Treatment of metabolic syndrome: drugs often but diet always - a case report

A case of a 32-year-old male with obesity and hypertension who was admitted to hospital with suspected acute myocardial infarction (MI) is presented. An initial diagnosis of MI was ruled-out, however, diabetes and marked hypertriglyceridemia were detected. Introduction of diet and proper diabetes control with insulin caused a marked decrease in triglyceride and cholesterol levels. After discharge the patient did not comply to dietary recommendations and stopped fibrates due to gastro-intestinal side effects which resulted in a marked elevation in lipid levels. Finally, statin therapy and better compliance to dietary recommendations resulted in the normalisation of cholesterol level, a marked decrease in triglyceride concentration and a loss of 5 kg of body weight. The need for combined treatment consisting of pharmacologic agents and life-style changes is stressed.     

Clinicopathological and ultrastructural study in two cases of chordoid glioma

Chordoid glioma is a rare benign neoplasm of uncertain histogenesis occurring in the third ventricle/ /suprasellar region. Recently, data have emerged suggesting that chordoid glioma is a variant of ependymoma related to a specialised ependyma of the subcommisural organ or the lamina terminalis area. In this study, we report clinicopathological and ultrastructural findings in two chordoid glioma cases. In case 1, a tumour (1.5 cm in diameter) in a 62-year-old man invaded the anterior-basal part of the third ventricle in the lamina terminalis region. In case 2, a large tumour in a 51-year-old woman occupied the whole third ventricle. The tumour attached to the medio-basal hypothalamic region. Histologically, both cases revealed a distinct chordoma-like pattern and glial immunophenotype of tumour cells. Under the electron microscope the tumour cells exhibited microvilli, intercellular lumina, intermediate type junctions and focal basal lamina formations. These findings were similar to those previously reported in the chordoid glioma cases. Moreover, the intracytoplasmic cilia and subplasmalemmal pinocytic vesicles or caveoles were observed. The study supports the view of ependymal derivation of chordoid glioma. Its relation to lamina terminalis or infundibular/median eminence area presumably reflecting tumour origin from the modified ependyma of circumventricular organs of the third ventricle is discussed.     

Sinus tympani in surgery of the middle ear and skull base

Tympanic sinus is located at the medial wall of the tympanic cavity. It's visualisation is difficult from most of approaches. Tympanic sinus is often filled with cholesteatoma in course of chronic otitis. Intraoperative assessment of tympanic sinus was performed in 29 patients with facial recess cholesteatoma, and in 20 patients with acoustic neuroma operated with translabyrinthine approach. In the group of patients with cholesteatoma four patients underwent canal wall up tympanoplasty with posterior tympanotomy, 25 underwent canal wall down tympanoplasty. Tympanic sinus was assessed during surgery with 30 degrees endoscope. In all cases depth of the sinus was measured with the use of calibrated hook. In 11 patients depth of the sinus exceeded 4 mm. In 6 among these features of bone destruction was found.     

Nicotinic receptor subtypes in human brain ageing, Alzheimer and Lewy body diseases

Human brain ageing is associated with reductions in a variety of nicotinic receptors subtypes, whereas changes in age-related disorders including Alzheimer's disease or Parkinson's disease are more selective. In Alzheimer's disease, in the cortex there is a selective loss of the alpha4 (but not alpha3 or 7) subunit immunoreactivity and of nicotine or epibatidine binding but not alpha-bungarotoxin binding. Epibatidine binding is inversely correlated with clinical dementia ratings and with the level of Abeta1-42, but not related to plaque or tangle densities. In contrast, alpha-bungarotoxin binding is positively correlated with plaque densities in the entorhinal cortex. In human temporal cortex loss of acetylcholinesterase catalytic activity is positively correlated with decreased epibatidine binding and in a transgenic mouse model over expressing acetylcholinesterase, epibatidine binding is elevated. In Parkinson's disease, loss of striatal nicotine binding appears to occur early but is not associated with a loss of alpha4 subunit immunoreactivity. Tobacco use in normal elderly individuals is associated with increased alpha4 immunoreactivity in the cortex and lower densities of amyloid-beta plaques, and with greater numbers of dopaminergic neurons in the substantia nigra pars compacta. These findings indicate an early involvement of the alpha4 subunit in beta-amyloidosis but not in nigro-striatal dopaminergic degeneration.     

Depression in patients with Parkinson's disease

The aim of our study was to assess the frequency of depression in group of patients with Parkinson's disease (PD) who fulfilled the diagnostic criteria of PD, had normal CT scans and responded well to L-dopa treatment. The sample consisted of 73 consecutive patients (34 women and 39 men), mean age 65.7 (41-81) years, mean duration of disease 6.7 years. Besides neurological examination, in all the patients the degree of motor impairment was evaluated using the UPDRS, H-Y, and SE scales. Moreover, a sociodemographic questionnaire, psychological tests (MADRS, MMSE), and a quality of life scale (PDQ-39) were used. Depression (MADRS scores > 19) was found in 25 (34.2%) of the patients, with major depression (scores > 28) diagnosed in 7 patients (9.5%) and moderate depression (scores between 20 and 28)--in 18 cases (24.6%). In comparison to non-depressed patients, those with depression were older by 0.9 years on the average, their onset of the disease occurred later by 1.7 years, and their mean duration of the disease was longer by 2.6 years. These differences were not statistically significant. Dementia (MMSE scores < or = 23) did not differentiate between the two groups: it was found in 27 depressed patients (37.4%) and in 26 (35.6%) of those without depression. Patients in the depressed group suffered statistically more often from sleep disorders (19 vs. 14; p < 0.001). In this group motor impairment was significantly more marked, as measured by the UPDRS (32.2 vs. 46.8; p < 0.001) and H-Y (2.54 vs 2.98; p < 0.007), and their quality of life as measured by PDQ-39 questionnaire was significantly lower (36.4 vs. 82.24; p < 0.00002). Our data indicate the presence of depression in 34.2% of the sample, i.e. a somewhat lower prevalence rate than that reported in other studies. This may be due to the fact that only outpatient population was analysed, and outpatients are seldom categorized as degree 4 and 5 on the H-Y scale. Depression on PD patients was correlated with their more severe motor disability and considerably lower quality of life. This may suggest a relationship with progression of the disease and more pronounced changes in cerebral neurotransmitters (i.e. endogenous origin), or PD patient's response to their limited mobility and isolation in later stages of the disease (i.e. reactive origin). However, the two factors--endogenous and reactive--may be overlapping, since a majority of PD patients suffer from mild to moderate depression.     

Additional pulmonary resections after pneumonectomy: actual long-term survival and functional results

Objective: Pulmonary resections after pneumonectomy due to metastases or metachronous non-small cell lung cancer (NSCLC) are rare because of the high potential risk of the second procedure and uncertain long-term results. On the basis of our series (largest in Europe) we tried to assess the long-term survival of patients treated in stage IV NSCLC. Methods: Retrospective analysis was carried out on 18 patients treated at our department by pneumonectomy followed by additional resection in the years 1981-2002 (15 males and 3 females, 44-69 years, mean 57). Eleven pneumonectomies were performed on the right side and seven on the left. Twelve squamous cell carcinomas and six adenocarcinomas were diagnosed. All patients were staged postoperatively as IIB-IIIA (four were N2). Their WHO status ranged between 0 and 1. The second surgical procedure (16 wedge resections, 2 chest wall resections) was performed 4-106 months later (mean 26). The patients staged N2 were radiated postoperatively. Results: There were no early postoperative deaths. The morbidity rate after second surgery was comparable to that observed after ordinary wedge resection. Histology of the lesions removed during the second operation was the same as after pneumonectomy in all patients. The pulmonary function tests (PFT) results worsened significantly but still reached 56-63% of the predicted values. Sixteen resected tumors of the remaining lung were staged T1 (<3cm), 2 - T3 (<3cm but infiltration of the parietal pleura on an area of 2-4cm(2)). Three patients revealed N2 disease (they were all N0 after pneumonectomy). All patients were considered M1 after second surgery. WHO status after the second procedure remained the same in 8 patients (44%) and worsened in 10 patients (56%). The survival rates were as follows: 11 patients survived 2 years (61%) while 8 patients survived 5 years (44%). The majority of patients died due to lung cancer (70%) but all the rest (30%) due to circulatory or respiratory insufficiency. There was a significant difference (p<0.05) in 5-year survival for N0-N1 vs N2 status (63% vs 14% - 1 patient) and also regarding the time interval between surgeries: less than 12 months vs more than 12 months (0% vs 63%). Conclusions: Pulmonary resections performed after pneumonectomy due to NSCLC are rare procedures but with an acceptable perioperative risk. The second procedure should be limited to wedge resection. The prognosis is poor for patients with N2 status and for those treated by second surgery earlier than 12 months after the first procedure.     

Apigenin inhibits TGF-β1 induced fibroblast-to-myofibroblast transition in human lung fibroblast populations

BackgroundFlavonoids are dietary plant compounds suspected to reduce the incidence of chronic diseases in several regions of the world. Due to anti-allergic and anti-inflammatory activities, apigenin (4’,5,7,-trihydroxyflavone) is thought to interfere with crucial events in the pathomechanism of asthma. However, the effect of apigenin on TGF-β-induced fibroblast-to-myofibroblast transition (FMT) in human lung fibroblast populations, a key event in asthma progression, has not yet been addressed.MethodsPrimary human bronchial fibroblasts (HBFs) propagated from ex vivo bronchial biopsies derived from patients with diagnosed asthma and human embryonic lung IMR-90 fibroblasts were cultured in vitro and treated with TGF-β₁ and apigenin. The myofibroblast fraction in fibroblast populations was evaluated by immunocytochemistry. Expression of α-smooth muscle actin (α-SMA) and tenascin C were assessed at the mRNA and protein level by real-time RT-PCR and immunoblotting, respectively. Additionally, proliferation and viability tests and time lapse-monitoring ofmovement of individual HBFs and IMR-90 cellswere evaluated.ResultsWe show that apigenin attenuates TGF-β₁-induced FMT in cultures of HBFs, and the magnitude of this attenuation was found to be similar to that observed in the established cell line of lung IMR-90 fibroblasts. Notably, FMT inhibition was observed at low (~10 μM), non-cytotoxic and non-cytostatic apigenin concentrations and could be correlated with the inhibition of α-SMA and tenascin C expression in HBFs at the mRNA level.ConclusionsOur data are the first to demonstrate that apigenin inhibits the TGF-β₁-induced expansion of hyper-contractile, α-smooth muscle actin – positive myofibroblasts within populations of HBFs derived from asthmatic patients. They also indicate the possible interference of apigenin with bronchial wall remodeling during the asthmatic process in vivo.     

The cost and appropriateness of health care technology in South Africa. A plea for the development of a local medical equipment industry

Some of the main reasons for the increase in the cost of health care technology are summarized. Local problems in the health care delivery system are not being solved effectively by imported medical equipment. The expertise required for the local solution of problems is available in the RSA and should be developed further. A private-sector consortium with matching funding from the State should serve as a clearing house for developing and evaluating assessment criteria, promoting the use of existing cost-efficient medical technologies, and identifying obsolete and inappropriate ones. The formation of a local health care technology corporation should be considered seriously.