. One hundred and forty-two patients had no history of upper gastrointestinal bleeding, while the remainder had bled in the past. Endoscopic appearances were recorded before starting patients on a sclerotherapy programme. Forty-four patients were re-evaluated after variceal eradication. The frequency of portal hypertensive gastropathy (PHG) and duodenopathy (PHD) was 61 and 14%, respectively. Mild PHG was present in 85% and was severe in the rest. Portal hypertensive duodenopathy was mild in 50%, while in the other half it was severe. There was no relationship of PHG and PHD to: (i) a history of upper gastrointestinal bleed; (ii) size of oesophageal varices; (iii) aetiology of liver cirrhosis; or (iv) liver function status as assessed by Child Pugh's scores (P=NS for all). The prevalence of PHG was higher in those patients with oesophagogastric varices (74 of 107; 69%) compared with patients with oesophageal varices alone (68 of 123; 55%; P<0.05). However, no such increase in frequency of PHD was noted in patients with oesophagogastric varices. Sclerotherapy increased the frequency of PHG. Twenty-four patients had PHG before starting sclerotherapy, while it was noted in 33 patients 1–3 months after variceal eradication (P< 0.05). In contrast, there was no increase in the prevalence of portal hypertensive duodenopathy after sclerotherapy (P=NS). There was no correlation between endoscopic and histological changes of PHG and PHD. In conclusion, PHG is quite frequent in patients with cirrhosis and its frequency increases with the presence of oesophagogastric varices and after sclerotherapy. However, the frequency of PHD is low and is not affected by the factors studied.     

Posttransplant T-cell lymphoproliferative disorders--an aggressive, late complication of solid-organ transplantation

T-cell non-Hodgkin's lymphomas are an uncommon occurrence after solid- organ transplantation. We describe a morphologically and immunophenotypically distinct group of T-cell lymphoproliferative disorders that occurred late in the course of six patients with solid- organ transplants. The patients ranged in age from 31 to 56 years (median, 43). Three were male; all were splenectomized. The interval from transplant to the diagnosis of lymphoma ranged from 4 to 26 years (median, 15). Symptoms at presentation were related to sites of involvement. Pulmonary, marrow, and CNS involvement were present in five, four, and one case, respectively. No patient had lymphadenopathy. Five patients had an elevated lactate dehydrogenase level (range, 226 to 4,880 IU/L; median, 1,220 IU/L). Five of six patients had a leukoerythroblastic reaction. All cases had large-cell histology and frequently contained cytoplasmic granules. Those cases tested expressed CD2, CD3, and CD8 and were negative for B-cell antigens. T-cell receptor beta- and gamma-chain genes were clonally rearranged in three of three and one of three cases, respectively. All T-cell posttransplant lymphoproliferative disorders (T-PTLDs) studied were negative for Epstein-Barr virus (EBV), human T-cell leukemia/lymphoma virus type 1 (HTLV-1), human T-cell leukemia/lymphoma virus type 2 (HTLV-2), and human herpes virus type 8 (HHV-8) genomes. Treatment with acyclovir (three patients) or chemotherapy (three patients) resulted in two responses. All patients had an aggressive course, with a median survival duration of 5 weeks. In conclusion, a clinically aggressive T- PTLD may be a late complication of solid-organ transplantation and does not appear to be related to EBV, HTLV-1, HTLV-2, or HHV-8 infection.     

The Post‐Deployment Mental Health (PDMH) study and repository: A multi‐site study of US Afghanistan and Iraq era veterans

The United States (US) Department of Veterans Affairs (VA) Mid‐Atlantic Mental Illness Research, Education, and Clinical Center (MIRECC) Post‐Deployment Mental Health (PDMH) multi‐site study examines post‐deployment mental health in US military Afghanistan/Iraq‐era veterans. The study includes the comprehensive behavioral health characterization of over 3600 study participants and the genetic, metabolomic, neurocognitive, and neuroimaging data for many of the participants. The study design also incorporates an infrastructure for a data repository to re‐contact participants for follow‐up studies. The overwhelming majority (94%) of participants consented to be re‐contacted for future studies, and our recently completed feasibility study indicates that 73–83% of these participants could be reached successfully for enrollment into longitudinal follow‐up investigations. Longitudinal concurrent cohort follow‐up studies will be conducted (5–10+ years post‐baseline) to examine predictors of illness chronicity, resilience, recovery, functional outcome, and other variables, and will include neuroimaging, genetic/epigenetic, serum biomarker, and neurocognitive studies, among others. To date, the PDMH study has generated more than 35 publications from the baseline data and the repository has been leveraged in over 20 publications from follow‐up studies drawing from this cohort. Limitations that may affect data collection for a longitudinal follow‐up study are also presented.     

Severe necrotizing stomatitis and osteomyelitis after chemotherapy for acute leukaemia

Background:  Leukaemia is a malignant neoplasm characterized by clonal proliferation of white blood cells within the bone marrow. Despite an increase in the white blood cell count, the leukaemic leukocytes are non-functional. The oral complications arising in leukaemic patients can be attributed to the direct and indirect effects of immunosuppressive chemotherapy.
Methods:  This case report describes severe maxillary and mandibular necrotizing stomatitis and osteomyelitis in a young female patient after chemotherapy for acute leukaemia. On physical examination, the patient presented malnourished with pale skin, cervical lymphadenitis, frequent fever and generalized pain. The intra-oral clinical examination found halitosis, multiple ulcers, necrotizing stomatitis and osteomyelitis located in the maxillary and mandibular regions. The necrotizing stomatitis and osteomyelitis were treated locally with atraumatic removal of the necrotized tissues. The patient received a daily preventive protocol consisting of oral hygiene care, including twice daily brushing, and mouthrinses with a solution of chlorhexidine. She was also treated with systemic metronidazole and amoxicillin for 21 days.
Results:  During the course of management the patient's oral condition improved with some re-epithelialization being noted. However, severe alveolar bone destruction remained evident. Thirty-two months after presentation of the initial symptoms, the patient died due to complications related to leukaemia recurrence (haemorrhage, sepsis and respiratory distress syndrome).
Conclusions:  Dental monitoring during cancer treatment is imperative in order to emphasize the importance of dental plaque control and the maintenance of a healthy periodontal condition throughout medical treatment.     

Twenty-Two-Year Follow-Up in the VA Cooperative Study of Coronary Artery Bypass Surgery for Stable Angina

We evaluated the 22-year results of initial coronary artery bypass surgery with saphenous vein grafts compared with initial medical therapy on survival, incidence of myocardial infarction, reoperation, and symptomatic status in 686 patients (average age 51) with stable angina in the Veterans Affairs Cooperative Study of Coronary Artery Bypass Surgery. Between 1972 and 1974, 354 patients were assigned to medical treatment and 332 to surgical revascularization. In the surgical cohort, 312 patients underwent operation (operative mortality 5.8%) and 25% subsequently underwent repeat operation (operative mortality 10.3%). In the medical cohort, 160 patients crossed over to surgery (operative mortality 4.4%) and 21% of these patients had reoperation (operative mortality 9.1%). Neither crossover nor reoperation was predictable by angiographic or clinical risk factors measured at baseline. The overall 22-year cumulative survival rates were 25% and 20% in the medical and surgical cohorts (p = 0.24). Corresponding rates in low-risk patients who had 1 or 2 vessels diseased, or 3 vessels diseased with normal left ventricular function were 31% and 24% (p = 0.024). Although significant at 10 years, there was also no long-term survival benefit for high-risk patients assigned to bypass surgery. The probabilities of remaining free of myocardial infarction and of being alive without infarction were significantly higher with initial medical therapy, 57% versus 41% (p = 0.02) and 18% versus 11% (p = 0.0031), respectively. This trial provides strong evidence that initial bypass surgery did not improve survival for low-risk patients, and that it did not reduce the overall risk of myocardial infarction. Although there was an early survival benefit with surgery in high-risk patients (up to a decade), long-term survival rates became comparable in both treatment groups. In total, there were twice as many bypass procedures performed in the group assigned to surgery without any long-term survival or symptomatic benefit.