Whats your serum ceruloplasmin level? Have you had a slit lamp eye exam looking for K-F rings??? Liver biopsy is the classic - conclusive test
I have done extensive research on Wiilson's Disease. These symptoms have been gleaned from 100s of reports, including medical and scientific. Since there is a character limit on how much can be sent through, I will send the symptoms through in stages.
About half the patients with Wilson's have neurological or psychiatric problems.
Neurological: movement disorders, migraines, insomnia, prolonged muscular contractions that may cause twisting (torsion) of body parts, repetitive movements, and increased muscular tone. Difficulty in articulating words, sometimes accompanied by drooling. Difficulty swallowing. Symptoms similar to multiple sclerosis. Tremors of head, arms, hands, or legs, impaired muscle tone, slowness of movements, slurred speech, difficulty controlling voluntary muscles
Psychiatric: depression, anxiety, behavorial changes (bizarre or inappropriate behavior), neurosis, psychosis
Neuropsychiatric: mild cognitive deterioration and clumsiness, as well as changes in behavior parkinsonism (increased rigidity and slowing of routine movements) with or without a typical hand tremor, ataxia (lack of coordination) or dystonia (twisting and repetitive movements of part of the body). Seizures and migraine appear to be more common in Wilson's disease.
SYMPTOMS of Wilson's Disease
Liver: jaundice, abdominal swelling, abdominal pain, vomiting of blood. Liver disease may present as tiredness, increased bleeding tendency , a tendency to bruise easily, or confusion (due to hepatic encephalopathy) and portal hypertension. The latter, a condition in which the pressure on the portal vein is markedly increased, leads to esophageal varices (blood vessels in the esophagus) that may bleed in a life-threatening fashion, splenomegaly (enlargement of the spleen) and ascites (accumulation of fluid in the abdominal cavity). On examination, signs of chronic liver disease such as spider naevi (small distended blood vessels, usually on the chest) may be observed. Chronic active hepatitis has caused cirrhosis of the liver in most patients by the time they develop symptoms. About 5% of all patients are diagnosed only when they develop fulminant acute liver failure, often in the context of a hemolytic anemia (anemia due to the destruction of red blood cells). This leads to abnormalities in protein production (identified by deranged coagulation) and metabolism by the liver.
Liver or spleen disorders: including cirrhosis and liver necrosis
SYMPTOM's of Wilson's Disease
Damage to the central nervous system: loss of coordination, loss of muscle control, muscle tremors, loss of cognitive and intellectual functions, loss of memory, confusion (delirium or dementia), other damage
Kidney problems: renal tubular acidosis, weakening of the bone, occasionally aminoaciduria; The Wilson disease gene is expressed in kidney tissue; therefore, any renal manifestations may be primary or secondary to release of copper from the liver.
Clinically, patients may resemble those with Fanconi syndrome, demonstrating defective renal acidification and excess renal losses of amino acids, glucose, fructose, galactose, pentose, uric acid, phosphate, and calcium. The frequency of renal manifestations is variable. Urolithiasis, found in up to 16% of patients with Wilson disease, may be the result of hypercalciuria or poor acidification. Hematuria (the presence of red blood cells (erythrocytes) in the urine) and nephrocalcinosis (a term originally used to describe deposition of calcium salts in the renal parenchyma due to hyperparathyroidism. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification on radiology. During its early stages, nephrocalcinosis is visible on x-ray, and appears as a fine granular mottling over the renal outlines. These outlines eventually come together to form a dense mass. It is most commonly seen as an incidental finding with medullary sponge kidney on an abdominal x-ray. However, it may be severe enough to cause (as well as be caused by) renal tubular acidosis or even end stage renal failure, due to disruption of the renal tissue by the deposited calcium) are reported, and proteinuria (the presence of an excess of serum proteins in the urine. The protein in the urine often causes the urine to become foamy) and peptiduria (protein having to do with the spleen) can occur both before treatment as part of the disease process and after therapy as adverse effects of D-penicillamine. The product of the Wilson disease gene is expressed in renal tissue, but whether the renal symptoms are primary or secondary to release of copper from the liver is unknown. Renal complications tend to be functional changes unrelated to identifiable histologic findings. Rarely, patients with Wilson disease develop renal stones and associated symptoms. Renal stones are precipitated by hypercalciuria (the condition of elevated calcium in the urine. Chronic hypercalciuria may lead to impairment of renal function, nephrocalcinosis, and renal insufficiency.) and poor urine acidification. Therapy with copper-chelating agents can improve renal function.
Eyes: Kayser-Fleischer rings, also associated with sunflower cataracts, brown or green pigmentation of the anterior and posterior lens capsule
Heart: cardiomyopathy, heart failure, cardiac arrhythmias, blood vessel and heart rupture, abnormal EKG's,
SYMPTOM's of Wilson's Disease
Hormones: hypoparathyroidism, infertility, habitual abortion (multiple miscarriages), gynecological problems, disrupted menstruation, irregular menstrual periods, estrogen production, helps maintain pregnancy, uterine fibroids, Endometriosis
[Copper is called the 'psychic' mineral, the 'intuitive' mineral, and a 'feminine' mineral because it is so important for the female reproductive system. Women tend to have higher levels of copper than men. Women also have more symptoms related to copper imbalance. These include yeast infections, migraine headaches, adult acne, various menstrual symptoms and depression. Copper-toxic women are often estrogen dominant.]
Other: abdominal bloating, alopecia (loss of hair), anxiety attacks, constipation, digestive distress, hypoglycemia, insomnia, loss of appetite, loss of smell, loss of taste, mental depression, panic attacks, elevated levels of serum cholesterol, triglycerides, and glucose, fungal and bacterial infections including yeast infection, gum disease, tooth decay, skin and hair problems, adrenal burnout, scoliosis; Other relatively uncommon findings include exotropic strabismus, optic neuritis or pallor of the optic disc, and nightblindness
Other physical findings include Azure lunulae of the fingernails and Arthropathy. An arthropathy is a disease of a joint. Although the terms "arthropathy" and arthritis have very similar meanings, the former is traditionally used to describe the following conditions: *) Reactive arthropathy (M02-M03) is caused by an infection, but not a direct infection of the synovial space. *) Enteropathic arthropathy (M07) is caused by colitis and related conditions. *) Crystal arthropathy (also known as crystal arthritis) (M10-M11) involves the deposition of crystals in the joint. *) In gout, the crystal is uric acid. In pseudogout/chondrocalcinosis/calcium pyrophosphate deposition disease, the crystal is calcium pyrophosphate. *) Diabetic arthropathy (M14.2, E10-E14) is caused by diabetes. *) Neuropathic arthropathy (M14.6) is associated with a loss of sensation.
The arthropathy of Wilson disease is a degenerative process that resembles premature osteoarthritis. Symptomatic joint disease, which occurs in 20-50% of patients, usually arises late in the course of the disease, frequently after age 20 years. The arthropathy generally involves the spine and large appendicular joints, such as knees, wrists, and hips. Osteochondritis dissecans (Patients with OCD complain of activity-related pain that develops gradually. Individual complaints usually consist of mechanical symptoms, including pain, swelling, catching, locking, and "giving way"; the primary presenting symptom may be a restriction in the range of movement., chondromalacia patellae, and chondrocalcinosis have also been described.)
I am pretty aware of the symptoms for "Wilson's" as I was tested for it. First by a ceruloplasmin level test , and then a liver biopsy. My dry copper weight was around 64ug/gm - which I have skewed low due to copious consumption of zinc (which can be a problem in and of itself)... A confirmation for wilson's would be 200 (or 250 ug/gm dry copper weight - depending on who's criteria) and above to confirm it.
Many diseases present with symptoms like Wilson's poses, but, again, if you have suspicion - do the blood test, do the Keyser-Fleischer test at the opthalmologist, and if they lead to further suspicion, ask a hepatologist about biopsy.
As far as any "link" between GB removal and WIlson's - Well, Im no MD, but the simple removal of the gall blad couldnt "trigger" wilson's - Now if you have underlying liver problems, that certainly (in my unprofessional opinion) aggravate your Gall-Bladder as they two or closely linked...