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Biomedical subjects

T D Nguyen

Publications and source records attributed to T D Nguyen.

At least 37 records · Page 2Linked to original sources
PubMed2001

Differential cellular accumulation of connective tissue growth factor defines a subset of reactive astrocytes, invading fibroblasts, and endothelial cells following central nervous system injury in rats and humans.

In brain injury, the primary trauma is followed by a cascade of cellular and molecular mechanisms resulting in secondary injury and scar formation. Astrogliosis and expression of transforming growth factor beta (TGF-beta) are key components of scar formation. A cytokine mediating the effects of TGF-beta is connective tissue growth factor (CTGF), a fibrogenic peptide encoded by an immediate early gene with suggested roles in tissue regeneration and aberrant deposition of extracellular matrix. In order to investigate CTGF in traumatic lesions, we evaluated 20 human brains with traumatic brain injury (TBI) and 18 rat brains with stab wound injury. Compared to remote areas and unaltered control brains, CTGF+ cells accumulated in border zones of the traumatic lesion site (p < 0.0001). In the direct peri-lesional rim, CTGF expression was confined to invading vimentin+, GFAP- fibroblastoid cells, endothelial and smooth muscle cells of laminin+ vessels, and GFAP+ reactive astrocytes. In the direct peri-lesional rim, CTGF+ astrocytes (>80%) co-expressed the activation associated intermediate filaments nestin and vimentin. In injured rat brains, numbers of CTGF+ cells peaked at day 3 and 7 and decreased to almost base level 3 weeks postinjury, whereas in humans, CTGF+ cells remained persistently elevated up to 6 months (p < 0.0001). The restricted accumulation of CTGF+-reactive astrocytes and CTGF+ fibroblastoid cells lining the adjacent laminin+ basal lamina suggests participation of these cells in scar formation. Furthermore, peri-lesional upregulation of endothelial CTGF expression points to a role in blood-brain barrier function and angiogenesis. In addition, CTGF appears to be a sensitive marker of early astrocyte activation.

Adult↗
PubMed2001

Distinct requirements for IL-6 in polyclonal and specific Ig production induced by microorganisms.

The role of IL-6 in Ig production induced in the mouse by lactate dehydrogenase-elevating virus (LDV), Toxoplasma gondii or lipopolysaccharide (LPS) was assessed. Following infection with LDV, a strong activator of B cells, an early and transient IL-6 production was observed, that originated predominantly from macrophages. Whereas LDV-induced B lymphocyte proliferation appeared independent of IL-6, mice deficient for this cytokine showed a marked reduction in their total T-dependent IgG2a production when compared to their normal counterparts. By contrast, specific responses directed against either LDV or non-viral antigens administered at the time of infection were not decreased in the absence of IL-6. Similarly, polyclonal, but not anti-parasite IgG2a production triggered by T. gondii infection was strongly dependent on the presence of IL-6. Finally, T-independent total IgG3 secretion triggered by LPS was also markedly reduced in IL-6-deficient mice. These results suggest that IL-6 plays a major role in T-dependent and T-independent polyclonal Ig production following B lymphocyte activation by viruses, and parasites, but not in specific antibody responses induced by the same microorganisms.

Animals↗
PubMed2001

Coronary MR angiography: selection of acquisition window of minimal cardiac motion with electrocardiography-triggered navigator cardiac motion prescanning--initial results.

The authors developed an electrocardiography-triggered M-mode navigator-echo technique to help monitor cardiac motion and identify the period of minimal cardiac motion in the cardiac cycle. Coronary magnetic resonance angiography was performed in eight healthy adult volunteers and one patient with heart disease. To minimize cardiac motion effects, trigger delays were estimated with the navigator-echo technique and two empirical formulas. The quality of images obtained with the different delay times was compared for clarity of depiction of the coronary arteries. Image quality was best with the delay calculated with the navigator-echo technique.

Adult↗
PubMed2001

P2Y(11), a purinergic receptor acting via cAMP, mediates secretion by pancreatic duct epithelial cells.

Pancreatic duct epithelial cells (PDEC) mediate the exocrine secretion of fluid and electrolytes. We previously reported that ATP and UTP interact with P2Y(2) receptors on nontransformed canine PDEC to increase intracellular free Ca2+ concentration ([Ca2+](i)) and stimulate Ca2+-activated Cl- and K+ channels. We now report that ATP interacts with additional purinergic receptors to increase cAMP and activate Cl- channels. ATP, 2-methylthio-ATP, and ATP-gamma-S stimulated a 4- to 10-fold cAMP increase with EC(50) of 10-100 microM. Neither UTP nor adenosine stimulated a cAMP increase, excluding a role for P2Y(2) or P1 receptors. Although UTP stimulated an (125)I(-) efflux that was fully inhibited by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM), ATP stimulated a partially resistant efflux, suggesting activation of additional Cl- conductances through P2Y(2)-independent and Ca2+-independent pathways. In Ussing chambers, increased cAMP stimulated a much larger short-circuit current (I(sc)) increase from basolaterally permeabilized PDEC monolayers than increased [Ca2+](i). Luminal ATP and UTP and serosal UTP stimulated a small Ca2+-type I(sc) increase, whereas serosal ATP stimulated a large cAMP-type I(sc) response. Serosal ATP effect was inhibited by P2 receptor blockers and unaffected by BAPTA-AM, supporting ATP activation of Cl- conductances through P2 receptors and a Ca2+-independent pathway. RT-PCR confirmed the presence of P2Y(11) receptor mRNA, the only P2Y receptor acting via cAMP.

Adenosine Triphosphate↗
PubMed2001

[Network of care for breast cancers: a prospective survey among general practitioners].

OBJECTIVE: To clarify the general practitioner (GP)'s current perception on a network dedicated to mammary cancers in a rural department. METHODS: A survey by questionnaire was carried out from March to September 1999. This questionnaire made of 3 different sheets and 4 parts entitled "your practice in oncology", the "partnership", "GPs and network", "expectations" respectively, was mailed to 233 GPs board certified by the Conseil Départemental de l'Ordre des Médecins. Questionnaire included space for free comments and a specification sheet. There was no letter of reminder following the first mail. RESULTS: The rate of spontaneous answers was 48% (112/233). Representativeness of the sample was considered coherent with age, sex-ratio, mean duration of setting up, practice modalities in the department of Aube. GPs took care, on annual average, over 6 patients with breast cancer. They generally referred their patients to the oncologist team at the Centre hospitalier général. Such a choice was mainly sustained by the quality of patient reception, the psychological support and the fraternal relationship. GPs were mostly concerned (76%) by the management of both chemotherapy side effects and psychological problems occurring in their patients. By popular request, they wished the setting up of a hot line and a systematic historical reminder of the adverse effects joined to the mail. As far as the network was concerned, 83% of the GPs thought it could be helpful, but only 60% would actively participate. Reasons for such a discrepancy are discussed taking free comments into account. CONCLUSIONS: GPs in the Aube department seem eager to practice in a more collective way, which places the patient in the heart of the medical approach. However they demand to play a key role according both to their knowledge of the whole file and to the trust the patients are putting on them.

Adult↗
PubMed2000

Persistent accumulation of cyclooxygenase-1 (COX-1) expressing microglia/macrophages and upregulation by endothelium following spinal cord injury.

Acute inflammation following spinal cord injury results in secondary injury and pathological reorganisation of the central nervous system (CNS) architecture. Cyclooxygenases (Prostaglandin Endoperoxide H Synthases, PGH) are key enzymes in the conversion of arachidonic acid into prostanoids which mediate immunomodulation, mitogenesis, apoptosis, blood flow, secondary injury (lipid peroxygenation) and inflammation. Here, we report cyclooxygenase-1 (COX-1) expression following spinal cord injury. In control spinal cords, COX-1 expression was localized by immunohistochemistry to ependymal cells, some neurons, inclusive dorsal and ventral root ganglion cells, few endothelial cells but rarely to brain microglia/macrophages. In injured spinal cords, COX-1(+) microglia/macrophages accumulated highly significantly (P<0.0001) at peri-lesional areas and in the developing necrotic core early after injury. Here numbers of COX-1(+) cells remained persistently elevated up to 4 weeks following injury. Further, COX-1(+) cells were located in perivascular Virchow-Robin spaces, between spared axons and in areas of Wallerian degeneration. Double labeling experiments confirmed co-expression of COX-1 by ED-1(+) and OX-42(+) microglia/macrophages. Transiently after infarction most COX-1(+) microglia/macrophages coexpress the activation antigen OX-6 (MHC class II). However, the prolonged accumulation of COX-1(+) microglia/macrophages at the lesion site enduring the acute post injury inflammatory response points to a role of COX-1 in tissue remodeling or secondary injury. We have identified and localized persistent accumulation of COX-1 expressing cells which might be a potential pharmacological target following spinal cord injury. Therefore, we suggest that approaches based on: (i) short-term; and (ii) selective COX-2 blocking alone might not be a sufficient tool to suppress the local synthesis of prostanoids.

Animals↗
PubMed2000

Isolation and heterologous expression of two genomic clones encoding Shaker-related potassium channels of trout CNS.

Two Shaker-related potassium channel genes (termed tsha1 and tsha2) expressed in the CNS of trout were cloned and sequenced. The coding regions of both genes were not interrupted by introns and exhibited a high overall sequence similarity to other members of the Shaker subfamily. By computer-assisted sequence alignments, tsha1 was identified as a fish homologue to the mammalian Kv1.2 subtype of potassium channels, whereas tsha2 did not show a preferential sequence homology but shared a uniform similarity to Kv1.1, Kv1.2, and Kv1.3. Upon heterologous expression in a mammalian glial cell line, both channels exhibited delayed rectifier current properties that differed from each other by their threshold potentials of activation and their pharamcological features: wheras the tsha1-mediated current was efficiently blocked by submicromolar concentrations of alpha-DTX but not by TEA, tsha2 was highly TEA-sensitive, correlating well with differences in the amino acid structure of the pore outer mouth region. As revealed by RT-PCR, Shaker-related potassium channels were sequentially expressed during trout brain development: tsha2 was found initially at stage 34, followed by tsha1 at stage 36, whereas two other members of the Shaker family (tsha3 and tsha4) were detectable much earlier (stage 30, hatching). In the mature brain tissue, no regional specialization of Shaker channel subtype expression was noted.

Amino Acid Sequence↗
PubMed2000

Selective accumulation of cyclooxygenase-1-expressing microglial cells/macrophages in lesions of human focal cerebral ischemia.

Cyclooxygenases (COX; prostaglandin endoperoxide H synthases) are key enzymes in the conversion of arachidonic acid into prostanoids which mediate inflammation, immunomodulation, mitogenesis, ovulation, fewer, apoptosis and blood flow. Here, we report COX-1 expression following focal cerebral infarctions (FCI). In healthy control brains, COX-1 was localized by immunohistochemistry to a few endothelial cells, single neurons and rare, evenly distributed brain microglia/macrophages. In infarctioned brains, COX-1+ cells accumulated highly significantly (P < 0.0001) in peri-infarctional areas and in the developing necrotic core early after infarction. Here, cell numbers remained persistently elevated up to several months post infarction. Further, clusters of COX-1+ cells were located in perivascular regions related to the Virchow-Robin space. Double-labeling experiments confirmed co-expression of COX-1 by CD68+ microglia/macrophages. Co-expression of the activation antigens HLA-DR, -DP, -DQ (MHC class II) or the macrophage inhibitor factor-related protein MRP-8 (S100A8) by most COX-1+ microglia/macrophages was only seen early after infarction. Thus, COX-1 appeared to be expressed in microglial cells regardless of their activation state. However, the prolonged accumulation of COX-1+ microglia/macrophages restricted to peri-infarctional areas enduring the acute post-ischemic inflammatory response points to a role of COX-1 in tissue remodeling or in the pathophysiology of secondary injury. We have identified localized, accumulated COX-1 expression as a potential pharmacological target following FCI. Therefore we suggest that therapeutic approaches based on selective COX-2 blocking might not be sufficient for suppressing the local synthesis of prostanoids.

Aged↗
PubMed2000

Lesion-associated accumulation of uPAR/CD87- expressing infiltrating granulocytes, activated microglial cells/macrophages and upregulation by endothelial cells following TBI and FCI in humans.

Urokinase-type plasminogen activator receptor (uPAR/CD87) together with its ligand, urokinase-type plasminogen activator (uPA), constitutes a proteolytic system associated with tissue remodelling and leucocyte infiltration. uPAR is a member of the glycosyl phosphatidyl inositol (GPI) anchored protein family. The functional role of uPAR comprises fibrinolysis by conversion of plasminogen to plasmin. In addition, uPAR promotes cell adhesion, migration, proliferation, re-organization of the actin cytoskeleton, and angiogenesis. Furthermore, uPAR is involved in prevention of scar formation and is chemoattractant to macrophages and leucocytes. In order to investigate the pathophysiological role of uPAR following human CNS injury we examined necrotic brain lesions resulting from traumatic brain injury (TBI; n = 28) and focal cerebral infarctions (FCI; n = 17) by immunohistochemistry. Numbers of uPAR+ cells and uPAR+ blood vessels were counted. Following brain damage, uPAR+ cells increased significantly within 12 h, reached a maximum after 3-4 days and remained elevated until later stages. uPAR was expressed by infiltrating granulocytes, activated microglia/macrophages and endothelial cells. Numbers of uPAR+ vessels increased in parallel subsiding earlier following FCI than post TBI. The restricted, lesion-associated accumulation of uPAR+ cells in the brain parenchyma and upregulated expression by endothelial cells suggests a crucial role for the influx of inflammatory cells and blood-brain barrier (BBB) disturbance. Through a failure in BBB function, uPAR participates in formation of brain oedema and thus contributes to secondary brain damage. In conclusion, the study defines the localization, kinetic course and cellular source of uPAR as a potential pharmacological target following human TBI and FCI.

Adolescent↗
PubMed2000

Connective tissue growth factor is expressed by a subset of reactive astrocytes in human cerebral infarction.

Connective tissue growth factor (CTGF), a transforming growth factor (TGF)-beta1 downstream mediator, is a secreted cell matrix-inducing peptide involved in both tissue regeneration mechanisms, such as wound repair, and also in aberrant deposition of extracellular matrix. The present study reports CTGF expression by cells associated with matrix deposition and glial scar formation in human cerebral infarction. CTGF was localized by immunohistochemistry in 17 brains of patients after focal infarction and in three neuropathologically normal control brains. CTGF expression was selectively localized to the cytoplasm of stellate reactive astrocytes. Compared to peripheral areas and brain controls without neuropathological findings, the total number CTGF+ astrocytes was significantly higher (P < 0.0001) in border zones adjacent to the core, corresponding to the penumbra. These numbers were significantly increased at day 1 and day 3 and remained persistently elevated up to several months post-infarction (P < 0.0001). The restricted expression and accumulation of CTGF+ reactive astrocytes adds convincing evidence for CTGF participation in the gliotic astrocyte CNS injury response involved in glial scar formation. CTGF can be considered a sensitive marker of early human astrocyte activation and a possible target for pharmacological intervention of aberrant matrix deposition.

Aged↗
PubMed2000

Panax vietnamensis protects mice against carbon tetrachloride-induced hepatotoxicity without any modification of CYP2E1 gene expression.

In order to explore the effect of Panax vietnamensis on carbon tetrachloride-induced hepatotoxicity, mice were pretreated for 7 days with either crude extract or total saponins. Crude extract and total saponins dramatically decreased carbon tetrachloride-induced increase of serum GST alpha level (-50.0%, -49.5% respectively). Serum AST level was significantly decreased only with total saponins (-52.2%) and ALT level was slightly modified. In vitro experiments shown that both preparations at high concentrations (> 2000 micrograms/ml) are able to inhibit CYP2E1 enzymatic activity in mouse and human microsomes. However, we did not observe any modification of Cyp2e1 gene expression (enzymatic activity, protein and mRNA levels) in mice treated with either crude extract or total saponins. Taken together, these data demonstrated that Panax vietnamensis could be used as an hepatoprotectant. However, the mechanism of action is not associated with CYP2E1 expression, as previously suggested in vitro in rat for total saponins from Panax ginseng.

Animals↗
PubMed2000

Immunohistochemical localization of MYOC/TIGR protein in the trabecular tissue of normal and glaucomatous eyes.

PURPOSE: To examine immunohistochemically the localization of myocilin/trabecular meshwork inducible glucocorticoid response (MYOC/TIGR) protein in the glaucomatous and normal trabecular meshworks. METHODS: Trabecular tissues were used from one eye with late-onset goniodysgenetic glaucoma, three with primary open angle glaucoma (one of which had the MYOC/TIGR gene mutation), two with exfoliation glaucoma and one without glaucoma. For light microscopic immunohistochemistry, frozen sections were stained by the avidin-biotin complex method using anti-MYOC/TIGR polyclonal antibody. For electron microscopic immunohistochemistry, the pre-embedding method using the same antibody was performed. Double immunostaining using both anti-MYOC/TIGR and anti-type VI collagen antibodies was done by the immunofluorescence method. RESULTS: With light microscopy, immunoreactivity was seen in the whole trabecular meshwork of each of the specimens. No notable differences were detected in staining among the types of glaucoma, or between the eyes with and those without the gene mutation. Under electron microscopy, immunoreaction products were observed not only in the cytoplasm of the trabecular cells but also in the extracellular matrix, where staining was associated with the long-spacing collagen, fine granular materials and possibly microfibrils. With double immunohistochemistry, MYOC/TIGR was colocalized with type VI collagen in the trabecular meshwork. CONCLUSIONS: In glaucomatous and normal trabecular meshworks, the MYOC/TIGR protein is distributed in the extracellular matrix colocalizing with type VI collagen.

Adolescent↗
PubMed2000

Regulation of exocytosis by protein kinases and Ca(2+) in pancreatic duct epithelial cells.

We asked if the mechanisms of exocytosis and its regulation in epithelial cells share features with those in excitable cells. Cultured dog pancreatic duct epithelial cells were loaded with an oxidizable neurotransmitter, dopamine or serotonin, and the subsequent release of these exogenous molecules during exocytosis was detected by carbon-fiber amperometry. Loaded cells displayed spontaneous exocytosis that may represent constitutive membrane transport. The quantal amperometric events induced by fusion of single vesicles had a rapid onset and decay, resembling those in adrenal chromaffin cells and serotonin-secreting leech neurons. Quantal events were frequently preceded by a "foot," assumed to be leak of transmitters through a transient fusion pore, suggesting that those cell types share a common fusion mechanism. As in neurons and endocrine cells, exocytosis in the epithelial cells could be evoked by elevating cytoplasmic Ca(2+) using ionomycin. Unlike in neurons, hyperosmotic solutions decreased exocytosis in the epithelial cells, and giant amperometric events composed of many concurrent quantal events were observed occasionally. Agents known to increase intracellular cAMP in the cells, such as forskolin, epinephrine, vasoactive intestinal peptide, or 8-Br-cAMP, increased the rate of exocytosis. The forskolin effect was inhibited by the Rp-isomer of cAMPS, a specific antagonist of protein kinase A, whereas the Sp-isomer, a specific agonist of PKA, evoked exocytosis. Thus, PKA is a downstream effector of cAMP. Finally, activation of protein kinase C by phorbol-12-myristate-13-acetate also increased exocytosis. The PMA effect was not mimicked by the inactive analogue, 4alpha-phorbol-12,13-didecanoate, and it was blocked by the PKC antagonist, bisindolylmaleimide I. Elevation of intracellular Ca(2+) was not needed for the actions of forskolin or PMA. In summary, exocytosis in epithelial cells can be stimulated directly by Ca(2+), PKA, or PKC, and is mediated by physical mechanisms similar to those in neurons and endocrine cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2000

IFN-gamma-independent IgG2a production in mice infected with viruses and parasites.

After infection with some viruses and intracellular parasites, antibody production is restricted to IgG2a. We first observed that, whereas live viruses such as lactate dehydrogenase-elevating virus (LDV) or mouse adenovirus induced mostly an IgG2a response, a large proportion of antibodies produced against killed viruses were IgG1. This IgG1 antiviral response was suppressed when live virions were added to inactivated viral particles. These results indicate that the IgG2a preponderance is related to the infectious process itself rather than to the type of antigen involved. Since IFN-gamma is known to stimulate IgG2a production by activated B lymphocytes and to be secreted after infection, we examined the role of this cytokine in the antibody isotypic distribution caused by LDV. Most IgG2a responses were relatively unaffected in mice deficient for the IFN-gamma receptor or treated with anti-IFN-gamma antibody. A similar IFN-gamma-independent IgG2a secretion was observed after infection with the parasites Toxoplasma gondii and Trypanosoma cruzi. However, the IFN-gamma-independent IgG2a production triggered by infection still required the presence of functional T(h) lymphocytes. Therefore, signal(s) other than IFN-gamma secretion may explain the T(h)-dependent isotypic bias in antibody secretion triggered by viruses and parasites.

Adenoviridae↗
PubMed2000

Degradation kinetics of leucine5-enkephalin by plasma samples from healthy controls and various patient populations: in vitro drug effects.

Incubation of [3H]tyrosine leucine5-enkephalin with platelet-poor human plasma (final concentration 1 x 10(-8) M; 1:9 ratio to Trizma base buffer, pH 7.4) resulted in rapid and complete peptide degradation in each of the subjects studied, with more than 95% of the initial labeled tyrosine consistently recovered as the free amino acid (< or =30 minutes). Essentially, and irrespective of the incubation time (1-180 minutes), tyrosine was the only Leu metabolite formed; we were unable to identify significant amounts (> or =3%) of any other possible labeled or nonlabeled Leu degradation fragments. Neither gender (64 men and 20 women; samples tested individually), age (men, 23-70; women, 25-65 years), nor the subjects' medical condition appeared to make a significant difference in either the t1/2 of Leu elimination, the initial velocity of this reaction (x +/- SD, median, minimum and maximum of 12.0 +/- 0.9, 12.0, and 10.6-13.7 minutes; 1.2 +/- 0.3, 1.1, and 0.6-2.0 pg/min, respectively), or in the Km and Vmax values for aminopeptidase Leu degradation (x +/- SD; 0.81 +/- 0.01 mM and 14.30 +/- 1.17 micromol/L/min, respectively). Subjects were diagnosed as chronic schizophrenics (n = 15), polydrug abusers including alcohol (n = 9) and polydrug abusers excluding alcohol (n = 8), chronic alcoholics (n = 12), and migraineurs (n = 10) during or outside an acute migraine episode; for comparison we used a group of gender-matched (20 men and 10 women), age-comparable, drug-free, healthy volunteers. Differences in plasma storage time or repeated sample freezing and thawing failed to alter significantly any of these kinetic parameters of Leu metabolism or to change the identity and/or relative ratio of the products formed. The Leu degradation rate was pH and temperature dependent (optimum, 7.4 and 37 degrees C, respectively). Leu degradation was strongly and similarly inhibited by puromycin, bacitracin, and bestatin (IC50 [+/- SD] of 1.4 +/- 0.2 micromol/L) and to a lesser extent by various L-tyrosine-containing Leu fragments. The kinetics of this reaction was not significantly affected by either thiorphan, N-carboxyphenylmethyl leucine, or any other of a number of monoamine neurotransmitters, substances of abuse, nonsteroidal anti-inflammatory agents, and miscellaneous compounds tested (concentration up to 10(-4) mol/L).

Adult↗
PubMed2000

[Linear radiodermatitis following total body electron beam therapy].

BACKGROUND: We describe herein a peculiar clinical presentation of a linear overlapping radiodermatitis, localized on the internal side of the limbs, following a total body electron beam therapy. CASE REPORT: A 68-year-old-man was treated in April 1998 by a total body electron beam therapy, for a stage I mycosis fungoides. Few days after the last irradiation, the patient suffered from a linear eruption localized on the internal side of the limbs and the external side of the abdominal wall. DISCUSSION: Total body electron beam therapy can be proposed in early stage mycosis fungoides with localized or generalized cutaneous lesions. Because penetration depth of electron is well controlled and is limited to the skin, usual side effects of total body electron beam therapy do not concern internal organs (bone marrow,.). We report here a peculiar clinical presentation of a linear radiodermatitis in frontal plane which has not been reported to date, to our knowledge. This radiodermatitis corresponds to overlapping of posterior and anterior fields of irradiation.

Aged↗
PubMed2000

Pharmaceutical sector in transition--a cross sectional study in Vietnam.

Increasing efforts are being made to improve pharmaceutical sector performance in low- and middle-income countries. An essential tool for such work is an objective and standard method of assessment which can be used to promote evidenced based National Drug Policy development and implementation. The average drug expenditure per capita has steadily increased in Vietnam and at the time of this study a National Drug Policy was being developed. This study assessed the Vietnamese pharmaceutical sector 1991-1994, focusing on the standard of the drug quality control system, availability of drugs and rational use of essential drugs in the private and public sectors by means of standardised indicators. The results from this study show that the quality control system is impaired and does not have capacity to quality control all drugs on the market. The availability of essential drugs is good whereas essential drugs are poorly prescribed, injections common and there is a high average number of drugs per prescription, both in the public and private sectors. Violations are common and enforcement of regulations weak. On top of this there is an active commercial advertising and marketing of drugs. These findings identify priorities for action to improve the present situation where the development and implementation of the Vietnamese National Drug Policy will be of major importance.

Cross-Sectional Studies↗