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Chest pain in achalasia is an age-dependent phenomenon
November 1999
Hepatic arterial minus hepatic venous oxygen tension and saturation before and during adenosine infusion were 7.0 ⫾ 2.8 and 6.5 ⫾ 2.4 kPa (NS) and 24.2% ⫾ 7.4% and 13.9% ⫾ 5.4% (P ⬍ 0.01), respectively. Adenosine-induced sinusoidal overflow by hepatic arterial blood and oxygen may explain the observed increase in hepatic venous oxygenation. Likewise, opening of arterial-hepatic venous as well as arterial-portal venous shunts by adenosine seems possible, leading to reduced rather than increased oxygen delivery to the hepatic parenchyma. Thus, our present findings neither support nor disprove the hypothesis that adenosine-induced vasodilation facilitates oxygen extraction in the cirrhotic liver. The functional benefit (if any) of hepatic arterial vasodilation in patients with cirrhosis remains to be clarified and is subject to an ongoing protocol in our unit. WOLFGANG E. FLEIG, M.D. GERHARD KLEBER, M.D. First Department of Medicine Martin-Luther-University Halle-Wittenberg Halle, Germany 1. Kleber G, Steudel N, Behrmann C, et al. Hepatic arterial flow volume and reserve in patients with cirrhosis: use of intra-arterial Doppler and adenosine infusion. Gastroenterology 1999;116:906– 914.
Chest Pain in Achalasia Is an Age-Dependent Phenomenon Dear Sir: Eckardt et al. have prospectively evaluated the long-term clinical course of chest pain in patients with achalasia.1 Patients with achalasia were followed up for a mean of 6.3 ⫾ 4.1 years to determine the probability of unaltered and remaining chest pain during long-term follow-up. Even though the conclusion that the frequency of chest pain diminishes with advancing age is supported by their data, it is equally important to recognize that this reduction in frequency of chest pain over the course of the follow-up is not related to the natural history of the disease. Kaplan–Meir estimates revealed that over 10 years some improvement in chest pain frequency would occur in 86% of the patients (shown in Figure 1).1 This may be due entirely to the age of the patients independent of the duration of the disease. We have performed a survey of 36 patients who had undergone successful pneumatic dilatation for achalasia. Each patient had the diagnosis of primary achalasia confirmed by radiographic, manometric, and endoscopic studies. Patients were requested to complete a detailed questionnaire in relation to their symptoms. At a median follow-up of 8.5 years (range, 1–22 years) after dilatation, 8 patients (22%) had some degree of chest pain. Persistence of chest pain was unrelated to the presence or absence of other esophageal symptoms such as heartburn, regurgitation, dysphagia, as well as changes in weight. Median age of patients with chest pain was significantly lower (median, 31.1 years; range, 20–42 years) than those without chest pain (median, 49.0 years; range, 17–86 years; P ⫽ 0.002). This is consistent with the findings of Eckardt et al. and suggests that ageing has an important effect on visceral perception and possibly protects from esophageal pain.2 Interestingly, in our patient group, patients with persistent chest pain had a longer duration of follow-up (median, 16 years; range, 2–22 years) than those without chest pain (median, 8 years; range, 1–18 years; P ⫽ 0.044). These findings suggest that progressive decline in the frequency and severity of chest pain in
CORRESPONDENCE 1259
patients with achalasia during the long-term follow-up after dilatation is unlikely to represent the natural history of the disease. DAVID L. NYLANDER Department of Gastroenterology Sunderland Royal Hospital Sunderland, England 1. Eckardt VF, Stauf B, Bernhard G. Chest pain in achalasia: patient characteristics and clinical course. Gastroenterology 1999;116: 1300–1304. 2. Lasch H, Castell DO. Evidence for diminished visceral pain with ageing: studies using graded oesophageal balloon distension (abstr). Gastroenterology 1992;106:A1035.
Reply. As with many data that are published in either abstract form or as letters to the editor, interpretation of Dr. Nylander’s findings is difficult. For example, he reports that after a median follow-up of 8.5 years, 8 (22%) of 36 initially treated patients had some degree of chest pain. Does this mean that 78% had lost this symptom? I suspect not, because he later indicates that he had studied two groups of patients, those with and without chest pain, the number of whom remains unknown. Furthermore, there is no information as to whether this was a prospective, longitudinal study or a retrospective observation. However, if one could assume the most optimal scenario, that all patients had chest pain to begin with and were studied prospectively in regular intervals, I would be unable to recognize any features in Dr. Nylander’s observation that would contradict our findings. In fact, his observation that chest pain affects mainly younger patients is unrelated to the intensity of other esophageal symptoms and diminishes after several years is in total agreement with our findings. Whether this decrease in chest pain over time is a function of age or caused by some other factor such as progressive neuronal degeneration remains to be established by future investigations. At present, however, there remains one important message for patients with achalasia who suffer from chest pain: therapy does little to improve this symptom and time may be the only cure. VOLKER F. ECKARDT Wiesbaden, Germany
Successful Use of Cyclosporine in the Treatment of Glucocorticoid-Resistant Nongranulomatous Chronic Idiopathic Enterocolitis Dear Sir: Although nongranulomatous chronic idiopathic enterocolitis occurs secondary to conditions such as celiac sprue, amyloidosis, hypogammaglobulinemia, and lymphoma, we refer to the study by Ruan et al.1 in the September 1996 issue of GASTROENTEROLOGY that provides support for it standing alone as a primary disease process. Clinically, it consists of chronic diarrhea, abdominal pain, and malabsorption. Endoscopic examination reveals multiple nonmalignant ulcers of the small and large intestine, and histology reveals a mixed inflammatory infiltrate of neutrophils, lymphocytes, and monocytes, as well as villous atrophy.2 Although frequently a fatal disease, Ruan et al. reported that 8 of 9 patients showed some response to glucocorticoid therapy (20–50 mg/day of prednisone). We now describe a patient who did not respond to daily 60-mg intravenous doses of methylprednisolone but showed almost complete clinical and histological resolution with cyclosporine. A 50-year-old man with a history of type 2 diabetes mellitus
Hepatic arterial minus hepatic venous oxygen tension and saturation before and during adenosine infusion were 7.0 ⫾ 2.8 and 6.5 ⫾ 2.4 kPa (NS) and 24.2% ⫾ 7.4% and 13.9% ⫾ 5.4% (P ⬍ 0.01), respectively. Adenosine-induced sinusoidal overflow by hepatic arterial blood and oxygen may explain the observed increase in hepatic venous oxygenation. Likewise, opening of arterial-hepatic venous as well as arterial-portal venous shunts by adenosine seems possible, leading to reduced rather than increased oxygen delivery to the hepatic parenchyma. Thus, our present findings neither support nor disprove the hypothesis that adenosine-induced vasodilation facilitates oxygen extraction in the cirrhotic liver. The functional benefit (if any) of hepatic arterial vasodilation in patients with cirrhosis remains to be clarified and is subject to an ongoing protocol in our unit. WOLFGANG E. FLEIG, M.D. GERHARD KLEBER, M.D. First Department of Medicine Martin-Luther-University Halle-Wittenberg Halle, Germany 1. Kleber G, Steudel N, Behrmann C, et al. Hepatic arterial flow volume and reserve in patients with cirrhosis: use of intra-arterial Doppler and adenosine infusion. Gastroenterology 1999;116:906– 914.
Chest Pain in Achalasia Is an Age-Dependent Phenomenon Dear Sir: Eckardt et al. have prospectively evaluated the long-term clinical course of chest pain in patients with achalasia.1 Patients with achalasia were followed up for a mean of 6.3 ⫾ 4.1 years to determine the probability of unaltered and remaining chest pain during long-term follow-up. Even though the conclusion that the frequency of chest pain diminishes with advancing age is supported by their data, it is equally important to recognize that this reduction in frequency of chest pain over the course of the follow-up is not related to the natural history of the disease. Kaplan–Meir estimates revealed that over 10 years some improvement in chest pain frequency would occur in 86% of the patients (shown in Figure 1).1 This may be due entirely to the age of the patients independent of the duration of the disease. We have performed a survey of 36 patients who had undergone successful pneumatic dilatation for achalasia. Each patient had the diagnosis of primary achalasia confirmed by radiographic, manometric, and endoscopic studies. Patients were requested to complete a detailed questionnaire in relation to their symptoms. At a median follow-up of 8.5 years (range, 1–22 years) after dilatation, 8 patients (22%) had some degree of chest pain. Persistence of chest pain was unrelated to the presence or absence of other esophageal symptoms such as heartburn, regurgitation, dysphagia, as well as changes in weight. Median age of patients with chest pain was significantly lower (median, 31.1 years; range, 20–42 years) than those without chest pain (median, 49.0 years; range, 17–86 years; P ⫽ 0.002). This is consistent with the findings of Eckardt et al. and suggests that ageing has an important effect on visceral perception and possibly protects from esophageal pain.2 Interestingly, in our patient group, patients with persistent chest pain had a longer duration of follow-up (median, 16 years; range, 2–22 years) than those without chest pain (median, 8 years; range, 1–18 years; P ⫽ 0.044). These findings suggest that progressive decline in the frequency and severity of chest pain in
CORRESPONDENCE 1259
patients with achalasia during the long-term follow-up after dilatation is unlikely to represent the natural history of the disease. DAVID L. NYLANDER Department of Gastroenterology Sunderland Royal Hospital Sunderland, England 1. Eckardt VF, Stauf B, Bernhard G. Chest pain in achalasia: patient characteristics and clinical course. Gastroenterology 1999;116: 1300–1304. 2. Lasch H, Castell DO. Evidence for diminished visceral pain with ageing: studies using graded oesophageal balloon distension (abstr). Gastroenterology 1992;106:A1035.
Reply. As with many data that are published in either abstract form or as letters to the editor, interpretation of Dr. Nylander’s findings is difficult. For example, he reports that after a median follow-up of 8.5 years, 8 (22%) of 36 initially treated patients had some degree of chest pain. Does this mean that 78% had lost this symptom? I suspect not, because he later indicates that he had studied two groups of patients, those with and without chest pain, the number of whom remains unknown. Furthermore, there is no information as to whether this was a prospective, longitudinal study or a retrospective observation. However, if one could assume the most optimal scenario, that all patients had chest pain to begin with and were studied prospectively in regular intervals, I would be unable to recognize any features in Dr. Nylander’s observation that would contradict our findings. In fact, his observation that chest pain affects mainly younger patients is unrelated to the intensity of other esophageal symptoms and diminishes after several years is in total agreement with our findings. Whether this decrease in chest pain over time is a function of age or caused by some other factor such as progressive neuronal degeneration remains to be established by future investigations. At present, however, there remains one important message for patients with achalasia who suffer from chest pain: therapy does little to improve this symptom and time may be the only cure. VOLKER F. ECKARDT Wiesbaden, Germany
Successful Use of Cyclosporine in the Treatment of Glucocorticoid-Resistant Nongranulomatous Chronic Idiopathic Enterocolitis Dear Sir: Although nongranulomatous chronic idiopathic enterocolitis occurs secondary to conditions such as celiac sprue, amyloidosis, hypogammaglobulinemia, and lymphoma, we refer to the study by Ruan et al.1 in the September 1996 issue of GASTROENTEROLOGY that provides support for it standing alone as a primary disease process. Clinically, it consists of chronic diarrhea, abdominal pain, and malabsorption. Endoscopic examination reveals multiple nonmalignant ulcers of the small and large intestine, and histology reveals a mixed inflammatory infiltrate of neutrophils, lymphocytes, and monocytes, as well as villous atrophy.2 Although frequently a fatal disease, Ruan et al. reported that 8 of 9 patients showed some response to glucocorticoid therapy (20–50 mg/day of prednisone). We now describe a patient who did not respond to daily 60-mg intravenous doses of methylprednisolone but showed almost complete clinical and histological resolution with cyclosporine. A 50-year-old man with a history of type 2 diabetes mellitus