Jay:
I was going to ask if you were some sort of engineer. I can usually spot them pretty easily (distinct personalities).
There is a difference between ITP and thrombocytopenia. Thrombocytopenia is usually defined as low platelets with a known primary cause such as viral infections, chemotherapy, heavy alcohol use, etc. These types will usually go away when the person recovers. If there is no known cause, the diagnosis is ITP which is autoimmune-related.
I have no idea if your low platelets were caused by heavy alcohol use or not. I will not deny the possibility. All you can do is change your lifestyle and wait it out. I do believe that lifestyle changes such as diet and stress management can make a difference.
Thrombocytopenia is a frequent complication of alcoholism, affecting 3 to 43 percent of nonacutely ill, well-nourished alcoholics and 14 to 81 percent of acutely ill, hospitalized alcoholics. Thus, apart from acquired immune deficiency syndrome (AIDS), alcoholism probably is the leading cause of thrombocytopenia. Except for the most severe cases, however, the patients generally do not exhibit manifestations of excessive bleeding. Moreover, alcohol-related thrombocytopenia generally is transient, and platelet counts usually return to normal within 1 week of abstinence.
Therefore, patients generally require no therapeutic intervention other than that needed to ease alcohol withdrawal. Only in patients whose thrombocytopenia is severe and associated with
excessive bleeding are platelet transfusions indicated. In many patients with thrombocytopenia, rebounding platelet numbers even exceed normal values. This rebound thrombocytosis after cessation of alcohol consumption also occurs in the majority of patients whose platelet
counts are normal at the time of hospitalization. In these patients, the extent of the excess in circulating platelets usually is higher than in patients presenting with thrombocytopenia.
The exact mechanisms underlying alcohol-related thrombocytopenia remain unknown. Some researchers
have suggested that alcohol intoxication itself, rather than alcohol-related nutritional deficiencies, causes the decrease in platelet numbers. This view is supported by findings that
thrombocytopenia developed in healthy subjects who received a diet containing adequate protein and vitamin levels (including large doses of folic acid) and consumed the equivalent of 1.5 pints (i.e., 745 milliliters) of 86-proof whiskey for at least 10 days (Lindenbaum 1987). The subjects’ platelet levels returned to normal when alcohol consumption was discontinued. Similarly, platelet counts can be reduced in well-nourished alcoholics who do not suffer from folic acid deficiency. The available data also suggest that alcohol can interfere with a late stage of platelet production as well as shorten the life span of existing platelets.
Individual drinkers appear to differ in their susceptibility to alcohol-induced thrombocytopenia. Thus, clinicians have noted that some people who consume alcohol in excess repeatedly develop thrombocytopenia (often severely), whereas other drinkers maintain normal platelet levels. In addition to differences in the quantity of alcohol consumed, inherited
or acquired variations in an individual drinker’s biochemistry may account for
these differences in susceptibility.
pubs.niaaa.nih.gov/publications/arh21-1/42.pdf