TL;DR: It is believed that most, if not all, patients in this group have degenerative Lewy body idiopathic Parkinson's disease, representing the lower end of a skewed deviation for age of onset of this disease.
Abstract: We describe a personal series of 60 cases of parkinsonism with onset under the age of 40 years. Known causes for early onset of secondary parkinsonism, such as Wilson's disease or encephalitis, were excluded in every case. Two groups were identified: those with onset after the age of 21 in whom no hereditary factors could be ascertained (56 cases), and those with onset before 21 years all of whom had familial parkinsonism. In neither group have we found any association with prematurely grey hair, hypertension, diabetes, pernicious anaemia, or thyroid disorder. Among their families, we have not found any association with diabetes, pernicious anaemia, or thyroid disorder. We propose that cases of apparent idiopathic Parkinson's disease beginning between age 21-40 years should be called "young onset Parkinson's disease." Twenty percent of such patients in our series had at least one first- or second-degree relative in the same or antecedent generations with parkinsonism, but only 1.5% of their relatives at risk had parkinsonism, which is similar to the prevalence in the general population. Ten percent of these patients had at least one relative with essential tremor, but only 1.6% of their relatives at risk had tremor, which again was similar to the prevalence in the population in general. These patients with young onset Parkinson's disease responded well to levodopa therapy. However, dyskinesias and response fluctuations occurred early and frequently. The prevalence of dyskinesias and response fluctuations was strongly correlated with the duration of levodopa treatment, but not with the duration (or probably the severity) of the disease before levodopa therapy was commenced. The involuntary movements often were severe and frequently were diphasic. Despite long disease duration, the incidence of dementia in young onset patients aged less than 65 years was negligible. We believe that most, if not all, patients in this group have degenerative Lewy body idiopathic Parkinson's disease, representing the lower end of a skewed deviation for age of onset of this disease. We have so far failed to identify any additional environmental factor which may have accelerated disease onset in these patients. In contrast, cases of parkinsonism beginning before age 21 years were invariably familial. We proposed that they should be called "juvenile parkinsonism." All affected relatives with parkinsonism also had young disease onset, and all but one were siblings. None of four such patients seen by us has demented, and computed tomography (CT) scan has been normal in all four. We believe that most such patients have some form of genetically determined secondary parkinsonism.
TL;DR: Pregnancy is associated with a greater thyroidal risk in women with TA, thereby emphasizing a potential link between pregnancy and thyroid disorders and it is recommended that patients with known, even subtle, thyroid abnormalities be closely monitored during pregnancy.
Abstract: A prospective study was undertaken during pregnancy in 120 euthyroid women presenting with mild thyroid abnormalities (TA): 11 with a past history of thyroid disorder, 44 with goiter, 20 with nodules, and 45 with thyroid autoantibodies. The aims of the study were to assess whether the pattern of thyroid alterations during gestation was different in women with TA compared to that in healthy control pregnant subjects and to evaluate possible obstetrical and neonatal repercussions. The overall prevalence of underlying subtle thyroid abnormalities in the cohort was 17%, probably as the result of the environmental moderately low iodine intake. Despite the intrinsic heterogeneity of the four groups of women with TA, the adaptation of the thyroid to the stress of pregnancy was different from that of the control subjects. Noteworthy were 1) the marked elevation of serum thyroglobulin in women with past history of thyroid disorder, goiter and thyroid nodules; 2) the increase in goiter size in a third of the goitrous women, associated with biochemical evidence of functional stimulation of the gland; 3) the indirect evidence of partial thyroidal autonomy in goitrous patients; and 4) the increase in the number and size of thyroid nodules during gestation. Taken together, the data indicated that pregnancy was associated with a greater thyroidal risk in patients with TA compared to healthy subjects. In relation to thyroid autoimmunity, most patients remained euthyroid during gestation, but in a few cases, TSH was elevated at delivery, suggesting diminished thyroidal reserve. Also, 40% of newborns from mothers with thyroid autoimmunity had elevated thyroid peroxidase antibody titers at birth, and there was a highly significant correlation between maternal and neonatal thyroid peroxidase antibody titers. Finally, thyroid autoimmunity was clearly associated with an increased risk of spontaneous abortion (13.3 vs. 3.3%; P < 0.001) Thyroid function in newborns from mothers with TA was normal and not different from that in controls; similarly, obstetrical features were similar in patients with TA and control subjects. In conclusion, pregnancy is associated with a greater thyroidal risk in women with TA, thereby emphasizing a potential link between pregnancy and thyroid disorders. It is recommended that patients with known, even subtle, thyroid abnormalities be closely monitored during pregnancy, in particular those with a goiter, nodules, or thyroid autoimmunity, especially in areas with a moderately low iodine intake, where the prevalence of mild thyroid disturbances is high.
TL;DR: The findings of this study revealed that a variety of systemic disorders may be present in association with different types of retinal vein occlusion and different age groups differs significantly, so as to imply that systemic diseases associated with various types of Retinal vein Occlusion can imply that unwarranted treatment for these diseases is likely to be expensive.
TL;DR: There are several interactions between thyroid and kidney functions in each other organ's disease states and a detailed knowledge of all these interactions is important for both the nephrologists and endocrinologists for optimal management of the patient.
Abstract: There are several interactions between thyroid and kidney functions in each other organ's disease states. Thyroid hormones affect renal development and physiology. Thyroid hormones have pre-renal and intrinsic renal effects by which they increase the renal blood flow and the glomerular filtration rate (GFR). Hypothyroidism is associated with reduced GFR and hyperthyroidism results in increased GFR as well as increased renin - angiotensin - aldosterone activation. Chronic kidney disease (CKD) is characterized by a low T3 syndrome which is now considered a part of an atypical nonthyroidal illness. CKD patients also have increased incidence of primary hypothyroidism and subclinical hypothyroidism. The physiological benefits of a hypothyroid state in CKD, and the risk of CKD progression with hyperthyroidism emphasize on a conservative approach in the treatment of thyroid hormone abnormalities in CKD. Thyroid dysfunction is also associated with glomerulonephritis often by a common autoimmune etiology. Several drugs could affect both thyroid and kidney functions. There are few described interactions between thyroid and renal malignancies. A detailed knowledge of all these interactions is important for both the nephrologists and endocrinologists for optimal management of the patient.
TL;DR: The data suggest that autoimmune processes precede onset of schizophrenia, but also non-affective psychosis and bipolar disorder, as well as a small role for genetic linkage.
Abstract: This paper extends earlier work on autoimmune diseases and schizophrenia (1) to bipolar disorder and disorders with features similar to schizophrenia, sometimes termed non-affective psychosis. This new analysis, with more than twice as many observations, allows comparison of bipolar disorder to schizophrenia, as well as facilitating more precise study of the temporal relationship of autoimmune disease and the first diagnosis of bipolar disorder, schizophrenia, and non-affective psychosis. The presentation of these disorders in parallel fashion facilitates assessment of the value of the nosologic distinctions between them.
The autoimmune diseases which have been studied most thoroughly in their relationship to bipolar disorder are the autoimmune thyroid diseases and multiple sclerosis (MS). The relationship between affective psychosis and thyroid disorder was noticed as early as 1888 (2). The metabolic slowing related to thyroid hormone deficiency could possibly be related to symptoms of depression (e.g., 3), but there is also a consistent association with psychosis, including a particular association, not always confirmed, with rapid-cycling bipolar disorder (4–6). The serotonin and thyroid systems are connected (7), and there are putative but unproven associations between antithyroid antibodies and mood disorders (8, 9). The effect of lithium on thyroid function was noticed years ago (10), but the observation may result in part from a constitutional factor which predisposes to bipolar disorder (11, 12).
The relationship of affective disorders to MS has been studied for decades (e.g., 13). To some extent, MS presents with affective symptoms, but there is comorbidity of the diagnosed cases as well as symptom overlap (14, 15). Three small family studies suggest a genetic relationship between the two disorders (16–18). As with bipolar disorder, the relationship is clouded by the possibility that treatment for MS is connected to affective state (19).
The literature on autoimmune diseases and schizophrenia has been reviewed previously (1). It is particularly rich for celiac disease (20), autoimmune thyroid disease (21), and rheumatoid arthritis (22). In our earlier work we showed that thyrotoxicosis, celiac disease, autoimmune hemolytic anemia, and Sjogren’s syndrome were more common in the family members of persons diagnosed with schizophrenia, prior to the diagnosis of schizophrenia in the case, and were more common in the cases of schizophrenia themselves as well, prior to the diagnosis of schizophrenia (1). A later study from Sweden showed that the risk of both schizophrenia and non-affective psychosis was raised by about 50% after the diagnosis of celiac disease, although the relationship was statistically significant only for the broader category of non-affective psychosis (23).