Pharyngeal involvement in tuberculosis is rare and is usually secondary to pulmonary tuberculosis. We report a very rare case of chronic granulomatous pharyngitis, which later turned out to be due to primary tuberculosis of the pharynx. The clinical presentation, diagnosis, treatment and complications of this rare clinical entity are presented.

Adult↗

PubMed1998

Retropharyngeal abscess: recent trends.

Retropharyngeal abscess (RPA) is relatively rare today. A study of 17 cases of RPA treated at our hospital in the past 10 years showed a shift in the disease from children below 6 years of age (41%) to older children and adults (58%). Upper respiratory tract infection (URTI) was found to be the commonest (52%) aetiological predisposing factor in all age groups. Other aetiological factors were septicaemia (11%) in children below the age of 6 years and trauma due to foreign body (35%) in the older children and adult age groups. Klebsiella, Staphylococcus and Streptococcus were the commonest species of microorganisms grown from pus. The changing clinical trends, microbiology, choice of antibiotics, usefulness of radiology, and complications of this potentially fatal illness are discussed.

Adolescent↗

PubMed1998

Teratocarcinosarcoma of the nasal cavity and ethmoid.

Sinonasal teratocarcinosarcoma is very unusual malignant neoplasm histologically consisting of an epithelial element and one or more mesenchymal components. This is a report of teratocarcinosarcoma, in a 74-year-old male, involving the right nasal cavity and ethmoids with intracranial extension. The tumour was totally resected via the craniofacial approach and the patient was given post-operative chemotherapy. Extensive tumour necrosis, rapid growth and local destruction are the prominent features of this tumour. The clinical presentation, pathological features and clinical course of this rare malignancy are discussed with a review of the literature.

Aged↗

PubMed1998

Transforming growth factor beta1 and recruitment of macrophages and mast cells in airways in chronic obstructive pulmonary disease.

Chronic airways inflammation is one of the features of chronic obstructive pulmonary disease (COPD). We demonstrated previously that bronchiolar epithelium in COPD contains increased numbers of macrophages and mast cells. Transforming growth factor beta1 (TGF-beta1) may be involved in this influx because it has chemotactic activity for macrophages and mast cells. In this study, we examined expression patterns of TGF-beta1, TGF-beta receptors type I and II (TGF-betaRI and TGF-betaRII) by immunohistochemistry and mRNA in situ hybridization in peripheral lung tissue of 14 current or ex-smokers with COPD (FEV1 < 75%) and 14 without COPD (FEV1 > 84%). In both groups, TGF-beta1 and its receptors are present in airway and alveolar epithelial cells, airway and vascular smooth muscle cells, and tissue and alveolar CD68(+) cells (considered herein to be macrophages). In subjects with COPD, a semiquantitative analysis revealed approximately twofold higher levels of TGF-beta1 mRNA and protein in bronchiolar and alveolar epithelium (p < 0.02) as compared with subjects without COPD. With regard to bronchiolar epithelial cells, we found a significant correlation between TGF-beta1 mRNA and protein expression (r = 0.62; p < 0.002), and between the FEV1 of all subjects together and TGF-beta1 protein (r = -0.60; p < 0.0002) and mRNA (r = -0.67; p < 0. 002) levels. The epithelial expression of TGF-beta1 mRNA and TGF-beta1 protein correlates with the number of intraepithelial macrophages (both: r = 0.44; p < 0.03) whereas intraepithelial mast cell numbers correlate with epithelial TGF-beta1 mRNA expression. These data suggest a role for TGF-beta1 in recruiting macrophages into the airway epithelium in COPD.

Adult↗

PubMed1998

Angiotensin II induces hypertrophy of human airway smooth muscle cells: expression of transcription factors and transforming growth factor-beta1.

Increased smooth muscle mass due to hyperplasia and hypertrophy of airway smooth muscle (ASM) cells is a common feature in asthma. Angiotensin II (Ang II), a potent vasoconstrictor and mitogen for a wide variety of cells, has recently been implicated in bronchoconstriction in asthmatics. However, a possible mitogenic role as well as underlying molecular mechanisms of this octapeptide in human ASM cells are not yet known. We studied the effects of Ang II on ASM cell proliferation and growth and on the expression of three transcription factors, egr-1, c-fos, and c-jun, as well as a cytokine, transforming growth factor-beta1 (TGF-beta1). Human ASM cells were isolated by enzymatic digestion of bronchial smooth muscle obtained from lung resection tissue. Confluent cells were growth-arrested and subsequently incubated with Ang II (100 nM) for different time periods and processed for the measurement of cell growth and gene expression. Ang II significantly induced DNA and protein synthesis in human ASM cells at 8 h, resulting in a net increase in the accumulation of protein over DNA (i.e., cellular hypertrophy) at 16 h of incubation. Cell counts and MTT-reduction assay, however, showed no increase in cell number as a result of Ang II stimulation. Ang II stimulated the expression of egr-1 and c-fos as early as 15 min, reaching maximum levels at 45 min, whereas the expression of c-jun peaked at 2 h of Ang II exposure. Furthermore, steady-state mRNA levels of TGF-beta1 were upregulated by Ang II after 4 h and reached peak levels at 16 h of incubation. Secretion of biologically active TGF-beta1 from human ASM cells was significantly (P <= 0.02) enhanced by Ang II incubation after 8 h, which remained elevated until 24 h. Our results suggest that the Ang II-induced transient early expression of transcription factors may regulate autocrine genes like TGF-beta1, of which the subsequent late upregulation could contribute to cellular hypertrophy during, for example, airway remodeling in asthma.

Angiotensin II↗

PubMed1997

Antrochoanal polyp--a rare paediatric emergency.

An antrochoanal polyp, a common clinical entity, with a rare presentation is being reported. A 12 year old boy was brought to Accident and Emergency department with an unusual sudden presentation of polypoidal mass filling the oral cavity up to his incisors as a result of which he could not swallow and speak. Prior to this episode he had no complaints of the disease. An emergency removal was planned and only during the operation could it be diagnosed as a antrochoanal polyp because of its pedicle in the lateral wall of the nose, which was confirmed by histopathological examination.

Aphonia↗

PubMed1997

Opioid receptor antagonists attenuate heat stress-induced reduction in cerebral blood flow, increased blood-brain barrier permeability, vasogenic edema and cell changes in the rat.

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Animals↗

PubMed1997

Involvement of nitric oxide in the pathophysiology of acute heat stress in the rat. Influence of a new antioxidant compound H-290/51.

The possibility that nitric oxide (NO) is involved in the pathophysiology of brain injury caused by heat stress (HS) was examined using immunohistochemistry of a constitutive isoform of neuronal nitric oxide synthase (c-NOS) in a rat model. In addition, to discover the role of oxidative stress in inducing c-NOS activity in HS, the effect of a new antioxidant H-290/51 on HS-induced expression of c-NOS immunoreactivity was examined. Subjection of conscious young animals to a 4-h HS in a biological oxygen demand (BOD) incubator at 38 degrees C resulted in marked upregulation of c-NOS in the cerebral cortex and hippocampus of stressed rats compared to normal rats kept at room temperature (21 +/- 1 degrees C). The c-NOS immunoreactivity was found in distorted neurons located in the edematous regions not normally showing c-NOS activity. Pretreatment with H-290/51 significantly attenuated the upregulation of c-NOS in animals subjected to HS, and the signs of neuronal distortion and edema were less pronounced. These results suggest that HS has the capacity to induce upregulation of c-NOS, and these effects can be reduced by prior treatment with H-290/51, indicating a possible neuroprotective effect of antioxidants in thermal brain injury.

Animals↗

PubMed1997

Topical application of insulin like growth factor-1 reduces edema and upregulation of neuronal nitric oxide synthase following trauma to the rat spinal cord.

The neuroprotective effects of insulin like growth factor-1 (IGF-1) on spinal cord injury induced edema formation, cell changes and profound upregulation of constitutive isoform of neuronal nitric oxide synthase (cNOS) was examined in a rat model. A focal spinal cord injury produced by making a lesion (about 2 mm deep and 5 mm long) of the right dorsal horn of the T10-11 segment resulted in a marked edema formation, cell injury and upregulation of cNOS following 5 h after trauma. In separate groups application of IGF-1 (0.1 microgram/microliter) topically on the exposed spinal cord (T10-11) starting from 30 min before injury (20 microliter), immediately before injury followed by 30 min, 60 min and thereafter every 1 h after injury until sacrifice resulted in significant attenuation of edema formation and cell changes. Immunohistochemistry showed a less pronounced expression of cNOS in the T9 and T12 segments of the cord in IGF treated rats compared to untreated traumatised controls. These results for the first time show that IGF treatment is neuroprotective and this effects of the IGF appears to be mediated via inhibition of NOS upregulation.

Administration, Topical↗

PubMed1997

Prostaglandins modulate constitutive isoform of heat shock protein (72 kD) response following trauma to the rat spinal cord.

The influence of prostaglandins on the constitutive isoform of heat shock protein (HSP 72 kD) response following a focal trauma to the rat spinal cord was examined using immunohistochemistry. A focal trauma to the spinal cord by making a longitudinal incision into the right dorsal (about 2 mm deep and 5 mm long) of the T10-11 segments, markedly enhanced the upregulation of HSP immunoreactivity in the traumatised as well as in the perifocal T9 and T12 segments. This upregulation of HSP was significantly reduced by pretreatment with indomethacin (10 mg/kg, i.p., 30 min before injury) an inhibitor of prostaglandin synthesis. These results show that blockade of PG synthesis prior to trauma has an inhibitory influence on the upregulation of HSP response, not reported earlier.

Animals↗

PubMed1997

Topical application of 5-HT antibodies reduces edema and cell changes following trauma of the rat spinal cord.

Involvement of serotonin in the early microvascular reactions and cell changes following trauma of the spinal cord was examined using topical application of serotonin antibodies to the traumatised cord in a rat model. A focal trauma of the spinal cord was produced by making an incision into the right dorsal horn of the T10-11 segments (about 2 mm deep and 5 mm long); the animals were allowed to survive 5 h after injury. Monoclonal 5-HT antibodies (1:20) were applied (25 microliters in 10 sec) to the traumatised spinal cord 2 min after injury. There was a significant reduction in the breakdown of the blood-spinal cord barrier, edema formation, and cell changes in the traumatised rats which received 5-HT antiserum compared to the injured rats given saline. These results show that 5-HT is an important mediator involved in the early pathophysiological responses of spinal cord injury.

Administration, Topical↗

PubMed1997

Substance P endopeptidase activity in the rat spinal cord following injury: influence of the new anti-oxidant compound H 290/51.

The influence of the new antioxidant compound H-290/51 was examined on the substance P endopeptidase (SPE) activity in a rat model of spinal cord injury. This compound (H-290/51) has neuro-protective effects on edema and cell changes in this model. Infliction of trauma to the cord by making an incision into the right dorsal horn of the T10-11 segment resulted in a marked upregulation of SPE in the segments rostral to the lesion. On the other hand, the injured and adjacent caudal segments exhibited a marked down-regulation of the enzyme activity. Pretreatment with H 290/51 increased the SPE activity in the T9 segment but downregulated the enzyme activity in the T10-11 and T12 segments. The drug induced enzyme activity change was not further influenced by the trauma of the cord. The results indicate that a focal trauma induces widespread alterations in spinal cord SPE activity which can be influenced by the anti-oxidant drug H 290/51, suggesting that SPE is somehow involved in cell injury.

Animals↗

PubMed1997

Benzodiazepine receptors influence spinal cord evoked potentials and edema following trauma to the rat spinal cord.

The possibility that diazepam will influence spinal cord evoked potentials (SCEP), edema formation and cell changes following spinal cord injury (SCI) was examined in a rat model. The SCI was produced in equithesin anaesthetised animals by making a longitudinal incision (about 2 mm deep and 5 mm long) in the right dorsal horn of the T10-11 segments. The SCEP were recorded from the epidural space of the T9 segment after stimulation of the right tibial and sural nerves. The SCEP consisted of a small positive peak followed by a broad and high negative peak. Infliction of trauma to the rats resulted in an immediate and pronounced decrease of the maximal negative peak (MNP) amplitude. The spinal cord edema and cell changes were markedly pronounced 5 h after injury. Pretreatment with diazepam attenuated the early SCEP changes induced by the trauma and reduced the later development of edema and cell injury. These results suggest that benzodiazepine receptors are involved in trauma induced alterations in SCEP changes, edema formation and cell injury, not reported earlier.

Animals↗

PubMed1997

Role of neurochemicals in brain edema and cell changes following hyperthermic brain injury in the rat.

The involvement of three potent neurochemical mediators of the edema formation such as serotonin, prostaglandins and opioids in the pathophysiology of hyperthermic brain injury was examined in a rat model using a pharmacological approach. Hyperthermic brain injury was induced in conscious young rats by exposing them to heat stress at 38 degrees C for 4 h. In these rats the blood-brain barrier (BBB) permeability, brain edema, cerebral blood flow (CBF), heat shock protein 72 kD (HSP) response and cell changes were examined. Pretreatment with ketanserin (a serotonin-2 receptor antagonist), indomethacin (prostaglandin synthesis inhibitor) and naloxone (opioid receptor antagonist) in separate groups of rats reduced hyperthermia and HSP response following heat stress and significantly attenuated changes in the BBB permeability, brain edema, CBF and cell reaction. These results suggest that the pathophysiology of hyperthermic brain injury is a complex mechanisms and several neurochemicals are involved in the brain pathology caused by heat stress.

Animals↗