Abdominal compartment syndrome--an old syndrome, a new perspective.

The abdominal compartment syndrome is a life threatening condition resulting from pathologic elevation of the intraabdominal pressure. Prompt diagnosis is required to avoid significant sequelae. Diagnosis of this syndrome is based on clinical findings and intra abdominal pressure monitoring. Treatment consists of decompressive laparotomy, which corrects the pathology. Various surgical techniques are described to manage the open abdomen. Despite considerable attention accorded to this disorder, it is still associated with high morbidity and mortality. This review article deals with the identification of risk factors, pathophysiology, diagnostic criteria and treatment of critically ill patients with the abdominal compartment syndrome.     

Concurrent exposure to lead,manganese, and cadmium and their distribution to various brain regions,liver, kidney,and testis of growing rats

Growing rats were exposed to 5 mg/L Pb,ad libitum in drinking water, and administered low or high doses of Mn and Cd intraperitoneal (i.p.) for 30 days. Some groups of animals were also administered combinations of Pb + Mn and Pb + Cd in an identical manner. Analysis of Pb, Mn, and Cd in tissue samples showed the expected dose-dependent accumulation when the metal was administered singly. However, combined treatment produced different types of metal shift in different tissues. Enhanced accumulation of all three metals in the brain, Mn in liver, Pb in kidney and Cd in testis and kidney after combined exposure may make target organs vulnerable to the toxic effects of metals, even when encountered at low concentrations. Further, the decreased levels of blood Pb after combined treatment with Cd or Mn suggests that the significance of blood Pb level as a diagnostic aid for Pb toxicity in coexposed conditions may not be of much value. Changes in the metallic distribution within the tissues after coexposure may be the result of a competition between the administered metals for common binding sites.     

Malate and lactate dehydrogenases of a freshwater catfish: impact of endosulfan

A sublethal concentration of technical grade endosulfan (END) inhibited 35 to 55% of the activities of cytoplasmic malate dehydrogenase (cMDH), mitochondrial malate dehydrogenase (mMDH), and lactate dehydrogenase (LDH) in the liver and the skeletal muscle of a freshwater catfish, Clarias batrachus, after 7 days of exposure. The activity remained in the inhibited state up to 28 days. The withdrawal of END from the medium after 1 week of exposure gradually restored the activities to control levels within 21 days in the skeletal muscle and 28 days in the liver. The administration of actinomycin D or cycloheximide between the 14th and the 21st day of the withdrawal of END almost completely inhibited the withdrawal-dependent recovery in the activities of all the three enzymes. This indicates de novo synthesis of the enzymes during the recovery period. A conjoint treatment of END and triiodothyronine (T3) raised the activities of cMDH, mMDH, and LDH in the liver and the skeletal muscle up to the control levels. This shows that the inhibitory effect of END may be relieved in presence of T3. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed few changes in the pattern of cytoplasmic proteins of the liver and the skeletal muscle in response to exposure to END.     

Occular loiasis in a Zambian woman

Asymptomatic infection with Loa loa, an eye worm, is reported in a 32-year old Zambian woman. The patient revealed up to 28% eosinophilia but microfileraemia was not noticed. One gravid female parasite 56 X 0.56 mm, extracted from lower lid of left eye of the patient, is described. Treatment with diethylcarbamazine (DEC) extended over three weeks was successful against another parasite in tissues.     

Hypersensitivity of diabetic human platelets to platelet activating factor.

Platelet activating factor (PAF) stimulated aggregation and [32P]-phosphatidic acid (PA) production was compared in normal and diabetic human subjects in platelet rich plasma. The concentration of PAF for half maximal (50%) aggregation of normal and diabetic platelets was 50 nM and 8 nM, respectively. PAF stimulated [32P]-PA production (a metabolite of phospholipase C pathway) was also greater in the platelets from diabetic subjects. This [32P]-PA production was inhibited by the PAF receptor antagonists SRI-63441 and SRI-63675. When the levels of glycosylated hemoglobin (HbA1c) were compared with the PAF stimulated [32P]-PA production a significant relationship was observed. These studies have demonstrated for the first time that diabetic human platelets show hypersensitivity to PAF in both aggregation and [32P]-PA production compared to normal subjects. This may be a result of some modification in phospholipid turnover mechanism and is receptor mediated. Further, the relationship of the degree of aggregation and [32P]-PA production to the level of HbA1c suggest that the insulin deficiency may contribute to these effects.     

Spontaneous regression of extramedullary plasmacytoma--a case report

A case of extramedullary plasmacytoma in the soft tissues of the posterior chest wall of an 80-year old man is reported herein. Immunofluorescence study showed that the tumor cells produced IgG lambda. An M-component was also detected in the patient's serum by paper electrophoresis. Two months following the open biopsy done to establish diagnosis, the tumor underwent spontaneous regression and the M-component in the serum also disappeared. This is the first case report of spontaneous regression of an extramedullary plasmacytoma and the probable reasons for this spontaneous regression are discussed herein.     

Lack of interaction between nefazodone and cimetidine: a steady state pharmacokinetic study in humans.

The steady-state pharmacokinetic interaction between nefazodone and cimetidine was evaluated in a three-period crossover study consisting of three treatments of 1 week duration with a 1 week washout between treatments. The 18 healthy, male study subjects received: nefazodone hydrochloride 200 mg twice daily (every 12 h) for 6 days; cimetidine 300 mg four times daily for 6 days; and 200 mg nefazodone hydrochloride twice daily + 300 mg cimetidine four times daily for 6 days. On day 7 of each treatment, only the morning dose was administered. Serial blood samples were collected for pharmacokinetic analysis after drug administration on day 7 of each treatment; blood samples for trough levels (Cmin) to assess attainment of steady state, were also collected just prior to the morning doses on days 2-7 of each study period. Plasma samples were assayed for cimetidine, and nefazodone and its metabolites hydroxynefazodone and m-chlorophenylpiperazine by specific, validated h.p.l.c. methods. Statistical analyses of Cmin data indicated that, regardless of treatment, steady state was achieved for cimetidine by day 2 and for nefazodone and its metabolites by day 3 of multiple dosing, and that there were no significant differences in Cmin levels between treatments. When nefazodone and cimetidine were co-administered for 1 week, no change in steady-state pharmacokinetic parameters for cimetidine, nefazodone or hydroxynefazodone was observed compared with each drug dosed alone.(ABSTRACT TRUNCATED AT 250 WORDS)