Menstrual-Linked Asthma

This study was conducted to determine the occurrence of menstrual-linked asthma (MLA) in India in 100 consecutive female asthmatics in the reproductive age group. The patients were required to respond to a questionnaire concerning the relationship between their asthma and the menstrual cycle. Twenty-three patients had subjective perception of deterioration in symptoms of asthma in relation to the menstrual cycle. Ten patients from both groups were also required to maintain a daily peak expiratory flow rate (PEFR) diary for 2 consecutive menstrual cycles. The mean total duration of illness in patients with MLA was significantly longer than in patients without cyclic exacerbation. Cough and breathlessness were also significantly more severe as was the disease. This was evidenced by the more frequent emergency room visits and hospitalizations in these patients. Menstrual-linked worsening of asthma was most common in the premenstrual week (17 patients). In 8 of these 17 patients, this phenomenon continued to occur during the menstrual week also. Interestingly, 1 patient complained of deterioration of asthma 2 days after menstruation was over. Such an observation is yet to be recorded. Fourteen patients reported an increase in symptoms with almost every cycle while 3 had worsening related to specific season only. Sixteen patients often required extra medication during the premenstrual and/or menstrual weeks. A significant association was also observed between severity of premenstrual syndrome and MLA. The mean PEFR values over 2 cycles revealed a significant fall in the morning as well as evening values in the premenstrual and menstrual weeks as compared to the midcycle week in patients with MLA. This fall was maximal in the premenstrual week. Such a fall was not observed in asthmatics without menstrual exacerbation of symptoms. MLA was detected in about a fourth of the female asthmatics in India and it appears to represent a more severe form of the disease. This study also documented that MLA was associated with an increase in airway resistance and was not simply due to an increased perception of symptoms during the premenstrual or menstrual weeks.     

Duodenogastric reflux after choledochoduodenostomy

Duodenogastric reflux (DGR) has been implicated in several disease processes. The present study was carried out to document the incidence and evaluate the clinical significance of DGR after choledochoduodenostomy (CDD). A total of 13 patients who had undergone cholecystectomy with a standard side-to-side CDD for choledocholithiasis or chronic pancreatitis were studied by symptom evaluation, scintigraphy, endoscopy, and gastric mucosal histology at least 6 months after surgery. The scintigraphic findings were then compared with those of 10 patients who had undergone cholecystectomy alone. Only two patients (15%) had mild dyspeptic symptoms. The incidence of DGR after CDD was 69% compared to 20% in the cholecystectomy alone group (P < 0.05). In the majority of patients the DGR was only mild to moderate and the severity correlated well with the degree of endoscopic gastritis, but not with the clinical symptoms or histological findings. These results indicate that while CDD is associated with a high incidence of DGR, its occurrence does not produce significant clinical symptoms.     

Growth hormone resistance in uremia

Growth retardation is a major complication in children with uremia. Protein restriction, calorie deficit, metabolic acidosis, renal osteodystrophy, and endocrinologic disturbances contribute to the growth failure. The effect of these factors on growth retardation can be attenuated in part by therapy with vitamin D metabolites, adequate nutrition, alkalization, and dialysis. Linear growth in children with uremia is markedly retarded despite normal or increased levels of circulating serum growth hormone. An increased growth hormone level in children with uremia is due to normal growth hormone secretion from the pituitary gland and impaired growth hormone clearance in the kidney. However, the elevated growth hormone level does not lead to a commensurate rise in serum insulin-like growth factor I (IGF-I); the serum IGF-I level is decreased or normal in relation to the degree of renal failure. This discrepancy suggests growth hormone resistance in the liver in uremia. Recent molecular techniques open a new era in studying the gene expression for growth hormone or IGF-I. There is no doubt today that growth hormone treatment has the beneficial effect of growth promotion in children with uremia, which also suggests endogenous growth hormone resistance in target organs or target cells in uremia.     

Experimental axonopathy induced by immunization with campylobacter jejuni lipopolysaccharide from a patient with guillain‐barré syndrome

Campylobacter jejuni (C. jejunj) infection is the most common antecedent in the axonal variant of Guillain‐Barré syndrome (GBS). Antibodies against nerve gangliosides found in GBS patients recognize cross‐reactive epitopes in the lipopolysaccharide (LPS) of C. jejuni. This led to the molecular mimicry hypothesis of GBS. We immunized eleven rabbits with a LPS extracted from HS:19 C. jejuni strain isolated from a patient with GBS and complete Freund's adjuvant (CFA)(group I). In a second experiment we immunized seven rabbits with LPS, CFA and keyhole limpet hemocyanin (KLH)(group II). All group I rabbits developed high titers of anti‐LPS, anti‐GM1, anti‐GD1b antibodies and lower titers of anti‐GD1a. One rabbit, 50 days after initial inoculation, showed tremor and weakness. All rabbits of group II developed high titres of antiganglioside antibodies and six animals showed weakness 59–113 days after initial inoculation. Two rabbits died. Pathology showed mild to moderate, tendentially grouped, axonal degeneration in sciatic nerves of four out of five animals. Control rabbits of group I (immunized with CFA only) did not develop antibodies, controls of group II (immunized with CFA + KLH) developed low titers of IgG anti‐GM1. None developed neurological signs or showed axonal degeneration. C. jejuni LPS is a potent B‐cell stimulator capable to induce a strong antiganglioside response in rabbits. However, to induce the neuropathy is crucial to employ KLH, a glycoprotein known to stimulate both humoral and cellular responses. This animal model reproduces the pathogenetic process hypothesized in axonal GBS with antiganglioside antibodies post C. jejuni infection.     

Rheumatic fever: clinical profile of the initial attack in India

The clinical profile of acute rheumatic fever in developing countries is frequently reported to differ from that in developed countries. This probably arose because a distinction was not made between the manifestations of the initial attack and those of a recurrence. Here, we report the patterns of presentation and clinical features of 100 cases of carefully determined initial attacks of rheumatic fever. As many as half the patients had carditis, and, of these, 50% exhibited congestive cardiac failure. This high incidence arises because in developing countries with limited health-care facilities patients continue to be physically active during the long pre-admission period. The study confirms that the clinical profile of the initial attack of rheumatic fever in developing countries is in most respects not unlike that in developed countries.