B-Lynch sutures for major primary postpartum haemorrhage at caesarean section.

This was a retrospective observational study of 11 consecutive patients of major primary postpartum haemorrhage (PPH) who had the B-Lynch suture at the time of caesarean section, performed between 1 March 2001 and 31 March 2004 at a teaching hospital in Scotland. Case-note review was performed in 123 patients, who had major primary PPH to identify patients who had B-Lynch sutures at the time of caesarean section. The patient's age, parity, gestation of pregnancy at which the B-Lynch suture was performed, the indication for caesarean section and the cause of primary major PPH were recorded. The operative details, intraoperative and immediate postoperative complications and the need for subsequent hysterectomy were noted. The patients were followed-up with clinic visits at 6 weeks and any further hospital referral for late postoperative complications and whether subsequent successful pregnancy was achieved, were documented. The incidence of major PPH in our centre was 0.5% of the total deliveries, of which 11 cases had the B-Lynch suture applied at the time of caesarean section. The patients were aged between 25 and 38 years old (mean 31 years). Parity ranged from 0 to 1 and the gestational age at which the procedure was performed ranged from 34 to 41 weeks (mean 38 weeks). Ten operations (91%) were performed by senior registrars supervised by the consultant on call and one (9%) case was performed by a consultant on call. All cases had the B-Lynch sutures performed for major primary PPH caused by uterine atony at the time of caesarean section. The weight of the babies delivered ranged between 2,110 - 4,820 g (mean 3,500 g). The total blood loss at surgery ranged from 2,000 - 10,000 ml (mean 3,500 ml). Only three patients (28%) required hysterectomy. All the patients made a good postoperative recovery. The hospital stay ranged from 4 - 24 days (mean 8 days). The patient who remained in hospital for 24 days did so because her baby was admitted into the neonatal unit. All the patients were reviewed 6 weeks postnatally. There was no significant morbidity. A subsequent successful pregnancy has been achieved in one patient.     

A Chinese adolescent girl with Fechtner-like syndrome

We describe a 15-y-old girl with Fechtner-like syndrome, who is the first Chinese reported to have this rare syndrome. She presented with left homonymous hemianopia and neuroimaging revealed haemorrhage in both parietal and occipital lobes. Peripheral blood smear showed macrothrombocytopenia and intracytoplasmic inclusion bodies inside leucocytes. Thrombocytopenia and proteinuria responded to intravenous immunoglobulin and pulsed methylprednisolone. This case illustrates that life-threatening haemorrhage can occur in patients with Fechtner syndrome. Although there was no effective treatment reported in the literature, high dose steroid and immunoglobulin seemed to be useful in our patient. Our patient also had nephritic-nephrotic syndrome with renal insufficiency, which is unusual in adolescent female patients.     

Occurrence of the t(2;5)(p23;q35) in non-Hodgkin's lymphoma

Primary CD30(Ki-1)-positive anaplastic large-cell lymphoma (ALCL) is considered by some to be a distinct clinicopathologic entity associated with the t(2;5) (p23;q35). However, the specificity of t(2;5) for ALCL has not been carefully studied. Therefore, we performed a detailed analysis of all cases of ALCL with abnormal cytogenetics results in the Nebraska Lymphoma Study Group registry, as well as all other cases of non-Hodgkin's lymphoma with t(2;5) in the registry. We found the t(2;5) in only five of 10 cases of ALCL, four of whom were young patients. However, we also found the t(2;5) in 11 other cases of nonanaplastic lymphoma, including eight children with typical peripheral T-cell lymphomas of various types. The t(2;5) was also found in three older adults with B-cell lymphomas of various types. Thus, the t(2;5) was not specific for CD30+ ALCL. However, t(2;5) may define a clinicopathologic entity in children and young adults characterized by variable morphologies with a T-cell or indeterminate phenotype, CD30-positivity, nodal disease with frequent extranodal involvement, advanced stage, and an excellent response to therapy, including bone marrow transplantation for relapsed disease. The clinical relevance of the t(2;5) in older patients requires further study.     

INVOLVEMENT OF NON-NMDA AND NMDA RECEPTORS IN GLUTAMATE-INDUCED PRESSOR OR DEPRESSOR RESPONSES OF THE PONS AND MEDULLA

1. Fifty-five intact and six baroreceptor denervated and vagotomized cats of either sex were anaesthetized intraperito-neally with urethane (400 mg/kg) and a-chloralose (40 mg/kg). Responses of the systemic arterial pressure (SAP), mean SAP (MSAP) and sympathetic vertebral nerve (VNA) and renal nerve activities (RNA) were recorded. 2. In intact animals, monosodium L-glutamate (Glu, 0.1 mol/L, 50 nL) was microinjected into pressor areas of the locus coeruleus (LC), gigantocellular tegmental field (GTF), rostral ventrolateral medulla (RVLM) and dorsomedial medulla (DM), and the depressor areas of caudal ventrolateral medulla (CVLM). The induced actions were compared before and after microinjection of either glutamate antagonists, glutamate diethylester (GDEE, 0.5 mol/L, 50–100nL), a competitive AMPA receptor blocker, or 2-amino-5-phosphonovaleric acid (D-AP5, 0.025 mol/L, 50–100 nL), a competitive N-methyl-D-aspartate (NMDA) receptor blocker. GDEE completely blocked the increases of SAP and VNA elicited from all pressor areas. D-AP5 only partially blocked the pressor but slightly blocked VNA and RNA responses from LC, GTF and DM, particularly those from RVLM. Neither GDEE nor D-AP5 blocked the depressor responses of SAP and two nerve activities elicited from CVLM. 3. In baroreceptor denervated animals, NMDA (2 mmol/L, 50–100 nL) and AMPA (0.2 mmol/L, 50–100 nL) were micro-injected into the same pressor areas of GTF, RVLM and DM and the depressor area of CVLM responsive to Glu activation (0.1 mol/L, 30 nL). In RVLM, DM and CVLM, the results of either NMDA or AMPA were similar to those induced by Glu. However, in GTF, microinjection of either NMDA or AMPA did not induce similar responses to Glu. This suggests that the nature of GTF may differ from RVLM and DM. 4. The above results suggest that the Glu-induced pressor responses from LC, GTF, DM and especially RVLM, are primarily mediated through AMPA receptors. The Glu-induced depressor responses from CVLM may not be predominantly mediated by either AMPA or NMDA receptors. 5. In both baroreceptor-intact and -denervated cats stimulation of the pressor areas often produced an increase of VNA and a decrease of RNA, while in the depressor CVLM decreased both VNA and RNA. The VNA, but not RNA were positively correlated with the pressor responses, while both VNA and RNA were positively correlated with the depressor responses. This may suggest that neurons of the sympathetic vertebral and renal nerves are topographically organized in the brain.     

The importance of seizure-inducing factors in youth

Of over forty known epileptogenic mechanisms, some eight involve transient conditions, the regulation of which necessarily involves the understanding cooperation of the patient/parents. Tension states, alterations of the wake-sleep cycle, fatigue and sleep deprivation, CNS stimulation by sensory or drug means, and shifts of the water and acid-base balances constitute the bulk of such seizure-inducing factors. The relative lack of CNS homeostatic control, due to immature development of the blood-brain barrier and cerebral maturation, serve to exaggerate these problems in childhood. In a referred group of 150 refractory epileptic children, the seizure-inducing mechanisms were found to be important (50% reduction of seizure incidence) in 20% and to be of "crucial" importance (complete control) in an additional 14%. These results indicate the importance of such mechanisms in selected children with epilepsy, who were only marginally or inadequately controlled by drug therapy. Reviews of the literature have suggested that this more comprehensive approach to the therapeutic management of epilepsy has not been adequately exploited.     

Induced luteolysis in the primate: rapid loss of luteinizing hormone receptors

The molecular mechanisms involved in luteolysis are still unclear in the primate. This study aimed to investigate the effect of induced luteolysis on the ovarian luteinizing hormone (LH) receptor and the steroidogenic enzyme, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) in the marmoset monkey. Luteolysis was induced in the mid-luteal phase either directly by systemic prostaglandin F2alpha (PGF2alpha), or indirectly by LH withdrawal using systemic gonadotrophin releasing hormone antagonist (GnRHant) treatment. The LH receptor was studied by isotopic mRNA in-situ hybridization and in-situ ligand binding and 3beta-HSD expression was studied using isotopic mRNA in-situ hybridization and immunohistochemistry. Induced luteolysis was associated with a reduction in the expression of LH receptor (P < 0.0001) and 3beta-HSD mRNA, closely followed by a reduction in the LH receptor (P < 0.05) and 3beta-HSD protein concentrations within 24 h. There were no differences in the findings whether luteolysis was induced with PGF2alpha or GnRHant. This study shows that disparate mechanisms to induce luteolysis in the primate result in an identical rapid loss of the LH receptor and 3beta-HSD. In conclusion, induced luteolysis leads to rapid loss of the steroidogenic pathway in luteal cells.