I have PE and i noticed it last year.My GP acted like it was no big deal. Also to go with it my blood Platelets were at 75 (should be 150-350 or higher)
He should have sent me to a hep specialist immediately. Do not pass go!
Instead he acted like all was fine.
I told him since the Harvoni is out now i need to find a hep dr and get on treatment.I found a hep specialist at Baylor hosp & transplant center.
I knew i wanted the best of the best.
As soon as the hep dr saw my last yrs blood work showing 75 on the platelets and the red palms he said and a few other things, looks like early stage cirrhosis. After the appointment i went down stairs and got the new blood work. Then a couple days later i got the Ultra Sound of the abdominal and i go in on the 30th of June which is day after tomorrow. I'm 63 and really never sick a day, so to speak. My wife of 20 yrs,sister 64,son 38 and i are going at 2:15 on Tuesday.
I'm terrified. I have read enough on the community blogs from others to know i may be a little decompansated and the news will be bad.The question is ...How Bad. It is the most life threatening / life changing thing i can imagine. So in closing,If you have red palms and hep c GO get it checked and go to a hep specialist. Don't rely on a GP to just watch it. A GP worth his salt will write you a referral to a hep specialist as soon as a hep c test saz you have hep c
All Best & God bless You All
RLP1952
I have to laugh when I read all the causes of PE. I was looking at my palms all day. Let us know how your biopsy turns out and take it easy on the 25th.
Jules
NAME: PURIBEN K PATEL AGE/SEX: 60/FEMALE
12th APRIL 2012 Test is done HCV (+VE)
30TH APRIL 2012 1) HCV VIRAL LOAD *42500
2)*GENOTYPE 3
15TH MAY 2012: TREATMENT PROTOCOL STARTED
Inj. Pegasys 180 mcg 1 per every week for 24 weeks
Cap. Ribavarin 200 mg 2-0-3 for 24 weeks
• After 4th week of treatment 12th JUNE 2012 – VIRAL LOAD *52
• After 12th week of treatment 26Th AUG 2012 – VIRAL LOAD *BELOW 15
• After 24th week of treatment 29Th OCT 2012 – VIRAL LOAD *BELOW 15
• After 24th week of treatment 29Th OCT 2012 – **NOT DETECTED
26TH APRIL 2013 (after 6 month of treatment) AGAIN TEST IS DONE
RESULT: - VIRAL LOAD *1,06,000
I have two doctors suggestion.
---->One doctor told repeat this Treatment again 48 weeks.But my mother is not acceptable for this treatment.
---->Second doctor was told---> not better result in this treatments and not acceptable this dose of patient of
this age.If you are collect medicine SOFOSBUVIR and treat this petient than
we hope better result.
Dear all,
Please help of this Case.
Thanks, I do have my biopsy scheduled for May 25. I have no other signs of cirrhosis so I will do my best not to worry until then.
When I first found out I had HCV and read about PE I was obsessed with looking at other peoples palms to see how red they were. Once I had a Fibroscn & biopsy showing minimal damage I realized my red palms were of no concern. Get a liver biopsy and find out for sure the state of your liver. This will put your mind at ease.
Best of luck
Maybe all that bike riding is just giving you a stronger circulation
I had read palms at the end of treatment. It really freaked me out. I knew that is was a sign of liver disease and I had just finished Hepatitis C treatment. My doctor didn't seem concerned. In fact I have had friends who have had unusually red hand and they just have red hands. I think in my case it was just the results of taking a massive amount of medication while treating hep c. This treatment has to have an effect on your liver. But
regardless, red hands can be just something you were born with. You should bring it to the attention of your doctor if your concerned. On the other hand :)
my doctor thought it wasn't that alarming and I have no history of red hands.
Best to You and Your Partner
I guess you're telling me it could be from a variety of causes, some unrelated to HCV? To be honest my palms don't look very red to me or to my partner. Actually his palms are much redder than mine and he's HCV-
Palmar erythema.
Serrao R, Zirwas M, English JC.
Source
Department of Dermatology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Abstract
Palmar erythema (PE), an often overlooked physical finding, is due to several physiologic or systemic pathologic states. PE can exist as a primary physiologic finding or as a secondary marker of systemic pathology. Primary or physiologic PE can be due to heredity, occurs in at least 30% of pregnant women as a result of associated alterations in the function of the skin and its microvasculature, or may be a diagnosis of exclusion (i.e. idiopathic PE). Secondary PE from systemic pathology encompasses a wide range of disease states. Twenty-three percent of patients with liver cirrhosis, from varying causes, can manifest PE as a result of abnormal serum estradiol levels. Patients with a rare neonatal liver disease such as Wilson disease and hereditary hemochromatosis may exhibit PE along with the other systemic manifestations of the genodermatoses. PE has been reported to occur in >60% of patients with rheumatoid arthritis and is associated with a favorable prognosis. Up to 18% of patients with thyrotoxicosis and 4.1% of patients with diabetes mellitus can have PE. This cutaneous manifestation of diabetes occurs more often than the more classic diseases such as necrobiosis lipoidica diabeticorum (0.6%). PE can be seen in early gestational syphilis and among patients with human T-lymphotrophic virus-1-associated myelopathy. Drug-induced PE with hepatic damage has been documented with use of amiodarone, gemfibrozil, and cholestyramine, while topiramate and albuterol (salbutamol) have been reported to cause PE in the setting of normal liver function. Fifteen percent of patients with both metastatic and primary brain neoplasms may have PE. Increased levels of angiogenic factors and estrogens from solid tumors have been postulated as the cause of PE in such cases. Erythema ab igne can mimic PE, and patients with atopic diathesis are more likely to have PE than matched control subjects. Smoking and chronic mercury poisoning are environmental causes of PE.No treatment of primary PE is indicated. If medication is the cause of PE, the drug responsible should be discontinued if possible. Identification of PE related to underlying disorders should be followed by treatment of the underlying condition. In light of the numerous etiologies of PE, this article reviews the current literature and provides a framework to help guide the clinician in determining the cause of PE in patients presenting with this finding.
www.ncbi.nlm.nih.gov/pubmed/18039017