Strong enough to get your ring around the collar, but not to cause dermatitis.

Little has been published on the effects of laundry detergents. However, physicians and Uncle Buck always ask if you have changed laundry detergent when you get a rash. So a multicenter study was conducted to evaluate the validity of this old adage. The study for allergic contact demratitis (ACD) involved the placement of 2 patch tests-a granular detergent and a liquid one. Reactions to other chemicals like fragrances and nickel were compared to the laundry detergent reactions. Over 700 patients volunteered, but only 5 had a postitive patch test to either or both detergents. 2 of these 5 patients could be evaluated further. Further testing showed that in 1 of the 2, reduplication of the dermatitis could not be elicited. Meanwhile, the other had a reaction to the controls and the detergents. For more details on the study and others like it, check out the citations below.

Information from:

Allergic contact dermatitis to detergents: a multicenter study to assess prevalence.

Belsito DV, Fransway AF, Fowler JF Jr, Sherertz EF, Maibach HI, Mark JG Jr, Mathias CG, Rietschel RL, Storrs FJ, Nethercott JR.

Division of Dermatology, University of Kansas Medical Center, Kansas City, KS 66160-7319, USA.

Study can be found at:

J Am Acad Dermatol. 2002 Feb;46(2):200-6. Links

Comment in:

OMIM

Just a reminder that OMIM is a great resource for information about genetic syndromes. I have found myself referring to it for both IM and Peds information.

For example,
Sandhoff Syndrome, which is clinically similar to tay-sachs

You get a decent clinical summary with references as well as the genetics.

Any other online genetics resources that people know of?

Who thought that botulinus intoxication was a good thing?

After having a CP patient with severe hypertonia, I wanted to find some treatment options and found this study to be interesting. After starting a registration program for all CP patients in Sweden in 1994, several treatment studies began. These studies are linked to the following article.

A study in southern Sweden was initiated to analyze the development of spasticity with age in all children with CP from 0 to 15 years during the period 1995-2006. Measurements of muscle tone in the gastrocnemius-soleus muscle according to the modified Ashworth scale were analyzed. The CP subtypes were classified according to the Surveillance of Cerebral Palsy in Europe network system based on 6218 examinations in 547. The degree of muscle tone increased up to 4 years of age, but decreased each year up to 12 years of age. The same tendency is seen in all spastic subtypes. The findings may have implications both for clinical judgement and for research studies on spasticity treatment.



The original article citation is: BMC Musculoskelet Disord. 2008 Nov 6;9(1):150.

Who gets HUS from E. coli 0157:H7?

We have an interesting patient on the service who has E. coli O157:H7. How can we predict who will get HUS?

I didn't find much on this question. A google scholar search for "predict HUS 0157" turned up this article. It is a quick and dirty study of 15 kids with 0157:H7, 5 with HUS, and 10 without. They looked at fever, vomiting, abdominal pain, tachycardia, and dehydration, and there was a significant p. value associated with dehyrdration at presentation and development of HUS.

Joishy, M. and Jauhari, P. and Mathew, A.A. and Rangarajan, T. "Can we predict the development of haemolytic uraemic syndrome in the early stage of Escherichia coli O157 infection?"Archives of Disease in Childhood, (2008) 93:2 180.

This article refers to this article, which is a nice review of 10 studies looking at the association between leukocytosis and development of HUS. A number of these studies were pediatric.
Anjay MA, Anoop P, Britland A, " Leukocytosis as a predictor for progression to haemolytic uraemic syndrome in Escherichia coli O157:H7 infection, 2007 Sep;92(9):820-3.

Cliff's:
Leukocytosis is a reliable early risk predictor
Absence of leukocytosis also has reliable NEGATIVE predictive value.

Schwachman-Diamond Syndrome

Schwachman-Diamond Syndrome was the topic of the question of the day yesterday, and my team and I bombed it badly. First I accused our chief resident of inventing the syndrome, but it turned out that the syndrome is real. The Diamond of Schwachman-Diamond fame is indeed the same Diamond as that of Diamond-Blackfan fame.

A quick google scholar search on Schwachman-Diamond Syndrome and the 2nd hit found a review article from 2002.

Cliff's Notes:

• The syndrome classically has three fundamental features:
• 1. pancreatic insufficiency
• 2. leukopenia
• 3. metaphyseal dysostosis

• It is the 2nd most common cause of pancreatic insufficiency in children (behind CF), and the third most common cause of inherited bone marrow failure behind Fanconi's anemia and Diamond-Blackfan.
• It is autosomal recessive.
• It is associated with MDS and AML
  
• Patients are susceptible to viral/bacterial/fungal infections secondary to a qualitative and quantitative immunodeficiency
• The pancreatic insufficiency is secondary to acinar maldevelopment
• Half of patients have the metaphyseal dysostosis , most commonly of the femoral head, and most commonly asymptomatic.
• Life expectancy is >35 years.

The original article citation is:
Shwachman, H., Diamond, L.K., Oski, F.A. & Khaw, K.-T. (1964) The syndrome of pancreatic insufficiency and bone marrow dysfunction. Journal of Pediatrics, 65, 645–663.

Pediatric Clostridium difficile colitis

We don't look for C. diff much in kids because kids don't get c. diff disease very often. In fact, simply having C. difficile is more often a sign of carrier status than of active disease. When we diagnosed a little girl on my service with c. diff, I thought I would see what I can learn. There is not much on pediatric C. difficile. I found the following:

McFarland, LV. “Pediatric Clostridium difficile: A Phantom Menace or Clinical Reality?.” Journal of pediatric gastroenterology and nutrition, v. 31 issue 3, 2000, p. 220.

High Points:

In the article, McFarland points out a number of pediatric c. difficile outbreaks. She separates positive C. difficile tests into four categories: "1) asymptomatic carriage, 2) acute and protracted diarrhea, 3) colitis (pseudomembranous colitis [PMC], fulminant colitis, toxic megacolon, and non-PMC colitis), and 4) recurrent infections."

Pediatric C. difficile may or may not be antibiotic associated.

High risk antibiotics are clindamycin, amoxicillin, ampicillin, and 2nd/3rd generation cephalosporins (our patient had had separate courses of two of these in the last month!).

I would add that the spores are not killed by alcohol hand rub, so soap and water is your friend in a C. difficile patient's room.

There was also a reasonably solid review article in the NEJM at the end of October this year.