Arterial fibromuscular dysplasia

Fibromuscular dysplasia is a nonatherosclerotic, noninflammatory vascular disease that involves primarily the renal and internal carotid arteries and less often the vertebral, iliac, subclavian, and visceral arteries. Although its pathogenesis is not completely understood, humoral, mechanical, and genetic factors as well as mural ischemia may play a role. The natural history is relatively benign, with progression occurring in only a minority of the patients. Typical clinical manifestations are renovascular hypertension, stroke, subarachnoid hemorrhage, abdominal angina, or claudication of the legs or arms. In patients with symptoms, percutaneous transluminal angioplasty has emerged as the treatment of choice in most involved vascular beds.     

Sudden infant death. Family and socio-cultural state and psycho-affective balance

This analysis presents 400 cases of children at risk for sudden infant death syndrome (SIDS) who were followed at the Port-Royal SIDS-clinic from 1981 to 1984. The 400 cases included: 107 children seen after a severe accident ("near-miss"), 20 twins from pairs stricken by 1 SIDS and 9 twins from near-miss pairs, 264 SIDS-siblings. The following risk factors were searched for: a) low socioeconomical level, b) marital difficulties, c) psychological or psychiatric disturbances in mother and/or father, d) pathological gynecologic and/or obstetric history (sterility, gestational and/or delivery accidents), e) unwanted pregnancy, f) perinatal morbidity. In deaths from SIDS or near-miss infants, 34% cumulated 2 factors, 26% 3 factors, 8% 4 factors; only 2% had no known factor. In addition, a few deaths or severe accidents occurred within a short delay after a travel or a change in daycare; the role of these coincidences should be studied; meanwhile, the authors emphasize the need for a special attention to the quality of the child's environment, as a basic factor for a harmonious development.     

Experimental group B streptococcal endocarditis treated with penicillin G versus ceftizoxime. In vitro-in vivo disparity

Aortic valve endocarditis due to a penicillin G (PNC) and ceftizoxime (CZ)-sensitive group B streptococcus (GBS) was induced in 72 rabbits. Animals received either procaine PNC (300 mg/kg per day) or CZ (150 mg/kg/day) for 3, 6, or 9 days. PNC rapidly sterilized blood cultures (less than or equal to 3 days) and significantly reduced vegetation GBS titers versus controls at all three sacrifice times (p less than 0.0005). In contrast, CZ exerted a slow in vivo bactericidal effect with vegetation titers not significantly different from controls until day 9 of therapy. By day 9 of therapy, 65/89 (73%) of vegetations were sterilized by PNC versus only 24/94 (26%) sterilized by CZ (p less than 0.0005). This marked in vitro-in vivo disparity in CZ-treated animals occurred despite 100% of individual serum bactericidal titers greater than or equal to 1:32 and 100% of individual CZ serum levels greater than or equal to 100 times the GBS MBC. The suboptimal CZ in vivo effect was not related to: (1) development of CZ resistance on therapy; (2) CZ inactivation, or (3) inoculum-growth phase effect.     

Estimation of Parkinson’s disease survival in Israeli men and women, using health maintenance organization pharmacy data in a unique approach

The aim of this work was to estimate in an incident cohort of pharmacy-based PD patients the survival of men and women accounting for age at treatment initiation and to compare their gender-specific survival with that of the general Israeli population. A population-based cohort of 4,848 incident pharmacy-based PD cases with definite/probable/possible certainty was previously identified using a drug-tracer approach for 1999–2008. Survival analysis was performed for two time scales: survival after treatment initiation (disease duration), and life-time survival (life expectancy). Kaplan–Meier curves and Cox regressions were used to compare survival across gender. Gender-specific SMRs were calculated from national rates and were compared using Poisson regression. During the follow-up from first purchase of any anti-parkinsonian drug (mean 4.0 ± 2.6 years, range 2 months–10 years), 1,266 (26 %) of the cases died. Younger age at first anti-parkinsonian drug purchase and female gender were associated with increased survival after treatment initiation (HR = 1.089, 95 % CI 1.080–1.098 for 1-year age increase; HR = 0.716, 95 % CI 0.640–0.800, females vs. males). Life-time survival increased with older age at first anti-parkinsonian drug purchase and female gender (HR = 0.759, 95 % CI 0.746–0.771 for 1-year age increase; HR = 0.694, 95 % CI 0.621–0.776, females vs. males). Sensitivity analysis on a sub-cohort of definite cases (n = 2501) yielded similar results. In comparison to the general Israeli population, mortality among pharmacy-based PD patients was significantly increased (SMR_men = 1.69, 95 % CI 1.57–1.81, SMR_women = 1.49, 95 % CI 1.37–1.62), differently between genders (p < 0.01). Female gender was associated with longer, perhaps more benign disease course, and longer life expectancy. Earlier age at anti-parkinsonian drug initiation increased disease duration, but was associated with shorter life expectancy.     

Effect of enalapril on haemoglobin and serum erythropoietin in patients with chronic nephropathy

It has been suggested that angiotensin-converting enzyme (ACE) inhibitors halt the progression of chronic renal failure. During the first months of a controlled trial of this hypothesis a fall in haemoglobin (Hb) was observed in patients treated with the ACE inhibitor enalapril. It was investigated whether this was related to changes in serum erythropoietin (EPO). Data were analysed in 59 consecutive patients during an observation period of 90 days. In enalapril-treated patients (n = 27) Hb fell gradually from a median value of 7.6 to 6.7 mmol/l at 90 days of treatment. In the control group of patients on conventional antihypertensive treatment (n = 32) median Hb was unchanged (7.6 mmol/l) throughout the observation period (p less than 0.001 enalapril vs control). In the enalapril-treated group median EPO concentration fell from 32 to 24 U/l at 90 days of treatment, whereas in conventionally treated patients median EPO was 34 U/l and 35 U/l, respectively (p less than 0.05 enalapril vs control). Neither glomerular filtration rate nor arterial blood pressure differed significantly in the two groups. Furthermore, there were no signs of bone marrow suppression, increased haemolysis or change in plasma volume. In conclusion, a decrease in Hb was found after start of treatment with enalapril in patients with progressive chronic renal failure, possibly caused by a suppression of EPO production.     

Albendazole sulfonation by rat liver cytochrome P-450c

The metabolism of albendazole (ABZ) was studied in perfused livers from control and ABZ-treated rats (10.6 mg/kg, per os, each day for 10 days). In the perfusion fluid, the concentration of ABZ-sulfoxide (SO-ABZ) remained unchanged in treated, as compared to control animals, whereas ABZ-sulfone (SO2-ABZ) was increased in treated animals. In bile, only SO-ABZ was present. The transformation kinetics of SO-ABZ to SO2-ABZ in microsomes from rats treated with ABZ, 3-methylcholanthrene, Aroclor and isosafrole were biphasic. This suggests that enzyme activity was a consequence of two enzyme systems, one characterized by low affinity and high capacity, the other by high affinity and low capacity, the latter could be induced by 3-methylcholanthrene, ABZ, Aroclor and isosafrole. Cytochrome P-450c was induced potently in vivo by ABZ as proven by increased monooxygenase (7-ethoxyresorufin and 7-ethoxycoumarin-O-deethylase) activities and by Elisa test (a 5-fold increase in hemoprotein concentration was observed). Purified and reconstituted cytochrome P-450c from 3-methylcholanthrene or ABZ-treated rat liver were able to produce SO2-ABZ (2.01 and 1.70 nmol/mg/15 min, respectively, whereas cytochrome P-450b produced 10 times less SO2-ABZ). Immunological assays, as well as activity measurements showed a relationship between cytochrome P-450c-3-methylcholanthrene and cytochrome P-450c-ABZ. We conclude that induction of cytochrome P-450c by ABZ is the probable explanation for the enhanced formation of SO2-ABZ in vivo.     

Effects of unilateral stereotactic posterior striatotomy on harmaline‐induced tremor in rats

Although long known and the most prevalent movement disorder, pathophysiology of essential tremor (ET) remains controversial. The most accepted hypothesis is that it is caused by a dysfunction of the olivocerebellar system. Vilela Filho et al. [2001; Stereotact Funct Neurosurg 77:149–150], however, reported a patient with unilateral hand ET that was completely relieved after a stroke restricted to the contralateral posterior putamen and suggested that ET could be the clinical manifestation of posterior putamen hyperactivity. The present study was designed to evaluate this hypothesis in the most often used model of ET, harmaline‐induced tremor in rats. Fifty‐four male Wistar rats were randomly distributed into three groups: experimental (EG), surgical control (SCG), and pharmacological control (PCG) groups. EG animals underwent stereotactic unilateral posterior striatotomy. SCG rats underwent sham lesion at the same target. PCG served exclusively as controls for harmaline effects. All animals received, postoperatively, intraperitoneal harmaline, and the induced tremor was video‐recorded for later evaluation by a blind observer. Thirteen animals were excluded from the study. Limb tremor was reduced ipsilaterally to the operation in 20 of 21 rats of EG and in two of nine of SCG, being asymmetric in one of 10 of PCG rats. Comparisons between EG × SCG and EG × PCG were statistically significant, but not between SCG × PCG. Limb tremor reduction was greater in anterior than in posterior paws. Lateral lesions yielded better results than medial lesions. These results suggest that the posterior striatum is involved with harmaline‐induced tremor in rats and support the hypothesis presented. © 2013 Wiley Periodicals, Inc.     

The role of the general practitioner in cancer care and the effect of an extended information routine

OBJECTIVE: To describe the role of the General Practitioner (GP) in the care of one specified cancer patient per GP, and to explore the GP's knowledge about that patient's disease and treatments, and what information she/he wanted versus received from the specialist clinic. A further aim was to evaluate the effects of an Extended Information Routine (EIR), including increased information from the specialist clinic to the GP. DESIGN: Semi-structured interviews with GPs about a patient randomised between an extended information routine and standard information from the specialist clinics. SETTINGS: Primary Health Care. SUBJECTS: 20 GPs, 10 who received extended information about the specified patient and 10 who did not. MAIN OUTCOME MEASURES: The extent of GPs' contact with the patient, GPs' potential or actual possibilities to support the patient, desired and received information from the specialist clinic. RESULTS AND CONCLUSIONS: GPs are commonly involved in the care of cancer patients, particularly in the diagnostics of the disease but also during the periods of treatment and follow-up. The information from the specialist clinic to the GP is insufficient in standard care. The extended information routine increased the GPs' knowledge of the disease and treatments, and facilitated their possibilities to determine patients' need for support.