2009 August 14

Minimal hepatic encephalopathy.

Indian J Gastroenterol Start a Discussion »

Aug 142009

Minimal hepatic encephalopathy.

Indian J Gastroenterol. 2009 Jan-Feb;28(1):5-16

Authors: Dhiman RK, Chawla YK

Minimal hepatic encephalopathy (MHE) is the mildest form of spectrum of hepatic encephalopathy (HE). Patients with MHE have no recognizable clinical symptoms of HE but have mild cognitive and psychomotor deficits. The prevalence of MHE is high in patients with cirrhosis of liver and varies between 30% and 84%; it is higher in patients with poor liver function. The diagnostic criteria for MHE have not been standardized but rest on careful patient history and physical examination, normal mental status examination, demonstration of abnormalities in cognition and/or neurophysiological function, and exclusion of concomitant neurological disorders. MHE is associated with impaired health-related quality of life, predicts the development of overt HE and is associated with poor survival. Hence, screening all patients with cirrhosis for MHE using psychometric tests, and treatment of those patients diagnosed to have MHE has been recommended. Ammonia plays a key role in the pathogenesis of MHE, which is thought to be similar to that of overt HE. Thus, ammonia-lowering agents such as lactulose and probiotics have been tried. These agents have been shown to improve cognitive and psychometric deficits, and have good safety profile. Future studies will better define the role of other drugs, such as rifaximin, acetyl L-carnitine and L-ornithine L-aspartate.

PMID: 19529896 [PubMed - indexed for MEDLINE]

Link to Article at PubMed

Hyperparathyroidism.

Lancet Start a Discussion »

Aug 142009

Hyperparathyroidism.

Lancet. 2009 Jul 11;374(9684):145-58

Authors: Fraser WD

Hyperparathyroidism is due to increased activity of the parathyroid glands, either from an intrinsic abnormal change altering excretion of parathyroid hormone (primary or tertiary hyperparathyroidism) or from an extrinsic abnormal change affecting calcium homoeostasis stimulating production of parathyroid hormone (secondary hyperparathyroidism). Primary hyperparathyroidism is the third most common endocrine disorder, with the highest incidence in postmenopausal women. Asymptomatic disease is common, and severe disease with renal stones and metabolic bone disease arises less frequently now than it did 20-30 years ago. Primary hyperparathyroidism can be cured by surgical removal of an adenoma, increasingly by minimally invasive parathyroidectomy. Medical management of mild disease is possible with bisphosphonates, hormone replacement therapy, and calcimimetics. Vitamin D deficiency is a common cause of secondary hyperparathyroidism, particularly in elderly people. However, the biochemical definition of vitamin D deficiency and its treatment are subject to much debate. Secondary hyperparathyroidism as the result of chronic kidney disease is important in the genesis of renal bone disease, and several new treatments could help achieve the guidelines set out by the kidney disease outcomes quality initiative.

PMID: 19595349 [PubMed - indexed for MEDLINE]

Link to Article at PubMed

Obesity hypoventilation syndrome.

Semin Respir Crit Care Med Start a Discussion »

Aug 142009

Obesity hypoventilation syndrome.

Semin Respir Crit Care Med. 2009 Jun;30(3):253-61

Authors: Berger KI, Goldring RM, Rapoport DM

The term obesity hypoventilation syndrome (OHS) refers to the combination of obesity and chronic hypercapnia that cannot be directly attributed to underlying cardiorespiratory disease. Despite a plethora of potential pathophysiological mechanisms for gas exchange and respiratory control abnormalities that have been described in the obese, the etiology of hypercapnia in OHS has been only partially elucidated. Of particular note, obesity and coincident hypercapnia are often associated with some form of sleep disordered breathing (apnea/hypopnea or sustained periods of hypoventilation). From a conceptual point of view, even transient reductions of ventilation from individual sleep disordered breathing events must produce acute hypercapnia during the period of low ventilation. What is less clear, however, is the link between these transient episodes of acute hypercapnia and the development of chronic sustained hypercapnia persisting into wakefulness. A unifying view of how this comes about is presented in the following review. In brief, our concept is that chronic sustained hypercapnia (as in obesity hypoventilation) occurs when the disorder of ventilation that produces acute hypercapnia interacts with inadequate compensation (both during sleep and during the periods of wakefulness); neither alone is sufficient to fully explain the final result. The following discussion will amplify on both the potential reasons for acute hypercapnia in the obese and on what is known about the failure of compensation that must occur in these subjects.

PMID: 19452386 [PubMed - indexed for MEDLINE]

Link to Article at PubMed

Alternative strategies for Clostridium difficile infection.

Int J Antimicrob Agents 1 Response »

Aug 142009

Alternative strategies for Clostridium difficile infection.

Int J Antimicrob Agents. 2009 Mar;33 Suppl 1:S51-6

Authors: Bauer MP, van Dissel JT

Although antibiotics are generally effective in achieving symptomatic recovery from Clostridium difficile infection, the disease frequently relapses, partly because antibiotics not only kill C. difficile, but also disrupt colonisation resistance of the gut microflora. Non-antibiotic strategies for the prevention and treatment of the infection include probiotics, deliberate colonisation by non-toxigenic C. difficile strains, toxin-binding agents, active immunisation, passive immunotherapy with intravenous immunoglobulin, monoclonal antibodies or bovine anti-C. difficile whey concentrate, and faecal transplantation. None of these alternative therapies has proven benefit in therapy or prevention, and prospective randomised trials are urgently needed.

PMID: 19303571 [PubMed - indexed for MEDLINE]

Link to Article at PubMed

Nosocomial and antibiotic-associated diarrhoea caused by organisms other than Clostridium difficile.

Int J Antimicrob Agents Start a Discussion »

Aug 142009

Nosocomial and antibiotic-associated diarrhoea caused by organisms other than Clostridium difficile.

Int J Antimicrob Agents. 2009 Mar;33 Suppl 1:S37-41

Authors: Gorkiewicz G

Most cases of nosocomial and antibiotic-associated diarrhoea are caused by alteration of the physiological gut microflora. This alteration leads to reduced microbial metabolism of carbohydrates and primary bile acids, resulting in osmotic or secretory forms of diarrhoea. Moreover, facultative enteropathogens may experience a growth advantage due to the antibiotic-induced microflora alteration that, in turn, can harm the gut mucosa by the toxins they produce. Clostridium difficile is the major infectious agent leading to pseudomembranous colitis. However, there is increasing evidence that certain other pathogens such as enterotoxin-producing Clostridium perfringens, Staphylococcus aureus and Klebsiella oxytoca can induce mucosal deterioration and diarrhoea after antibiotic use. But, as with C. difficile, these facultative enteropathogens can also be found in the healthy population. Their contribution to disease is, therefore, controversial and their presence in the stools of antibiotic-associated diarrhoea patients is often claimed to be mere colonisation. In this respect, the causal relationship of each suspected pathogen with the development of intestinal disease has to be proved clinically and experimentally.

PMID: 19303568 [PubMed - indexed for MEDLINE]

Link to Article at PubMed

Recurrent Clostridium difficile infection: causality and therapeutic approaches.

Int J Antimicrob Agents Start a Discussion »

Aug 142009

Recurrent Clostridium difficile infection: causality and therapeutic approaches.

Int J Antimicrob Agents. 2009 Mar;33 Suppl 1:S33-6

Authors: Johnson S

Recurrent diarrhoea after successful treatment of the primary episode is a common complication of Clostridium difficile infection (CDI) and may be increasing in frequency. Evidence suggests that persistent alterations in the indigenous bowel flora and failure to mount an effective antibody response to C. difficile toxins are the main mechanisms whereby recurrent CDIs occur. Treatment of the first recurrence with the same agent used for the treatment of the primary episode is reasonable, but a different approach is needed for patients with multiple CDI recurrences. Prolonged, repeated courses of metronidazole are discouraged, but a practical first option in these patients is to use tapered-dose oral vancomycin followed by a pulsed-dose regimen. Other potential options include probiotic approaches, restoration of the normal flora, immunological approaches, toxin-binding approaches, and serial therapy with vancomycin followed by rifaximin. Randomised studies including a sufficient numbers of patients have not yet been conducted for the treatment of recurrent CDI and are needed to help guide the formulation of effective recommendations.

PMID: 19303567 [PubMed - indexed for MEDLINE]

Link to Article at PubMed

Older Entries

M	T	W	T	F	S	S
« Jul				Sep »
					1	2
3	4	5	6	7	8	9
10	11	12	13	14	15	16
17	18	19	20	21	22	23
24	25	26	27	28	29	30
31