Treating nondementia illnesses in patients with dementia

Physicians increasingly are called on to provide primary care for the growing population of people with Alzheimer-type dementia. However, little attention has been paid to the care of nondementia illnesses in this group of patients. To illustrate how presence of dementia can alter the risk-benefit ratio of treatment of a common medical problem, we present a case study in which a patient with dementia developed disastrous adverse effects to a drug commonly used to treat osteoporosis. This case and 2 composite vignettes illuminate how presence of dementia should influence the decision-making process for treatment of nondementia illnesses. We address issues such as decreased decision-making capacity, problems with reporting adverse effects, decreased cognition leading to problems with treatment adherence, and the role of screening and basic questions about acceptable burdens of treatments in patients with limited prognosis. We suggest ways to improve communication with patients with dementia in an effort to minimize complications and improve care, as well as policy changes to include patients with dementia in clinical trials. JAMA. 2000;283:3230-3235     

Tissue Inhibitor of Metalloproteinase-1 Concentrations are Attenuated in Peritoneal Fluid and Sera of Women with Endometriosis and Restored in Sera by Gonadotropin-Releasing Hormone Agonist Therapy

Objective: To establish tissue inhibitor of metalloproteinase-1 (TIMP-1) concentrations in peritoneal fluid (PF) and sera of women with endometriosis and compare them to disease-free controls.

Design: Prospective randomized study.

Setting: Academic medical center.

Patient(s): Women with laparoscopically documented endometriosis and disease-free women of reproductive age.

Intervention(s): Peritoneal fluid and sera were collected, and some women received gonadotropin-releasing hormone agonist (GnRH-a) therapy for endometriosis.

Main Outcome Measure(s): Peritoneal fluid and sera TIMP-1 concentrations were measured with a specific RIA.

Result(s): The TIMP-1 concentrations were significantly lower in PF and sera of women with endometriosis compared with disease-free women. The GnRH-a therapy restored serum TIMP-1 concentrations.

Conclusion(s): Aberrant expression and localization of TIMP-1 may derange the proteolytic milieu of the peritoneal cavity and contribute to the etiology and underlying physiologic sequelae associated with endometriosis. Measurement of TIMP-1 in serum may aid in diagnosing endometriosis and assist with monitoring treatment efficacy in women with this disease.     

Treatment of HAART-induced lactic acidosis with B vitamin supplements.

Lactic acidosis, a rare but life-threatening condition is fairly common in HIV-infected individuals. The cause of lactic acidosis appears to stem from the use of HAART, causing mitochondrial dysfunction and the depletion of flavoprotein cofactors necessary for electron transport. Deficiencies of riboflavin or thiamin can contribute to the development of hyperlactic acidemia. Further, the high incidence of liver disease (hepatitis B or C and alcoholic liver disease) in this population predisposes HIV patients to metabolic abnormalities. Supplementation with thiamin or riboflavin, depending on the individual patient's condition, can reduce elevated lactic acid levels.     

What constitutes a true hyperdense middle cerebral artery sign?

OBJECTIVES: The 'hyperdense MCA sign' refers to an appearance of increased attenuation of the proximal middle cerebral artery (MCA) that is often associated with thrombosis of the M1 MCA segment and may be the only diagnostic feature on computed tomography early after ischaemic stroke. False positives are recognized, and correct recognition of this sign has, therefore, assumed greater importance with the advent of thrombolytic therapy for stroke. We sought to define objective criteria for hyperdensity of the MCA. METHODS: Brain computed tomographs obtained by a standard protocol in a neuroradiology department were analyzed by a single observer. All consecutive scans reported as exhibiting a hyperdense MCA were compared to controls reported as having normal scans. Ovoid regions of interest were placed over the vessels and cerebral cortices, and the attenuation in Hounsfield units (HU) measured. Absolute attenuation and ratios of one side to the other were compared. RESULTS: MCA attenuation was unrelated to age in cases (n = 18) and controls (n = 80). The mean MCA attenuation was greater in the affected MCA of cases as compared with controls [54.0 HU (99% confidence interval CI 46.7-61.2) vs. 41.3 HU (99% CI 39.7-43.0); p < 0.00001]. Cases were subdivided into true and false positives by the ratio of denser:less dense MCA (within or without the 95% prediction interval for controls). In all true positives, the MCA ratio was > 1.2. 9 of 10 true positives had acute ischaemic stroke; 1 patient had herpes simplex encephalitis, but had MCA attenuation within the 95% CI for controls. False positives had mature cerebral infarction or non-ischaemic pathologies. The ratio of MCA attenuation to adjacent cerebral cortex was significantly higher in both true and false positives than in controls. CONCLUSIONS: Hyperdense MCAs associated with acute ischaemic stroke can be distinguished from normal vessels and false positives by measurement of absolute attenuation of affected and normal vessels: an absolute density of >43 HU and a MCA ratio of >1.2 defined hyperdensity and excluded all other pathologies. Confirmation in other centres is required.