The abdominal wall: an overlooked source of pain.

When abdominal pain is chronic and unremitting, with minimal or no relationship to eating or bowel function but often a relationship to posture (i.e., lying, sitting, standing), the abdominal wall should be suspected as the source of pain. Frequently, a localized, tender trigger point can be identified, although the pain may radiate over a diffuse area of the abdomen. If tenderness is unchanged or increased when abdominal muscles are tensed (positive Carnett's sign), the abdominal wall is the likely origin of pain. Most commonly, abdominal wall pain is related to cutaneous nerve root irritation or myofascial irritation. The pain can also result from structural conditions, such as localized endometriosis or rectus sheath hematoma, or from incisional or other abdominal wall hernias. If hernia or structural disease is excluded, injection of a local anesthetic with or without a corticosteroid into the pain trigger point can be diagnostic and therapeutic.

Initial experience with high-dose radioimmunotherapy of metastatic medullary thyroid cancer using 131I-MN-14 F(ab)2 anti-carcinoembryonic antigen MAb and AHSCR.

UNLABELLED: This phase I study was initiated to determine the toxicity and therapeutic potential of high-dose 131I-MN-14 F(ab)2 anti-carcinoembryonic antigen monoclonal antibody (MAb) combined with autologous hematopoietic stem cell rescue (AHSCR) in patients with rapidly progressing metastatic medullary thyroid cancer. METHODS: Twelve patients were entered into the study. Dose escalation was based on prescribed radiation doses to critical organs (i.e., kidney, lung, and liver). Starting doses were 900 cGy to the kidney and no more than 1200 cGy to the lung and liver, with dose increments of 300 cGy until the maximum tolerable dose is determined. Tumor targeting was assessed by external scintigraphy, toxicity was assessed according to the common toxicity criteria of the National Cancer Institute, and therapy responses were assessed by CT, serum carcinoembryonic antigen, and calcitonin. RESULTS: One patient received 9.95 GBq 131I-MN-14 F(ab)2, for an initial dose of 656 cGy to critical organs, 8 received 900 cGy (8.69-17.98 GBq), and 3 received 1200 cGy (15.17-17.69 GBq). The MAb scans of all patients showed positive findings. Autologous hematopoietic stem cells were given to all patients 1-2 wk after therapy, when the total body radiation exposure was less than 5.2 x 10(-7) C/kg/h. Dose-limiting toxicity, defined as grade 3 or 4 nonhematologic toxicity, was not seen in the patient who received the 656-cGy dose, and only 1 of the 8 patients treated at the 900-cGy dose level had grade 3 toxicity, which was gastrointestinal and reversible. No dose-limiting toxicity was seen in the 3 patients treated at the 1200-cGy dose level. Except for the instance of grade 3 gastrointestinal toxicity, nonhematologic toxicity was relatively mild, with only grade 1 or 2 toxicity observed in 9 patients. No renal toxicity was seen. Of the 12 patients, 1 had partial remission for 1 y, another had a minor response for 3 mo, and 10 had stabilization of disease lasting between 1 and 16 months. CONCLUSION: The results show the safety of administering high myeloablative doses of 131I-MN-14 F(ab)2 with AHSCR in patients with metastatic medullary thyroid cancer. The antitumor responses in patients with aggressive, rapidly progressing disease are encouraging and warrant further research to optimize the effectiveness of this new treatment.

Pharmacokinetics, dosimetry, and initial therapeutic results with 131I- and (111)In-/90Y-labeled humanized LL2 anti-CD22 monoclonal antibody in patients with relapsed, refractory non-Hodgkin's lymphoma.

The pharmacokinetics, dosimetry, and immunogenicity of 131I- and (111)In-/90Y-humanized LL2 (hLL2) anti-CD22 monoclonal antibodies were determined in patients with recurrent non-Hodgkin's lymphoma. Fourteen patients received tracer doses of 131I-hLL2 followed 1 week later by therapeutic doses intended to deliver 50-100 cGy to the bone marrow. Another eight patients received (111)In-hLL2 followed by therapy with 90Y-hLL2 also delivering 50 or 100 cGy to the bone marrow. The blood T(1/2) (hours) for the tracer infusions of 131I-hLL2 was 44.2 +/- 10.9 (mean +/- SD) compared with 54.2 +/- 25.0 for the therapy infusions, whereas the values were 70.7 +/- 17.6 for (111)In-hLL2 and 65.8 +/- 15.0 for 90Y-hLL2. The estimated average radiation dose from 131I-hLL2 in tumors >3 cm was 2.4 +/- 1.9 cGy/mCi and was only 0.9-, 1.0-, 1.1-, and 1.0-fold that of the bone marrow, lung, liver, and kidney, respectively. In contrast, the estimated average radiation dose from 90Y-hLL2 in tumors >3 cm was 21.5 +/- 10.0 cGy/mCi and was 3.7-, 2.5-, 1.8-, and 2.5-fold that of the bone marrow, lung, liver, and kidney, respectively. No evidence of significant anti-hLL2 antibodies was seen in any of the patients. Myelosuppression was the only dose-limiting toxicity and was greater in patients who had prior high-dose chemotherapy. Objective tumor responses were seen in 2 of 13 and 2 of 7 patients given 131I-hLL2 or 90Y-hLL2, respectively. In conclusion, 90Y-hLL2 results in a more favorable tumor dosimetry compared with 131I-hLL2. This finding, combined with the initial anti-tumor effects observed, encourage further studies of this agent in therapeutic trials.

The low birth-weight infants of Saudi adolescents: maternal implications.

Maternal factors and perinatal outcome of low birth-weight (less than or equal to 2,500 g) infants of 46 adolescent mothers was studied and compared with 160 adolescents who delivered infants weighing greater than 2,500 g. The significant factors found in the low birth-weight group were anaemia, small maternal physique and preterm delivery. Expectedly, the perinatal mortality rate was significantly increased in low birth-weight infants.

PIP: From 1981-1985, researchers studies pregnancy outcomes of 206 female adolescents (= or 17 years old at the time of 1st hospital visit) at King Fahd Hospital in Al-Khobar, Saudi Arabia. 23% of all infants born to adolescents were classified as low birth weight (= or 2500g). 17.4% of these mothers were 15 years old or younger, 39.1% were 16, and 43.5% were 17. For mothers who delivered an infant 2500g, 17.5% were 15, 26.9% were 16, and 55.6% were 17. Mothers who had low birth weight infants (mean weight 53.48k) tended to weigh less at time of delivery than those who had infants 2500g (61.89kg; p.005). Further, the stature of 31.1% of those in the low birth weight group was 150cm whereas only 13.5% of the remaining mothers were 150cm. 64% of mothers who had low birth weight infants delivered before 37 weeks gestation (p.005). Anemia (Hb10.6g/dl) was the most significant complication contributing to low birth weight (38.6%; p.005). This suggests that many adolescent mothers did not take iron and vitamin supplements and that they did not take iron and vitamin supplements and that they did not eat adequately during pregnancy. Even though toxemia also contributed significantly to low birth weight (9%; p.05), its overall prevalence was markedly low (1.9% in 2500g group). The mode of delivery did not affect birth weight. Perinatal mortality for low birth weight infants stood at 14.6%. None of the .2500g infants died. All adolescent mothers should receive early prenatal care. In addition, more health education of health professionals and adolescents is needed to stress the importance of regular prenatal care, liberal hospitalization, intensive antepartum and intrapartum fetal monitoring.

Petroleum hydrocarbon toxicity in vitro: effect of n-alkanes, benzene and toluene on pulmonary alveolar macrophages and lysosomal enzymes of the lung.

The in vitro effects of straight chain alkanes (nC6-nC10), benzene and toluene on pulmonary alveolar macrophages (PAM) of rats and rabbits was studied. The concentrations used ranged from 0.02 to 1.0 mM. All hydrocarbons used in the study were cytotoxic to isolated cultured PAM cells in a dose-dependent manner. The LC50 for these hydrocarbons towards rat PAM cells was estimated to be 1.0 mM for nC8, 2 mM for nC7, 5 mM for nC9 and 10 mM for nC6, nC10, benzene and toluene. Rabbit PAM cells were more sensitive to the hydrocarbons, resulting in and LC50 half that for rat PAM cells. Hydrocarbons also caused extracellular release of the lysosomal enzymes cathepsin D (EC 3.4.23.5) and cathepsin B (EC 3.4.22.1) in a manner corresponding with cell damage. There was more cathepsin D activity released from cells than cathepsin B. In addition, hydrocarbons also caused the release of cathepsin B and D from isolated lysosomes, and there was 10-15% more enzyme activity released in the culture medium of lysosomes exposed to concentrations of 0.5 and 1.0 mM compared to PAM cell cultures of either rats or rabbits. Hydrocarbons also caused loss of cell respiration and stimulated a dose-dependent and a time-dependent increase in lipid peroxidation. The two alkanes nC7 and nC8 caused the greatest increase in lipid peroxidation and the greatest loss of cell respiration. The results indicate that there is a relationship between chain length of alkanes and their cytotoxicity to PAM cells.(ABSTRACT TRUNCATED AT 250 WORDS)