I really don't have any recipes to contribute because I don't know the carb counts of most of the things we eat.  We just kind of wing it around here . . . 

But . . .I did have a chance to make Lorraine's Special Fried Rice last weekend and it was pretty fabulous!

Jim and I both went back for seconds. 

Ok, so my pictures are not as pretty as Lorraine's but here is my attempt at pictures of our Chicken Fried Rice -

Chopping Broccoli (& other yumminess)

The Final Product

Looks Good!!

Most Important - Nate Loved It!!

Our family gave it 4 Thumbs Up - Emma was our lone hold out only because as she put it "broccoli makes me gag!".  Ehhh - I'll leave the broccoli out of hers next time for the 5 Thumbs Up!

Last week I was asked to take part in study being conducted by Schlesinger and Associates.  They were looking for caregivers of children with diabetes (CWD).  Hey - that's me!  I have a CWD so I was more than happy to participate.

They asked me to make a collage about diabetes and bring it to the meeting.  So, the above picture is what I made and took into the meeting. Pretty cute - no?  I mean if you have to make a picture about diabetes - it's pretty cute.  Oh wait - maybe it's just my adorable son, Nate that makes it so cute!!  :)

Anyway, I have no idea who or what the research was for but I hope that I was able to help in some way because ONE DAY I WOULD LOVE TO SAY THAT MY SON USED TO HAVE DIABETES!

Seriously, thank you all for your words of support and encouraging comments.  I let it all out and am feeling much better today.  And . . . I am very pleased to announce that after my grandmother prayed a good, long prayer for me she has forgiven me for saying BULLSHIT in my blog  - - - and I could not be happier!  :)

For all the new peeps that commented on this post --- thank you - thank you - thank you.  After a good nights sleep tonight I fully intend on stopping by your blogs and show you the same amount of love you showed me today,  Thanks again!!

Last week we (The Houston Five + Poppa DeJulius) attended the JDRF Walk to Cure Diabetes Kick Off Dinner. I promised myself - no crying!  Dang!  As soon as the Nick Jonas video started playing - I was CRYING! [Click HERE to see video]

And then again when all of these young children were on stage . . .

Lots of Cute T1 Peeps you may know in this picture.

 We have Elise from Death of a Pancreas , Liam from Sticking it to Diabetes , and Miss J and Miss G from 2 Green Eyed Girls (& their daddy too)


Look at these cuties. . .

Liam, Elise and Nate

Why do I still cry and get so emotional when discussing diabetes? Why?
I have friends and family members that have had T1 for years and are totally fine.  I read blogs written by men and women that have had T1 for as long as they can remember and they are living happy, healthy, and successful lives.  So, WHY do I CRY?

Well, sit down just a spell and let me tell you why -


Because diabetes SUCKS.  That's right I said it - it sucks.

Sometimes I wonder if I cry more for me or for Nate?  Well, some days I think I do cry for me and some days I cry for Nate.

On September 17th of 2009 - everything changed in my life.  Everything.

My life is hard.  Yep - I said it.  It's hard.  Not easy  --- not a lot of easy over here at the Houston house.
Sometimes I just get sad.  Sometimes I get mad.  Pretty damn mad!  Sometimes I just think - you know what?  This is bullshit!  Yep - I said bullshit.

It's BS that I have to use a lancet to cut my son's finger 12 times a day, make him bleed, so that I can test his blood glucose.  Yes, that is BS.  Nate doesn't even flinch - he's so strong and so tough and he is ONLY 2 years old.  That is BS.  If you are reading this and your 2-year old does NOT have diabetes - what do you think your child would do if you cut his finger and made him bleed even 1 time?

It's BS that a drug that smells like a big band-aid is infused into my son's body all day long and that stinky drug called insulin keeps him alive.  It's BS that if I make just 1 tiny mistake with that insulin pumping through his body - he could DIE.  See what I mean -  total BS!

It's BS that I NEVER sleep.  Seriously - Never!  Anyone that knows me well knows that is not a good thing.  It is my job to keep my son alive and it is a 24/7 job.

It's BS when people ask me - - - 'Why are you still checking him at night?' or 'When will you be able to stop checking him all night?'.  I want to ask them when they would stop?!?!  Would that be rude?  If your child had a disease that could potentially kill them - when would you stop checking?


It's BS when people tell me --- Oh, my cousin's brother's son was diagnosed with T1 a couple of years ago.  They're fine.  Everything is fine.  They have it totally under control.  OK - calling BS on that.  First of all if you tell me 'they have it under control' then you have no idea what the heck you are talking about.  A person with diabetes can have good control but there is NO such thing as total control. Everything is a roller coaster with T1 especially with children.  Another big fat BS when you tell me that 'they are fine'.  Really? You know that for a fact?  Or do you just assume because everything looks ok from the outside that everything is fine?  I can pretty much GUARANTEE that everything is not fine on the inside --- I don't care how long it's been since the diagnosis there are still good days and bad days.  I can GUARANTEE that every mom of a T1 still cries every now and then ---- if she doesn't then there is something wrong!!

It's BS that I am begging people for money to support the JDRF because MY son has diabetes.  It's BS because I am asking (begging) my friends and my family to walk with us, support us and donate but I feel like I'm asking strangers. It's BS because I never see my friends anymore and when I do I'm sure they are sick and tired of me and my tired ass begging them to support MY cause.  But what is NOT BS is that my son needs a cure and that is why I will keep begging anyone and everyone to help.

It's BS that I miss my normal, boring life.  I miss my friends.  I miss girls night out.  I miss hanging out and chatting with other moms.  Even when I try to do these things my brain is such mush from all of the numbers swirling around and the lack of sleep I feel like I'm not really there.

It's BS that I have to weigh, measure and count every little thing that goes into Nate's mouth.  Seriously - it is SO much harder than it sounds.

It's BS that I cannot get insurance for my children.  Yes, I know there are options out there but the options are BS.

It's BS that my 6 year old asked me the following question "Mom, if Nate has diabetes and Sophie has Crohn's --- what am I going to get?".  That is BS.



Here's why I still cry - - - because when I look at my son he looks so healthy and beautiful but I know that his BG jumping all over the place. I know that that 325 that I saw on the meter this morning is BAD!   It's really bad.  I know that his life expectancy is shorter than you son's life expectancy --- what mom doesn't cry about that?  A child's mortality is something a parent should NEVER have to think about and yet I think about it every day.

I cry because I want a cure so bad that I can almost taste it and yet somehow I won't allow myself to think about it.

I cry because I want to take this stupid disease away from my son --- I just want to grab it and take it away.

I cry because type 1 diabetes is so misunderstood and I want to tell the world all about it but when I try to discuss it all I can do is CRY.

That is all.
Tomorrow I will be back to sunshine and rainbows.

I LOVE these magnets and I love that all of the proceeds go to JDRF.  My awesome D-Mom pal, Jill over at Diabetes Sweeties sent me one for Christmas and my mom was green with envy.  She was on a mission to find one for her truck!!  Now I am normally the more internet savvy one but I have to hand to to my mom --- she searched high and low and finally found the site that sells them.

You can order them at:

http://juvenilediabetesmagnets.homestead.com/

Christi and her mom, Laura (awesome name) will hook you up!!


I'm so glad she did because now our trucks look like this:

FAIL. 

I am super excited about D-Feast Friday and I am super sad that I am not participating.  Here's the deal - - -
I've been sick all week, I've got the diabetes blues and I am pretty sure there is not a recipe that I can offer that doesn't spike Nate's bg to the MOON! Even the bacon and eggs he had this morning sent him off the charts - - - I give up!

Maybe he's getting sick - I don't think so.  Maybe he's growing - could be!  Maybe diabetes sucks - yep I think that's it!! 

I am already seeing fantastic recipes popping up on my blog roll so please take a look on the left hand side of my blog and check out all of the awesome bloggers that are participating!

Thank you Karen, Lorraine and Elizabeth for coming up with D-Feast Friday - you girls are AMAZING!!

How can you not insure these 2 adorable children?


That is all.

Thank you,

Laura Houston

Nate and Sophie have been taking swim lessons from the same lady that taught me (A VERY LONG time ago).
Sophie loves it. Nate hates it.

Here is a video of Nate - he learned survival first and has now moved on to swimming. This video is of Nate floating for survival.



What does swimming do to his bg you ask?? Well, when he is swimming at home he drops like a ROCK - I'm talking CARBOPALOOZA baby (yep, I stole that word from Meri) and zero basal but when he is at swim class he goes high as a kite because he gets SO MAD!! Nothing is ever the same or easy with diabetes!!

And this is why Nate needs to be able to survive in the water (see picture below) - - - 
I was watching him from the next room. He moved Barbie's pretty, pink RV over to the door, stood on his tip toes and figured out the child-proof lock on the back door.  Can I just say that my girls NEVER did that!?!?  NOT ONE TIME!!




Nate has never been away from me since his dx so he is a MOMMA'S BOY! All that crying is not about the swimming or the floating - - - it is about him wanting his MOMMA!!

I told Jim that I really don't think I've ever had a boy quite so smitten with me. :)
It's starting to reach stalker status - - - I can't even pee in peace. It's gotten ridiculous in a good way. I love my little momma's boy!!


Ms. Sophie loves to swim too!! Here she is with her new BFF, Hannah -




Sophie was not swimming at all at the beginning of the summer and now she can swim the length of the pool.  I am so proud of her. She has worked so hard to learn to swim and feel confident in the water. Yea Sophie!!



2 Little fishies!!!

I seriously feel like that is all Nate's DexCom does.  BEEP!  I changed some settings and things have gotten better. But I had this idea while driving down the road with Nate and his DexCom was beep beep beeping!!

Since he is only 2 and still in a car seat he could not get to the receiver and even if he could I really would not want him chunking it at my head while driving!  So, I would like to develop a CGM specifically designed for children (the concept would work for adults too) and make the receiver a wristwatch. With a range more like the Navigator or even further!! I (mom or T1 Peep) could be wearing the watch and when an alarm goes off I could take a quick looksie (while driving, cooking, sleeping, in a meeting,  . . . whatever) and figure out a plan of action! It's quick, it's easy and it's a watch!!  I mean I like a nice watch just like the next person so if you want bling on your new CGM watch - - - I think bling should be an option!  Design your own CGM watch!!.  Wouldn't you rather wear a blingy (or design of your choice) watch CGM rather than a spibelt?

Because here is what happened when momma did not know which alarm was going off while driving (I haven't learned the different alarm sounds just yet).

Ms. Emma never gets any face time on this blog so I thought I would give her a shout out.  Emma just finished a great swim season with the BT Bullets!!  She is one fast little swimmer!!  She has been sick for the past 5 days but she wanted to swim in the championship meet anyway.  She swam on Monday morning and rocked it at the meet then came home and collapsed with a 103 degree fever.

Here are some pics of Ms. Emma . . .

After our perfect night that looked like this -



Nate checked his own bg today . . .

Thank you all for you words of encouragement about our insurance situation.  I know we will be fine. 
Insurance for Me, Jim and Emma is a done deal.  Sophie and Nate are another story.  I have been stockpiling test strips and insulin as best I can and I will get another 3-month supply before the coverage ends so we should be ok for a while.  The hard part is that it looks like we will have to take Nate off of the OmniPod.  If we have to pick our expenses --- Insulin is his life so we will have to have that! Test strips are our next priority so pumping will have to wait.  Plus, Sophie's expenses are not exactly light on the pocketbook.  She has a daily maintenance medicine that she has to take 3 times per day and if things don't get a lot better we may have to move on to a very expensive treatment plan for her. 

I am in a good place right now.  I'm not stressing or freaking out (too much) but I am very sad that we will have to stop pumping (podding).  We fought so hard to get Nate on the OmniPod and goodness knows we have worked our tails off getting basals sets, ratios figured out, and correction factors correct!!  Going back to shots may kill me (oh yea and I'm sure Nate won't like it too much either!).

Don't even get me started about being without the DexCom ---- no pump and no Dex.  I will feel like I am stepping back into the dark ages!!  --- The last statement in  no way implies that people that choose not to pump or use a CGM are living in the 'dark ages' --- it is just how I will feel after having what has become such luxuries for us.  :)  I've become quite spoiled!

There are options out there (surely there are!) but the problem is even if we get Nate and Soph on a plan they exclude all expenses of their preexisting condition for at least a year!  It is a frustrating system but it is what it is and like I said I am not going to let this get me down.  We will get through this and be just fine --- just another new kind of fine! 

The good news is we still have our 'beep-beep' (Nate's name for his PDM) and pods for now so I am going to enjoy the heck out of them while I can!!

Nate's alkaline phosphatase results came back much lower today and all of the other results were completely normal. It looks like we have a case of Benign Transient Hyperphosphatasemia which really means that his alkaline phosphatase was elevated for no good reason but should go down and cause absolutely no problem whatsoever.

That's all I've got for now.

Thank you as always for all of the comments, prayers and support . . . it really takes a village!

Ummm - yea - whatever that means!  I'm seriously not that sure what it is but I am sure hoping that Nate has it!

Last week we took Nate to his endo for his quarterly appointment.  At his new practice they do not do a finger stick HBA1C like they did at his previous practice.  They do a full blown blood draw and run 'the works' to make sure everything is on track.  Nate has not had his blood drawn since his diagnosis and even at that time we were never given any information on what tests were run or what the results were. 

Type 1 diabetics run the risk of several other endocrine issues so I was thrilled to get a full work up and anxious to get the results back.  Almost everything looks pretty good.  His A1C is down an entire point, no thyroid problems, his cholesterol is good.  A few issues --- his triglyceride results are high and his HDL is low which apparently is somewhat normal for T1 children. His alkaline phosphatase results came back extremely high and when I say HIGH --- I'm not even kidding.  They should be somewhere between 200 - 400 and his came back at 3,017.  What does this mean?  I honestly just don't know - I've been on Dr. Google all day and I can't wrap my head around all of the things that it could mean but for now Nate's dr. is running more tests which should give us more answers soon.

And . . . if all of the the test results come back normal then they think he may have a case of Benign Transient Hyperphosphatasemia.


________________________________________
Here is the information that I was sent - It's a lot to digest so please feel free to bypass.  :)


Transient hyperphosphatasemia (TH) of infancy and early childhood is characterized by a marked elevation of serum alkaline phosphatase in the absence of detectable liver or bone disease, and a return to normal levels within weeks or months. The condition is thought to be benign; thus, this disorder is also called benign transient hyperphosphatasemia. Recognition of this phenomenon permits avoidance of unnecessary procedures and concerns, provided that underlying liver and bone disease are appropriately excluded.


The clinical presentation and evaluation of an infant or young child with marked elevation of serum alkaline phosphatase will be reviewed here. Evaluation of an older child or adult with elevated alkaline phosphatase, or of any individual with elevations of multiple liver enzymes, is discussed separately. (See "Alkaline phosphatase and other enzymatic measures of cholestasis" and "Approach to the patient with abnormal liver function tests".)
Serum AP levels gradually return to normal within two to three months but have persisted as long as six months in a few cases [9,10]. The half-life of AP ranges from 5 to 25 days, depending upon coexisting morbidities [11]. In series reporting the results of long-term follow-up, no clinical sequelae were noted up to four years after the episode of TH [12,13].
The prevalence of TH is not known. In a series of 260 healthy infants, three (1.5 percent) had unexplained and transient elevations in serum AP, all more than three times the upper limit of normal for the assay [14]. Similar prevalence rates were seen in a separate study in which serum alkaline phosphatase levels >1000 U/L (2.5 times the upper limit of normal) were found in 2.8 percent of healthy children under two years of age. More moderate elevations of alkaline phosphatase, between 400 and 1000 U/L, were found in 5.1 percent of the subjects [15].
Most children with TH are healthy, although TH has occurred in association with a variety of clinical conditions, including gastroenteritis, respiratory infection, failure to thrive, and asthma. TH has also been reported with viral infections such as respiratory syncytial virus [16-18], enteroviruses [19], and HIV [20]; following liver [21,22] or kidney transplant [21]; and in children receiving chemotherapy for leukemia and lymphoma [11,23]. Some of these apparent disease associations may reflect more frequent laboratory testing to monitor the underlying disease. Indeed, in the largest study that prospectively evaluated a healthy population of infants and toddlers, no association with growth parameters was found [15]. A seasonal distribution of cases has been noted in some series, with more cases identified in late summer and early fall [5,11].
The cause of the increased sialylation remains uncertain. By definition, TH is not caused by vitamin D deficiency. However, one hypothesis is that TH develops because there is increased production of AP during a period of catch-up growth after weight loss or vitamin D insufficiency, at a rate that overwhelms the mechanisms that normally desialylate the enzyme [11]. If so, children with TH might display subclinical vitamin D insufficiency at the time of diagnosis. However, this was not the case in one series of healthy infants and children, in which there was no difference in serum levels of vitamin D, parathyroid hormone, calcium, or phosphorus among subjects with TH as compared to those with normal AP levels [15].
Risk factors for nutritional rickets should be assessed, including exclusive breast feeding or intake of less than one liter of vitamin D-fortified formula or milk daily, dark skin pigmentation, low exposure to sunlight, or prematurity. These infants and children are at risk for rickets unless given vitamin D supplements of at least 400 IU daily. (See "Overview of rickets in children".)
A normal result for each of these tests is adequate to establish a provisional diagnosis of TH in an otherwise healthy infant or young child. Of note, the serum GGT activity is six to seven times the upper limit of the adult reference range in normal full-term neonates; levels decline and reach adult levels by five to seven months of age [24].
Measurement of alkaline phosphatase isoenzymes by electrophoresis can be helpful if this test is available. The presence of excessive bone and liver fractions supports the diagnosis of TH and argues against primary hepatic or bone disease. (See "Alkaline phosphatase and other enzymatic measures of cholestasis".)
The possibility of rickets should be raised by low serum levels of 25-hydroxyvitamin D with low serum calcium and/or phosphorus, elevated levels of PTH, a history of risk factors for vitamin D deficiency (exclusive breast feeding without vitamin D supplementation), or typical skeletal abnormalities. Any of these findings should prompt further evaluation for rickets, with radiographs of long bones. (See "Overview of rickets in children".)
Bone pain or other bone abnormalities should be evaluated radiographically for evidence of tumor, fracture, or juvenile Paget disease (a rare autosomal recessive disorder of bone turnover associated with bone deformities and susceptibility to fracture). Limb pain also can be caused by a variety of orthopedic, infectious, rheumatic, and neoplastic disorders, as discussed separately. (See "Clinical manifestations and diagnosis of Paget disease of bone" and "Clinical assessment of the child with suspected cancer", section on 'Bone and joint pain' and "Overview of the causes of limp in children".)
Follow-up to document return of serum alkaline phosphatase (AP) levels to normal is critical for confirmation of the diagnosis of TH [25]. In our practice, we repeat serum AP measurement in a child with the provisional diagnosis of TH within two weeks, and then monthly until a downward trend is noted and normal values are attained. Sustained serum AP elevation beyond three to four months should prompt reconsideration of other causes of hyperphosphatasemia, including the bone disorders mentioned in the preceding section.

• Transient hyperphosphatasemia (TH) of infancy and early childhood is characterized by a marked elevation of serum alkaline phosphatase (AP) in the absence of detectable liver or bone disease. Almost all cases occur in infants and children younger than five years of age. (See 'Clinical presentation' above.)

• In TH, the serum AP is typically elevated four to five times the upper limit of the pediatric reference range, and gradually returns to normal within two to three months. (See 'Clinical presentation' above.)

• Serum AP activities are higher in children than in adults because of physiological osteoblastic activity. The upper limit of the pediatric reference range is up to three times higher than in adults, peaking in late infancy and again during puberty (graph 1). (See 'Normal ranges for serum AP' above.)

• TH is characterized by elevations in both bone and liver alkaline phosphatase isoenzymes. The pathogenesis has not been fully established, but is thought to include reduced clearance of AP due to increased sialic acid content, perhaps caused by or compounded by a transient surge in alkaline phosphatase production. (See 'Pathogenesis' above.)

• The evaluation should include a history and physical examination to assess for evidence of primary liver or bone disease. Laboratory testing should include measurement of serum aspartate aminotransferase, alanine aminotransferase, bilirubin, calcium, phosphorus, 25-hydroxyvitamin D, parathyroid hormone, blood urea nitrogen, and creatinine. In addition, measurement of either gamma-glutamyl transpeptidase (GGT) or 5'-nucleotidase helps to exclude liver disease. (See 'Evaluation and management' above.)

• The possibility of rickets should be raised by low serum levels of 25-hydroxyvitamin D, calcium or phosphorus, elevated serum parathyroid hormone, a history of risk factors for vitamin D deficiency such as exclusive breast feeding without vitamin D supplementation, or typical skeletal abnormalities. Any of these findings should prompt further evaluation, including radiographs of long bones. (See 'Laboratory testing' above and "Overview of rickets in children".)

• Even if rickets is excluded, all children should be evaluated to ensure adequate intake of vitamin D and supplemented with at least 400 IU daily if needed. Steps should also be taken to ensure adequate intake of calcium. (See 'Monitoring' above.)

• If there is no evidence of liver or bone disease in an infant or young child, then the provisional diagnosis of TH can be made. Repeat measurement of serum AP should be performed at intervals until normal values are attained. (See 'Monitoring' above.)

1	Rosalki, SB, Hurst, NP. Transient presence in serum of an atypical alkaline phosphatase. Clin Chim Acta 1976; 73:149.
2	Schambeck, CM, Kopp, A, Mora-Maza, G, Keller, F. Transient alkaline hyperphosphatasaemia in an adult: biochemical peculiarities. Eur J Clin Chem Clin Biochem 1997; 35:441.
3	Rosalki, SB, Foo, AY, Went, J, et al. "Transient hyperphosphatasemia of infancy and childhood" in an adult. Clin Chem 1991; 37:1137.
4	Onica, D, Torssander, J, Waldenlind, L. Recurrent transient hyperphosphatasemia of infancy in an adult. Clin Chem 1992; 38:1913.
5	Behulova, D, Bzduch, V, Holesova, D, et al. Transient hyperphosphatasemia of infancy and childhood: study of 194 cases. Clin Chem 2000; 46:1868.
6	Stein, P, Rosalki, SB, Foo, AY, Hjelm, M. Transient hyperphosphatasemia of infancy and early childhood: clinical and biochemical features of 21 cases and literature review. Clin Chem 1987; 33:313.
7	Rosalki, SB, Foo, Y. Transient hyperphosphatasemia of infancy: four new cases, and a suggested etiology. Clin Chem 1980; 26:1109.
8	Kruse, K, Kracht, U. [Isolated elevation of serum alkaline phosphatase]. Dtsch Med Wochenschr 1985; 110:669.
9	Garrote de, Marcos JM, Molina Arias, M, Echavarri Olvarria, F, Arregui Sierra, A. [Benign transient hyperphosphatasemia: the contribution of 20 new cases]. An Esp Pediatr 1996; 44:112.
10	Carroll, AJ, Coakley, JC. Transient hyperphosphatasaemia: an important condition to recognize. J Paediatr Child Health 2001; 37:359.
11	Crofton, PM. What is the cause of benign transient hyperphosphatasemia? A study of 35 cases. Clin Chem 1988; 34:335.
12	Steinherz, PG, Steinherz, LJ, Nisselbaum, JS, Murphy, ML. Transient, marked, unexplained elevation of serum alkaline phosphatase. JAMA 1984; 252:3289.
13	Posen, S, Lee, C, Vines, R, et al. Transient hyperphosphatasemia of infancy--an insufficiently recognized syndrome. Clin Chem 1977; 23:292.
14	Asanti, R, Hultin, H, Visakorpi, JK. Serum alkaline phosphatase in healthy infants. Occurrence of abnormally high values without known cause. Ann Paediatr Fenn 1966; 12:139.
15	Huh, SY, Feldman, HA, Cox, JE, Gordon, CM. Prevalence of transient hyperphosphatasemia among healthy infants and toddlers. Pediatrics 2009; 124:703.
16	Goto, M. [Is respiratory syncytial virus one of the causative agents for transient hyperphosphatasemia?]. Rinsho Byori 2002; 50:1146.
17	Holt, PA, Steel, AE, Armstrong, AM. Transient hyperphosphatasaemia of infancy following rotavirus infection. J Infect 1984; 9:283.
18	Schonau, E, Herzog, KH, Bohles, HJ. Transient hyperphosphatasaemia of infancy. Eur J Pediatr 1988; 148:264.
19	Suzuki, M, Okazaki, T, Nagai, T, et al. Viral infection of infants and children with benign transient hyperphosphatasemia. FEMS Immunol Med Microbiol 2002; 33:215.
20	Fennoy, I, Laraque, D. Benign transient hyperphosphatasia and HIV infection. Clin Pediatr (Phila) 1989; 28:180.
21	Ranchin, B, Villard, F, Andre, JL, et al. Transient hyperphosphatasemia after organ transplantation in children. Pediatr Transplant 2002; 6:308.
22	Arikan, C, Arslan, MT, Kilic, M, Aydogdu, S. Transient hyperphosphatasemia after pediatric liver transplantation. Pediatr Int 2006; 48:390.
23	Massey, GV, Dunn, NL, Heckel, JL, et al. Benign transient hyperphosphatasemia in children with leukemia and lymphoma. Clin Pediatr (Phila) 1996; 35:501.
24	Cabrera-Abreu, JC, Green, A. Gamma-glutamyltransferase: value of its measurement in paediatrics. Ann Clin Biochem 2002; 39:22.
25	Tolaymat, N, de Melo, MC. Benign transient hyperphosphatasemia of infancy and childhood. South Med J 2000; 93:1162.

Ok - peeps!  I am not doctor and I have no ambitions of being one . . .I'm just a mom, a pancreas and a night time (wanna-be) nurse but I will try to give you some more information on Apidra and how it is working for Nate.  Ok, just trying to cover my you know what here!! 

Apidra (insulin glulisine [rDNA origin] injection from the makers of Lantus

'ALL ABOUT APIDRA' from Diabetes Reference Guide from Sanofi Aventis:


Apidra is a rapid-acting insulin that works like your body's natural insulin to help manage your blood sugar.  It comes in a standard vial or the optiClik pen, and it also works well in your insulin pump. In fact, Apidra is shown to have low rates of pump clogs and infusion site reactions.


Apidra also gives dosing flexibility because you can dose within 15 minutes before or 20 minutes after you start a meal.




______________________________________________


More Apida information from their handout about pediatric indication - - -



Apidra is a rapid-acting human insulin analog indicated to improve glycemic control in adults with type 2 diabetes mellitus or adults and children (4 years and older) with type 1 diabetes mellitus.

Apidra has a more rapid onset of action and shorter duration of action than regular human insulin.  Apidra should normally be used in regiments that include a longer-acting insulin or basal insulin analog.




** As with all insulin preparations, the time course of Apidra action may vary in different individuals or at different times in the same individual and is dependent on site of injection, blood supply, temperature, and physical activity.


Ok - I think I hit the highlights from Apidra literature. 

Now here are some answers to the questions from my last post:

* We currently have Nate's DIA (Duration of Insulin Action) on his OmniPod set to 3.5 hours. Once I get a better feel for the new insulin in his pump I may kick it down to 3 hours.

* We previously had it set at 5 hours with Novolog (very conservative) when we 1st started pumping and then changed it to 4 hours before we made the change to Apidra.

* Our Co-Pay is about the same.  We use CVS/Caremark and fill our Rx 3 months at a time and there is a minimum difference in co-payment

* We didn't make any other pump setting changes due to the Apidra. We were/are still working on his breakfast ratio and correction factor but the changes had nothing to do with the insulin change.  We were experimenting with our AM bolus before we officially made the change. 

*  The dosing is the same unit for unit for Nate.

I hope this helps at least a little - - -
For more information check out www.apidra.com

____________________________________________________________

For the record - - -

the day that I wrote the Apidra post Nate's numbers looked like this:

225a - 108
323a - 74 (treated with 7g)
700a - 209 (huh?) breakfast bolus and correction
842a - 168
938a - 100 (woot-woot) bolus for snack
1037a - 120
1133a - 170 lunch bolus
338p - 108 snack bolus
506p - 122 dinner bolus
721p - 152 bedtime snack bolus
825p - 191
1032p - 192


and then I posted this little statement on my blog:
"We bolus Nate right before he eats and we still have great numbers."

Why would I write that?  Why would I even think about putting that out there?  Why didn't I knock on the big hunk of wood that is my desk???  Why??

Because the next bg check looked like this:

224a - 335   WTH?  Corrected very conservatively because well because it's 224a!!
331a - 301   Nate woke up crying, thirsty, we rocked and fell asleep in his rocking chair
720a - 400   OMG! Freaking out - haven't seen a number with a 4 in front in a LONG time (knock-              knock-knocking on wood right now)
900a - 439   Because I'm a nerd I didn't use his PDM because I didn't want to see another bad number in the history.  I know - I'm a nerd that way.
1025a - 286   Yippee!
1111a - 121   Wow - that was fast! We were at playtime with our local D friends so treated with 10g

1146a - 143 lunchtime bolus, lunch, then off to play in the Chic-fil-A play area!! 
156p - 99 Nice number since we were at his endo appointment!!!!   :)