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PubMed1999

[Anatomical-clinical conference: mediastinal mass].

A 56 years-old man developed a pneumonia. An anterior mediastinal mass is fortuitly found on the chest X-ray and the patient is hospitalised for further investigations. Differential diagnosis of mediastinal masses is discussed.

Biopsy↗
PubMed1997

[Anatomo-clinical conference: bronchiolo-alveolar cancer and confusion].

A 67 year old man is admitted with mental confusion. He has been treated 10 months before the present complication for a diffuse bronchiolo-alveolar carcinoma with a good response to chemotherapy. Brain imaging shows symmetrical lesions in the periventricular areas and in the semi-oval centers. A test will allow to obtain the diagnosis.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed2001

[A 68-year-old man with speech disturbance as the initial symptom followed by bradykinesia and dementia. Clinical conference].

We report a 68-year-old man with progressive speech disturbance and dementia. He was well until 1995, when he noted an onset of difficulty in speech. He was able to name simple objects and understand language, however, he showed great difficulty in spontaneous speech. In 1998, he visited our service. He was alert and oriented, but he showed moderate degree of dementia. He did not appear to have aphasia but he showed marked dysarthria and slurred speech. He showed limb-kinetic apraxia in his right hand. He showed moderate restriction in his vertical gaze, masked face, and dysphagia. He walked normally. No rigidity, ataxia, or abnormal involuntary movement was noted. He showed grasp response and he was bradykinetic. He was treated with levodopa without effect. His condition deteriorated slowly and he was admitted to our service because of fever on February 13, 1999. He was alert but almost mute. He was unable to look upward or downward. Oculocephalic response was preserved. Axial rigidity was noted but no limb rigidity was present. He walked with small steps. Retropulsion was present. Deep tendon reflexes were diminished and the plantar response was flexor bilaterally. Laboratory examinations were unremarkable and his fever went down within a few days by supportive treatment. He was discharged to his home, where his condition deteriorated further. He developed cardiopulmonary arrest on May 3, 1999 and was brought into ER again. Cardiopulmonary resuscitation was unsuccessful and he was pronounced dead at 7:30 in the morning on the same day. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that this patient had corticobasal degeneration. But he felt that the differential diagnosis from atypical progressive supranuclear palsy, in which cortical pathology and symptoms predominated as in corticobasal degeneration, would be extremely difficult. Most of the participants felt that this patient had corticobasal degeneration, but a few thought that he had atypical PSP. Post-mortem examination revealed asymmetric cortical atrophy, which was accentuated in the left motor cortical area. Microscopic examination of the precentral cortex revealed neuronal loss and gliosis. Ballooned neurons and astrocytic plaques were also seen. The substantia nigra showed marked neuronal loss. Neuropil threads were observed in the nigra. Those threads were positive for anti-tau immunohistochemistry. The internal segment of the globus pallidus, the subthalamic nucleus, and the cerebellar dentate nucleus showed mild to moderate neuronal loss. A few neurofibrillary tangle-positive neurons were seen in these structures. Neuropil threads were also seen throughout. Pathologic changes were consistent with the diagnosis of corticobasal degeneration. One of the participants pointed out that he was able to walk at the time when he was showing marked speech disturbance and limb-kinetic apraxia, which was rather unusual for PSP suggesting corticobasal degeneration.

Aged↗
PubMedDate not supplied

Might the M184V substitution in HIV-1 RT confer clinical benefit?

The M184V substitution in HIV-1 RT develops rapidly following initiation of therapy with 3TC and confers high-level phenotypic resistance to this drug both in vitro and in vivo. Interestingly, the presence of M184V is also associated with alteration of several mechanisms relating to RT function that include decreased RT processivity, reduced nucleotide-dependent primer unblocking, increased fidelity, hypersensitization to other NRTIs, impaired viral fitness, and delayed appearance of mutations in RT that are responsible for resistance to thymidine analogues (i.e. thymidine-associated mutations or TAMs). Collectively, these factors might explain the residual antiviral effect and clinical benefit observed with continued use of 3TC in combination therapy regimens following the emergence of M184V. Indeed, the results of numerous controlled as well as observational clinical studies are suggestive of improved therapeutic outcome associated with continued usage of 3TC and maintenance of the M184V mutation. However, several of these trials did not possess adequate statistical power to resolve whether or not continued use of 3TC provided actual benefit, nor were they specifically designed to test the M184V benefit hypothesis in prospective fashion. There is a need for randomized clinical trials of this type in order to validate the potential benefit of maintenance of M184V and whether continued use of 3TC is the only means of attaining this objective.

Amino Acid Substitution↗