Labeling may be an important cause of reduced quality of life in chronic hepatitis C

226

Letters to the Editor

AJG – Vol. 98, No. 1, 2003

REFERENCES 1. Kaplan MM. Primary biliary cirrhosis. N Engl J Med 1987; 316:521–8. 2. Elster AD, Chen MY. Chiari I malformations: Clinical and radiological reappraisal. Radiology 1992;183:347–53. 3. Oakes WJ. Chiari malformations, hydromyelia, syringomyelia. In: Wilkins RH, Rengachary SS, eds. Neurosurgery. New York: McGraw-Hill, 1996:3593–616. 4. Alexander GE, Provost TT, Stevens MB, Alexander EL. Sjo¨ gren syndrome: Central nervous system manifestations. Neurology 1981;31:1391–6. 5. Konttinen YT, Kinnunen E, von Bonsdorff M, et al. Acute transverse myopathy successfully treated with plasmapheresis and predonisone in a patient with primary Sjo¨ gren’s syndrome. Arthritis Rheum 1987;30:339 –44. 6. Rutan G, Martinez AJ, Fieshko JT, Van Thiel DH. Primary biliary cirrhosis, Sjo¨ gren’s syndrome, and tranverse myelitis. Gastroenterology 1986;90:206 –10. 7. Wakatsuki T, Miyata M, Shishido S, et al. Sjo¨ gren syndrome with primary biliary cirrhosis, complicated by transverse myelitis and malignant lymphoma. Intern Med 2000;39:260 –5. 8. Blagodatskii MD, Larionov SN, Manokhin PA. Clinico-immunological and pathomorphological correlations in syringomyelia. Zh Nevropatol Psikhiatr Im S S Korsakova 1991;91: 6 –11. 9. Newman PK, Wentzel J, Foster JB. HLA and syringomyelia. J Neuroimmunol 1982;3:23–6. 10. Ishchenko MM, Degtiar VV, Komorovskaia IAM. Four cases of familial syringomyelia in a single generation. Zh Nevropatol Psikhiatr Im S S Korsakova 1976;76:662–5. Reprint requests and correspondence: Hiromasa Ohira, M.D., Department of Internal Medicine II, Fukushima Medical University School of Medicine, 1-Hikarigaoka, Fukushima 960-1295, Japan. Received Aug. 15, 2002; accepted Aug. 19, 2002.

Labeling May Be an Important Cause of Reduced Quality of Life in Chronic Hepatitis C TO THE EDITOR: The mechanisms by which hepatitis C virus (HCV) infection causes a decrease in health-related quality of life (HRQL) are unknown (1). A recent hypothesis has proposed that the cerebral effects of HCV may be responsible for the reduced HRQL (2). However, the reduction of HRQL may not be caused by the biological consequences of HCV infection. Chronic hepatitis C may impair HRQL simply because of the effects of “labeling” (3), which refers to the impact on HRQL of the consequences of establishing the diagnosis. An approach to evaluate the magnitude of labeling is to investigate HRQL in altruistic blood donors. We assessed HRQL in HCV-infected donors who completed the Short Form (SF)-36 questionnaire at the time of the diagnosis (group A: 14 men, three women, 40 ⫾ 11 yr) and in HCV-infected subjects (group B: 28 men, 44 women, 58 ⫾ 5 yr) identified at the same blood bank 5 ⫾ 3 yr before and who had periodical medical visits at our liver unit. Patients

Figure 1. Scores of the SF-36 health survey questionnaire (mean ⫾ SD) in HCV-positive blood donors investigated after the medical assessment that followed the diagnosis (group B, n ⫽ 72) were lower than HCV-positive blood donors investigated at the time of the diagnosis (group A, n ⫽ 17; p ⬍ 0.05).

with alcohol intake over 20 g/day, treatment with interferon during the prior 2 yr, and comorbidities were excluded. SF-36 scores in group A were within the normal range when compared with an age- and gender-adjusted Spanish population; however, SF-36 scores in group B showed a moderate but significant decrease (Fig. 1), comparable with the one observed in previous studies. As in prior studies, we could not find any significant relationship between the results of the SF-36 and parameters of liver function or viral infection (ALT 50 ⫾ 46 IU/L, genotype 1 75%, previous treatment with interferon 43%, Ishak’s fibrosis stage 2 ⫾ 1.6, Ishak’s necroinflammatory activity 4 ⫾ 1.6). Our observations support the interpretation that the medical process that patients with HCV infection undergo has important consequences on their HRQL. We have observed a decrease in HRQL in patients with chronic hepatitis C identified upon blood donation who followed a medical assessment similar to that of any HCV-infected patient. Because blood donors were asymptomatic at the time of the diagnosis and HRQL did not relate to parameters of liver function, the decrease in HRQL probably reflects the effects of the medical process that follows labeling. In accordance with our observations, a recent study in HCV patients found a relationship between the number of medical visits, life expectancies, and emotional distress (4). Similarly to what has been proposed for arterial hypertension (5), the effects of labeling probably depend on the characteristics of the medical process that follows the diagnosis. A medical process that includes frequent medical visits, blood tests, and possibly a liver biopsy may worsen the appreciation of the long-term consequences of HCV infection. Although it is difficult to modify this process, it is important to recognize its effect when designing strategies aimed at improving HRQL. There is no doubt that eliminating the burden of HCV infection will have beneficial

AJG – January, 2003

Letters to the Editor

consequences on the health of the entire population. However, when facing the individual patient diagnosed with a screening test, it would be desirable to identify those who will never note a negative effect on their health. The development of tools to identify these subjects may avoid the long medical process that follows the diagnosis and its negative effects on quality of life. Juan Co´ rdoba, M.D. Josep Reyes, M.D. Juan Ignacio Esteban, M.D. Liver Unit Hospital Universitari Vall D’Hebron Barcelona, Spain Jose´ Manuel Herna´ ndez, M.D. Centre de Transfusio´ i Banc de Teixits Barcelona, Spain

REFERENCES 1. Koff RS. Impaired health-related quality of life in chronic hepatitis C: The how but not the why. Hepatology 1999;29: 277–9. 2. Forton DM, Taylor-Robinson SD, Thomas HC. Reduced quality of life in hepatitis C—Is it all in the head? J Hepatol 2002;36:435–8. 3. Rodger AJ, Jolley D, Thompson SC, et al. The impact of diagnosis of hepatitis C virus on quality of life. Hepatology 1999;30:1299 –301. 4. Fontana RJ, Hussain KB, Schwartz SM, et al. Emotional distress in chronic hepatitis C patients not receiving antiviral therapy. J Hepatol 2002;36:401–7. 5. Wenger NK. Quality of life issues in hypertension: Consequences of diagnosis and considerations in management. Am Heart J 1988;116:628 –32. Reprint requests and correspondence: Juan Co´ rdoba, M.D., Liver Unit, Hospital Universitari Vall d’Hebron, Pg, Vall d’Hebron 119, Barcelona, Spain 08035. Received Aug. 15, 2002; accepted Aug. 19, 2002.

A Rare But Endocrine Cause of Chronic Diarrhea TO THE EDITOR: A 41-yr-old man was referred for evaluation of chronic diarrhea, which lasted since early infanthood. He complained about frequent (15 of 24 h) watery stools, which persisted during fasting, slight abdominal pain, and bloating. The patient denied significant weight loss, fever, or night sweats. Nine yr ago, he was treated for presumptive Crohn’s disease with steroids (30 –50 mg prednisolone/day) over a period of several wk without any improvement. The past medical history comprised unclassified hypothyroidism, recurrent muscle cramps attributed to hypocalcemia of unknown cause, and a congenital lym-

227

phatic edema on the left leg. The current medication consisted of levothyroxine (150 ␮g/day), recently calcitriol (1.5 ␮g in three divided doses daily), oral supplementation of calcium (2–3 g/day, divided in several doses a day, unregular intake), magnesium (40 mval/day), and potassium (40 mmol/day). Additionally, the patient used loperamide and simethicon as needed. The round-faced patient had a short stature and a body mass index of 24.5 kg/m2 with normal vital signs. Apart from the lymphatic edema of the left leg and two cafe´ -au-lait spots on his arm, the physical examination was normal. However, his intelligence was below average. The laboratory results were remarkable with respect to calcium 1.3–1.86 mmol/L (normal range 2.15–2.60), serum albumin 1.8 g/dl (3.8 –5.1), total serum protein 3.5 g/dl (6 – 8.5), parathyroid hormone 118.2 pg/ml (5– 65), folliclestimulating hormone 24.1 U/L (1–10), luteinizing hormone 14.3 U/L (1–10), normal testosterone (574 ng/dl), insulinlike growth factor-1 83 ng/ml (93–302), human growth hormone 1.0 ng/ml (0.5–5), colecalciferol 35 nmol/L (50 – 300), vitamin B12 113 pg/ml (250 –1100), thyroid-stimulating hormone 10.85 ␮E/ml (0.4 – 4) with unbound T3 and T4 in the normal range under substitution with levothyroxine 150 ␮g/day. During previous yr, the patient had already underwent an extensive evaluation comprising repeat upper and lower GI tract endoscopies with multiple biopsy specimens, abdominal magnetic resonance imaging and CT scan, albumin scintigraphy, lactose and glucose breath tests, and repeated stool cultures, which did not reveal any abnormalities. The clue to the diagnosis in the present case was the fact that the patient displayed consistently decreased systemic calcium paralleled by normal phosphate values (2.4 –3.3 mg/dl) and elevated parathyroid hormone. Hypocalcemia resulting from malabsorption may lead to secondary hyperparathyroidism, which in turn causes increased urinary output of phosphate. Thus, normal phosphate concentrations are usually not found in patients with severe enteropathy with hypocalcemia. Hence, the elevated values for parathyroid hormone seen herein are not caused by a malabsorption. Taking into account the elevated thyroid-stimulating hormone levels despite normal values for T3 and T4 (which were attributed to the comparable high substitution dose of levothyroxine), the elevated follicle-stimulating hormone and luteinizing hormone concentrations with normal testosterone and the impaired insulin-like growth factor-1 values, the diagnosis was compatible with a distinct form of pseudohypoparathyroidism (Albright syndrome type I). In his original description, Albright characterized this form of pseudohypoparathyroidism by a failure to respond to administration of exogenous parathyroid hormone by a rise in the urinary excretion of phosphate and of serum calcium levels (1). Characteristic clinical features in some, but not all the patients with pseudohypoparathyroidism comprise short stature, brachymetacarpia, and brachymetatarsia, a round face, obesity, and reduced intelligence. Autosomal-domi-